Monthly Archives: November 2011

Adrenal glands – applied aspects

Dr P Muhammed Muneer BHMS,MD(Hom)

The two adrenal glands : each of which weighs about 4 grams – lie at the superior poles of the two kidney.
Each gland is composed of two distinct parts, the adrenal medulla and the adrenal cortex.
The adrenal medulla, the central 20% of the gland is functionally related to the sympathetic nervous system; It secretes the hormones epinephrine and nor epinephrine in response to sympathetic stimulation.

The adrenal cortex secretes cortico steroids hormones. The hormones are all synthesized from the steroid cholesterol.
The Corticosteroids are
1. Mineral corticoids – Especially affect the electrolytes of the extra cellular fluids sodium and potassium.
2. Glucocorticoids – They exhibit important effects that increase blood glucose concentration also effect on both protein and fat metabolism.
3. Androgen

Synthesis and secretion of Adreno cortical Hormones
The adrenal cortex has there distinct layers – They are zona glomerulosa, Zona fasciculate and Zona reticularis.
(i) Zona glomerulosa – Constitutes 15% of the adrenal cortex (lies just underneath the capsule)
– Secretes aldosterone (which is the principal mineral corticoid)
– Contain the Enzyme aldosterone syntheses which is necessary for synthesis of aldosterone.
– The secretion of these cells in controlled mainly by the extra cellular fluid concentration of angiotensin II and potassium, both of which stimulate aldosterone secretion.

II. Zona fascicutala :
– Middle and widest layer
– Constitute 75% of adrenal cortex
– Secretes the glucocorticoids cortisol and cortico sterone.
Small amounts of adrenal and conges and estrogens.
– The secretion of these cells is controlled in large part by the hypothalamic – pituitary ancis ulia – adreno corticotropic hormone (ACTH)

III. Zona reticulose
– Deep layer or cortex
– Secretes the adrenal and rogens dehydroepiandro sterone and androstenedione.
– Small amounts of estrogens and gluco corticoids
– ACTH – regulates secretion of these cell
– Cortical and rogen stimulating hormones released from pituitary may also regulate secretion.

Adreno cortical hormones are Steroids Derived from Cholesterol
Although the cells of the adrenal cortex can synthesis small amonts of cholestrol from acetale, approximately 80% of cholestrol used for steroid synthesis is provided by low density liporesteins (LDL) in the circulating plasma.
The important cortico steroid hormones; including synthetic ones, are the following.

Mineralo Corticoids
1. Aldosterone (very potent, accounts for about 90% or all mineralo corticoid activity)
2. Desoxy cortico sterone (1/30 as potent as aldosterone, but very small quantities secreated)
3. Corticosterone (sught mineralo corticoid activity)
4. 9x – Fluorocortisl (Synthetic, slightly more potent than aldo sterone)
5. Cortisol (Very slight mineral corticoid activity, but large qty secreted)
6. Cortisone (Synthetic, slight mineralo corticoid activity)

Glucocorticoids
1. Cortisol (very potent, accounts for about 95% of all glucocorticoid activity)
2. Cortico sterone (Provides about 4 percent of total gluco corticoid activity, but much less potent than cortisol)
3. Cortisone (Synthetic, almost as potent as cortisol)
4. Prednisonce (Synthetic, four times as potent as cortisol)
5. Methyl prednisone (Synthetic, five times as potent as cortisol)
6. Dexamelthsone (Synthetics, 30 times as potent as cortical)

It is clear from this list that some of these hormones have both glucocortioid and mineralo corticoid activity. It is especially significant that corisol has a small amount of mineralo coticoid activity, because some syndromes of ecers cortisol secretion can cause significant mineral corticoid effects, along with its much more potent gluco corticoid effects.
The intense glucocorticoid activity of the synthetic hormone dexamethasone, which has almost zeor minerl corticoid activity, makes this an especially important drug for stimulating glucocorticoid activity.
The Normal concentration of aldosterone in blood is about 6 nanograms per 100 ml and the secretory rate is 150 to 250 mg / day.
The concentration of cortisol in blood everages 12 mg / 100 ml and the secretary rate averages 15 to 20 mg / day.

Functions of the Mineralo corticoids – Aldosterone
1. Renal and circulatory effects of aldosterone –
Aldosterone increases renal tubular ……….. of sodium and secretion of potassium.
Aldosterone causes sodium to the conserved in the extra cellular fluid while increasing potassium exertion in the urine.
A High concentration of aldosterone in the plasma can transiently decrease the sodium loss into the urine to as little as little as a few mill equivalent day. At the same time potassium loss into urine increases several fold. Therefore, the net effect of excess aldosterone in the plasma is to increase the total quantity of sodium in the extra cellular fluid while decreasing the potassium.
Total loss of adrenal cortical secretion usually causes death with 3 days to 2 weeks unless the person receives extensive salt therapy or injection of mineralo corticoid without mineralo corticoids potassium ion concentration of the extra cellular fluid rises markedly. Sodium and chloride are rapidly lost from the body, and the total extra cellular fluid volume and blood volume become greatly reduced. The person soon develops diminished cardiac output; which progresses to a shockhi… state followed by death. The entire sequence can be previated by the administration of aldosterone or some other mineralo corticoid. Therefore mineralo corticoild … said to be the acute life saving portion of the adreno cortical hormones.

2. Excess aldosterone increases extra cellular fluid volume and arterial pressure.
An aldosterone – mediated increase in extra cellular fluid & volume lasting more than 1 to 2 days also leads to an increase in arterial pressure. The rise in arterial pressure then increases kidney excretion of both salt and wakes called pressure natriuresis and pressure …….. respecting thus after the extra cellular fluid volume increases 5 to 15 percent above normal, arterial pressure aldo increases 15 to 25 mm of Hg and this elevated blood pressure returns the several output of salt and water to normal despite the excess aldosteron. This return to normal of salt and water excretion by the kidneys as a result of pressure …. And ….. is called aldosterone escape.

Conversely when aldosterone secretion become zero large amounts of salt are lost in the urine not only diminishing the amount of sodium chloride in the extra cellular fluid volume the result is severe extra cellular fluid dehydration and low blood volume, leading to circulatory shock. Without therapy this usually causes death within a few days after the adrenal glands suddenly stop secreting aldosterone.

3. Excess aldosterone causes Hypokalemia and muscle weakness; too little aldosterone causes Hyperkalemia and cardiac toxically.
4. Excess aldosterone increases tubular Hydrogen ion secretion with resultant mild alkalosis.
5. Aldosterone stimulates sodium and potassium transport in sweat glands, salway glands, and intestinal epithelial cells.
Aldosterone also greatly enhances sodium absorption by the intestines, especially in the color, while prevent loss of sodium in the stools.

Regulation of Aldosterone secretion
1. Increased potassium ion concentration in the extra cellular fluid greatly increases aldosterone secretion.
2. Increased actively actively of the rennin – angio tension system also greatly increase aldosterone secretion.
3. Increased sodium ion concentration in the extra cellular fluid very slightly decreases aldosterone secretion.
4. ACTH from the anterior pituitary gland is necessary for aldosterone secretion but has little effect in controlling the rate of secretion.

Functions of the Glucocorticoids
Effects or cortisol on carbonytrate metabolis.
Stimulate ….. (Formation of carbohydrate from proteins and some other substances) by the liver often increasing the rate of gluconeogenesis as much as 6 to 10 fold this results mainly from two effect of cortisol.
(i) Cortisol increases the enzyme required to convert aminoacids into glucose in the liver cells.
(ii) Cortisol causes mobilization of aminoacids from the extra hepatic tissues mainly from muscle.

Decreased glucose utilization by the cells
Cortisol also causes a moderate decrease in the rate of glucose utilization by most cells of the body.
A suggested mechanism is based on the observation that glucocorticoids depress the oxidation of incotinamide adenine dinuceleotide (NADH) to form NAD. Because NADH must be oxidized to allow glycolysis this effect could account for the dimmished utilization of glucose by the cells.
Elevaled Blood Glucose concentration and Adrenal Diabetes
Both the increased rate of gluconeogenesis and the moderate reduction in the rate of glucose utilization by the cells cause the bllod glucose concentration to rise the rise blood glucose in turn stimulates secretonsy insulin. The increased plasma levels of insulin, however are not as effective in maintaing plasma glucose as they are under normal conditions.
The increase in blood glucose concentration is occasionally great … (50 percent or more above normal) that the condition is called adrenal diabetes.

Effects of Cortisol on Protein Metabolism
(i) Reduction in cellular protein : Reduction of protein stores is essentially all body cells except those of the liver this is caused by both decreased protein synthesis and increased catabolism of protein already in the cells.
Cortisol also depress the formation of RNA and sub sequent protein synthesis is many extrahepatice tissues especially is musles and lymphoid tissues. In the presence of great excess of cortiol, the muscles can become so weak that the person cannot rise from the squatting position.
i. Cortisol increases liver and plasma protein.
Coincidentially with the reduced proteins elsewhere with body, the liver protein become enhanced further more, the plasma proteins are also increased.
ii. Increased Blood Aminoacids
iii. Diminished transport of aminoacids … extra … cells & enhanced transport .. hepatic cells.

Effects of cortisol on fat metabolism
i) Mobilisation of fatty acids
It promotes mobilization of fatty acids from adipose tissue. This increases the concentration of free fatty acids in the plasma.
The increased mobilization of fats by cortisol, combined with increased oxidation of fatty acids in the cells, helps shift the metabolic system of cells in times of starvation or other stresses from utilization of glucose for energy to utilization of fatty acids. This cortisol mechanism, homener requires several hours to become fully developed.
ii) Obesity caused by excess cortisol: Despite the fact that cortisol can cause a moderate degree of fatty acid mobilization from adipose tissue, many people with excess cortisol secretion develop a peculiar type or obesity with exess deposition of fat in the chest and head regions of the body giving a buffalo like torso and rounded moonface. Althoug the cause in unknown it has been suggested that this obesity results from excess simultaneously food intake, with fat being generated in some tissues of the body more rapidly than it is mobilized & oxidized.

Cortisol is important in resisting stress and inflammation
Almost any type of stress, whether physical or neuogenic, cause an immediate and marked increase in ACTH secretion by the anterioc pilu….. gland followed within minutes by greately increased adreno cortical secretion of cortisol.
Anti……. Effects of cortisol
The administration of large amounts of cortisol can usually block in lamination or even reverse many of its effects once it has begun.
Cortisol causes resolution of inflammation

Regulation of cortisol secretion
ACTH stimulates cortisol secretion
Secretion of cortisol is controlled almost entirely by ACTH secreted by Anterior pituitary gland. This hasmore also called corticotrophin or adreno cartico trop in also enhances the production of adrenal and origins.
ACTH secretion is controlled by corticotrophin releasing factor from hypo thalamus
Physiologic stress increases ACTH and adreno cortial secretion.
Inhibitory effect of cortisol on hypothalamus and on the anterior pitulary to cause decreased ACTH secretion
When ACTH is secreted by the anterior pituitary gland several other hormones that have IIIrd Chemical structure are secreted simultaneously.

Adrenal Androgens
Several moderate actine male sex hormones called adrenal and rogens and are continually secreted by the adrenal cortex especially duty fetal life.
Abnormalities of Adrenocortex secretion
Hypoad renalism – Addison’s Disease.
Addissions disease results from failure of adrenal cortices to produce adreno cortial hormones.
Causes I) Primary atrophy of the adrenal cortices.
ii) Tuberculosis destruction of – (cause autoimmunity 80%) the adrenal glands.
iii) Invasion of the adrenal cortices by cancer.

Disturbances in Addisons disease
i) Mineralo corticoid deficiency :
Decrease renal tubular sodium reabsorption be lost into urine in great profusion. The net result is greatly decreased extra cellular fluid volume futhere more Hypontremia, Hyperkalemia and mild alkalosis develop.
As the extra cellular fluid becomes depleted, plasma volume falls, RBC concentration rises, cardiac output decreases, and patient dies in shock death usually occurring in the interacted patient 4 days to 2 weeks after cessation of ineralo corticoid secretion.

ii) Gluco corticoid deficiency
Loss of cortisol secretion makes it impossible for a person with addisson’s disease to maintain normal blood glucose concentration between emals because he or she cannot syntheisse significant quantities of glucose by gluconeogensis. Further more lack or cortisol reduces the mobilization of both proteins and fats from the tissue.
Lack of adequate glucorticoid secretion also makes to person with addison’s disease highly susceptible to the deteriorating effects of different types of stress, and even a mild respiratory infection can cause death.

iii. Melanin pigmentation : of the mucous membranes and skin Melanin is not always deposited evenly but occasionally in the thin skin areas, such as the mucous membranes of the lips and the thin skin of the nipples.

Treatment
An untreated persons with total adrenal destruction dies within a few days to a few weeks because of consuming weakness and usually …… shock. Yet such a person can live for years it small quantities or mineralo corticoids and glucorticoids are administrated daily.

Addisonian crisis
Great quantities or glucocorticoids are occasionally secreted in response to different types of physical or mental stress. In a person with addissons disease, the output of gluco corticoids does not increase during stress. Yet whenever different types of trauma, disease or other stresses, such a surgical operations. Supervence a person in likely to have an acute need for excessive amount of glucocorticoids and often must be given 10 or more times the normal quanitites of glucoroticoids to prevent death.
This critical need for extra gluco corticoids and associated severe debility in times or stresses called an addissonian crisis.

Hyperadrenalism – Cushing’s Syndrome
Causes: 1) Adenomas of anterior pituitary that secrete large amount of ACTH.
2). Abnormal function of the Hypothalamous that causes high levels of or corticotrophin releasing hormones.
3). Ectopic secretion of ACTH by a tumour elsewhere in the body such as an abdominal carcinoma.
4). Adenomas of the adrenal cortex when Cushing syndrome is secondary to excess secretion of ACTH by the anterior pituitary is called cushing’s disease.
5). Cushing syndrome can also occur when large amount of gluco corticoids are administrated over prolonged periods for therapeutic purpose. (for eg RA)

A special characteristic of Cushing syndrome is mobilization of fat from the lower part of the body, with consonants extra depositon of fat in the ….. and upper abdominal regions, giving rising to buffalo torso. The excess secretion of steroid also lead to an edematous appearance of the face, and and rogence potency os some of the hormones sometimes causes acne and hirsutism (excessing growth of facial haia) the appearance of the face in frequently described as moon face”.

Effects of carbohydrate & Protein metabolism
i) Blood glucose concentration – (High as 200 mg/ dl after ….)
ii) Losing protein from muscles in particular causes severe weakness.
iii) Loss of protein synthern in the lymphoid tissue leads to suppressed immune system so many patient dies of infection
Even the protein collagen fibers in the subcutaneous tissue are diminished so that the subcutaneous tissue Teac earily, resulting in development of large purplish striac where they have torn apart in addition severely diminished protein deposition in the bones often causes severe osteoporesis consequent weakness of the bones.

Treatment of cushings syndrome
i) Removing of adrenal hum our.
ii) Hypert….. pitutitary gland or even small tumouss in the pituitary that oversecrete ACTH can sometimes be surgically removed or destroyed by radiation.
If ACTH secretion can not easily be decreased, the only satisfactory treatment is … bilateral partial (or even total) ……….. followed by administration of adrenal steroid to make up for any insufficiency that develops.

Primary Aldosteronism (conn’s syndrome) occasionally a smell tunes of the zone glo… cells occurs and secretes large mounts of alsosterone; the resulting condition is called primary alsosteronism of conn’s syndroeme.
The most important effects are hypokalemine, stright … is ECF volume blood volume, very shaguf increase is plasima sodium… usually not one 4-6 m eq/l increase) and almost always hypertension. Especially inlauesting in primary aldosteronium are occasional period of muscel … caused by hpyothalmous.

Applied Anatomy of Facial Nerve

Dr P Muhammed Muneer BHMS,MD(Hom)

Anatomy of Facial Nerve
The facial nerve has a motor and sensory root, the latter being the nervus intermedius. The two roots emerge at the caudal border of the pons lateral to the recess between the inferior olive and inferior cerebellar peduncle, the motor part being medial; the vestibulocochlear nerve is lateral to the sensory root. The nervus intermedius usually cleaves at first to the vestibulocochlear rather than the facial nerve, passing to the latter as it approaches the internal acoustic meatus.

The motor root supplies: the muscles of the face, scalp and auricle, the buccinator, platysma, stapedius, stylohyoid, and the posterior belly of digastric.

The sensory root: conveys from the chorda tympani gustatory fibers from the presulcal area the tongue and, from the palatine and greater petrosal nerves, taste fibres from the soft palate. It also carries preganglionic parasympathetic innervation of the submandibular and sublingual salivary glands, lachrymal gland and glands of nasal and palatine mucosa.

Course of Facial Nerve
From their emergence from the brain, the roots pass anterolaterally with the vestibulocochlear nerve to the internal acoustic meatus; here the motor root is in an anterosuperior groove on the vestibulocochlear nerve, with the sensory root between them. At the lateral end of the meatus the nerve enters the facial canal and then descends to the stylomastoid foramen. Emerging from the foramen the nerve runs forwards in the parotid gland crosses the styloid process, retromandibular vein and external carotid artery and divides behind the neck of the mandible into branches which pierce the anteromedial surface of the parotid gland and diverge under cover of it. They form a network known as parotid plexus which supplies the facial musculature.

The Branches of Facial Nerve

In the facial canal – Nerve to stapedius
Chorda tympani

At exit from stylomastoid foramen – Posterior auricular
Digastric, posterior belly
Stylohyoid

On the face –  Temporal
Zygomatic
Buccal
Marginal Mandibular
Cervical

Applied Anatomy
Facial paralysis, often unilateral, may be due to:
(1) Supranuclear lesions in the cortico nuclear fibers from the frontal lobe, variably combined with numerous other descending fibers converging in the facial nucleus.
(2) Nuclear or infranuclear lesions involving lower motor neurons.

Supranuclear facial paralysis involving “upper motor neuron” pathways is usually a part of hemiplegia. Movements in the lower part of the face are usually more severely affected, voluntary movements being weak or absent though emotional expression is little affected. Electrical reaction of affected muscles are unaltered. Occasionally supranuclear lesions may abolish or weaken emotional movements but not voluntary movements. This dissociation shows that the supranuclear control of expressive movements is separate from the corticonuclear path for voluntary movements.

Nuclear or infranuclear lesions vary in their effects according to the lesion’s site. If the nucleus or facial pontine fibres are involved, neighbouring structures are inevitably also involved. Facial muscles are represented in cell groups within the nucleus; their degree of involvement governs the extent of paralysis, which is ipsilateral. Lesions due to adjacent damage include paralysis of the lateral rectus because of involvement of the abducent nucleus around which the facial nerve loops.

The involvement of the motor trigeminal nucleus causes paralysis of masticatory muscles.Sensory loss on the face are caused by the involvement of the principal sensory and spinal trigeminal nuclei or spinothalamic tract and paralysis of the upper and lower limbs due to corticospinal lesions. Due to proximity of facial sensory root the vestibulocochclear nerve, lesions in the posterior cranial fossa or in the internal acoustic meatus may cause loss of taste in the part of tongue with ipsilateral deafness and facial paralysis. When damage is in the temporal bone, the chorda tympani is involved and in petrous temporal fractures the vestibulocochlear nerve is involved.

Bilateral facial paralysis are caused by
(1) Bilateral infranuclear lesion’s :
• Acute idiopathic polyneuritis
• Leprosy
• Leukemia
• Syphilitic or meningococcal meningitis
• Double otitis media
• Rheumatic
• Post diphtheritic
• Bell’s Palsy
• Uveoparotid paralysis
(2) Muscle diseases:
• Myasthenia gravis/ myotonic dystrophy
• Facio-scapulo humeral dystrophy

Signs: Flattening of all normal folds, sagging of corners of mouth, fixed expression less mask like face, no voluntary movements of facial muscles. White of eye seen when patient attempts to close them. Patient talks as if he had severe stomatitis.

BELL’S PALSY
Is an acute apparently isolated LMN facial palsy for which no cause can be found.
Aetiology:
(a) Associated known clinical condition – Diabetes Mellitus, severe hypertension in last trimester of pregnancy, dental anesthesia.
(b) Causes – (i) Exposure to cold, oedema and subsequent compression of the nerve trunk within rigid fallopian canal causes circulatory disturbance, (ii) other important causes of acute facial palsy include suppurative otitis media, herpes zoster, head injury, Guillian-Barre syndrome, sarcoidosis and multiple sclerosis.

Symptoms:
sudden following exposure to chill or without any apparent precipitating cause, maximum paralysis in twenty-four hours. Post auricular pain is common and many precede paralysis by two days. There may be spontaneous loss of sense of taste, hyperacusis and watering of eyes. Sweating is less on affected side.

Signs:
Forehead cannot be wrinkled, frowning lost, eyes cannot be closed. On attempting closure eye ball turns upwards and outwards, known as Bell’s phenomenon. On showing teeth, the lips do not separate on affected side. Whistling not possible. Articulation of labial components difficult. Nasolabial fold flattened out. Angle of affected side droops with dribbling of saliva. Cheeks puffs out with expiration because of buccinator paralysis. Food collects between teeth and paralysed cheek. Fluid runs out while drinking. Base of tongue lowered.Vesicles within the external auditory meatus and ear drum in Ramsay Hunt Syndrome. Pain may precede facial weakness. Deafness may result.

Investigations
: Electromyography.
Management: Local heat.
Local treatment of muscles.
Protection of eye.

Reference
1. Gray’s anatomy
2. Harrisson’s Principles of internal medicine .15th edition
3. Last’s anatomy

Applied physiology of thyroid gland

Dr Smitha Madavan  BHMS,MD(Hom)

It is highly vascular , largest endocrine ductless gland lies deep to the sternothyroid and sternohyoid muscles from the level of C5-T1 vertebrae.It consists of two lobes right and left anterolateral to the trachea and larynx. An isthmus unites the lobes over the trachea usually to the 2nd -3rd tracheal rings. The thyroid is surrounded by a thin fibrous capsule. External to the capsule is a loose sheath found by a visceral layer of the pretracheal deep cervical layer. Dense connective tissue attaches the capsule of the thyroid gland to the cricoid cartilage and the superficial tracheal rings.

The thyroid is divided into lobules composed of about 20-40 evenly disperse follicles. The follicles range from uniform to variable in size and lined by cuboidal to low columnar which is filled with thyroglobulin. In response to trophic factors from the hypothalamus, TSH is released by thyrotrophs in the anterior pituitary into the circulation. TSH act on the thyroid and convert thyroglobulin into thyroxine – T4 & lesser amounts of triodothyroidin – T3 and are released into the systemic circulation. The binding proteins serve to maintain the serum free T3 & T4 concentration in narrow limits yet ensure that the hormones are readily available to the tissues. In the interfollicular stroma the thyroid gland also contains a population of parafollicular cells or C cells which synthesis and secrete the hormone calcitonin. This hormone promotes the absorption of calcium by the skeletal system and inhibits the reabsorption of bone by osteoclasts.

Arterial supply:superior and inferior thyroidal arteries.
Venous drainage: Three pairs of veins drain the thyroid gland; superior, middle and inferior thyroidal veins.
Nervous supply: nerve fibres from the cervical sympathetic ganglion indirectly influence thyroid secretion by acting on blood vessels.

The functional liability is reflected in transcient hyperplasia of the thyroidal epithelium. At this time thyroglobulin is resorted and the follicular cells become tall & columnar, sometimes forming small unfolded buds or papillae. When the stress abates involution occurs, ie, the height of the epithelium falls, colloid accumulates and the follicular cells resume their normal size and architecture. Failure of this balance between hyperplasia and involution may produce major or minor deviations from the usual histologic pattern. Thyroid abnormalities are relatively common in the general population.

Clinical conditions related to Thyroid
1. Hyperthyroidism–Toxic goitre
2. Hypothyroidism
• 1o—-defect in the thyroid gland
• 2o— defect in the thyroid hormone synthesis
• 3o— defect in the hypothalamus / pituitary

3.Thyroiditis

  •  acute thyroiditis
  •  riedel’s thyroiditis
  •  hashimoto’s thyroiditis
  •  subacute granulomatous thyroiditis
  •  subacute lymphocytic thyroiditis

4.Goitre

  • non-toxic— parenchymatous goitre

             — diffuse colloid goitre
— nodular goitre

  • toxic–1— diffuse toxic goiter—Grave’s disease

         2— nodular goitre—Multinodular goitre

5.Neoplasms
• adenoma
• carcinoma—papillary
— follicular
— medullary
— anaplastic

6.Congenital anomaly—thyroglossal cyst

Investigations
1) TFT
2) BMR
3) ECG
4) FNAB & Cytology
5) USG
6) Serum creatinine
7) Serum Cholesterol level
8) Serum Colloidal gold test
9) Iodine uptake
10) Urinary excreation of radioactive iodine
11) Radioiodine scan / scintiscan
12) Radiography
13) Laryngeoscopy
14) Tendon reflex
15) Thyroid antibodies
16) Protein bind plasma activity
17) Precipitin test
18) Tumour marker

Manifestations of the thyroid disease
I)Hyperthyroidism:it is a hypermetabolic state caused by increased levels of circulating tri-iodothyronine (T3) and thyroxine(T4). When the elevated levels arise from hyperfunction of the thyroid gland–Hyperthyroidism. If it is due to excessive leakage of hormone out of non-hyperactive gland-thyrotoxicosis.

Causes:
• diffuse hyperplasia of the thyroid gland
• ingestion of exogenous thyroid hormone
• swellings hyperfunctional mononodular goiter
adenoma of thyroid
thyroiditis

Primary—Hyperthyroidism arising from an intrinsic thyroid abnormality.
Secondary—Hyperthyroidism arising from a process outside the thyroid eg., pituitary tumour.

Manifestations:

  • Nervousness 
  • Palpitations
  • Rapid pulse
  • Fatigue
  • Muscular weakness
  • Weight loss with good appetite
  • Diarrhea
  • Heat intolerance
  • Warm skin
  • Excessive perspiration
  • Emotional liability
  • Menstrual changes
  • Tremor
  • Eye changes:
  • Wide eyed gaze
  • Lid lag-von graefe’s sign
  • Graves disease
  • Ophthalmopathy
  • Lid retraction 

Neuromuscular:

  • Fine tremor
  • Emotional liability
  • Anxiety
  • Inability to concentrate
  • Insomnia
  • Proximal muscle weakness
  • Skin:warm moist and flushed
  • Increased sweating
  • Absence of wrinkling of skin of forehead—joffrey’s sign

GIT:

  • Increased mobility
  • Increase in appetite but weight loss
  • Skeletal :osteoporosis
  • ardiac:tachycardia
  • Palpitation
  • Atrial arrhythmias
  • Cardiomegaly
  • CCF
  • Sleeping pulse rate is increased 

Lab diagnosis:
serum T3 ↑
serum T4 ↑ –primary hyperthyroidism

serum TSH ↓–primary /secondary hyperthyroidism. To differentiate primary /secondary hyperthyroidism TSH levels after the injection of TRH (TRH stimulation test) is used in the evaluation of cases of suspected hyperthyroidism with equivocal changes in the baseline serum TSH level. A normal rise in TSH after administration of TRH excludes secondary hyperthyroidism ie.,the defect is in thyroid.
Measurement of radioactive iodine uptake level provides an additional direct indication. Weyne’s diagnostic index

II) Hypothyroidism: it is a hypometabolic state caused by deficiency of circulating thyroid hormones.
Causes:
• insufficient thyroid parenchyma due to non goitrous
goitrous—dyshormogenesis
drug induced
deficiency of iodine
postablative—after surgery
radioactive
developmental defect
• Interference with thyroid hormone synthesis due to enzyme deficiency
• Suprathyroidal lesions—vascular damage to anterior pituitary gland

Aetiology:
Hereditary influence
Predominance in females
Usually after the age of 35

Manifestations—1)cretinism 2)myxoedema

Cretinism: the severity of the mental impairment appears to be directly influenced by the time at which thyroid deficiency occurs in utero impaired development of skeletal system and CNS.

Manifestations:

  • Mental retardation
  • Short stature
  • Dry rough skin 
  • Wide set eyes 
  • periorbital puffiness 
  • enlarged protruded tongue
  • Umbilical hernia 
  • cold intolerance 
  • pot belly
  • Delayed bone age
  • New born 
  • Lethargic 
  • Flaccid
  • seldom crying

Myxoedema –hypothyroidism developing in the older child or adult. In longstanding cases it is characterised by the deposition of mucinous material causing swelling of the skin and subcutaneous tissues.

Manifestations

  • Decreased physical and mental activities
  • Fatigue
  • Cold intolerance
  • Apathy
  • Speech and intellectual functions slowed listless
  • Overweight
  • Constipated
  • ↓sweating
  • carpal tunnel syndrome
  • skin cool pale
  • dull expression 
  • bloated look 
  • pouting lips
  • signs
  • periorbital oedema
  • coarsening of skin
  • facial features
  • cardiomegaly
  • pericardial effusion
  • hair loss
  • vitiligo
  • cold extremeties
  • malar flush
  • yellowish tint to the skin

Lab diagnosis:
1)serumT3↓
serum T4↓ — primary hyperthyroidism
serum TSH↑

2) serumT3↓
serum T4↓ —secondary hyperthyroidism
serum TSH (WNL /<(N)

3)serum cholesterol— primary thyroid failure
4)ECG—bradycardia
low voltage complexes
flattened or inverted T waves
5)tendon reflex—prolonged duration
6)thyroid antibodies–+ in hashimoto’s disease

III) Thyroiditis:
inflammation of the thyroid gland
a)acute infectious disease:caused by infectious agents like staphylococcus aureus, streptococci, salmonella, enterobacteria, mycobacteria, fungi, haematogenous in origin, manifests as hot , painful enlargement of gland.

b)Riedel’s thyroiditis:progressively increasing sclerosis, replacing thyroid parenchyma by dense fibrous tissue penetrating the capsule extend beyond trachea,stony hardness of the gland. Usually males are affected. Manifestations include glandular atrophy and hypothyroidism. Iodine uptake studies (N) thyroid scan no uptake of the hormones.

c)Hashimoto’s thyroiditis: :exclusively in females. It is the most common cause of goitrous hypothyroidism in regions where dietary iodine is adequate. Manifests as symmetrical diffuse, painless enlargement of the gland with well defined margin and of rubbery consistency.

Pathogenesis:R elated to the defect in function of thyroid specific suppressor T cells, resulting in the emergence of CD4 + helper T cells directed at thyroid and the production of autoantibodies to various components of the thyroid.
It is associated with other autoimmune disease.

Genetic component: goitrous form is associated with HLA-DR5. Atrophic form is associated with HLA-DR3.

Morphology: goitrous form characterised by the enlarged asymmetric gland with intact capsule, the parenchyma is generally paler than normal microscopic changes include exuberant infiltrate of lymphocytes plasma cells and macrophages often with germinal centres abundant eosinophilic granular cytoplasm in residual follicular cells and delicate fibrosis. Atrophic form with extreme fibrosis and less inflammation size of the gland is reduced.

Lab diagnosis:
serum T3 ↑
serum T4 ↑
serum TSH ↓
radioactive iodine uptake↓

d) subacute lymphocytic thyroiditis: : common in females especially in the post partum family history of autoimmune disease often seen along with viral infection. Antibodies to viruses demonstrable in half of the cases. Self limited form.
Manifestations:
Palpitation tachycardia
Tremor weakness
Fatigue
Lab diagnosis:
serum T3 ↑
serum T4 ↑
serum TSH ↓
radioactive iodine uptake↓

e) subacute granulomatous thyroiditis: self limiting form female of second fifth decade, after viral infection with HLAB35 antigen is formed from virus induced host tissue damage. This antigen stimulates the form of cytotoxic T lymphocytes with then damage thyroid follicular cells. the immune response is limited. This transcient hyperthyroidism usually diminish in 2-6 weeks which results in release of excessive thyroid hormones in 6-8 weeks thyroid function returns to normal. Clinical features:
painful enlargement of thyroid ,upper jaw, throat , pain in ears while swallowing
acute fever illness with raised ESR. Fatigue, malaise, myalgia
Lab diagnosis:
serum T3 ↑
serum T4 ↑
serum TSH ↓
radioactive iodine uptake↓
thyroid antibodies ↑

Grave’s disease:previously healthy gland is now characterized by hyperthyroidism due to a hyperfunctioning diffuse goiter, infiltrative ophthalmopathy, oedematous dermopathy (localized myxoedma) female predominance, history of stress and strain.
Pathogenesis: autoimmune process initiated by IgG antibodies against portions of the TSH receptor.
Morphology: mildly & symmetrically enlarged with an intact capsule and soft parenchyma. Microscopic changes include wide spread hypertrophy & hyperplasia of follicular epithelium manifested by crowding of columnar cells into irregular pappilary folds-colloid is substantially decreased ,interfollicular parenchyma contains hyperplastic lympjhoid tissue & increased number of blood vessels.

Manifestations:
Ophthalmopathy
Dermopathy,
Diffuse hyperplasia

Characteristics:
exophthalmos, goiter, tachycardia, tremor,the volume of the pretibial myxoedema –minority both retro-orbital of patients –orange peel texture and connective tissue and extra ocular muscles and is increased due to inflammation of extracellular matrix components including proteoglycans and hyaluronic acid.

Lab diagnosis:
serum T3 ↑
serum T4 ↑
serum TSH ↓
radioactive iodine uptake↓

IV) Goiter: most often caused by dietary Iodine deficiency or goitrogens. It decrease the thyroid hormone production. Compensatory increase in the TSH with resultant hyperplasia and hypertrophy of the gland. Female predominance. Usually those around puberty, during pregnancy, at menopause which subsides itself or with iodine therapy.
Diffusely enlarged, no evidence of hyper or hypothyroidism sporadically it caused by biosynthetic defects .
Morphology—massive enlargement of gland secondary to accumulation of colloid and variable atrophy of follicular epithelium. Palpable smooth , painless move with deglutition due to persistently fluctuating TSH stimulation.
Nodular goiter:sporadic form seen as single nodule at the junction of the isthmus and one lateral lobe. Complication—haemorrhage, calcification, secondary toxicosis and carcinoma.Sudden haemorrhage will lead to tracheal compression leading to dyspnoea demanding immediate tracheostomy.

Multinodular goiter : endemic nontoxic with hyper irregular nodular with focal haemorrhage, fibrosis, calcification and cystic changes include a variable degree of colloid accumulation follicular epithelial hyperplasia and follicular involution massively enlarged. >2000gm and extend behind sternum (retrosternal goiter)—substernal, plunging type,purely intrathoracic
Clinical features:
Dyspnoea
Dysphagia
Cough
Stridor
Engorgement of the neck veins
Recurrent laryngeal nerve paralysis
Lab diagnosis:
serum T3 ↑
serum T4 ↑
radioactive iodine uptake uneven

V) Neoplasms :
characterized by fixity to the underlying structures. More than
90 % are prone to be adenomas. There are certain clinical features helps in evaluation.Solitary nodule may be neoplastic.Functioning hot nodules on scintiscans are more likely benign than malignant. Nodules in younger patients < 40 and in males. FNAC is useful in evaluation of thyroid nodules.

Benign adenoma: multiple histologic variant.
Gross appearance : well demarcated solitary lesion occasionally accompanying fibrosis, haemorrhage or calcification 1)papillary type 11)follicular type
Microscopic:sharp demarcation from adjacent parenchyma by a fibrous capsule. Architecture distinct from that of adjacent compression of the surrounding gland by adenoma absence of multinodularity in the remaining gland.
Histologic:hurthle cell adenomas feature granular eosinophilic cells contain abundant mitochondria .
Clinical features:
Focal mass must be differentiated from carcinoma. Haemorrhage into adenoma may produce rapid painful enlargement of the gland .TSH dependent tumour. Most are cold on scans rarely with hyperthyroidism.

Malignant nodule:papillary-75-85%

  • Follicular: 90% are well differentiated lesions. Pathogenesis related to head and neck irradiation during the first two decades of life.
  • Papillary carcinoma —common form in 3rd % 5th decades.
  • Gross features :infiltrative lesion with calcification or cystic change.
  • Microscopic —papillary with predominance of follicular elements.
  • Hypocromatic empty nuclei devoid of nucleoli—(orphan annie eyes)nuclear grooves, Eosinophilic intranuclear lesions.inclusions-psamoma bodies
  • Histologic variants include encapsulated follicular tall cell
  • Clinical features:
  • First mass in cervical node
  • Dyspnoea
  • Dysphagia
  • Cough
  • cold mass on scitiscans
  • Prognosis :generally excellent 90% survival rate if >20 years
  • Favourable factors include
  • Well differentiated histology
  • Female sex
  • Age less than 20 years
  • Confinement of lesion to thyroid

Follicular carcinoma
Female predominance in fifth, sixth decade, Multinodular goiter predispose to follicular carcinoma ,Apparent encapsulation, Colloid filled follicles, Metastases by haematogenous spread.Prognosis depend upon
-Size of the lesion
-Presence or absence of capsular invasion
-Presence of metastasis
-Degree of histologic anaplasia

Medullary carcinoma

  • Represent neuroendocrine tumours originating from the parafollicular or C cells of the thyroid. Distinctive features include secreation of calcitonin, prostaglandin
  • Clinical features:
  • Dysphagia 
  • Hoarseness 
  • cough
  • Prognosis variable
  • Malignant lymphoma:very rare and very difficult to differentiate from anaplastic CA

VI) Congenital anomaly

  • Thyroglossal cyst
  • Cyst developing from thyroglossal tract
  • common sites: beneath hyoid
  • In the region of thyroid
  • Above thyroid
  • Located in middle or just lateral to it involves on deglutition and moves upward when the tongue is protruded due to attachment of foramen caecum
  • Histolgy
  • Squamous epithelium

Specific investigations

  • BMR

This is estimated by determining the Oxygen consumption of the patient in the basal state.The reading obtained is compared with a normal standard and the difference is recorded as a % .Normally the rate varies from –20% — +20%
In thyrotoxicosis 80—90 % myxoedema –45 %

  • Serum creatinineà0.6mg / 100ml—thyrotoxicosis
  • Diagnosis is confirmed if the level falls after thyouracil therapy.
  • Blood cholesterol level decreased in hyperthyroidism increased in hypothyroidism
  • Serum colloid gold test +in hashimotos disease
  • Precipitin test-when the antibodies produced in hashimotos disease are mixed with thyroglobulin or saline extract of the thyroid gland precipitation occurs.
  • Iodine uptake

The functions of the thyroid gland is better understood by its capacity to concentrate iodine(10000 times more than the normal tissue.The patient who has not received any medication for at least 1 month is given a tracer quantity of radioactive iodine(ie., 25 microcuries in 100 ml of water for a normal sized gland the dose should be increased when the gland is larger than normal and the uptake is directly measured by Gieger muller counter 24 hours after the dose induced. In healthy subjects the iodine uptake is about 20- 40% , ie., this amount is retained by the thyroid gland and rest is excreted. An uptake of 55% or more indicates hyperthyroid and uptake of 20% or less indicates hypothyroidism.

Protein bound plasma activity: the patient who has not taken iodine for at least 2 weeks is given a dose of 10 -20 microcuries of radioactive iodine and 10 ml of blood is taken 48 hours later. Normal range—0—0.4 % dose found in 1 litre of plasma.Thyrotoxicosisà >0.4%

Urinary excretion of radioactive iodine-urine samples in next 48 hours is collected in 3 samples .
Normal range—35-70% of the dose.
Hyperthyroidism—5-35%
Hypothyroidism—70-97% of the dose.
Laryngioscopy
Involvement of recurrent laryngeal nerve
Radiography—determining the position of trachea which may be displaced or depressed.

Wrist joint – applied anatomy

Dr  Jyothi K  BHMS, MD(Hom)

Wrist joint
This joint is also called radio-carpal joint. It is a synovial joint of ellipsoid type, formed by the articulation of the distal end of the radius and the triangular articular disc with the scaphoid, lunate and triquetral. It provides a stable, mobile platform on which the hand can perform. It comprises the carpal bones scaphoid, lunate, triquetral, trapezium, trapezoid, capitate and hamate.

The fibrous capsule of the wrist joint is lined by synovial membrane. The capsule is strengthened by palmar radiocarpal, dorsal radiocarpal and radial and ulnar collateral ligaments. The deep fascia of forearm is thickened posteriorly at the wrist to form a transverse band known as extensor retinaculam which retains the extensor tendons in position. Anteriorly at the wrist the deep fascia is thickened to form flexor retinaculam which converts the anterior concavity of the carpus into a carpal tunnel through which the flexor tendons and median nerve pass.

Arterial supply : by the articular branches derived from the dorsl and palmar carpal branches.
Nerve supply : anterior interosseous nerve (branch of median nerve) and posterior interosseous nerve (branch of radial nerve).
Ossification of carpal bones : All the carpal bones appear after birth and usually ossifies from one centre. Capitate ossifies at second month, hamate at 2-4 months, triquetral at 2-3 years, lunate 2-4 years, scaphoid, trapezium, trapezoid at 2-4 year and pisiform at 8-12 years.

Movements at the wrist joint
The wrist comprises two distinct components,
1) the radiocarpal joint (including the intercarpal joints) allowing flexion, extension, abduction and adduction.
2) the inferior radio ulnar joint allowing supination and pronation.
The movements at each component must be examined separately.

1. Extension (Dorsiflexion)
: to judge the range of extension ask the patient to place the palms and fingers of the two hands in contact in vertical plane and to lift the elbows as far as he can while keeping the heels of the hands together. The normal range of extension is 90o

2. Flexion (Palmar flexion) : To judge palmar flexion the above test is reversed, that is the patient places the backs of hands together with the fingers directed vertically downwards and lowers the elbow as far as he can. The angle between the hand and forearm is compared on both sides. The normal range of flexion is 80o.
3. The range of adduction or ulnar deviation is about 35o abduction radial
deviation is about 25o .
4. The normal range of pronation and supination is 90o and the patient’s elbow must be rotated to a right angle in order to eliminate rotation at the shoulder.

Imaging:
RADIOGRAPHIC EXAMINATION : Routine radiographs should include antero- posterior & lateral view projections of wrist. For detailed study of the carpal bones additional oblique projections are required.
Other investigative procedures are MRI, isotope bone scanning, wrist arthroscopy and electrophysiology.

Clinical conditions affecting wrist joint:
injuries of the wrist
Fractures of distal radius.

Adults children
1. Colle’s fracture. 1. Fracture distal radial epiphysis
2. Smith’s fracture. 2. Fracture distal radial mataphysis
3. Barton’s fracture.
4. Radial styloid fracture.

Injuries of the carpus :any of the bones of the carpus may be injured or dislocated. The common and important injuries are,
1. Scaphoid fracture.
2. Lunate dislocation.
3. Peri-lunate dislocation.
4. Dorsal chip fracture.

Colle’s fracture
This is fracture of the distal end of the radius produced by a fall on to the palm of the outstretched hand. This injury is uncommon below the age of 50 years. After this, it is one of the commonest fracture, particularly common in women, the high incidence being related to the onset of postmenopausal osteoporosis. Fracture line about 2 to 2.5 cm proximal to the distal articular surface of radius. Distal fragment is shifted dorsally, proximally into the shaft, angulated radially and supinated. There is always an associated injury to the inferior radio-ulnar joint.

Clinical features :
a) The appearance of wrist is typical and described as a ‘dinner – fork’ deformity. Viewed from the side the dorsal aspect of the wrist is unduly prominent, viewed from the dorsum the lateral aspect of the wrist is slightly prominent and hand is radially deviated.
b) The fracture site is tender.
c) The radial styloid process is no longer distal to the ulnar styloid process, instead the two styloid processes are approximately at the same level.
Diagnosis by x-ray wrist A-P and lateral view.
Complications : malunion, stiffness of wrist, shoulder and fingers, carpal tunnel syndrome.

Smith’s fracture
This is the reverse of Colle’s fracture, the distal fragment is flexed rather than dorsiflexed. It is uncommon. It is due to a fall on the dorsum of the palmar – flexed wrist or due to a backward fall on the outstretched hand.

Barton’s fracture:
This is an intra articular fracture of the distal radius with anterior displacement of a small fragment along with the carpus. Redisplacement is very common after closed reduction. The fracture is best managed by open reduction and application of an Ellis T – plate.

Radial styloid fracture (chauffer’s fracture):
This injury occurs following a direct blow on wrist or occasionally following a fall on the wrist . The fracture line is transverse extending laterally from the articular surface of radius and the fracture is more often undisplaced.

Fractures in children
Fracture distal radial epiphysis :
This is child’s Colle’s fracture. Due to separation of the distal radial epiphysis resulting in a displacement similar to the Colle’s fracture.

Fracture distal radial metaphysis:
This may occur at any level proximal to the epiphyseal plate. The fracture may be of the greenstick variety or may be complete.

Scaphoid fracture
The commonest injury of the carpus. Injury occurs following a fall on the outstretched hand, typically in young adults.
Clinical features : patient presents with pain in the wrist, but function of the wrist may not be grossly impaired. On examination, there will be a tenderness over the scaphoid in the anatomical snuff box, a little swelling and no bruising. These physical signs suggest a ‘sprained wrist’ rather than a fractures.

Radiologically examination : AP view, lateral view and two oblique view should be taken to confirm the diagnosis.
X-ray may not display the fracture immediately after injury since no displacement occurs at the fracture site. Repeated X-ray after one or two weeks when the suspicion still remains after negative X-ray. The fracture may be in the proximal pole, waist, distal pole or tubercle of scaphoid and may be displaced or undisplaced.

Complications : Non union, avascular necrosis of the proximal fragment.

Lunate & perilunate dislocation:
The mechanism is fall on the palm of outstreched, dorsiflexed hand which displaces the whole of carpus backwards leaving only the lunate in contact with radius called perilunate dislocation. The dislocation may reduce but displaces the lunate forward out of position causing lunate dislocation. This may be associated with fracture of scaphoid.

Clincal features :
The wrist and fingers are stiff and the wrist is swollen and tender. If the lunate has dislocated, it may compress the median nerve to cause median nerve signs. A well centered lateral X ray clearly reveals the dislocated lunate in front of the carpus. The AP view is important to exclude the associated fracture of scaphoid and close inspection of X ray AP view will show that the bones of the proximal row of carpus (scaphoid, lunate, triquetral) are not disposed round the head of the capitate with the intervention of a regular joint space as in the normal wrist. If lunate is displaced , it appears triangular rather than quadrangular in outline.

Dorsal chip fracture
This ligamentous or capsular avulsion of a flake of bone from the dorsal aspect of the carpus.It results from forced palmar flexion of the wrist.

Articular disorders of the wrist
1. Deformities
2. Arthritis
3. Miscellaneous

I DEFORMITIES: some rare disorders are ,
1. Carpal fusions
: Coalescence of two or more of the carpal bones. It is the commonest congenital abnormality. Inherited as autosomal dominant trait and may be bilateral and often associated with other abnormalities. Will not cause problems and treatment is not necessary.

2. Radial club hand : The infant is born with the wrist in marked radial deviation. There is absence the whole or part of the radius and usually also the thumb or the entire first two rays of the hand. It may occur as an isolated abnormality or as part of a generalised dysplasia.
Treatment : Gentle manifestation and splintage. Operation to centralise the carpus over the ulna probably before the age of three years.

3. Madelung’s deformity: It is the congenital subluxation or dislocation of lower end of ulna from malformation of the bones. There may be minor generalised abnormalities of bone structure often with short stature. It may be also be caused by disease or fracture – a fracture at the lower end of the radius with upward displacement of the lower fragment. The deformity varies in degree from a slight prominence of lower end of ulna at the back of the wrist to complete dislocation of the inferior radio- ulnar joint with marked radial deviation of the hand. The more sever form is associated with congenital absence of the radius.

4. Ulnar club hand
: Ulnar deviation present at birth and is due to partial or complete absence of the ulna. The radial head may dislocate as the child grows.

5. Distal ulnar dysplasia : In older children with hereditary multiple exostoses there is dispropotionate shortening of ulna, its distal end becomes carrot – shaped and the radius is bowed.

6. Wrist drop
: radial nerve palsy : With radial nerve palsy the wrist drops into the flexion and active extension is lost.

II ARTHRITIS:
1. Pyogenic arthritis :
Pyogenic arthritis of the wrist is uncommon. Infection may be haematogenous or it may be introduced through a penetrating wound.
Clinical features : Acute onset with constitutional symptoms, pain and swelling about the joint, increased local warmth and marked impairment of movement.

Radiographic features : In the early stages X rays do not show any alteration from the normal. Later, if the infection persists there is diffuse rarefaction with loss of cartilage space and some destruction of bones.

2. Rheumatoid arthritis :
It commonly affects the wrist and hands and is a major cause of serious loss of function and ugly deformities.Affected joints are swollen from synovial thickening and movement is restricted. In the later stages articular cartilage and the underlying bones are eroded and the fingers tend to deveiate medially – ulnar deviation.

X- ray : Radiography do not show any abnormality at first. Later there is diffuse rarefaction of the bones. As the disease progresses there will be destruction of cartilage leading to narrowing of the joint space & subchondral bone erosion.

3. Osteoarthritis :
It is uncommon and develops as a sequel of injury. The commonest predisposing factors are fracture of the lower end of the radius with involvement of articular surfaces, fracture of scaphoid bone complicated by avascular necrosis of the distal fragment, dislocation of the lunate bone, Kienbock’s disease of the lunate bone and long established rheumatoid arthritis. Predominant pathological change is degeneration and wearing away of the articular cartilage lining the joint surfaces. Patient complains of gradully increasing pain and stiffness of wrist worse on activity. Movements are markedly limited and painful if forced at the extremes. The skin temperature is normal.
X- ray : narrowing of the joint space & spurring or sharpening of bone at joint margins.

III. MISCELLANEOUS :
Kienbock’s disease:
It is a rare affection of the lunate bone characterised by softening, fragmentation & liability to deformation . Later it may lead to osteoarthritis of the wrist. Exact aetiology is unknown. Repeated injury is a predisposing factor.

Clinical features : pain in the wrist, most marked at the centre of the joint over the lunate area which is worse during active use of wrist. Strength of the grip is impaired due to pain.
X –ray : Lunate appears slighly more denser than surrounding bones, later the bone has a fragmented appearance.

EXTRA-ARTICULAR DISODERS ABOUT THE WRIST:
1. Chronic infective tenosynovitis:
Chronic inflammation of flexor tendon sheath in the lower forearm and hand occuring in response to low grade infection. Flexor sheaths are commonly affected. The affected sheaths are greatly thickened and show changes of chronic inflammation, contain excess of fluid. Patient presents with gradual onset of swelling with mild aching pain, in the region of the affected tendon sheath. The function of the fingers and thumb impaired. Affects the lower 5 or 6 cms of the front of the forearm and proximal part of palm.
Treatment : Of mild cases – wrist and forearm immobilisation.

2. Stenosing tenovaginitis:
This is a condition of unknown aetiology in which the sheath of a tendon thickens spontaneously, so as to entrap the tendon.

a) De Quervain’s tenovaginitis: the common sheath of abductor pollicis longus and extensor pollicis brevis tendons at the wrist are affected. Women between 40 – 50 years are usual victims.
Pateint complains of pain andd difficulty in abducting and extending the
thumb. A bulge is detected on examination on the tendons over the radial
styloid process.

b) Trigger finger : The fibrous sheaths of the flexor tendons of the fingers and thumb are involved. The flexor tendons gradually develops a constriction under the retinaculum and a bulge distal to it. Patient complains of tenderness at the base of the affected finger and locking of finger in full flexion. The locking can be overcome either by a strong effort or by extending the finger passively with the other hand, then the flexion is released with a distinct snap, like a trigger of a pistol.
Treatment : Dividing appropriate retinaculum

3. Carpal tunnel syndrome :
The carpal tunnel is formed by the flexor retinaculum anteriorly and by the distal row of the carpus posteriorly through which flexor tendons and median nerve passes. Any swelling likely to result in compression and ischaemia of median nerve in carpal tunnel – this may occur in acromegaly, myxoedema, multiple myeloma, rheumatoid arthritis, pregnancy, osteoarthritis of wrist etc. causes carpal tunnel sydrome.

Clinical features
: tingling, numbness or discomfort in the radial three and half digits and difficulty in carrying out fine movements. Shaking the hands in the air gives relief – flick test. Flexion of wrist for 60 sec causes pain – Phalen’s sign. Tinel’s sign – sharp, shooting pain along the distribution of median nerve when the flexor retinaculum is tapped gently.

Treatment : longitudinal incision of flexor retinaculam gives relief.

4. Dupuytren’s contracture:
There is localized thickening and contracture of the palmar fascia and there may be nodules in the fascia or in the subcutaneous tissue. This condition mostly affects the medial part of the palmar fascia in which the ring finger and less often little finger become flexed. Aetiology is not clearly known. There is hereditary predisposition. It is seen in cirrhotics and epileptics who takes sodium hydantoin and may also develop in diabetics.

Treatment : Night splintage and gentle stretching by the patient and excision of fascia.

5. Ganglion :
This is a tense and cystic swelling containing gelatinous material in it. Mostly arises from the capsule of joint or tendon sheath. Commonly seen on the dorsum of the wrist or the palm of the hand. They are caused by the myxoid degeneration of fibrous tissue of capsule, ligaments and retinaculae, sometimes predisposed by injury. If it originates from a tendon sheath it can be moved sideways slightly but not at all along the length of the tendon particularly when the tendon is made taut. There is chance of reccurence of ganglion after surgical excision.

Applied Anatomy of Inferior Vena Cava

Dr.Anitha MA   BHMS,MD(Hom)
Dr Padiyar Homoeopathic Medical College. Kerala

The inferior venacava conveys blood to the right atrium from all the structures below the diaphragm. It is formed by the union of common iliac veins at fifth lumbar vertebral level. Then it ascends up anterior to the vertebral column, passing through the posterior surface of the liver, pierces the diaphragm and ascends up and reaches the inferoposterior part of the right atrium. It has got 2 parts —1.Abdominal part 2.Thoracic part

RELATIONS
Abdominal part

  • Anteriorly— Root of mesentry with its vessels, head of pancreas, superior part of duodenum. Above the duodenum it is covered by peritoneum of posterior surface of epiploic foramen. Above this the liver is anterior.
  • Posteriorly— Lower three lumbar intervertebral bodies, anterior longitudinal ligament and right psoas major muscle.
  • Right lateral— Right ureter, descending part of duodenum, medial border of right kidney and right lobe of liver.
  • Left lateral— Aorta and caudate lobe.

Thoracic part
It is partly outside and partly inside the pericardial sac. The extra pericardial sac is separated from right pleura and lung by right phrenic nerve. The intra pericardial part is covered except posteriorly by inflected serous pericardium.

SURFACE ANATOMY
It begins just below the transtubercular plane, ends behind the sternal end of sixth right costal cartilage.
Variations
1. May be placed below the level of renal veins.
2. Complete visceral transposition, inferior venacava is situated left of aorta.

Superficial connections
Epigastric vein, circumflex iliac vein, lateral thoracic vein, thoracoepigastric vein, internal thoracic vein, lumbovertebral anastomotic vein.
Deep connections
Azygos vein, hemiazygos vein and lumbar veins.
Tributaries—
Common iliac vein, lumbar veins, right testicular or ovarian vein, renal vein, right suprarenal vein, inferior phrenic and hepatic veins.

CLINICAL ANATOMY
1. Thrombosis of veins
Thrombosis of inferior venacava is usually presented as swelling of either one leg or both legs and back without ascites and increase of temperature. Collateral circulation is soon established by the enlargement of deep and superficial veins.
Deep vein thrombosis is a life threatening condition. Main site of thrombosis is the lower limbs. It is usually unilateral but may be bilateral when they are extensive and extends into pelvis and inferior venacava.

Factors leading to venous thrombosis—
1. Change in the vessel wall with damage to endothelium due to injury or inflammation.
2. Dimnished rate of blood flow in veins, occurs during and after operation and in debilitating conditions like stroke and myocardial infarction.
3. Increased coagulability of blood following surgery in thepresence of infection or systemic malignancy.

Causes of swollen leg
1. Venous thrombosis.
2. Calf haematoma.
3. Cellulitis.
4. Baker’s cyst rupture.
5. Pelvic disease obstructing lymphatic or venous return.
6. Hypoalbuminaemia

Investigation of venous diseases
1. Venography.
2. Doppler ultrasound.
3. Photoplethysmography
4. Duplex ultrasound imaging

Management of Deep vein thrombosis
1. Heparin therapy.
2. Prevent pulmonary embolism.
3. Compression stockings.
4. Avoid prolonged standing.
5. Keep the limbs elevated.

2. Portal hypertension
Prolonged elevation of portal venous pressure(normal 2-5 mm of Hg) above 12 mm of Hg. Increased portal vascular resistance is the main factor causing portal hypertension.
Causes—
1. Extrahepatic post-sinusoidal — Budd-Chiari syndrome.
2. Intrahepatic post-sinusoidal — Venoocclusive disease.
3. Sinusoidal — Cirrhosis.
4. Intrahepatic presinusoidal — Sarcidosis, Schistosomiasis.
5. Extrahepatic presinusoidal — Portal vein thrombosis.
Due to increased portal vascular resistance, there will be development of collateral vessel, bypassing the liver and enters the systemic circulation through the inferior venacava. Main site of collateral vessel formation are at lower end of oesophagus, stomach, rectum, anterior abdominal wall and renal, lumbar, ovarian and testicular vasculature.

Clinical features
1. Splenomegaly.
2. Hypersplenism.
3. Thrombocytopenia.
4. Caput medusa.
5. Bleeding varices.
6. Fetor hepatis.

3. Thrombophilia
Condition in which severe deficiency of antithrombin III, protein C and protein S leads to episodes of venous thrombosis.

4. Pulmonary embolism
Fatal complication of lower limb deep vein thrombosis. Aclot from the lower limb vein detached from its site and passes via the inferior venacava and right heart to pulmonary arteries.

References
1.Clinically oriented anatomy by Keith.L.Moore. 2. Gray’s anatomy.
3.Grant’s method of anatomy 4. Davidson’s principles and practice of medicine.

Pharynx – Applied aspects

Dr Binu K BHMS,MD(Hom)
The pharynx is a wide muscular tube situated behind the nose, the mouth, and the larynx. Clinically it is considered as a part of upper respiratory passage where infections are common. The upper part of the pharynx transmits only air, the lower part(below the inlet of the larynx) only food, but the middle part is a common passage for both air and food(but only one at a time).

Dimensions:-

Length is about 12-14 cm
The upper part is widest (3.5cm) and non collapsible. Middle part ia narrow, the lower part is the narrowest of gastro intestinal tract (except for the appendix).

Boundaries:-
Superiorly : Base of the skull including the posterior part of the nbody of sphenoid and basilar part of the occipital bone in front of the pharyngeal tubercle.
Inferiorly : The pharynx is continuous below with the oesophagus at the level of C6 corresponding to the lower border of the cricoid cartilage.
Posteriorly : The pharynx glides freely on the prevertibral fascia which separates it from the vertebral spine.
Anteriorly : It communicates with the nasal cavity, oral cavity and the larynx. (thus the anterior wall of the pharynx is incomplete). It is attached from above downwards on each side to the medial pterygoid plate, pterygomandibular raphae, mandible, tongue, hyoid bone, and thyroid and cricoid cartilages. Laterally it communicates with the tympanic cavities through the auditory tubes and is in relation with the styloid process and their muscles, the common, internal and external carotid arteries and some of the branches of the latter artery.

The pharynx consists of 3 parts : nasal, oral and laryngeal.

Nasal part of pharynx:-

  • This is the upper part of pharynx behind the nose and above the lower border of the soft palate.
  • It resembles the nose structurally and functionally. a)it is respiratory in function. c)its walls are rigid and noncollapsibleb)it is lined by ciliated columnar epithelium. d)its mucous membrane is supplied by trigeminal nerve.
  • The wall of nasopharynx is formed by pharyngo basilar fascia and the posterior median pharyngeal ligament.
  • Anteriorly, it communicates with the nasal cavities;
  • Inferiorly, with the oropharynx.
  • The lateral wall presents the following a)the pharyngeal opening of the auditory tube b)tubal elevation c)salpingopharyngeal fold d)the levator palate and e)pharyngeal recess.

The roof and the posterior wall form a a continuous slope opposite the posterior part of the body of sphenoid., the basiocciput and the anterior arch of atlas. Under the mucous membrane, opposite the occiput, there is a collection of lymphoid tissue called pharyngeal tonsil (naso pharyngeal tonsil).
The nasopharyngeal tonsil is better developed in children. A pathologically enlarged pharyngeal tonsil is called adenoids. Its presence make nasal breathing impossible.
There is another collection of lymphoid tissue in the nasopharynx behind the tubal opening. It is called tubal tonsil. It is continuous with the lateral part of the pharyngeal tonsil.

Oral part of pharynx (Oropharynx) :-
This is the middle part of pharynx situated behind the oral cavity. Above it communicates with the nasopharynx, in front with the oral cavity. Below it opens into the laryngopharynx at the level of the upper border of epiglottis. Behind it is supported by the body of the axis vertebra and upper part of the body of C3. Its lateral wall presents the palatine tonsil(tonsil) which lies in the tonsillar fossa. This fossa is bounded anteriorly by the palatoglossal arch and posteriorly by the palatopharyngeal arch. The wall of the oropharynx is formed posteriorly by the superior, middle and inferior constrictors of the pharynx.

Waldeyer’s lymphatic ring :-
In relation to the oropharyngeal isthmus, there are several aggregations of lymphoid tissue that constitute Walceyer’s lymphatic ring. The most important aggregations are right and left palatine tonsils. Posteriorly and above there is pharyngeal tonsil. Laterally and above tubal tonsil; inferiorly lingual tonsil. Outer to this ring there are retropharyngeal, jugulodigastric, submandibular and submental lymphnodes.

Palatine tonsil (The tonsil):-
The palatine tonsil occupies the tonsillar sinus(fossa) between the palatoglssal and palatopharyngeal arches. It can be seen through the mouth.
The tonsil is almond shaped. It has 2 surfaces- medial and lateral; 2 borders- anterior and posterior and 2 poles- upper and lower. The medial surface is covered by stratified squamous epithelium which is continuous with that of the mouth.The lateral surface is covered by a sheet of fascia which forms the capsule of the tonsil. The anterior border is related to the palatoglossal arch with its muscle. The posterior border is related to the palatopharyngeal arch with its muscle. The upper pole is related to the soft palate and the lower pole to the tongue.
There are several pitted depressions on the surface of the tonsil, they are called crypts. The intratonsillar cleft is the largest crypt of the tonsil. It is present in its upper part. A peritonsillar abscess(quinsy) often begins in this cleft.
The bed of the tonsil is formed by: a) the pharyngobasilar fascia; b) the superior constrictor and palatopharyngeus muscles; c)the buccopharyngeal fascia; and d) in the lower part the styloglossus and the 9th cranial nerve.

Arterial supply of tonsil:-
1) Main source: tonsillar branch of facial artery.
2) Additional sources: (a)ascending palatine branvh of facial artery; (b)dorsal lingual branches of the lingual artery; (c)ascending pharyngeal branch of the external carotid artery; and (d) the greater palatine branch of the maxillary artery.

Venous drainage:-
One or more veins leave the lower part of the deep surface of the tonsil, pierce the superior constrictor and join the palatine, pharyngeal or facial veins.
Lymphatic drainage:-Lymphatics pass to the jugulodigastric nodes
Nerve supply:-Glossopharyngeal and lesser palatine nerves

Applied anatomy:-

The tonsils are large in children. They retrogress after puberty. The tonsils are frequently sites of infection. Infection may spread to surrounding tissue by forming a peritonsillar abscess.
Laryngeal part of pharynx (Laryngopharynx):- This is the lower part of the larynx situated behind the larynx. It extends from the upper border of epiglottis to the lower border of the cricoid cartilage’
The anterior wall presents a)inlet of larynx b) posterior surfaces of the cricoid and arytenoids cartilages.

brain (2)

Functional areas of brain

brain (2)Dr Bindu K   BHMS,MD(Hom)
Functions of brain can be studied by dividing it into different lobes (frontal lobe, parietal lobe, temporal lobe and occipital lobe.) or by dividing it into different areas based on histological structural differences (ie-Brodmann’s areas—47 areas)

BROADMANN’S CLASSIFICATION OF FUNCTIONAL AREAS
It was a mere historical accident that Broadmann in his original study of the monkey brain started to cut the serial sections in the horizontal plane. He named the first cell mass that he encountered as area one(1). The subsequent groups of cells that he visualized were called in ascending numerical order. In the finalized map that is seen today the numbrers occur in a jumbled manner because of the fact that reading is done in an anterior-posterior direction. There are nearly 5 areas described by Broadmann.

The workers who came to the field later used rather artificial methods to subdivide Broadmann’s areas into smaller and smaller subdivisions so that they ended up by describing a mosaic pattern consisting of quiet a large number of islets with a confusing array of numerical labels. There has been a conscious attempts at simpliflying and rationalizing the Broadmann map by various workers,like Vogt,Von Bonin and Bailey.

Classification of Von Bonnin and Bailey
The area FA of Von Bonnin and Bailey corresponds to area 4 of Broadmann. It is the agranular cortex in the depth in the central fissure and extending anteriorly to the frontal surface of the pre-central gyrus. The gray mater is quiet thick in this area and the anterior border is determined by the presence of the giant pyramid cells of Betz in the 5th layer. FB roghly corresponds to Brodmann’s area 6, the is still thick and agranular but lacks Betz cells. FC is analogous to area 8 and is a transitional band with an illdeveloped granular layer.

 The reminder of the frontal lobe designated as FD corresponding to areas 9 to 12 is quiet uniform in structure. PB lies almost entirely buried in the depth of the central fissure and consists of dust-like cells(Konio cortex) of sensory cortex. PC occupying the free face of the post-central gyrus looses the excessive granulation and the six layers are more or less uniform size and character. According to Von Bonin and Bailey,there is no distinct area 2, and thus PB and PC will correspond to areas 3 and 1 of Brodmann. The areas OC,OB and OA in the occipital lobe correspond to 17,18 and 19 of Brodmann. While OC is a sharply defined area, OB merges in sensibly with OA. The temporal lobe which does not contain motor cells is divided into TA,TE and TC.

Methods of localization of cerebral cortex

A rough and ready method is to divide them into anatomical, physiological, pathological and clinical methods. The anatomical method may further be subdivided into macroscopical and microscopical observations and the other methods can be split up further.
The gyri and sulci and the fissures and lobes which are outstanding features on the surfaces of the cerebral cortex provide very convenient landmarks for labeling the cerebral cortex. Thus the pre central gyrus has been conferred with the role of centre of voluntary motor activity and the occipital lobe with the interpretation of visual sensation. The simplicity of this method limits its usefulness as an exact scientific tool in the study of cortical function. The microscopic method, on the other hand, provides the most elegant means of outlining cortical activity and has been extensively used in this area of investigation. Areas with large pyramidal cells (agranular cortex) would control motor function, while konio-cortical areas (granular cortex) would subserve the function of sensory appreciation. A group of cells may have more than one function, and all functions need not be represented by differing cell patterns.similarly, the fibre tracts gives an indication of the associative function the connected areas. 

Major fissures and sulci of the brain
There are six main fissures and sulci:-

  • the longitudinal cerebral fissure
  • the transverse cerebral fissure
  • lateral sulcus (fissure)
  • the central sulcus
  • the parieto occipital sulcus, and
  • the calcarine sulcus.

The longitudinal cerebral fissure (sagittal fissure)
It partially seperates the cerebral hemispheres. In situ, this contains the falx cerebri. The longitudinal cerebral fissure seperates the cerebral hemispheres in the frontal and occipital regions, but between these parts of the brain, the fissure extends only as far as the corpus callosum.

The transverse cerebral fissure
It seperates the cerebral hemisphres superiorly from the cerebellum, mid-brain and diencephalon inferiorly. The tentorium cerebelli lies in the posterior part of this fissure.

The lateral sulcus
It begins inferiorly on the inferior surface of the cerebral hemispheres as a deep furrow and extends posteriorly, seperating the frontal and temporal lobes.posteriorly, the lateral sulcus seperates partly the parietal and frontal lobes.

The central sulcus
It is a prominent groove running infero-anteriorly from about the middle of the superior margin of the cerebral hemispheres, stopping just short of the lateral sulcus.
The central sulcus is an important landmark of the cerebral cortex because the motor cortex (pre-central gyrus) lies anterior to it and the general sensory cortex (post-central gyrus) lies posterior to it. The superior end of the central sulcus is located about 1 ¼ cm posterior to the mid-point of a line joining the inion and the nasion and its inferior end is about 5 cm superior to the external acoustic meatus.

The parieto-occipital sulcus
It seperates the parietal and occipital lobes of the brain on the medial aspect of the brain. It extends from the calcarine sulcus to the superior border and continues for a short distance on the supero-lateral surface.

The calcarine sulcus
It is on the medial surface of the brain. It commences near the occipital pole and runs anteriorly, taking a curved course and joining the parieto-occipital sulcus at an acute angle.

The main lobes of the cerebral hemispheres.
There are four main lobes of the cerebral hemispheres.

The frontal lobes
They are the largest of all the lobes of the brain. They form the anterior parts of the cerebral hemispheres. The frontal lobes lie anterior to the central sulci and superior to the lateral sulci. Their lateral and superior surfaces extend posterior to the coronal sulcus.the basal surfaces of the frontal lobes rest on the orbital parts of the frontal bone in the anterior cranial fossa. The orbital gyri form impressions in the orbital plates of the frontal bone. The olfactory bulbs rest on the cribriform plates.

The parietal lobes
The parietal lobes are related to the internal aspects of the posterior and superior parts of the parietal bones. Each parietal lobe is bounded anteriorly by the superior part of the line joining the parieto-occipital sulcus and the pre-occipital notch. The inferior boundary of each lobe is indicated by an imaginary line extending from the posterior ramus of the lateral sulcus to the inferior end of the posterior boundary.

The temporal lobes
The temporal lobes lie inferior to the lateral sulci. Their convex anterior ends, called, temporal poles, fit into the anterior and lateral parts of the middle cranial fossa. Their posterior parts lie against the middle one-third of the inferior part of the parietal bone.

The occipital lobes
These are small and are located posterior to the parieto-occipital sulci. They rest on the tentorium cerebelli, superior to the posterior cranial fossa. They contain the visual cortex.

Functions of certain specific cortical areas

Post-central gyrus – primary sensory areas
Pre-central gyrus – voluntary motor area (primary motor area)
These primary sensory and motor areas have highly specific functions, while other areas of the cortex perform more general functions that we call association or cerebration.

Specific functions of the primary sensory areas
The primary sensory areas all have certain functions in common. For instance, somatic sensory areas, visual sensory areas and auditory sensory areas all have spatial localizations of signals from the peripheral receptors.
The functional ability of the parietal cortex is recognising the following types of functions.
1. tactile discrimination
2. tactile localisation
3. thermal perception of minute changes
4. weight discrimination (stereognosis)
5. vibratory sensation
6. taste sensation

All the sensory tracts after successive relays at different levels end in different parts of the cerebral cortex. The somaesthetic sensations are relayed to the post-central cortex.(areas 3,1,2) of the parietal lobe. The body is represented in a reverse order in areas 3,1,2. The extent of representations varies depending upon the type of function. The sensation from the tongue or face has wider representation than that from the limbs.
Besides the above functions of the parietal cortex, it is observed that the post-central gyrus is also involved in the modulation of afferent input.
Apart from areas 3,1 and 2 of the parietal cortex, additional sensory cortices are also found in the motor cortex and in the ectosylvian gyrus.

Secondary sensory area
The secondary sensory area or sensory association areas extend 1 to 5 cms in one or more directions from the primary sensory areas. Each time a primary sensory area recieves a sensory signal, secondary signals spread, after a delay of a few milli-seconds into the respective association areas as well. Part of this spread occurs directly from the primary area through subcortical fiber tracts, but a major part also occurs in the thalamus, beginning in the sensory relay nuclei, passing next to corresponding thalamic association areas, and then travelling to the association cortex.

The general function of the sensory association area is to provide a higher level of interpretation of the sensory experiences.

Destruction of the sensory association areas greatly reduces the capability of brain to analyze different characteristics of sensory experiences. For instance, damage in the temporal lobe below and behind the primary auditory areas in the dominant sphere of the brain often causes a person to lose his ability to understand words or other auditory experiences even though he hears them.

Like wise, destruction of the visual association area in Broadmann’s area 18 & 19 of the occipital lobe or the presence of a brain tumour or other lesions in these areas, does not cause blindness or prevent normal activation of the primary visual cortex but greatly reduce the person’s ability to interpret what is seen. Such a person often loses the ability to recognize the meanings of words, a condition that is called “ word blindness” or dyslexia.

Destruction of the somatic sensory association area in the parietal cortex posterior to primary somatic area 1 causes the person to lose spatial perception for location of the different parts of the body. In the case of the hand has been “lost”, the skills of the hand are greatly reduced. Thus, this area of the cortex seems to be necessary for interpretation of somatic sensory experiences.

Interpretative function of the posterior superior temporal lobe – the general interpretative area (wernicke’s area)
The somatic, visual and auditory association areas, which can actually be called interpretative area, all meet one another in the posterior part of the angular gyrus where the temporal, parietal and occipital lobes all come together. This area of confluence of the different sensory interpretative areas is especially highly developed in the dominant side of the brain – the left side in the right-handed persons. And, it plays the greatest single role of any part of the cerebral cortex in the higher levels of brain function that we call cerebration. Therefore, this region has frequently been called by different names suggestive of the area having almost global importance. The knowing area, the tertiary association area and so forth. The temporal portion of the general interpretative area is called Wernicke’s area in honor of the neurologist who first described its special significance in intellectual processes.

Following severe damage in the general interpretative area, a person might hear perfectly well and even recognize different words but still might be unable to arrang these words into a coherent thought. Like wise, the person may be able to read words from the printed page but be unable to recognize the thought that is conveyed. In addition, the person has similar difficulties in understanding the higher levels of meaning of somatic sensory experiences, even though there is no loss of sensation itself.

Dominant hemisphere: The general interpretative functions of Wernick’s area and of the angular gyrus and also the functions of the speech and motor control areas are usually much more highly developed in one cerebral hemisphere than in the other. This is called the dominant hemisphere. In at least 9 or 10 persons the left hemisphere is the dominant one. At birth, Wernicke’s area of the brain is often as much as 50 percent larger in the left hemisphere than in the right. Therefore, it is easy to understand why the left side of the brain might become dominant over the right side. However, it for some reason the dominant Wernicke’s area is removed in early childhood, the opposite side of the brain can develop full dominant characteristics.

Wernicke’s area in the non-dominant hemisphere: when the Wernick’s area in the dominant hemisphere is destroyed, the person normally loses almost all intellectual functions associated with language or symbolism, such as ability to read , ability to perform mathematical operations, and even the ability to think through logical problems. How ever, other types of interpretative capabilities, some of which undoubtedly utilize the temporal lobe and angular gyrus regions of the opposite hemisphere are retained. Psychological studies in patients with damage to their non-dominant hemispheres have suggest that this hemispheres may be especially important for understanding and interpreting music, non-verbal visual experiences, spatial relationships between the person and the surroundings, and probably also interpreting many somatic experiences related to use of the limbs and hands. Thus, even though we speak of the dominant hemisphere, this dominance is primarily for language or symbolism- related intellectual functions, the opposite hemisphere can actually be dominant for some other types of intelligence.

An area for recognition of faces.
An interesting type of brain abnormality called prosophenosia is the inability to recognize faces. This occurs in persons who have extensive damage on the medial undersides of both occipital lobes and along the medioventral surfaces of the temporal lobes. Loss of these face recognition areas, strangely enough, results in very little other abnormality of brain function.
The occipital portion of this area is contiguous with the primary visual cortex and the temporal portion is closely associated with the limbic system that has to do with emotions, brain activation and control of one’s behavioral response to the environment.

Prefrontal areas
The prefrontal areas is the most anterior part of the cerebral cortex and is a highly developed portion of the cerebral outgrowth. It consists of areas 9 to 12,13 & 14,23 and 24,32 and 44 to 47 and was formerly called the “silent areas” of the brain. This area has a control of some types of behaviour, especially choice of behavioural options for each social or physical situations. One of the outstanding characteristics of a person who has lost the prefrontal areas is the ease with which he can be distracted from a sequence of thoughts. The person without prefrontal areas ordinarily acts precipitously in response to incoming sensory signals, such as reacting angrily to slightest provocations. Also he is likely to lose many or most of his morals; he has little embarrassment in relation to his excretory, sexual and social activities; and he is prone to quickly changing moods of sweetness, hate, joy, sadness, exhilaration and rage. In short he is a highly distractible person with lack of ability to pursue long and complicated thoughts.

Physiological anatomy
of the motor areas of the cortex and their pathways to cord
The motor cortex lies anterior to the central sulcus, is characterized by large pyramid shaped cells. This area is usually referred to simply as area IV which is the number of the area in the Broadmann classification of the cortical areas. It is frequently also called the primary motor cortex or pyramidal area. The anterior portion of the motor cortex is usually referred to as area VI because it is mainly composed of area VI in Broadmann’s classification. It is also frequently referred to as either the motor association area or the pre-motor area.

The pyramidal area and the pyramidal tract (corticospinal tract)
This area in each hemisphere contains approximately 34,000 giant Betz cells or giant pyramidal cells, for which reason it is called the pyramidal area. The pyramidal tract passes downwards through the brainstem, then it decussates mainly to the opposite side to form the pyramids of the medulla. By far the majority of the pyramidal fibres then descend in the lateral corticospinal tracts of the cord and terminate principally on interneurons at the bases of the dorsal horns of the grey matter. A few fibres, however, do not cross to the opposite side but pass ipsilaterally down the cord in the ventral corticospinal tracts and then mainly decussates to the opposite side farther down the cord.

Collaterals from the pyramidal tracts in the brain.
Even before the pyramidal tract leaves the brain, many collaterals are given off as follows:
1. the axons from the giant Betz cells send short collaterals back to the cortex itself. It is believed that these collaterals mainly inhibit adjacent regions of the cortex. When the Betz cells discharges, thereby, “sharpening” the boundaries of the excitatory signals.
2. A large body of collateral fibres pass into the striate body and putamen. From here additional fibres extend through several neurons down the brain stem and then into the spinal cord through the extra pyramidal tracts.

3. A moderate number of collaterals pass from the pyramidal tract into the red nuclei. From these additional pathways pass down the cord through the rubrospinal tract.
4. A moderate number of collaterals also deviate from the pyramidal tract into the reticular substance of the brain stem; from here signals go to the cord via reticulospinal tracts and others go to the cerebellum via reticulocerebellar tracts.

5. A tremendous number of collaterals synapse in the pontile nuclei, which give rise to the pontocerebellar fibres. Thus, whenever signals are transmitted from the motor cortex through the pyramidal tract, simultaneous signals are transmitted into the cerebellar hemispheres.
6. Many collaterals also terminate in the inferior olivary nuclei and from here secondary olivocerebellar fibres transmit signals to most areas of the cerebellum.

Thus, the basal ganglia, brain stem and the cerebellum all receive strong signals from the pyramidal tract every time a signal is also transmitted down the spinal cord to cause a motor activity.

Importance of the area pyramidalis:
The giant pyramidal cells of the area pyramidalis are very excitable. A short train of stimuli almost always elicits discrete movements of muscles on the opposite side of the body. In almost no other region of the cortex can one be certain of achieving a motor response with such weak stimuli.

Extra pyramidal tracts:
The extra pyramidal tracts are collectively, all the tract besides the pyramidal tract itself that transmit motor signals from the cortex to the spinal cord.

Primary motor cortex (area IV)
The different muscle groups of the body are not represented equally in the motor cortex. In general, the degree of representation is proportional to the discreteness of movement required of the respective part of the body. Thus the thumb and fingers have large representations, as is true also of the lips, tongue and the vocal cords. The topography of the cortical motor areas shows that the body is represented in an inverted pattern. The parts of the body represented in this cortex are as follows from above downwards. Toes, ankle, knee, hip, abdomen, thorax, arm, hand, fingers 5, 4, 3, 2 and thumb, face and tongue. Recent work has shown that the arm area intervenes between the face and the trunk areas. While there is generalized invasion of the entire body, the parts of the face are in the normal erect orientation.

Supplementary motor area
Areas on the medial surface rostral to the central sulcus is the supplimentary motor area or area 2. The entire body is represented in this area also, the head and upper extremity in the anterior part and close to the edge of the hemisphere while the lower extremity is more posterior and nearer to the corpus callosum. The threshold of stimulation of this area is higher than the primary area. It is suggested by Smith et al that the supplementary motor area functions by its relay through area 4.

Pre-motor area (area 6)
Rostral to pre-central gyrus lies an area, which when stimulated, produces movement in the opposite arms and rotation of head and trunk to the opposite side. This is designated area 6. These effects are seen even after the ablation of the area 4. The control of muscular groups by area 6 is mediated through the extra pyramidal tracts. It is generally accepted that area 6 is an integrated center for adaptive motor activity.
Area 6 has normally an inhibitory control on some primitive reflexes. Voluntary movements tends to become apraxic in man, ie, inability to execute purposeful movements when area 6 is affected. If the area 6 along with area 4 on both sides is removed, some more motor defects are seen, though posture and locomotor activities are unaffected. Also, Hypertonicity in all the limbs. Some reflexes like flexor reflexes are exaggarated, when areas 4 and 6 are removed together.

Suppressor areas

First described by Vogt and Vogt. They found that movements were inhibited on stimulation of these areas. They are 2, 8,19 and 24.

Clinical signs of lesion’s of motor cortex
Lesions of motor cortex consequent to vascular accidents results in contra lateral paralysis. Commonest cause of such a lesion is thrombosis or hemorrhage of middle cerebral artery which supplies that portion of motor cortex. The ensuing paralysis is called hemiplegia. This involves the face, the limbs and the trunk muscles on one side of the body. The paralysis is typical of an upper motor lesion. The predominant feature is spasticity of the muscles. Lesions at the internal capsule, even though small, results in an extensive hemiplegia. This is due to the fact that the fibers are concentrated in a compact bundle in the internal capsule.

Hemiplegia is characterized by loss of voluntary movement on one side. Facial muscles also show failure of movements of movement on volition but muscles contract during emotional expressions like laughter, anxiety or anger. Respiratory and other bilaterally innervated muscles do not show any impairment of movement. The tone of the muscles is excessive leading to a clasp knife rigidity. There is not much of waisting, except a slight amount of atrophy due to prolonged disuse.
The deep reflexes are exaggerated with prolongation of relaxation. The typical extensor plantar reflex (Barbinski’s sign) is seen. This reflex is a part of a general withdrawal reflex and is seen in lesions of cortico spinal pathway. This reflex can be elicited by stroking with a sharp object, the lateral aspect of the sole of the foot, when there is dorsiflexion of the big toe and fanning of the lateral toes. Such a reflex is seen in babies where it is attributed to the yet unmyelinated pyramidal tract. Sometimes, an extensor pattern is observed in deep sleep also. Patellar and ankle clonus may be present. Superficial reflexes are also lost on the affected side.

Involvement of facial muscles either on the same side or on the opposite side depends on the level of the lesion. If the lesion is supranuclear (above the facial nucleus), there will be hemiplegia with facial palsy on the opposite side of the lesion, ie, on the same side of the paralysed limbs. If the lesion is at the level of the facial nerve nucleus, there is hemiplegia on the opposite side with facial palsy on the same side of the lesion. Aphasia is seen if the lesion is cortical and involves Broca’s area (area 44)

Voluntary movement
For the execution of movement, cortex plays an important role. The motor cortex is the upper motor key board which activates the lower motor key board (spinal cord) for the necessary movement. In a voluntary act both pyramidal and extrapyramidal systems are involved. The postural back ground for every voluntary act is controlled by the extra pyramidal system.

Integrating the two hemispheres into a single mind.
Corpus callosum is not only a communicating link between the two hemispheres, but it also co-ordinates behaviour. Though there are two hemispheres in the brain, each is capable of neuronal processing. We act as though we have only one mind and not two.

References
1. Gray’s Aanatomy
2. Grant’s method of Anatomy
3. Baily and Love’s – Short practice of surgery
4. Keeth. L .Moore – Clinical Anatomy

Cranial Nerves – applied anatomy

Dr Ameer Khalid BHMS,MD(Hom)

Olfactory Nerve CN – I
Purely sensory and are concerned with smell.
The olfactory cells reside in the mucosa of the superior nasal concha & the upper part of the nasal septum.
Nerve fibre arising in this mucosa collect bundles that together constitute an olfactory nerve. The axons of these cells pass through the sieve like cribriform plate of the ethmoid bone, pierces the duramater & arachnoid of the brain to reach the overlying olfactory bulb to the medial surface of the cerebral hemisphere & the temporal lobe. The most important of these is entorhinal area made up of the uncus and the anterior part of the paraphippocampal. gyrus.

Lesions of the olfactorty Nerve results in
Lloss of sense of smell – Anosmia (Olfactory anaesthesia). Smell is also responsible for the finer appreciation of taste.

Causes of Anosmia
1)Head Injuries : A sudden shift of the cerebral hemispheres results in avulsion of Olfactory bulb from the brain or from the cribriform plate.
The olfactory Nerve may also be damaged by a fracture of the ciribriform plate. The subarachnoid space on the cranial side of the cribriform plate is located in close approximation to the olfactory mucosa. A fracture through the cribriform plate that tears the mucosa can result in leak of CSF through the nose – CSF Rhinorrhoea.
This condition can result in meningitis caused by spread of micro organisms from the nose to CSF
2) CVA-Effusion of blood into base of frontal lobe.
3) Tumours of the Frontal lobe, or those arising near the pituitary gland
4) Infections –c/c tuberculous meningitis & other infections like common cold, Viral Hepatitis, syphilis, osteomyelitis of frontal or ethmoidal regions.
Unilateral Anosmia may be of diagnostic significance in localizing brain lessons.

Optic Nerve – CN II

  • Special sensory nerve conveying information related to special senses.
  • (Olfactory Nerve, optic Nerve & Cochlear Nerve)
  • The nerve mediate vision.

Optic Nerves-

  • Not strictly a nerve, but a tract of nerve fibres of CNS. Leave the retina at the optic disc (Blind Spot) courses through the optic canal to Optic Chiasm
  • About 5cm in length; is slightly longer than the distance it travels; that it permits free movement of eyeballs.
  • These tracts are complete with dura, arachnoid, subarachnoid space & pia.
  • There is a myelin sheath for the fibres of this nerve, but there is no neurolemmal sheath. So there is no regeneration of Optic Nerve Fibres after injury or destructive diseases.
  • Lesions of optic nerve distal to chiasm cause Ipsilateral blindness
  • Some disease processes involving optic nerve can affect some fibres but spare other & instead of total blindness there usually are areas of lost function in the central or peripheral parts of fields of vision of each eye. An area of depressed function in the visual field is called a scotoma

At the optic chiasm
Here pathways from both retinas are sorted so that the same visual fields project the opposite side of the brain.

  • (a) Pathways from temporal ½ of each retina remain ipsilateral. Pathways from nasal ½ cross in optic chiasm.
  • (b) ) Hemianopsias HEMI =1/2 .AN – No, OPSIS –Vision

Optic chiasm sits above pituitary fossa, so that a pituitary tumour may press on optic chiasm
(i) Bitemporal Heteronymous Hemianopsia (Tunnel Vision)-Results from medial compression of optic chiasm,interrupting input from the nasal half of retina of both eyes with loss of both temporal visual fields.
(ii) Ipsilateral Nasal Hemianopsia -: Results from lateral compression of uncrossed nerves, interrupting input from temporal retina of one eye with loss of one nasal visual field. A Localised dilation or Aneurysm of Internal carotid Arterty, superior to cavernous sinus, could exert this king of pressure on optic chiasm which cause nasal hemianopsia

Optic tracts
Pass posteriorly from optic chiasm conveying common visual field to the lateral geniculate body of thalamus (LGB’s)

Optic Radiations :
From each LGB, project to the primary visual area of each occipital lobe in the region of calcarine fissure.
Lesions of optic tracts, optic radiations or occipital cortex result in Cortical Blindness with Contralateral homonymous hemianopsia.(loss of contralateral ½ of the visual fields of both eyes.)
Optic Nerve is peculiarly liable to Neuritis (Inflammation)-
Papillitis – Inflammation of optic Nerve head
Retrobulbar Neuritis – Neuritis behind the eyeball optic neuritis results in atrophy.
Retrobulbar neuritis involving the optic nerve/tract is commonly caused by Multiple sclerosis.
Optic Atrophy – Any damage of optic Nerve is followed by its atrophy. Results in diminished visual aquity or blindness.
Primary or simple optic atrophy is caused by processes that involve optic nerve such as adjacent tumours.

Tumours

Rare : Glioma & Meningioma
Papilloedema– Non inflammatory oedema of optic disc.

Vestibulocochlear Nerve-CN XIII

  • A sensory nerve consisting of 2 components :
  • Fractures of the middle cranial fossa which involve the internal acoustic meatus may cause permanent deafness.
  • Lesions of the Cerebellopontine angle :-
  • An acoustic neuroma is a slowly growing tumour that arises from Schwann cells in the sheath of nerve VIII close to the attachment of the nerve to the brainstem. Tumour exerts pressure on the lateral region of the caudal part of the pons near the cerebellopontine angle.
  • At first, symptoms are those of VIII Nerve damage
  • Progressive deafness, spontaneous horizontal nystagmus and if tested, absence of normal labyrinthine (Vestibular) response (By placing cold or warm water in the ear& observing the patient for nystagmus)
  • Later, Cerebellar ataxia appears on the side of the lesion owing to compression of cerebellar peduncles.
  • If tumour becomes extremely large, damage to spinal tract & nucleus of Nerve V can occur, abolishing corneal reflex & causing decreased pain & temperature sensibility over the face on the side of injury.
  • A peripheral type of facial paralysis, also on the side of the lesion, can result from damage to fibres of Nerve VII.

Trigeminal Nerve – CN V

  • Largest of the 12 cranial Nerve
  • Called so because it consist of 3 main divisions
  • The principal general sensory nerve to head, particularly the face and it is the motor nerve to the muscles of mastigation.

1. Ophthalmic Nerve:
Superior division of trigeminal nerve
Smallest of the 3 branches
Wholly sensory; supplies the area of skin derived from embryonic frontonasal prominence
Divides into 3 branches
a) Nasociliary
b) Frontal
c) Lacrimal
Takes part in the sensory supply to the skin of the forehead, upper lid & nose.

II . Maxillary Nerve:
Intermediate division of trigeminal
Has 3 cutaneous branches that supply the area of skin derived from the embryonic maxillary prominence

III. Mandibular Nerve :

Inferior division of Trigeminal.It has 3 sensory branches that supply the area of skin derived from embryonic manidbular prominence of first branchial arch.
Also supplies Motor Fibres to muscles of mastication.

Trigeminal Neuraligia (TIC Douloureaux) – Condition characterized by sudden attacks of excruciating pain, brought on by a mere touch in area of distribution of one of the divisions of trig nerve usually CNV2. It mimics toothache
Sensory & Motor nuclei of CNV may be involved in degenerative or other lesions in brain stem or intracranial positions of nerve may be affected by trauma or a tumour.
If motor fibres are affected, muscles of mastication will be weakened or paralysed causing deviation of mandible to affected side.
When mouth is opened, In paralysis of pterygoid muscle of one side, chin is pushed to paralysed side muscle of side.

Lesions of peripheral branches of CNV are not common, but may result from
(a) Traumatic injury to face
(b) Tumours
(c) Fractures of bones of skull
Infra orbital nerve is commonly injured in fracture of maxilla , Mandibular, Nerve may be damaged by Fracture of ramus of mandible.

Herpes Zoster
– A virus infection also affects the trigeminal ganglia. Inflammation of ganglia may result in necrosis of some ganglion cells, which usually produces typical herpetic eruptions in one or more of the 3 divisions of the nerve Herpes zoster of the face usually involves the region supplied by ophthalmic nerve.
Aneurysm of Internal Carotid Artery
May involve CNV particularly lesion interior to anterior clinoid process. When aneurysm is located near the foramen lacerum, it often affects all 3 divisions of CNV

Pain arising in structure supplied by nerve may be felt in an area of skin supplied by another branch- Referred pain
(a) Caries tooth in lower jaw (supplied by inferior alveolar nerve) causes pain in ear (Auriculotemporal nerve)
(b) If ulcer of Cancer on tongue (Lingual Nerve affected) Causes pain over ear & temple)
(c) Frontal sinusitis – Sinus supplied by a branch from supra orbital nerve – pain referred to forehead (Skin supplied by supra orbital nerve)

Facial Nerve – VII
Has a large MOTOR a small sensory root
The fibres forming the motor root arise from the motor nucleus which lies in the lower part of the pons.
Facial nerve runs superficially within parotid gland before giving rise to 5 terminal branches
-Temporal
-Zygomatic
-Buccal
-Mandibular
-Cervical
It supplies the superficial muscles of the neck ie the platysma, muscles of facial expression, auricular muscles & scalp muscles (occipitofrontalis muscle.The fibres of Sensory root (also called the Nerves are the axons of cells situated in the Facial (Geniculate) Ganglion which lies within a canal in the temporal bone.

Clinical Application-
1. Peripheral facial paralysis may be caused by chilling of the face, middle ear infections, tumours, fracture & other disorders. About 75% of all Facial Nerve lesions are of the type. Types of signs & symptoms depend upon location of the lesion.
2. As the Facial nerve runs superficially within the parotid gland, it may be infiltrated by malignant cells (eg: from a carcinoma of the parotid gland). This commonly result in incomplete paralysis (paresis of the muscles of facial expression). Care must be taken to preserve the facial nerve & its branches during excision of these tumours.
3. On rare occasions, parotid inflammation (eg : Mumps) may temporarily affect the Facial Nerve.
4. There is fan like distribution of the branches of Facial Nerve. So avoid vertical incisions in the parotid gland (eg : for drainage of pus. Short incisions parallel to the courses of the branches are less likely to produce a noticeable effect on the functioning of facial muscles. Weakness rather than complete paralysis of muscle usually results from injury to the branches of facial nerve because of the overlapping distribution of its branches
5. As the Mastoid process of the temporal bone is not present at birth,facial nerve may be easily injured by forceps during delivery of a baby.
6. Following a stroke or CVA, one side of the body is paralysed however there is usually some preservation of movement of muscles of forehead on the paralysed side because superficial part of the motor nucleus of the facial nerve is bilaterally controlled from the cerebral cortex.
7. Sudden facial paralysis often follows exposure to cold- BELL’S PALSY- An infra nuclear type of paralysis . Motor supply to the muscles of one half is severely affected. Paralysis of muscles of facial expression causes an expressionless look. On that side of his face, inability to whistle, puff his cheek or close that eye.

Vagus Nerve – CN X

The vagus, as its name implies, is a wandering or vagrant nerve, in the sense that it travels far afield its branches go to many parts of the body. passes through the thorax into the abdomen, in its course give branches to lungs, heart, stomach, intestines etc.
Contains –
• Motor
• Sensory
• Secretory &
• Vasodilator fibres

Vagal Trunk branches takes part in the formation of cardiac plexus.Function of vagus nerve is to slow the heart and reduce the force of its beat.
Recurrent laryngeal nerve which is a branch of vagus is motor to all muscles of larynx except cricothyroid Damage to recurrent laryngeal nerve – will result in the cord being pulled by the cricothyoid muscle into the paramedian position. This decreases the airway.
If both recurrent laryngeal nerves are injured, vocal cord is fixed in the intermediate or cadaveric position. Airway is good but patient is unable to approximate the vocal cords , resulting in a poor voice.

Vagus& recurrent laryngeal nerve-

Damage to these nerves may produce an alternation in the voice.
Temporary paralysis of these nerves may occur as a result of post-operative oedema.
As the vagus nerve largely control the secretion of acid by parietal cells of stomach ,an excess acid secretion is associated with peptic ulcers. Section of vagus nerve (Vagotomy) as they enter the abdomen is sometimes performed to reduce acid production. Often only the gastric branches of vagus nerve are cut (selective vagotomy)
Thereby avoiding adverse effects on other organs (eg : dilatation of gall bladder)

Glossopharyngeal Nerve-IX CN
Arises from the lateral aspect of medulla just caudal to pons
Predominantly a sensory nerve, but also contains voluntary motor fibres to the stylopharyngus muscle& Preganglionic parasympathetic fibre
Lesions : Rare in isolation
Interruption of all fibres result in
(A) Loss of sensation including that of taste in posterior 1/3rd of tongue
(B) Unilateral loss of gag reflex (produced by stimulating the posterior pharyngeal wall)
(Glossopharyngeal Nerve : Afferent to that region
Vagus Nerve : Efferent to that region)
(C) difficulty with swallowing
Glossopharyngeal Neuralgia : Very rare. Paraxysms of pain felt in sensory distribution of nerve.
Glossopharyngeal Nerve to the tongue accompanies the tonsillar artery on the lateral wall of pharnyx. As the wall is thin, CN IX is vulnerable to injury during tonsillectomy. Also odema around this nerve following tonsillectomy may result in temporary loss of taste.

Accessory Nerve – CN XI
Has 2 distinct parts
1) Spinal Root
2) Cranial Root
Lesion of the nerve is rare

May be damaged by
1) Traumatic Injury
2) Tumours at the base of the skull
3) Fractures involving the Jugular foramen
4) Neck laceration
Injury to spinal accessory nerve results in paralysis of sternocleido- mastoid causing weakness on turning the head against resistance away from the paralysed muscle.
Paralysis of Trapezius muscle causes downward & outward rotation of the upper part of the scapula, sagging of the shoulder & weakness on attempting to shrug the shoulder.The normal nuchal ridge formed by Trapezius muscle is also depressed & dropping of the shoulder is an obvious sign of injury to spinal root of nerve.
Isolated Lower Motor Neuron lesion of Accessory Nerve may occur after Lymph node dissection of the neck. The function of CN XI may also be interfered with by inflamed lymph nodes in the neck. This can cause a/c torticollis (WRY NECK) or drawing of the head to one side.

Hypoglossal Nerve – CN XII

  • A purely motor nerve
  • CN XII supplies all the intrinsic & extrinsic muscles of the tongue except palatoglossus
  • To test the nerve : – Ask the patient to protrude the tongue. In a normal person, protruded tongue lies in the midline. If the CN XII is paralysed, tongue deviates to the paralysed side.
  • Trauma such as fractured jaw may injure the CN XII causing paralysis of tongue musculature.
  • Neck Lacerations – often with major vessel damage, and basal fracture of skull also cause CN XII injuries. Moderate dysarthria may result.

Occulomotor, Trochlear & Abducent Nerves – III, IV, VI CN
All the 3 cranial nerves supply the muscles of the eyeball

Occulomotor Nerve
Occulo Motor = Related to movements of eye
This nerve is the motor nerve to the levator palpebrae superioris muscle of the eyelid ,the superior, medial & inferior rectus & inferior oblique muscles of the eyeball.

Lesions of the Occulomotor nerve results in-
1. Ptosis : Levator palpebrae muscle is involved & upper eyelid is in complete ptosis ie, the eye is partially closed & upper lid cannot be raised voluntarily (unlike ptosis due to lesions of cervical sympathetic trunk where the voluntary motor supply is intact).
2. Outward deviation (abduction) of the eye (External strabismus) because of the unopposed action of the lateral rectus muscle & inability to turn the eye vertically or inward.
3. Dilatation of the pupil (Mydriasis) because of the unopposed action of the radial muscle fibres of the iris, which are supplied by the sympathetic system. A light shone in either eye produces no constriction of the dilated pupil.
4. Patient is unable to look up, down or medially with the affected eye.
5 .The patient with a lesion of the occulomotor nerve complains of a drooping lid & double vision. Incomplete lesions produce partial effects. There may be some weakness of all functions, or one symptom may appear without the others (eg : dilatation of the pupil without paralysis of eye movements)
Patient with diabetes mellitus are prone to develop vascular lesions of the occulomotor nerve with loss of all functions except for papillary responses.

Abducens Nerve – VI CN
This is the motor nerve to the lateral rectus muscle. It has the longest intracranial course of cranial nerve & can be damaged in the brain stem or more often in its intracranial course.

Lesions of Abducens nerve –
Abducens nerve paralysis result in the patient being unable to turn the eyeball laterally on the affected side. The imposed pulls of the medial rectus muscles cause the eye to turn inward (adduct) thereby producing on internal strabimus. Strabrimus / Squint, is an abnormality of eye movement in which the axis of the eyes are not parallel. When strabimus occurs from a nerve VI lesion visual images do not fall on corresponding points of the left & right retinas, as a result, the images cannot be fused properly. The result is Diplopia (Double Vision), which worsens when the patient attempts to gaze to the side of the lesion. The 2 images are seen side by side, thus the disorder is termed Horizontal Diplopia.

The patient usually attempt to minimize the diplopia by rotating the head so that the chin turns towards the side of lesion Tentorial herniation may result in abducens nerve paralysis . It is seen more commonly with posterior fossa lesion, such as a slowly accumulating posterior fossa haematoma which results in reversed tentorial coning. The patient may remain conscious while the nerve palsy occurs which makes diplopia an important symptom.
A carotiocavernous fistula may also result in abducens nerve paralysis.

Trochlear Nerve – IV
The trochlea is a motor nerve which supplies the superior oblique muscle. Paralysis of superior oblique muscle –
The ocular muscles do not act individually, but contract in groups and the action of a muscle at any moment will depend on the position of the eye when muscle contraction occurs.
When the trochlear nerve is injured, there is limitation of movement when the patient is asked to look downward with the eye adducted; in this position the action of the inferior rectus is minimal while that of the superior oblique muscle should be maximal. The patient is unable to look at the tip of the nose. Complaints of vertical diplopia & tilts the head in order to align the eyes & thereby eliminate the diplopia .

References-
1.Clinically oriented anatomy by Keith.L.Moore.
2.Gray’s Anatomy
3.Grant’s method of Anatomy
4. Bailey&Love’s short practice of surgery
5.Last’s Anatomy

face (2)

Arteries of the face

face (2)Dr Anitha MA   BHMS,MD(Hom)
Dr.Padiyar Homoeopathic Medical College. Kerala

The two principal arteries that supply the face are the facial artery and superficial temporal artery. In addition many branches of the ophthalmic and maxillary arteries that accompany Cutaneous branches of the trigeminal nerve add to the rich vascular supply to the face

1. FACIAL ARTERY
The facial artery supplies the muscles and tissues of the face, the sublingual gland, the tonsil and the soft palate.

Facial artery arises from the front of the external carotid artery in the carotid triangle above the lingual artery, and immediately above the greater cornu of the hyoid bone. Medial to the ramus of the mandible it arches upwards and grooves the posterior border of the sub mandibular gland. It next turns downwards and forwards between the gland and the medial Pterygoid and reaching the lower border of the mandible hooks round it at the anterior edge of the masseter and enter the face.

On the face it passes forwards and upwards across the mandible and buccinator almost to the angle of the mouth where the pulsations can be felt if the cheek be grasped lightly between finger and thumb. It then ascends the side of the nose and ends at the medial palpebral commissure to supply the lachrymal sac and anastamoses with the dorsal nasal branch of the ophthalmic artery.

The facial artery is remarkably tortuous in the neck to accommodate itself perhaps to the movement of the Pharynx during deglutition and on the face to the movement of the mandible, lips and cheeks.

Its branches can be divided into cervical and facial groups

Cervical branches
1. The ascending palatine artery
2. The tonsillary artery
3. The glandular branches
4. The submental artery: It branches off as it quite the sub mandibular gland; it runs forwards upon the mylohyoid below the body of the mandible. It supplies the surrounding muscle and anastamoses with sublingual branches of the sublingual artery and the mylohyoid branch of the inferior alveolar artery.

At the chin it turns upwards over the base of the mandible and divides into superficial and deep branches which anastamoses with interior labial and mental arteries, supplying the chin and lower lip.

Facial branches
1. The interior labial artery : Arises near the angle of the mouth; it passes upwards and forwards under cover of the depressor anguli oris and penetrating the orbicularis oris, runs in a tortuous course near the edge of the lower lip between this muscle and the mucous membrane.

It supplies the glands, mucous membrane, and muscle of the lower lip and anastamoses with artery of the opposite side and with the mental branch of the inferior alveolar artery.

2. The superior labial artery: It follows a similar course near the edge of the upper lip, lying between the mucous membrane and the orbicularis oris, and anastamoses with artery of the opposite side.
It supplies the upper lip, and gives off a septal branch, which ramifies on the lower and front part of the nasal septum and an alar branch, to the ala of the nose.

3. The lateral nasal branch. Is derived from the facial artery as the vessel ascends along the side of the nose.

It supplies the ala and dorsum of the nose, anastamosing with its fellow with the septal and alar branches of the superior labial artery; with the dorsal nasal ramus of the ophthalmic artery; and with the infra orbital branch of the maxillary artery.
The lateral nasal artery may be represented by several small ramii it may alternatively arise from the superior labial artery, diverging from its septal branch.

The Anastamoses of the facial artery are very numerous, not only within the branches of the vessel of the opposite side, but in the neck.
With sublingual branch of lingual
With the ascending pharyngeal and
With palatine branch of maxillary

On the face
With the mental branch of the inferior alveolar
The transverse facial branch of the superficial temporal
The infra orbital branch of the maxillary and
The dorsal nasal branch of the ophthalmic artery.
The anastamoses across the midline between the superior and inferior labial arteries are by their main trunk, an important fact in the treatment of split lip.

Variations
The facial artery not infrequently arises in common with the lingual artery, constituting the linguo – facial trunk. It varies in size and in the extend to which it supplies the face:
It occasionally ends by forming the submental artery and not infrequently extends only as high as the angle of the mouth or nose.
The deficiency is then compensated for by enlargement of one of the neighboring arteries.
In a series of 110 human fetuses a common linguo-facial – trunk occurred in 43 percent. In 42 percent it did not reach the medial orbital angle, terminating as the superior (20 percent) or inferior (22 percent) labial artery.

Applied anatomy.
The superior and interior labial branches supply the lips and lie in the submucous tissue. During operations on the lips these vessel may be controlled by an assistant who grasps the lip between his finger and thumb, or they may readily be occluded by spring clamps which take the whole thickness or the lip.
The superior labial gives a small artery to the nasal septum and troublesome epistaxis may occur from the vessel as a result of small septic ulcer of the anterior portion of the septum. The epistaxis may occur from the vessel as a result of small septic ulcer of the anterior portion of the septum. The epistaxis may be temporarily arrested by compressing the labial trunk in the upper lip of the affected side.

2. The superficial temporal artery
Arises in the parotid gland as one of the two terminal branches of the external carotid artery. It emerges from the superior aspect of the parotid gland in front of the ear. It is accompanies in its course by the auriculo temporal branch of V3. The artery divides into a frontal and parietal branch above the zygoma and is distributed to the scalp overlying the frontal and parietal bones, respectively. A transverse facial artery may arise from the superficial temporal artery within the parotid. The transverse facial artery course between the parotid duct and the zygomatic arch to supply the facial tissue over the body of zygoma.

A temporal pulse is frequently taken by compressing the superficial temporal artery against the Squamous part of the temporal bone above the ears.

3. The posterior auricular artery ( Branch of ext. carotid artery)
Arises posteriorly from the external carotid artery it ascends between the superior surface of the posterior belly of the digastric muscle and the parotid gland. It grooves the base of the skull between the mastoid process and auricle.

4. The maxillary (internal maxillary) artery 
It runs anteriorly out of the retromandibular position of the parotid gland to supply the deep face as well as portion of the nasal and oral cavities.
(a) The first (Mandibular) portion of the maxillary artery lies on the deep surface of mandibular ramus. Most of its branches pass through the foramina. Its branches are
i) Middle meningeal artery
ii) Interior alveolar artery and tiny tympanic branches and an accessory meningeal artery.
(b)The second (Pterygoid) portion of maxillary artery passes deep to the inferior head of the lateral Pterygoid. its branches
Muscular branches : Include the masseteric, buccal, temporal and pterygoid arteries.
(c) The third (Pterygopalatine or terminal) portion of the maxillary dives into pterygo maxillary fissure to enter the pterygopalatine fossa. Branches are pharyngeal branch, posterior superior alveolar arteries, Sphenopalatine artery supplying the medial wall of the nasal cavity by way of the naso palatine artery and the lateral walls by way of the lateral nasal arteries, the descending palatine artery, and infra orbital artery (supplying facial structures, and anastamosing with branches of the facial artery.

The Internal Carotid Artery
Gives rise to the ophthalmic artery. Its supra trochlear and supra orbital branches supply the forehead and anterior scalp. It anastomoses with superficial temporal, facial and posterior auricular branches of the external carotid artery.

Altered Hydrocephalus

Dr Anitha M.A MD(Hom)
DrPadiyar Memorial Homoeopathic Medical College.Kerala

The term hydrocephalus refers to an excessive amount of cerebro spinal fluid with consequent dilatation of the ventricular system usually accompanied by increased intra cranial pressure.

THE CEREBRAL VENTRICULAR SYSTEM
Within the brain there are four irregular shaped cavities. These cavities are called ventricles. The ventricles contain cerebro spinal fluid. The ventricles are: –

  • Right & left lateral ventricles
  • Third ventricle
  • Fourth ventricle

The lateral ventricles: The lateral ventricles lie within the cerebral hemispheres separated by the septum lucidum, one on each side of the median plane just below the corpus callosum. They communicate with the third ventricle through the inter ventricular foramen.

The third ventricle: The third ventricle is situated below the lateral ventricles between the two parts of the thalamus. It is connected with the fourth ventricle by a canal – the cerebral aqueduct or the aqueduct of midbrain.

The fourth ventricle : The fourth ventricle is a lozenge shaped cavity below & behind the third ventricle, between the cerebellum & the pons.
The fourth ventricle is continuous below with the central canal of the spinal cord and communicates with the subarachnoid space by a single median aperture called the foramen of Magendie and two lateral openings on the roof called the foramina of Luschka.

THE CEREBRO SPINAL FLUID
The cerebro spinal fluid is an ultrafiltrate of the plasma, which is a clear fluid and contains water, mineral salts, glucose, plasma proteins, small amounts of albumin and globulin, creatinine, and urea. It is secreted by the choroids plexus which is constituted by a tuft of capillaries covered by the ependyma. These capillaries differ from the normal capillaries in the sense that they lack the blood brain barrier.

The cerebro spinal fluid is secreted into the ventricles. From the roof of the fourth ventricle the cerebro spinal fluid flows into the subarachnoid space and completely surrounds the brain and spinal cord. The movement of the cerebro spinal fluid is aided by the pulsating blood vessels, respiration, and change of position. In certain places especially the base of the brain, the arachnoid mater and dura mater are separated and these result information of pools of cerebro spinal fluid which protects large veins, arteries and cranial nerves.

The cerebro spinal fluid is secreted at a rate of 0.5ml/mnt which accounts to 720 mls/day. Even then the amount of circulating cerebro spinal fluid is kept constant at 120 mls by maintaining the balance between secretion, and absorption.

The normal cerebro spinal fluid pressure is 10 cms of water on lying and 30 cms of water when sitting up. When the cerebro spinal fluid pressure reaches a threshold level, it passes back into the blood by the tiny diverticula named arachnoid villi, which project into the venous sinuses of the brain. When venous pressure is large the arachnoid villi collapse, preventing the flow of blood constituents into the cerebro spinal fluid. Some amount of cerebro spinal fluid is absorbed by the ventricular walls.

Functions of the cerebro spinal fluid :-
1. It supports and protects the brain and spinal cord.
2. Maintains uniform pressure around delicate structures.
3. Acts as a cushion and shock absorber.
4. Maintains moisture and helps inter change of substances between the cerebro spinal fluid and nerve cells

Hydrocephalus
Incidence : Hydrocephalus is found in 2-5 among 10,000 children.

Presence of excessive amounts of the cerebro spinal fluid can be due to:-
a. Increased production of the cerebro spinal fluid.
b. Block in the flow of the cerebro spinal fluid.
c. Impaired absorption of cerebro spinal fluid.

Etiology
:
I. Overproduction of the cerebro spinal fluid : Choroid plexus papillomas usually in the fourth ventricle produces the cerebro spinal fluid in large quantities.
II. Impaired absorption of the cerebro spinal fluid : The causes are necessarily acquired as in complications of subarachnoid haemorrhage, meningitis,& spread of a tumour within the subarachnoid space.

III. Block in the flow of the cerebro spinal fluid is observed in:-
1. Meningitis
2. Tumours
3. Congenital cerebral cysts
4. Congenital occlusion of the inter ventricular foramina
5. Abnormalities of the cerebral aqueduct
6. Blood clots following intra cerebral haemorrhage
7. Absence of the foramina of Magendie & Luschka
8. Agenesis of subarachnoid space

Predisposing Factors :
1. Physical injury
2. Irradiation
3. Nutritional deficiencies
4. Chemicals
5. Drugs
6. Intrauterine viral infection- toxoplasmosis

Factors like parental age, parity, previous still births, smoking, Diabetes mellitus, epilepsy, X-rays, hypertension, medications etc. have been found to have no influence on the occurrence of hydrocephalus.

Depending upon the exact etiology, hydrocephalus could be classified into:-
1. Congenital
2. Traumatic
3. Inflammatory
4. Neoplastic
5. Degenerative

Clinical Features :-
The clinical features vary from infants to older children and adults.
Infants :
1. Large size of the head.
2. Fontanelles become large and bulge out : If the rate of enlargement of the head is more than 2cms/ month at any time of life it is suggestive.
3. Scalp becomes shiny and thin.
4. Scalp veins become distended because of communication with intra cranial veins by the emissary veins.
5. Eyes & ears appear low set.
6. Weakness of upward gaze produces the setting sun sign.
7. The eyeballs are rolled downwards with the supracorneal sclera becoming more prominent.
8. Excessive irritability, Apathy, & Stupor.
9. Inability to retain fluids.
10. Retardation of milestones.

O/E – Head circumference increased
Mac Ewan’s Sign is positive. ( Percussion of the head reveals a cracked pot sound).
Papilloedema
Transillumination gives valuable results
Older children :-
1. After closure of the fontanelle, there are symptoms of raised intracranial pressure.
2. Deterioration of visual acuity.
3. Transient or permanent blindness.
4. Optic atrophy & papilloedema.
5. Difficulty in feeding & suckling because of stretching of the cortico bulbar tracts.
6. Hoarse hydrocephalic cry.
7. Quadriparesis – stretching of the pyramidal tracts.
8. Tendon jerks are exaggerated & plantar responses extensor.
9. Failing mental functions, behavioral abnormalities.
10. Endocrine abnormalities due to pressure on the pituitary,including obesity,small stature, precocious puberty,
adiposo genital atrophy, primary amenorrhoea and Diabetes incipidus

Investigations :-
CT Scan
Magnetic Resonance Imaging
Diagnostic ultra sound

Treatment
:-
Prophylaxis-Multi vitamin supplementation
Surgical – To remove the cause for obstruction, like benign tumours, cysts, Choroid plexectomy. 

Personal materia medica – a new concept

Dr  Shiv Dua
Any new idea or concept is a matter of controversy and is subject to criticism. Healthy criticism is always welcome since it is a ladder to acceptance.

“Personal Materia Medica (MM)” is not the MM that we purchase for our personal use or refer to on our computers. Personal MM is the individual MM that we have prepared ourselves in our memory with the help of our knowledge as conceived in practice and is without our knowing stored in our subconscious/memory. Everyone differs in knowledge and experience and hence everyone has made a different personal MM for his or her exclusive personal use. Sentiments/expressions like Love, hate, fright, horror, grieving, regrets, sadness, sympathy, confidence, disappointment, envy, innocence, suspicion and surprise etc. are not recorded in Personal MM because these notions are produced spontaneously upon circumstances. If someone has met with an accident near a cinema hall, every time he goes near this cinema hall, he is reminded the accident he had. He does not recall the accident always. Sentiments are also reminders. Personal MM is an expertise developed thru practical experience and observation. The most important of it is that it is changeable unlike book MM. On each new experience with medicine, the old conception changes. Concept of personal MM is what you deserve most. If you settle for less than you deserve, you get even less than you settled for. 

Difference between book MM and Personal MM
Book MM as explained in aphor 143 of Organon says that it should not have imaginary symptoms. Personal MM has symptoms that are ‘experienced’. Personal MM is invisible but not imaginative because it exists in our memory. Symptoms of a remedy, we have experienced, symptoms we have innovated, symptoms that are additional to what exist in book MM and symptoms that have been removed from a medicine after finding them obsolete make a perfect personal MM. Book MM prepares the student as a ‘doctor’. Personal MM prepares one a ‘successful doctor’ because he is experienced. Theoretically all the Doctors go thru same rigor of studies in colleges but what makes the difference to be successful in long run is through “Personal MM” which is developed over a period.

Sachin Tendulkar vs Vinod Kambli is perfect example of difference between book MM and “Personal MM. They studied in same school, had same trainer for cricket, played in the same ground together and shared blessing of their coach equally but Sachin excelled. Kamble is known as friend of Sachin. He has not reached the height of Sachin in cricket.

Take a mobile phone for example. Book MM is like ‘sim’ memory’ and personal MM is like memory- card. Data of Memories are interchangeable. Matter from book MM can be sent to personal MM. When we record new data from internet, it can be stored in memory card. When we experience some new symptom that is not in book MM, we store the same in personal MM. Book MM is theory, personal MM is practical experience stored in memory.

Key characteristics of Personal MM
Without good memory, no one can become a homoeopathic doctor. We know that every mind differs and hence quantum of memory differs. With different attitudes, different methods of conceiving, variable approach, and individual methods of prescribing and diagnosing make every doctor different. If there is any similarity between the doctors, it is the basic intelligence by dint of which you have become homoeopaths. Memory has direct relation with the intelligence. According to an article published in journal ‘Nature’, Bernard Devlin concluded that genes account for 48 percent of intelligence and 52 percent of it is through combining of parental care, environment and education. A homoeopath is no exception. His intelligence is both inherited or acquired intelligence. In his acquired intelligence he four qualities that make him/her possess a good personal MM.

These four make a good personal MM in an individual.

Objectivity – It means not getting influenced by personal opinion of others. For example if a doctor asks another doctor as to what potency he uses while giving nitric acid, and if the reply is 200 is the best, the enquiring doctor should not get influenced by this and start using 200 potency in his or her prescription.

Comprehension– It means understanding with intelligence. For example, we must correctly know the origin of the medicine so that its main features are known. If the medicine belongs to vegetable kingdom, it effect on the metabolism would be sober or mild, if it from mineral kingdom, the effect on metabolism would be hard and if it from from animal kingdom, its effect would be destructive if given wrongly. This is understanding the medicine or comprehension. 

Reasoning – It means motive, cause or justification. Reasoning is not causation. It is justification. If we give a medicine, we must have at least one strong symptoms of the medicine which could justify the prescription.

Judgment – It is authoritative opinion or a decision. Suppose we have selected three medicines in a case and now one is to be given to the patient. We have to see which medicines fit most to the symptom of the patient. This is decision or judgment.

“Judgment” is key driver in personal MM. Here is a short story to prove the point.

There were three medical students going out on the road. They saw a man walking ahead of them. He was limping, walking slowly and at times, stopping. They were final year students. The first student asked the other two to guess as to what was the reason for this man’s unnatural gait. The second student guessed. ‘It is some injury on his knee or leg that has changed his gait’. The third student guessed, ‘no, it is hydrocele that has changed his pace’. Now was the turn of first student. He finally declared, ‘well both of you are wrong. I can bet that it is due to piles’. They could not reach any decision and approached the man who was limping and walking. They told him that they were medical students and wanted to know the reason as to why he was limping. ‘What have all of you guessed?’ said the stranger. The students told him the conclusions of injury, hydrocele and piles. The stranger laughed and said, ‘well, all of you have failed to guess my problem’. In fact, I could not control my stools and have spoiled my pants. Now I am trying to balance the stool so that it does not fall out till I reach my home’.

So, if judgment of selection of remedy is right, everything goes right. A doctor who judges best in his selection of remedy is best homoeopath

How to build good Judgment
Judgment requires knowing all the three medicines we have selected in a case. For knowing we have study the medicines individually. For this we have to select some books to study. We should have two books with us to study medicines. ‘Leaders’ of Nash and Allen’s Keynotes. Select 40-50 medicines and read them in Nash every day turn by turn. Now take Allen keynotes and start reading the same medicines every day. It is a long term plan. Continue it and one day you will master those medicines. You can now do acute –prescribing without the help of any book. Better continue study of medicine as and when you get time in between gap of two patients. Good judgment comes through study of medicines. One must snatch some time each day to study medicines. This would strengthen our memory in our personal MM.

Group of medicines and personal MM
It is impossible for any one to memorize the symptoms of all the medicines in our book MM. But beauty is that we all remember a group of remedies related to a disease. If I ask a doctor as to what is the group of medicines that cure piles, he/she can answer with number of medicines without any discomfort or referring to the MM.  Now if I ask another doctor the same question, he/she will also answer but with a difference.

There will be difference of medicines in both the cases. For example one may include aesculus and the other may exclude it. Some may cite five medicines; some may name ten medicines for piles. Everyone has a different set up of memory even for disease-wise group of medicines. This also means that everyone has been taught differently in different institutes. Their teachers have been different having different views about remedies. Moreover, the student has individual capacity to conceive according to his/her ability. This difference of conception is not knowledge received from the teacher but one’s personal capacity to absorb. Memory is sharp in recollecting group of medicines. It means we have stored it in our personal MM. We have faded memory of symptoms of each medicine and hence it is not in our personal MM until we experience it in our cases. Memory developed during studies does not make personal MM but it is made during practice after experience. All life lessons are not learnt in colleges, life teaches them everywhere.

What influences or does not influence Personal MM?
Symptoms that influence Personal MM are pains, old and new symptoms, resembling symptoms, obsolete symptoms and additional symptoms. Medicines that influence personal MM are favorite medicines and theory of single medicine. Features that do not influence Personal MM are potency decision, specific medicines and frequency/repetition of medicines. Now we shall discuss the above one by one.

Understanding symptom
Reading the symptoms of medicine in the book is not understanding symptoms. We interpret them in different ways individually. I remembered to had started my thesis of ‘symptomology in Homoeopathy’ in HMD with these lines ‘Your dealings and behavior is your introduction’. From how one deals and behaves we can find out the symptoms. One person can be defined in tens of interpretations. Our most difficult job is to compare symptoms of body with symptoms of medicines. A patient has few physical and narrated symptoms but the MM book has many more symptoms as proved by the prover of remedy. The prover might have different constitution than that of our patient. We are trained to resort to totality of symptoms. Patient’s totality is not totality of symptoms in book MM. What should we do? Even if few symptoms of the patient bear similarity from total symptoms of MM, medicine is supposed to work and will work in majority of cases.

What matters for us is individuality. There are many ways to ascertain individuality. I am giving two major interpretations as per my personal MM recording in my subconscious.

  • A patient who is in a hurry, does not wait for his turn, wants to return to his home/office will give minimum symptoms to doctor.
  • A patient whose hair are not combed or had not a timely hair cut, has not shaven, has not used hair dye since long, his shoes are not polished, nails are not cut will give maximum symptoms to doctor

Record this in your personal MM.

New and old symptom
The symptoms of medicines written in MM are old enough. The reason is that they do not coincide with present day era. We believe in what we read.  Our minds are prejudiced that whatever is written in MM is authentic. Do we remember that the era in which these books were written and medicines were proved has dramatically changed? Now we are in progressive era. Phones have become wireless. Distant viewing and conferences are viable. Mobile phones and internet has given us opportunity to widen our thinking. Science has reached a new height but our medicines have not attained new values or changes. What is the impact of this?

Our speakers in seminars show the old versions of medicine and its application. The repertization of a case is from old repertory. Has any speaker given us clue of some new symptom of a medicine and by dint of which has he solved any case. Speakers are shy to tell what they achieved in experience with medicine. Success with old symptoms written in MM is not an achievement.

There should be entry of new symptoms in personal MM if experienced. How? Here is what we should do.

Obsolete symptoms
How old symptoms of medicines are to be replaced by new symptoms? New entry of medicines is upon proving new symptoms. This is not an overnight job. But we have some obsolete symptoms in our books which can be erased. Sometimes the given symptoms of a medicine in book MM become obsolete and still the medicine works. This is the beauty.

Let us have an example. General uncleanliness of the body is an important symptom of capsicum. When a patient with capsicum symptoms like bleeding piles, thirst after stool, cough with pain in distant part of body etc. is enquired about his general cleanliness of body, the patient refuses to be unclean. Naturally we have not enquired directly about his uncleanliness and simply wanted to know whether he takes regular baths or whether he likes to clean the body if it gets dirty due to pollution or taking part in some games etc. Still the patient would not agree that he allows his body to remain unclean. He may also say that he takes bath daily. If the patient tells a lie, we can observe his clothes, his palms, nails and its cleanliness. Amazing, we find they are also clean. The reason is that he is compelled to be a clean – personality to his office mates including women. He is a tem leader in a multinational company. So his profession is not allowing him to be unclean.

Now there is another great symptom of capsicum- the home sickness. The patient says he is not homesick. The reason is his laptop. He goes to ‘skype’ and enjoys talking with his family and seeing them too.

This anomaly confuses us. All the symptoms of capsicum are there except ‘uncleanliess and homesickness’. We ignore these symptoms and give capsicum basing upon other symptoms. And the patient gets well. This has been experienced by many of us. You must have experienced such obsolete symptoms in many remedies. So, old symptoms written in MM do change with the change in life style of people. The era has changed when the remedy was proved and the relevant symptoms have become obsolete.  

Now capsicum in my experience becomes innovative medicine. This is our ‘additional knowledge’ and can be stored in our personal MM. Since you have experienced it, this makes automatic entry in our memory of personal MM.

Pain, a great symptom.
While discussing about group of medicines, we talked about how group of medicines over the name of disease is easy to recollect. We talked about piles. On the name of this disease, one doctor prescribes aesculus, the other prefers nitric acid to the same patient with same symptoms. Why? Again question of understanding symptom

There is severe pain in rectum with prolapse after stool. It is in both aesculus and nitric acid. This is what the patient tells. He would not tell pain as sensation of full of sticks as in aesculus. He will not tell violent ‘cutting’ pain as in nitric acid. He will say, ‘ Bahut zayada dard hai doctor sahib’. Even if we insist to tell the type of pain, he will not speak the language of MM. There are  118 types of pains like stitching, throbbing, cutting, piercing, digging, drawing, griping, gnawing, crushing, crippling etc. as coined by  Boenghausen. How many of us give a remedy on description of pains? None. We take help of its locality and modality. Pain is a great symptom provided it is identified by modality and locality.

Understanding pains.
Let us return to aesculus and nitric acid. Suppose the patient tells that he has pain and prolapse of rectum.

This is aesculus. But if the pain is prolonged and with prolapse. It is N-acid. If the patient tells that his pains are prolonged, only then one can judge but this is not possible. On the question of pains best is to enquire about bleeding and non-bleeding nature of piles. Both the remedies have bleeding. Now ask if the bleeding is less or profuse and also about tolerance of pain. This can be easily told by the patient. In aesculus, the bleeding would be very less due to strain on the haemmoriodal veins and pain would be severe. In nitric acid, the bleeding would be profuse due to fissures but pain could be tolerated. When discharges occur, the pain gets less.

This experience of asking to the point questions to the patient comes after experience. This ‘to the point’ quarry should be recorded in our personal MM.

Favored or favorite medicines
Some times the symptoms of a medicine go direct to our mind and appeal us much. This is the reason many of us have a favorable medicine which we prescribe frequently even if the totality of symptoms is not there. How this ‘liking’ is developed. For this we have to return to Book MM. During the frequent referring of MM, we start relying on authenticity of  some medicine especially when we have tasted success with it in our cases. Now what happens when success is tasted? We start liking this very medicine. When we like something, we favor its use even when the totality of symptoms do not warrant for its use. This is against aphor.257 which forbids favoritism. It also says that it is found to have good results. In that case the doctor misses use of rare remedies that may have been appropriate to use.

If you tell a boy not to pluck mangoes from the garden, he will do it to have taste of mangoes. This is natural. We know use of favorite medicine is prohibited, we use it since we taste success. We do it in acute cases only and our reputation increases in success. Today is the period of commercialism. If you do not believe in it, do not give favorite remedies.  If we go on getting success in our cases, we do enter in our Personal MM. If the success is followed by failures, it should be erased from personal MM.

Single remedy
These days we hear about use of single remedy in our seminars. You have heard many homoeopaths in seminars showing complete cure of a long standing disease by single dose of a remedy of 30 or 200 potency. In support they produce documents, slides and videos of a patient. Everybody has right to claim  success. Audience has right to encourage. Rarely such claims are challenged. Truth is something else. Single dose of a remedy rarely cures a long standing disease. The surprise is that we see all familiar faces in the seminars time and again. How is it that they only get success with single dose and not others?

As per aphor 280 of Organon, if a single dose is giving beneficial results, it is to be continued in gradually ascending magnitude. Again aphor 281 says that if the disease exists, high potency should be given. This aspect is neglected in many seminars. As per aphor 171, in non-veneral chronic diseases that arise from psora, several anti-psoric remedies are to be given one after the other to cover remaining symptoms of the disease.

Single dose
On single dose, I quote E.B. Nash, ‘Rarely will a case come out so clearly that the cure can be performed with one remedy. Successions of remedies are needed and here is where the so-called complementary remedies are skillfully applied.  About chronic and acute diseases, he says, ‘The old saying used to be and is also sanctioned by Hahnemann that acute diseases generally tend to recover but not the chronic diseases. There is much truth in it. None but the true homoeopathic physician realizes the importance of thoroughly taking and working out such cases. There is always need to give two or more medicines in chronic cases. Rarely does one remedy works in rare cases’. How can single remedy go on working when its action of duration has ended. You may not agree with me but think over it.

Giving single, two or multiple remedies are not recorded in personal MM since the choice is variable. Choice is upon experience. We shall talk about this experience later.

Resembling symptoms
Resembling symptoms are mostly found in medicines having drug affinities of each  considered medicine. Affinity is relationship. Let us consider symptoms of Ant-C. You will recall them from book MM such as loss of appetite, desire for pickles, headache on taking bath, thickly coated white tongue, alternate diarrhea and constipation etc. and so on. We shall take up resembling symptoms of AC in sul, puls and ipec. Although ars, brom, bismuth, hep, sep and merc have also some resembling symptoms with AC. Lips are dry in all these medicines. No stools alike in all these medicines. White coated tongue is in all the four. Two of them also have resembling symptoms. Bad smell in nose is in puls and sul. Loss of appetite is in AC and sulpher. We identify them by differences . Sulpher has white tongue but its tip is red. Puls has white tongue with mucous. In modality, both AC and puls are worse from heat and evening. They are better in open air. AC is better during rest but puls is better in motion. Resembling symptoms confuse and confusions do not get entry in our personal MM. Best is to consult MM on your table or computer for solving resembling symptom- confusion 

Additional symptoms
Additional symptom of a remedy is what we experience during practice and what is not written in book MM. When found, it goes direct to the personal MM. This is a key point of personal MM. See the example. By mistake, once I gave AC to a patient who had cracking in the middle of lower lip (Puls).  AC has lips cracking at the corners of mouth. But the beauty is that the patient got cured with AC. Now what is the impact of such an anomaly?

I tasted success with AC and  started giving AC to all my patients of lips cracking irrespective of different locality.

This means that AC has an ‘additional’ symptom of lips which is  cracking in the centre. This has gone into my personal MM but it can change if the forthcoming experiences fails in curing cracks in centre of lips. In the same way you might have experienced additional symptoms of a remedy. It is indeed recorded in your personal MM.

Additional knowledge
We discussed that obsolete symptom of a medicine is our additional knowledge. Now see another example.

Suppose a patient has aggravation of pains on movement (bryonia, nux and ars.). Another patient is having amelioration of pains on movement (rhus tox, puls, lyco and ferrum).

One fine morning we get a patient who  tells that he has pains that aggravate on movement and on rest. What do we give? We think of Phytolleca that has symptoms in between bryonia and rhus tox.  But see how medicines defy our conceived rules due to this experience. During my practice of more than three decades, I have cured such patients with RT. Whenever there is little doubt about narration by the patient, I do not hesitate to break rules and give both RT and Bry. RT 200/TDS and BRY 200/HS. The relief comes after 3 days after which it is replaced by SL. The theory of single remedy is good but at times, I prefer to violate the rules. After all cure is our primary aim. I am here to tell my opinion. But you are free to have your different opinion.

A case of additional knowledge
When I was writing this talk on my computer, a patient Mr. A , m/52 years of Faridabad consulted me in my clinic. Following is his history as recorded on page five of my patient document dtd 20.10.11-

20.10.11- Pain left shoulder and left side of neck when moving the head sidewise and pain during rest at night as well. He was on allopathic pain killers since a week but no relief. Occipital pain <thinking and pain< lying on occipit, constipation normal, Thirst normal, salt, sweet, desire normal. He was given RT200/tds and Bry200/hs for three days.  25.10.11- Relief of pain. Medicines discarded. He was given S.L. in place.

After three days he returned to thank me. Additional knowledge makes a good entry in our Personal MM.

Dil se dawa dijiye
Let us ponder over the justification of giving both RT and BRY. We have another medicine for the above symptoms. It is Paris quardrifolia. It has symptom of thinking aggravates. Thinking aggravates the pain has 21 remedies but Bry and RT are not in this list. If we go by symptom, lying on occipit aggravates the pain, it has ten remedies. Bry is there but RT is not in the list. (Reference: Phatak’s repertory). Not once but many a times my personal MM has proved success in such cases. In many cases location and modality works but ignoring all such parameters, best is to give the medicines that appeal you much as per your personal MM. Rare remedy occasionally works, not always.

‘Voh dawa deejiye jo dil kehta ho’, is an old saying. ‘Kabhi kabhi dimag se dil achha kaam karta hai’. You will find success with this type of prescribing provided your personal MM also permits. Permission is always based upon your experience. Personal MM is ‘Dil se’ as well.

Itching to innovate
Every one has some type of itch. Some itch for success, some for money and some for innovations. Itching for innovation is what we, in homoeopathy, need. We are having many experiences with medicines. Experience the medicine and then attempting to achieve something is ‘itch’. To do something new is ‘itch’. Itch or ‘khujali’ is essentially with each one of us. ‘Khujli and chughli’ na bhi chaho to ho jati hai’.  We do it but we do not reveal it. Years pass by and we go on doing this ‘khujli’ of finding additional and new symptoms of medicines. We store all this itch in our personal MM. Advantage is that with this new itch, we do not need consulting any MM for acute diseases. Many of us are not consulting any book MM for prescribing in acute cases. Let me reveal the type of itch I have innovated during my experience time. Your itch during practice is valuable and you must reveal the same in scientific sessions of monthly meetings so that every one gains by your experience.

Itch –my experience
In almost seventy percent of cases of vertigo, I have been prescribing conium 30 without going in for modalities. Conium is my first medicine. Some one from you must have read my article in vital informer a few years back. It was a case of a person who came to my clinic with the body support of his wife. He could not walk independently. He had vertigo on standing, on starting to move and on walking. His cat scan and other tests were normal and  he was in the hospital for a day before coming to me. He was given conium 30, six doses in a day and next day he returned to the clinic driving his car by himself. Some times you experience miraculous results of a remedy and it is here that you start believing in its efficiency. Conium has vertigo on lying down and when turning over in bed. After this case and later in many cases I witnessed the wonderful results of conium. Now I give conium to all vertigo cases as my first medicine. Very rarely it fails. Try it and you will find the truth.

So conium is my  ‘khujali’  medicine for vertigo. One thing you must remember that before giving conium to all vertigo patients, you must check his blood pressure. If it is on lower side, do not hesitate to give conium. It will work wonderfully.

Similarly, in all cases of constipation, I give nux and sulpher to start with. Nux three times a day and sulpher in the morning. This works well in the first week but does not cure constipation completely. Now I change the medicine on changed symptoms. In all cases of patients who have taken lot of allopathic drugs, I give Nux as first medicine. Nux is a clear case of ‘khujali’ for most of us and many of us give it.  The beauty of this type of ‘khujali’ is that it is not written in any MM and still we follow it. It is because some senior writers have mentioned this after they experienced success in it. If I am not wrong, the pioneers of such an anomaly were E.B. Nash, R.B. Bishambhar Das, R.P. Chatterjee and J.N. Shingle. Nux is now stored in my personal MM as antidote of allopathic drugging.

I again repeat that it is my itch and you need not care about this itch. You may have difference of opinion over this issue. Itch is the primary entry in our personal MM since it is earned by experience. Experience is what personal MM is made of. 

Potency decision –not in personal MM
Suppose we give Natrum mur 30 to a patient for sun headache and it does not work, this failure is not recorded in our personal MM but a faded memory remains for some days. Mostly we register success in cases more in personal MM. Within these ‘some’ days, if  some other patient reports same problem, the failure of Natrum mur 30 comes back to mind. This time we give NM 200 and the case gets cured. Now this success is recorded in our personal MM with a bang. We come to  know  NM 200 potency works well instead of 30 potency for sun headache. Why this decision? Because nothing succeeds like success. But the fact remains that potency decision is a staggering decision depending upon the type of patient, nature of disease, age and vitality of patient besides your very liking. Hence potency does not get registered in our personal MM. 

Specific medicines-not in personal MM
Like potencies, Specific medicines are not entered in our personal MM. The method of giving specific disease- wise medicines instead of adhering to  totality of symptoms is very much common for all of us.

For example: If Stool slips back, we give silicea. Ineffectual urging for stool is Nux, Lyco, or sul. Even soft stool needs effort to expel, it is Alumina. Slender long stool expelled with difficulty is Phos. And so on we prescribe specific  medicines.

Busy doctors who have a long queue of patients waiting outside their clinics cannot resist prescribing  specific medicine for specific symptoms of the kind as mentioned above. It might be their first medicine before going in for detailed treatment.  Their success is not granted and hence Specific medicines are not included in personal MM.

Frequency/repetitions
Frequency is not written clearly against each medicine in book MM except a few medicines like belladona and aconite. Some deep medicines do not require repetitions. There are many conceptions we have learnt from books.

From experience we have more of notions. For example, Lyco when given in single dose works better than nux given three or four times a day. Similarly we find that among burners, sulpher  given in single dose works better than arsenic or apis in frequent doses. Such experienced facts are stored in personal MM after we  experiment with it on our patients. Generally we do not fare well in using any stable method and hence do variations in frequency and repetitions.

About repetition, there is a general rule. In acute cases, doses should be repeated every 1,2,3 or 4 hours. In fatal illness, every 10, 15 and 20 minutes, the potency being increased after two unsuccessful doses and in chronic cases, once or twice a week.

Respected medicines
We have very respectable Indian medicines in the MM that could be used on patients provided we read their culture carefully. We have Neem, Jamun, Arjun chhal, Brahami, Amla, Babool, Peepal, Barh, Ghrit Kumari and Kalmegh etc.in India. They are respectable plants religiously and people offer prayers to many of them.  Dr. P. C. Majumdar, A.C. Bhaduri,D.N. Roy, S.C. Ghosh, K.K. Bhattacharya and others of Bengal and Assam proved these plants and called them respectable medicines. (K.N. Basu’s book Bhartiya Aushdhawali ka sankshipt Bheshaj Tatava’, (HahnemannPublishing House, Kolkatta)

Homoeopaths in Bengal use these herbal medicines. We know them by Latin names. All herbal medicines of Indian origin are respectable and most of us do not use them. Once we start using them, we can reach a new height of achievement. There is need for entry of Indian drugs in our personal MM.

Spice in your life
Not only Homoeopathy, every Profession or business becomes boring after some years. A stagnation point comes when doctor feels like leaving the profession since it becomes a routine. It turns monotonous. At this juncture, one has to find ways to bring spice in profession. Variety is in many ways.

In the clinic, change setup of furniture, color of curtains or wall pictures. Introduce computer. Steve Jobs says on computers, ‘you go to your TV to turn the brain off-you go to the computer when you want to turn your brain on’.

If you are coming to clinic from your residence on one fixed route, change it. Come by other alternative route for some days. If you are driving car, go to clinic on bike. If you are not having any weekly off, start it or at least make one holiday essential on last day of month. People are out of budget on last day of month and visit doctors less. This way you can divert your time to your family. Or you can invent many ways to enjoy and break the monotony in the profession.

In clinic practice, you have better methods to invent. First week, start giving medicines in thirty potency to all your patients. Watch the results and record the success rate. Next week, start giving medicines in 200 potency to all your patients. Again record the results and the success rate.

Similarly bring variation in medicines. First fortnight, give single medicine to all your patients.  Next fortnight, give two remedies at a time. Third fortnight, give multiple remedies at a time. Compare which method brought you most of success. Even if you have not decided which method is best, you will know the results of using different methods. Innovation or creative ideas come when experiments are conducted. Such derived at conclusions would enhance entries in our personal MM. 

Conclusion
Before concluding I would pay my respects to all senior homoeopaths and my colleagues here. It is the experience that speaks truth. Experience is what is written in personal MM. Personal MM is practical, creative and innovative. One must possess this and with pride it should be revealed to all. Late Dr. Rastogi had this quality. He had a vast personal MM from which he used to quote in his speeches.  I remember he had talked from this SDHA platform about rare remedies without referring to any documents. It was his unique collection of memory.

Please recall our last Kent lectures seminar. We had enjoyable acquaintance and encounter with Dr. S. Haque whose tips were most favoured one by the audience. These tips are always floating in his mind. He has a big volume of tips based upon his personal MM. Such doctors become very popular since their tips work as well. I remember that one of the organizer of conference hall wanted some medicine for stiffness and pain of his knees. I was talking with Dr. Haque then. He collected a piece of paper and a pen to write some medicines. This was without any help of book or any enquiry of pains. Naturally he has deep knowledge lying in his personal MM.

Be your own boss in your clinic to learn from within you which is reverence to formulating your personal MM. You are the learner, the guide, and the caretaker. Believe in your capacity and what ever you do will be success.

Thank you.

Abstract of the talk and discussions on 13.11.11 in conference hall of Nehru Homoeopathic Medical College, New Delhi with honored members of South Delhi Homoeopathic Association.(SDHA).

This article is open to criticism – Readers are requested to post their comments and suggestions here

State Govts told to shut down 14 homoeopathy colleges

In a delayed move, the Health Ministry has directed the State Governments to shut down 14 homoeopathy colleges in their respective areas for providing substandard education.

The move came after the Ministry found that the institutes, despite being given an opportunity to upgrade their infrastructure, did not do so thus putting the future of hundreds of students in jeopardy.

“Though they were given sufficient time to improve their infrastructure including faculty they failed to comply. Now, we have asked the State Governments to take action against their respective defaulter colleges within next three months or their licence will stand cancelled automatically,” said a senior Health Ministry official.

These institutes are situated across states like Bihar, Jharkhand, Madhya Pradesh and Rajasthan among others.

Interestingly, just six months ago, the Ministry had brushed aside the recommendations of the Central Council for Homeopathy (CCH) which had called for closure of these institutes for acute paucity of teaching staff and other infrastructure as prescribed in the rules.

“But MoS for Health S Gandhiselvan preferred to give them another chance for the academic year 2011-12,” sources pointed out. However, the amnesty failed to deliver results as fresh inspections by the Ministry found that these colleges remained short of meeting minimum educational standards.

The Ministry has now also asked the CCH to conduct a survey, by even engaging government teachers as inspectors, of all the homeopathy medical colleges across the country every year.

Source : http://dailypioneer.com/nation/23261-state-govts-told-to-shut-down-14-errant-homoeopathy-colleges.html

Four Common Meds Send Thousands of Seniors to Hospital: CDC

Blood thinner, aspirin, insulin and oral diabetes drugs account for two-thirds of nearly 100,000 hospitalizations.

An estimated 100,000 older Americans are hospitalized for adverse drug reactions yearly, and most of those emergencies stem from four common medications, a new study finds.

The four types of medication — two for diabetes and two blood-thinning agents — account for two-thirds of those drug-related emergency hospitalizations.

“Of the thousands of medications available to older patients, a small group of blood thinners and diabetes medications caused a high proportion of emergency hospitalizations for adverse drug events among elderly Americans,” said lead study author Dr. Daniel Budnitz, director of the U.S. Centers for Disease Control and Prevention’s medication safety program.

Medications previously designated “high-risk” were implicated in only 1.2 percent of hospitalizations, the study found.

Working with a nationally representative database, CDC researchers identified more than 5,000 cases of drug-related adverse events that occurred among people aged 65 and older from 2007 to 2009 and used that to make their estimates for the whole population.

Nearly half (48 percent) of the hospitalizations occurred among adults 80 and up, according to the study, published in the Nov. 24 issue of the New England Journal of Medicine. Nearly two-thirds (66 percent) were the result of unintentional overdoses.

The four medications, used alone or together, most often cited:

  • The blood thinning medication warfarin (Coumadin, Jantoven), which is used to treat blood clots, was involved in 33 percent of emergency hospitalizations.
  • Insulin, used to control blood sugar in diabetes patients, was involved in 14 percent of cases.
  • Antiplatelet drugs such as aspirin and clopidogrel (Plavix), which are used to prevent blood clots, were involved in 13 percent of cases.
  • Oral hypoglycemic agents — diabetes medications taken by mouth — were involved in 11 percent of cases.
  • With antiplatelet or blood thinning drugs, bleeding was the main problem. For insulin and other diabetes medications, about two-thirds of cases involved changes in mental status such as confusion, loss of consciousness or seizures.

“These are important findings,” said Dr. Michael Steinman, an associate professor of medicine in the division of geriatrics at the University of California, San Francisco, who is familiar with the research. “This study highlights a few key issues that are important for doctors and patients to be aware of. The first is that serious adverse reactions to drugs are common among older people, particularly among people over 80. But even those 65 and older are at substantial risk of having an adverse effect from their drugs.”

One challenge for doctors and patients is that the medications may be necessary, Budnitz said.

“These are often critical medicines for patients’ health,” he said. “Patients who are on these medicines should tell all their doctors what they are taking and work together with their doctors and pharmacist to make sure that they are taking these medicines correctly.”

Among U.S. adults aged 65 and up, 40 percent take five to nine medications and 18 percent take 10 or more, according to the study authors. Prior research has also found that older adults are nearly seven times more likely than younger people to have an adverse drug event that requires hospitalization. “As most people age, there often are changes in how their kidneys, liver, heart, and other organs work that can make them more susceptible to adverse drug events,” Budnitz said.

And though taking lots of pills raises safety issues, in 82 percent of cases the treating physician attributed the overdose to a single drug, Budnitz added.

To reduce risks, Steinman said doctors and patients need to discuss whether the drug is truly necessary. For people with very high blood pressure or blood sugar, “the answer is almost always ‘yes,’ you should treat it,” Steinman said. “But if you have only mildly elevated blood pressure or blood sugar, the benefits of treating it versus the harms start to shift. Do these drugs really provide enough benefit that it’s worth taking them?”

SOURCES: Daniel Budnitz, M.D., M.P.H., director, medication safety program, U.S. Centers for Disease Control and Prevention; Michael Steinman, M.D., associate professor, medicine, division of geriatrics, University of California, San Francisco, and San Francisco VA Medical Center; Nov. 24, 2011, New England Journal of Medicine

Source : http://www.nlm.nih.gov/medlineplus/news/fullstory_119037.html

DEC Guidelines for offering Online Programmes

The following seven key areas are being identified and described as the requirements for ensuring quality of teaching and learning in Online Education.

ORGANIZATIONAL STRUCTURE
The organizational structure of the institution willing to offer Online Programmes should be according to the DEC NORMS FOR ENSURING QUALITY IN OPEN AND DISTANCE LEARNING (ODL) SYSTEM

However, in addition there should be the following human resource support:

  • A Person in-charge of Online Programmes to coordinate the programmes, human resources and technology infrastructure.  In Open Universities, this person may be designated as Director (Online Programmes).
  • There should be 1-2 technical persons to administer the technology and provide instructional design support on the LMS.
  • Adequate staff should be there to develop e-content (if in-house development is carried out).  In case of outsourcing of e-content development, sufficient project managers may be appointed to liase with the teachers and the outsourced agency.
  • Online Learner Help Desk (24X7) in the form of Call Centre may be there. 

PLANNING AND DEVELOPMENT OF ACADEMIC PROGRAMMES – COURSEWARE

  • Planning a suitable online courseware format
  • Selection of appropriate authoring tools and relevant hardware (Server, LMS platform, etc.);
  • The online programme should emanate from/ be a part of the perspective plan;
  • Development of online programmes should go through three stages namely: Programme formulation, Instructional Design and  Development of courseware.

3. DESIGN OF E-CONTENT

  • Courseware developed should be in self-learning format having adequate hyperlinks pointing to relevant resources and could be in the form of a media mix comprising of text, audio, video animations, etc.
  • Production of courseware may be outsourced to professional agencies in case in- house facilities are not available, Also adequate training should be given to faculty on design and development of E- content.
  • Relevant approach may be followed with provision of multiple entry/ exit points, leading from lower to higher qualifications
  • Curriculum should be pitched at the level of the programme i.e. certificate/diploma/UG/PG/etc.
  • UGC model curriculum may be a point of reference, however, to meet the specific needs of learners and demands of the society (at large) is recommended
  • Expert Committees, with experts drawn from industry as well, should be constituted for the development of curriculum and the design of online programme
  • The programme should be approved by Statutory bodies of the University
  • Nomenclature of the degrees must be as per UGC guidelines
  • Courseware  should be uploaded before the launch of programme;
  • Courseware should be periodically updated;
  • Study input for each programme should be well defined in terms of credits (1 credit =30 study hours) depending on the level of the programme as given in Table1
  • Courseware should be available online 24X7  
  • E-content could be in the form of text, audio, video and animation.  The LMS used should integrate all learning objects.
  • Credit value of the programme to determine the number of units Online counseling forum with chat area for interacting with faculty and peers, assessment and evaluation through assignments as proposed   
  •  Online Courseware should follow the principles of self learning materials.

4. STUDENT ADMISSION

  • Online admission facility may be provided;
  • Prospectus and application form containing criteria for admission, fee and duration should be available online;
  • Online deposit of student fee and generation of fee receipt for the learner for his/her records may be made available;
  • Issue of personal passwords to all learners.

5. LEARNER SUPPORT SERVICES

  • Organized learner support through Online chat rooms, email facility, bulletin boards, video conferencing with the faculty and university Administration;
  • Help Desk to provide both academic and administrative support services, such as dissemination of information, counseling and tutoring services, vocational guidance, multimedia support, library services,  evaluation of assignments, feedback, guidance of project work, organization of  seminars, conduct of online examinations, etc.;
  • Information of available support services should be prominently displayed /flashed on the website;
  • The University/ Institution should also cater to the special needs and requirements of diverse online learner groups including women, physically challenged, economically weaker sections of the society and other deprived and denied groups by adopting a diversified delivery approach
  • Institution to make arrangements for digital library facility to be accessed by enrolled learners
  • Online tutors be provided to handle chat and discussion forum online
  • Adequate training should be given to online tutors
  • The Help Desk Centre would be available to learners 24X7 to solve technical and administrative problems
  • Institution  to maintain online records pertaining to:
  • Tutor- Counsellors and Staff
  • Students Registered
  • Counselling Sessions
  • Assignments Received, Evaluated and Returned
  • Student Queries
  • Administration and Finance
  • Student feedback about the course, delivery, counsellor/teacher, facilities, environments, etc.
  • Access to the above data should be restricted to the University/ Institution Administration.  Learner data should not be shared without permission of the Vice Chancellor
  • A time frame policy should be in place for replying to the student queries within the stipulated time
  • Periodic feedback to be obtained from the online students related to quality of courseware, quality of tutor support and quality of administrative support
  • Periodic webinars on contemporary or significant topics should be conducted by the institution
  • Information about such webinars should be displayed on the website and e-mailed to all the concerned faculty and learners
  • Such webinars would be free of cost for registered students of the institution.  Fee may be charged from those if they are interested to participate
  • The tutor student ratio should not exceed 1:20 in a semester/cycle for discussion forum and chat session
  • Institution should get the assignments evaluated within maximum 4 weeks from the date of receipt and provide feedback to the learners highlighting the deficiencies and strengths.

6. LEARNER ASSESSMENT AND EVALUATION

  • Assessment should be both formative as well as summative.
  • Formative assessment should be through online computer marked assessment, tutor marked assignments projects, discussion forum, and webinars linked to the objectives and desired competencies / skills or expected learning outcomes.
  • Turn around time for providing feedback on performance to the learners should not exceed 2 weeks and definitely before the terminal exam commences.
  • Formative assessment should contribute to 25% to 30% weightage in the overall assessment;
  • Summative assessment should be in the form of online exams for or any other comprehensive method of assessment
  • Students should be able to submit tutor marked assignments online and receive feedback within reasonable time
  • Formative assessment descriptive and objective and application oriented contributing to 70%-75% in the overall assessment.  This may be conducted online in a proctored system
  • Tools of assessment should be prepared by empanelled experts;
  • All tools of assessment should be moderated before being administered to ensure reliability and validity and standards as per the level of the programme
  • Term-end examination should be held twice a year and the timetable should be circulated to the learners 3 months in advance and put on the website and e-mailed to all the learners
  • Accurate compilation/ tabulation of grades/ marks by the exam unit for each learner, course wise need be maintained
  • Evaluation of term end exam papers, assignments, projects etc. should be done by empanelled evaluators, it should not be outsourced
  • Time schedules should be adhered to particularly in the declaration of results within a period of 4 weeks.
  • Dispatch of provisional certificates to learners immediately after declaration of results
  • Timely award of Degrees or Diplomas

7. Technology Infrastructure and Use 

  • Every University/ Institution should have its own Website ;
  • All the relevant information, about various, courses, fee structure,     rules,  Examination, etc. must be available on the Website;
  • The institution  should inform the prospective learners about the technical requirements to join an online programme;
  • The institution should create access centres to facilitate easy access to internet
  • The institution should have access to a LMS installed on their own server or outsourced from other service providers
  • The institution should provide an e-mail account to all enrolled learners through its institutional mail server
  • There should be appropriate bandwidth available to allow easy access of the website/LMS to the learners
  • There should be a user policy regarding use of the institutional website/ LMS to prevent misuse, and all users must agree to the policy
  • User password shall be protected by the institution, and only the user should be able to change it
  • IP capturing may be considered to ensure security
  • Users (both learners and teaches) may be provided regular orientation on technology use

Electronic service delivery Bill to be placed before Cabinet

The Electronic Service Delivery Bill – which mandates all government organisations to deliver public services through electronic mode – will be sent for Cabinet approval before the Winter session of Parliament.

This was stated by the IT and Communications Minister, Mr Kapil Sibal, at the Economic Editors Conference here.

The public services delivered through the electronic mode would include receipt of forms and applications, issue of any licenses, permits, certificates, or approvals and the receipt or payment of money, according to the draft Bill.

Time frame
The Bill proposes a five-year timeframe for transitioning to the e-delivery mode. The cut-off date is extendable by up to another three years.

It also says that in 180 days of the Bill coming into effect, the individual Government agencies will have to list out the public services that are to be delivered through the electronic mode, and indicate the timeline for e-enabling each of these service. They will also have to outline the framework for grievance redressal mechanism in case of user complaints.

“We are in the process of drafting a Public Service Delivery Bill which hopefully will go to the Cabinet before the Winter Session…If possible, we will try and introduce it in the Winter Session of the Parliament,” Mr Sibal said.

Draft electronics policy
The Minister also stressed on the need to encourage electronics manufacturing in the country. Mr Sibal, earlier this month, had released a draft electronics policy that talked of incentives to create over 200 electronics clusters, and a ten year stable tax regime for electronics design and manufacturing.

“The electronics manufacturing sector needs to be given an impetus…If it does not happen, it will upset all our technology plans,” he said. India cannot afford to be in a situation where electronics imports exceed oil imports, he pointed out.

“Electronics industry will be at the heart of everything…If we do not prepare ourselves (to address the situation), the electronics import bill will be $400 billion by 2020,” he added.

Links

sciatica

Recommendations for the Management of Neuropathic Pain

sciaticaRecommendations for the Management of Neuropathic Pain Associated With Peripheral Nerve Entrapment.

Peripheral nerve entrapment is often associated with neuropathic pain symptoms. These recommendations – an update of the recommendations first published in 20051—describe the management of some of the more common causes of neuropathic pain due to peripheral nerve entrapment. The recommendations are structured by nerve level as follows:

  • Root level
    – Cervical radiculopathy
    – Lumbar radiculopathy
    Less common causes
    – Brachial plexus injury
    – Thoracic outlet syndrome
  • Peripheral nerve level
    – Carpal tunnel syndrome
    – Cubital tunnel syndrome
    – Other sites
    Less common cause
    – Radial tunnel syndrome.

Treatment of neuropathic pain associated with peripheral nerve entrapment differs from other neuropathic pain conditions, such as post-herpetic neuralgia, painful diabetic neu­ropathy and trigeminal neuralgia, in that surgical decompression is often a first-line treatment option, rather than pharmacological treatment. Nerve repair may be required in cases of nerve injury; these procedures are beyond the scope of this paper. In the presence of a definite mechanical compression, the primary goal is surgical decompression of the nerve. However, conservative treatment and pharmacotherapy tend to be more effective when neuroimaging shows no significant compression on the affected nerve root. Neuropathic pain sometimes persists following surgical decompression or repair of com­pressed or damaged nerves. In these cases, pharmacotherapy is an appro­priate treatment option.

Treatment
Conservative treatment: This may include short-term use of a cervical collar during the acute phase (a soft collar will in most cases be sufficient for conservative treatment), oral non­steroidal anti-inflammatory drugs (NSAIDs), neck care exercises, postural training and activity modification, and intermittent cervical traction. While many cases of cervical spondylosis respond to conservative treatment, patients with cervical radiculopathy may require surgical decompression of the nerve root.

Patients with painful cervical radiculopathy and neuropathic pain symptoms may improve with phar­macotherapy, such as antidepressant or anticonvulsant agents. A recently published observational, prospective study in the treatment of painful cervical or lumbosacral radiculopathy in a primary care setting revealed that pregabalin monotherapy or add-on therapy, versus non-pregabalin phar­macotherapy, for 12 weeks resulted in improvements in pain, anxiety symptoms, depression, sleep dis­turbance, general health and level of disability; improvements were sig­nificantly greater in the pregabalin groups.4

There is some evidence for a role for epidural corticosteroids in the man­agement of cervical radiculopathy.5,6 One systematic review concluded that there is moderate evidence for cervical interlaminar and transforaminal epidural steroid injections in providing long-term relief.6 However, care must be taken with these procedures, with some evidence for rare, but severe, neurologic complications reported for transforaminal cervical epidural steroid injection.A review of complications of interlaminar cervical epidural steroid injections revealed that it is a relatively safe procedure, with most adverse reactions being minor and transient, but serious complications may also result.Hence, patients should be referred to experienced physicians for epidural corticosteroid injection.

Surgical interventions: Surgery is indicated when other treatments have failed. The main aim of surgery in patients with cervical myelopathy and radiculopathy is decompression of the spinal cord or nerve root. However, surgical interventions are associated with complications (1% to 8% of patients), including death (0% to 1.8%).Complications resulting from damage to the spinal cord include tetraplegia, and those resulting from damage to the nerve root include muscle weakness. Patients with pain only are the most difficult group to treat; surgery tends to be more beneficial in patients with severe neu­rological deficits.

Surgical decompression of the nerve root is often achieved via an anterior approach (with removal of the intervertebral disc and osteophyte), or a posterior approach (with laminectomy). A 2002 Cochrane review on the role of surgery in cervical spondylotic radiculomyelopathy iden­tified two controlled trials involving 130 patients.The most common surgical interventions were via an anterior cervical approach with spinal fusion. Patients receiving surgery via a posterior approach underwent laminectomy. Control interventions included physiotherapy, hard or soft cervical collar, anti-inflammatory drugs, intermittent bed rest and pre­vention of vigorous activities. Surgery patients had greater improvements in pain, weakness and sensory loss in the short term than control patients. However, after 1 to 2 years’ follow-up, there were no significant differences observed between groups. The authors concluded that there was inadequate data with which to determine whether surgical interventions were superior to more conservative therapy.

Read full article : http://www.cimsasia.com/

Joint American Homeopathic seminar 2012 Washington

7th Joint American Homeopathic seminar 2012 organized by National Center of Homeopathy, USA to be held at Washington DC in April 2012. Happy to have an opportunity to meet 2008 noble prize recipient for medicine Dr.Luc Montagnier and speak in the advance seminar segment

Speakers
This year’s (2012) conference promises to be a spectacular, world-class event. We have a roster of speakers that reads like a “Who’s Who” of world-class teachers. We are especially honored that Dr. Luc Montagnier, recipient of the 2008 Nobel Prize for his discovery of the HIV virus, will present live, in person, at this year’s conference. Dr. Montagnier is just one of the world-class presenters on the roster for our 2102 conference.

JAHC 2012 is a gathering of the entire homeopathic community: practitioners from all of the professional organizations, including NASH, AIH, HANP, and HNA; students; and interested members of the public. Alongside the advanced and introductory workshops, this year’s special events include film previews and a thought-provoking panel discussion by some of today’s leading homeopathic thinkers. A vendor exhibit area, Friday evening reception and a roundtable luncheon round out this not-to-be missed 3-day weekend!

Whether you’re a homeopathy student, a professional homeopath, or someone who treats family and friends at home – there’s a place for you at the Annual Joint American Homeopathic Conference this coming April 20-22.

Introductory Seminars – Saturday and Sunday

  • On Saturday and Sunday, April 21st & 22nd  Topics include:
  • No More Morning Sickness!
  • Integrating Homeopathy with Nutrition, Herbal and Allopathic Medicine
  • Your Beautiful Bones
  • Homeopathy in Times of Crisis
  • Homeopathic Insights in Dentistry
  • Fun with First Aid

Discounts
Senior Citizens may take 10% off conference seminar fees if in financial need. Please provide proof of age (65+). Students in financial need may contact NCH regarding possible discounts.

Special Needs
Persons with disabilities may request reasonable accommodations (e.g. sign language interpreter) by contacting NCH. Requests should be made as early as possible.

National Center for Homeopathy
101 S. Whiting St., Suite 315, Alexandria VA 22304-3416
Phone (703) 548-7790
Toll Free (877) 624-0613
Fax (703) 548-7792
office@nationalcenterforhomeopathy.org
www.nationalcenterforhomeopathy.org

Mind Technologies by Hompath nominated for eIndia 2011

Homoeopathy, using technology of remote support, in this project we have treated nearly 14300 patients. With the vision of reaching the poor and needy, an initiative was undertaken by Mind Technologies for the state of Tripura.

For this work they have been nominated for a prestigious award at the eIndia 2011, they  need your whole hearted support to win – please cast your online vote.  

About eINDIA Awards
The eINDIA Awards have been instrumental in promoting the most innovative initiatives in the domain of ICTs (Information and communications technology) for Development and to spread awareness about the role of ICTs in addressing social concerns.

Kindly follow the below steps to give your valuable vote to our Tele-homeopathy project which has been nominated for ‘eINDIA 2011 Awards’

  1. Open the Link http://www.eindia.net.in/2011/
  2. Click on Vote Now! Box at top middle.
  3. Click on eHealth Awards. Vote Now.
  4. Enter mandatory details & Click on Next button.
  5. Go to the last option “Best Private Sector Initiative of the Year”.
  6. Select Tele-Homoeopathy project implementation in rural India :: Mind Technologies, Mumbai which is seen in the end in the list. Please vote here and help us to work for the cause of humanity
  7. After this click on Done button. You will get the Successful voting message.
  8. Click on Done button on this page.

Mind Technologies has once again proved that they are true pioneers in combining healthcare and technology. ‘Health For All’ which seemed a remote likelihood by the end of last century can now be fulfilled soon by making ‘The E-Medicine Revolution’ happen in India.

Right, affordable and efficient medical service to all, provided at the right time, has the potential to deliver this promise through Telemedicine. For the first time in history of Homoeopathy, using this technology of remote support, the project has screened nearly 14300 patients. With the vision of reaching the poor and needy, an initiative was undertaken by Mind Technologies for the state of Tripura. Mind Technologies, lead by Dr. Jawahar Shah, M.D. (Hom.) has taken the first step towards making this dream a reality.

We hereby request and urge you to visit the link given above and vote for Tele-Homoeopathy project implementation in rural India – Mind Technologies and help Homeopathy reach masses.

This is our opportunity to give back something to our valuable science and make it the first choice of treatment. Moreover, This will help people accept Homoeopathy and avail of it at a much affordable cost. It will overcome all geographic, economical and social barriers faced by the rural citizens and help them obtain quality preventive and curative services through Homoeopathy.

Dr. jawahar Shah www.hompath.com

web

National Online Exam System launched

webOnline examination system to pave the way for a clean, fair, fast and efficient examination and evaluation process

The government on Monday launched a national online examination system which can be adopted by colleges and universities to make tests hassle-free and more transparent.

“The conventional paper-oriented manual examination system is time-consuming, inefficient and unfriendly to the environment,” a statement by the C-DAD quoted HRD Minister Kapil Sibal, who launched launched the system, as saying. “The online examination system will pave the way for a clean, fair, fast and efficient examination and evaluation process,” the release said.

The Centre for Development of Advanced Computing’s (C-DAC) Director General Rajat Moona said with the use of the system, the time taken from publication of advertisement to declaration of the final results will be around 45 days for large recruitment drives. The system permits candidates to select the date, time slot and venue.

The online examination system has been developed by C-DAC under the sponsorship of the Department of Information Technology. The release said the online system can be adopted by colleges and universities for conducting national-level entrance tests. The system has been extensively tested for more than one year and has been found to be quite robust in performance, Moona said.

Source : http://governancenow.com/gov-next/egov/national-online-exam-system-launched

Complete Dynamics New Version released

Released Complete Dynamics version 11.7.
This version contains a pre release of the Complete Repertory edition 2012.

Strongly improved the program speed and reduced the use of computer memory.
Homeopaths that work with the HFA method (facial analysis) can use a pre release of remedy coloring in the analysis (contact us for details).

  • Additions for all of Clarke’s Dictionary of Practical Materia Medica (smaller and medium sized remedies completed).
  • A three year project in total!
  • More information on Nosodes and Bowel nosodes.
  • Corrections and improvement in structure of repertory rubrics.
  • Remedies: 2.353.017, sources: 4.485.984 (of which Clarke 377.341), rubrics with remedies: 208.825.
  • No new provings, but many remedies updated with 40 % or more information.

New development

  • We will be adding important new functions to Complete Dynamics in early 2012.
  • And for the remainder of 2012, we have also planned very important new features for the Practitioner Edition!
  • At this moment, we can not reveal yet what that will be…(we have been warned that the competition is watching us very carefully).

What is happening with Radar and MacRep?
Many people ask us if whether we know what is happening to Radar and MacRepertory. They seem to be worried about the future of these products.

If you want to read what we know about it, please visit this page.

Visit us at www.completedynamics.com
Complete Repertory website www.morphologica.com

Source : Complete Dynamics info@completedynamics.com news letter

Tripura received international award for tele-homoeopathy

 Agartala, Nov 23 (IANS): Tripura has become the only NE State to receive an international award for tele-homoeopathy, where patients in rural areas are diagnosed bydoctors through video-conferencing, a minister said here on Wednesday.

“Tripura recently received the international award at the Health World Expo-2011 in New Delhi for successful implementation of THTM (tele-homeopathy treatment method),” state Health Minister Tapan Chakraborty told reporters.

“The tele-homoeopathy treatment project was launched in Tripura in February last year and so far 21,550 rural people, 60 percent of them women, have been treated,” the minister added.

The project was initiated in different parts of the country by the Ayurveda, Yoga and Naturopathy, Unani, Siddha and Homoeopathy (AYUSH) department under the union ministry of health and family welfare.

Patients and doctors sitting in different places, including Kolkata and Delhi, can interact with each other through the THTM. He said that the medicines are provided free of cost to the patients.

Chakraborty said tele-homoeopathy facilities have been extended in ten rural locations in Tripura following an agreement between Tripura government, Kolkata-based National Institute of Homoeopathy and private firm Infrastructure Leasing and Financial Services Limited (IL&FS).

“Patients of polyarthritis, women’s gynaecological disorders, anaemia, pregnancy-related diseases, acute and chronic respiratory disease, gastro-intestinal diseases, geriatric problems, skin disorder, and communicable diseases have found exceptional results through the THTM,” the minister added.

Source : http://www.assamtribune.com/scripts/detailsnew.asp?id=nov2311/at045

job16

CGHS Empanelment for AYUSH Hospitals – application invited

job16It has been decided to have CGHS empanelment of AYUSH Hospitals will be made a continous process. Interested hospitals could apply for empanelment and these hospitals would be inspected by Quality Council of India(QCI) for verification of their infrastructure, facilities and staff as per prescribed norms/requirements. If found complying, such hospitals would be empanelled.

CGHS is also in process of encoragement of Accreditation of AYUSH Hospitals with NABH.

Director CGHS has invited sealed tenders from Ayurveda, Yoga & Naturopathy, Unani , Siddha and Homeopathy Hospitals for determination of rates for various procedures/treatment to be provided to CGHS beneficiaries/Central Government employees and their eligible family members covered under CS(MA) rules 1944.

Important Dates:

  • Date of issue of tender: From 8-11-11 to 17-12-11
  • Last Date of submission of Completed Tender:  22-12-11( 4 pm)

Eligibility criteria

Private Homeopathy & other AYUSH  Hospitals and teaching institutions, who full fill

  • 1. Hospitals must have 20 beds or more
  • 2. Hospital must have infrastructure and man power as mentioned
  • 3. Dedicated personal computer
  • 4. Internet connectivity

Contact :  Dr.Anand.T.Gudivada,C.M.O.I/c, AMSD.CGHS.HQ.

Email : firefox_anand@yahoo.co.in

More details: www.similima.com/pdf/cghs-ayush-tenders.pdf

Application : www.similima.com/pdf/cghs-ayush-advertisement.pdf

Website : http://msotransparent.nic.in/cghsnew/index.asp

NB: In the interest of the development of AYUSH industry, please circulate this information to your colleagues and friends so that maximum can be benefited