Cranial nerves- A comprehensive study

Dr. Achamma Lenu Thomas BHMS,MD(Hom)
Medical Officer, Dept. of Homoeopathy, Govt. of Kerala

We know that there are 12 pairs of cranial nerves and 31 pairs of spinal nerves. Cranial nerves carry information to and from the brain.

Cranial nerves contain 2 types of fibers
1) Sensory fibers – that relay sensory information
2) Motor fibers – that relay motor information
Sensory nerves – carry only sensory information
Eg – olfactory, optic & vestibulocochlear nerve.
Motor nerves – carry only motor information
Eg – hypoglossal & spinal accessory
Mixed nerve – These nerves have both sensory & motor fibres


  • 1st and 2nd – forebrain
  • 3rd and 4th – midbrain
  • 5th – pons
  • 6,7,8 – inferior surface of pons.
  • 9-12 – Medulla oblongata

The central sulcus divides the cerebum into two – a portion anterior to it called motor area or motor cortex and a portion posterior to it called sensory cortex.

Motor pathway of cranial nerves
From the motor cortex fibers called the corticonuclear fibres arise and they end in the cranial nerve nuclei. These form the UMN pathway. From the cranial nerve nuclei fibers arise and they end in different parts of body. These form the LMN pathway.

Sensory pathway of cranial nerves
Sensory fibers originates from the sensory organs. They form the first order neurons and their axons terminate in brainstem. From there second order neurons arise and they terminate in thalamus. From there 3rd order neurons arise and their axons end in sensory cortex.

Olfactory nerve
The olfactory mucus membrane in the upper part of the nasal cavity contains olfactory receptors. The central process of these receptors forms the olfactory nerve fibers. These olfactory nerve fibers passes through the cribriform plate to the olfactory bulb, then it forms the olfactory tract. Olfactory tract passes posteriorly and divides into the medial and lateral olfactory straie. Medial olfactory straie gets connected to the olfactory tract of opposite side. The lateral olfactory straie carries the fibers to the primary olfactory cortex in the temporal lobe.

Local causes which impair the sense of smell like rhinitis, sinusitis and gross deviation of septum should be looked for and excluded before testing the smell.
Each nostril is tested separately after occluding the other one, by using substances with mild aroma like coffee, powder, peppermint, clove etc.
The patient is asked to close his eyes and mouth and inhale the odour of the test substance and identify it. Ability to perceive the smell and to differentiate one smell from the other is taken as normal even though proper identification may not be sometimes possible. Substance which give pungent smell such as ammonia, chloroform etc should not be used because they stimulate the trigeminal nerve endings and irritate the nose even when the sense of smell is absent.

Disorders of olfaction includes, loss of smell -anosmia, reduction of smell – hyposmia, increased smell – hyperosmia, distortion of smell – parosmia and illusions and hallucinations of smell.

  • Parosmoia – Head injury or local abnormalities of nose
  • Hyperosmia – In psychiatric patients
  • Olfactory hallucinations & delusions – epilepsy, migrane , psychatric patients.
  • Anosmia – Head injury of cribriform plate
  • Aneurynsms of circle of Willis
  • Anterior communicating artery
  • Ophthalmic artery
  • Tumors
  • Olfactory groove meningioma
  • Pituitary tumors
  • Frontal lobe glioma
  • Frontal lobe abscess
  • Frontal bone osteoma
  • Increased ICP(rarely)

Optic nerve
Retina is formed by rods and cones, these synapse with the bipolar cells, these in turn synapse with the ganglionic cells. The fibers of the ganglionic cell forms the optic nerve. The optic nerve leaves the orbit through optic foramen, it unites with the other optic nerve at optic chiasma. Only the fibers of the nasal ½ of the retina passes to the other side while the fibers from the temporal half passes straight. Then it forms the optic tract. Optic tract comes to the lateral geniculate body. A few fibers leaves the tract before reaching the lateral geniculate body and pass to the superior colliculus – these fibers are those which are concerned with light reflex. From the lateral geniculate body the fibers get fanned out. This is called optic radiation. In optic radiation fibers which carry information from the lower ½ of visual field passes through the parietal lobe and fibers which passes information through the upper ½ of visual field passes through the temporal lobe. It is important that the ocular system reverses the image. The nasal side of the fundus picks up the temporal image and temporal side of the fundus picks up the nasal image. Damage to nasal side of retina will produce a temporal visual defect and vicevera.

Lesion of optic nerve
Complete lesion of optic nerve leads to total visual loss. Usually it starts as a central scotoma (area of defective vision) and then progresses to complete loss of vision. Some disease of optic nerve affects some fibers only and spares other fibres. So instead of total blindness there are areas of loss of vision in central and peripheral fields.

Optic nerve is peculiarly liable to Neuritis (Inflammations)
1) Papillitus – inflammation of optic nerve head
2) Retrobulbar neuritis – neuritis of optic nerve just behind the eyeball
3) Optic atrophy – any damage to optic nerve later leads to optic atrophy
4) Optic nerve compression – leads to atrophy
Optic nerve damage starts as scotoma
1) Centro caecal scotoma – When the scotoma extends to involve the blind spot it is called centrocaecal scotoma. It is characteristic of toxic ambylopia, – alcoholism, tobacco
2) Arcuate scotoma – When the scotoma extends from the blind spot and follows the course of the nerve it is called arcuate scotoma seen in glaucoma, choroiditis.

Lesion at optic chiasma
1) Medial compression of optic chiasm interrupts fibers from both nasal ½ of retina this leads to bitemporal visual loss – This is called bitemporal hemianopia. Hemianopia means loss of one half of the visual field. Loss of both temporal ½ or both nasal ½ of visual field is called – heteronymous hemianopia.
2) Lateral compression of optic chiasm – results in interruption of uncrossed nerves. This leads to ipsilateral nasal hemianopia.
3) Pituitary adenoma, nasopharynageal carcinoma, sphenoid sinus mucocele leads to compression of optic chiasma from below it leads to involvement of upper quadrants first & leads to bitemporal quadratopia.
Involvement of lower quadrants indicate compression of optic chiasma from above leads to bitemporal quadrantopia causes: craniophrayngioma or third ventricular tumor.

Lesion of optic tract & lateral geniculate body
Results in loss of vision of nasal half .This is called homonymous hemianopia. Because of relative rotation of nasal & temporal fibers in optic tract the defect will be in congruous.
Lesion in optic radation
Fibers fan out in optic radiation along the temporal and parietal lobes. Fibers of the upper ½ of the visual field pass through the temporal lobe and lesion of optic radiation along temporal lobe leads to upper quadrantanopia. The fibres of lower ½ of visual field passes through the parietal and any lesion of parietal lobe causes lower quadrantopia.

Tubular contraction of visual field
In this condition the visual field is constructed as if the patient looks through a tube. It occurs in frontal lobe lesions, also in hysteria.

Spiral contraction of visual field
When the visual fields are repeatedly tested on one sitting it may be seen to constrict progressively. It is usually a hysterial phenomenon, it can also occur due to fatigue and rarely in frontal lobe lesions.

Testing visual fields
Visual fields can be central and peripheral. Visual field extending up to 30ο from the point of fixation is called central visual field and the rest is called peripheral visual field.

Assessment of peripheral visual field – is by confrontation method. In this method visual field of the patient is compared with the visual field of the examiner. The examiner positions himself face to face in front of the patient in such a way that the eyes of the patient and examiner are almost at the same level. Each eye is tested separately while the other eye is covered. Patient fixes his eyes on the eyes of the examiner. Examiner brings an object from the periphery to the center and asks the patient to say ‘yes’ as he sees the object. Thus the upper nasal, lower nasal upper temporal and lower temporal areas are tested.

If the patient is totally bedridden, uncooperative demented subject, defensive eye blinking brought by moving the examiner’s hand rapidly from periphery towards patients eye can by tested. Absence of expected response should suggest loss of vision in that part of visual field.

Visual inattention is often tested by confrontation test. Here two eyes are kept open and two identical objects (examiners index finger) are presented simultaneously in corresponding positions of both visual fields. If visual inattention is present, the patient appreciates the finger only on one side.

Assessment of central vision
Central visual field can be assessed by red pin test. Since the central portion of retina is rich in rods and cones and is color sensitive, a red pin can be used for confrontation test. A red pin is brought from periphery to the center in all quadrants. Scotomas can be detected by this. If the red pin is of 3mm size at the area of blind spot (place where rods & cons are absent) the pin disappears. Blind spot can be seen.

Field of vision can also be detected by using perimeter. A point of light is moved centrally from the extreme periphery. The position at which the patient observes the target is marked on the chart. Repeated testing from multiple directions provides an accurate record of visual fields.

Visual acuity – Visual acuity tests the central vision. Visual acuity is the resolving power of eye for the central vision. Both the eye is assessed separately. Both near and distant vision is tested.

If there is severe visual impairment v.a can be assessed by asking the patient whether he can appreciate light. If not it is written as no P.L. Ask whether the patient can see hand movement. If not it is written as ‘no H.M.’. Ask if the patient can count fingers if not it is written as ‘no C.F.’.

If the patient can read, near vision and distant vision is tested. Near vision is tested by using an Jaeger type card. It is held 35cm from the patients eye. To exclude the difficulty due to refractory errors a pin hole card can be used. The patient is asked to look through a 1mm size pin hole punched in a card. The pinhole allows the light to fall only on the central part of the retina. If the visual acuity which is originally impaired improves on pin hole test, the visual impairment is due to refractive errors and not due to neurological causes.

Distant vision is tested using the snellen’s chart. Visual acuity is expressed as ‘d/D’. d is the distance of which the patient sits is 6m. ‘D’ no of the line that patient can read.
Optic fundus examination can be done using an ophthalmoscope
Color vision is tested. Ask whether the patient can appreciate colors. Color vision is also tested by using Ishiara’s chart.

Occulomotor , abducent and trochlear
The occulomotor abducent and trochlear are described together as these three nerves and the muscles innervated by them together participate in the smooth and coordinated movements of the eyes.

Course : occulomotor nerve
Occulomotor nerve has got two nuclei , main motor nuclei and Edinger-Westphall nuclei . This nerve arises from the anterior surface of the mid-brain in the interpeduncular fossa . It ends by entering the orbit and all its way supplies leavator palpebra superioris , all ocular muscles except superior oblique and lateral rectus . It also supplies ciliary muscles and constrictor pupillae . Affection of leavator palpabre superioris leads to ptosis . When extra ocular muscles are involved it leads to diplopia, strabismus and defective ocular movements. Involvement of constrictor pupillae and ciliary muscles leads to loss of light reflex.

Course : trochlear nerve
It is the smallest of all cranial nerves .It arises from the midbrain immediately above pons . It ends by entering the orbit and supplying the superior oblique muscles .

Course : abducent nerve
This nerve arises from the brain stem at the pontomedullary junction . It has the longest intracranial course and ends by entering the orbit at the superior orbital fissure . It supplies the lateral rectus muscle .

Test for levator palpabrae superioris
Levator palpabrae superioris helps to elevate the upper eye lid. Paralysis of levator palpabrae superioris leads to ptosis
Ask the patient to look at a distant object then ask him to elevate the upper eye lid .
Ptosis can be due to other causes such as sympathetic palsy, myasthenia gravis and partial ptosis due to trachoma and tumors of eyelids .

Test for ocular movements
Steady the patient’s head and ask him to follow an object held at arm’s length .Observe the full range of vertical and horizontal eye movements . The vertical and horizontal eye movements made from the mid position of gaze are called the cardinal movements . Then examine the other directions of gaze .

  • Upward movement is called elevation- Superior rectus and inferior oblique .
  • Downward movement is called depression –Inferior rectus and superior oblique .
  • Lateral movement is abduction – Lateral rectus.
  • Medial movement is adduction – Medial rectus .
  • Looking up and out – Superior rectus .
  • Looking up and in – Inferior oblique .
  • Looking down and out – Inferior rectus .
  • Looking down and in – Superior oblique .

Nerve supply of the muscles .
All the muscles are supplied the occulomotor nerve except the superior oblique which is by trochlear and lateral rectus by abducent.
So in the fourth cranial nerve lesion the patient cannot turn the eyes inwards . Patient will have difficulty in reading and going downstairs, in case of which he will have to tilt his head .
In the sixth cranial nerve palsy the patient will not be able to turn the eyeball to the lateral side . The imposed pull of medial rectus muscle causes the eye to turn inwards thereby producing internal strabismus .

Total paralysis of the 3rd,4th& 6th cranial nerves is known as the internal opthalmoplegia . Paralysis of the extra occular muscles is called the external opthalmoplegia . Paralysis of the intrinsic muscles of the eye ( ciliary muscles and constrictor pupillae) is called the intrinsic opthalmoplegia.

Supranuclear mechanisum of eye movements
1) Pursuit movement – tract –occipito mesencephalic tract .
These are the slow movements accurately tracing a moving object .
2) Saccadic movement – Fronto mesencephalic pathway
These are rapid eye movements on shifting from one point of fixation to other .
3) Convergence mechanism – Ask the patient to look at a distant object then at your finger kept at few centimeters in front of the nose The center for convergence movement is at the occipital cortex. Lesion at occipital cortex leads to impaired convergence mechanism
3) Position maintenance mechanism
Ability of the eyes to fix at a stationary object . tract is the occipito mesencephalic tract . Lesion of this tract leads to impaired fixation .
4) Reflex mechanisum
Occipitocephalic reflex : eye balls reflexively deviate according to the movements of the head.
Doll’s eye movement :
Eyeballs move in a direction opposite to the movements of the head., when the head is passively moved. Presence of doll’s eye movements indicates supra nuclear lesions .
Occulovestibular reflex: Reflex eye movements occur when the external auditory canal is irrigated with warm or cold water .
Absence of reflex movements suggests brain stem lesions . Midbrain and pontine lesions will produce failure of upwards and downward gaze . Impaired vertical movements is common in extra pyramidal diseases.

Diplopia is said to be present when the patient complains of seeing two images when he looks at an object . This is due to the paralysis of one or a group of extra ocular muscles . When the eyes are fixed on an object the image falls on the macular area in normal eyes and outside macular area in the parietic eye .Thus two images of an object are perceived The image which is seen by the parietic eye is called the false image and by the normal eye is the true image. The patient s asked to look at all directions of gaze and determine in which position maximum separation of true and false images occur. Maximum separation occurs in which direction of gaze , the muscle responsible for gaze in that direction is the parietic one .The abnormal eye can be determined by covering one eye and noting the effect on diplopoia . If this results in disappearance of false image then the paretic muscle belongs to that eye.

Refers to the abnormal deviation of eye. The abnormal deviation of eyes can be divergent , convergent , upwards or downwards . When squinting is noticeable ,if both eyes are open it is called manifest squint . If squinting is noticed on covering one eye , it is called latent squint .

Squinting is due to the paralysis of extra ocular muscles . Abnormality is seen when the eyes are in the resting position but it becomes more obvious when the eyes are turned in the direction of the action of paralysed muscle .The images of the object fail to fall on corresponding points in the retina of both eyes and this also leads to diplopia .In paralysis of medial rectus and superior oblique the squint is divergent due to the unopposed action of lateral rectus .In paralysis of lateral rectus the squint is convergent due to the unopposed action of medial rectus .
We have to differentiate it from the squint that occurs not due to the paralysis of extra ocular muscles

Nystagmus is defined as the involuntary to and fro movement of the eye in the horizontal vertical ,rotatary or mixed direction .Occular posture or tone of extra ocular muscles is normally maintained by the impulses which reach the eye from the retina , labyrinth, cerebellum and midbrain .


  • I – Nystagmus is present only when the eyes are deviated to one side .
  • II – Nystagmus produced in mid position and also when the eyes are deviated to one side.
  • III – Nystagmus present in all direction of gaze .

Nystagmus can be pendular – eyes found to drift in one direction giving rise to a slow phase as a corrective phenomenon they are quickly brought back into the neutral position – Quick phase
.Nystagmus can be of eqnal amplitude to both sides

1) Retinal nystagmus : Vision is defective & fixation is impaired rapid pendular nystagmus occurs
2) Vestibular nystagmus:- Any damage to labrinth or veatibular nerve leads to vestibular nystasgmus .Slow phase towards side of lesion and quick phase to normal side .
3) Labrynthine disease – Nystagmus occurs when the patient assumes certain postures . This is known as positional nystagmus .To elicit this suddenly reposition the patient . After several seconds nystagmus develops and on repeated testing it disappears .
4) Posterior fossa lesion – In posterior fossa lesions positional nystagmus occurs .
5) Cerebellar damage – In cerebellar damage nystagmus occurs with fast phase towards the side of lesion .
6) Vestibular nuclei or brainstem lesion- Here the fast phase of nystagmus occurs towards the direction of gaze .
7) Medial longitudinal fasiculus – A lesion in medial longitudinal fasiculus leads to dissociate nystagmus .Nystagmus is present in one eye and not in other eye .( A lesion in MLF leads to internuclear ophtalmoplegia . MLF are a bundle of fibers which connect some of the cranial nerve nuclei together viz. 3,4 5 , 6. 8., 11, and 12th cranial nerves.These bundles have connections also with brainstem and motor nuclei of the upper cervical nerves ).

7) Lesion in cervico medullary junction – Downbeat nystagmus.
8) Lesion in upper midbrain – Convergence nystagmus.
9) Lesion in sellar & para sellar region – See-saw nystagmus .

Occular bobbing ( up & down motion of the eye )
is seen in large pontine lesions . Opsoclonus ( rapid jerky movements of the
eyes ) is seen in brain stem lesions.

Test for pupils

1) Size of pupil – Normally both pupils are equal in size . Difference in
the size of the pupil is called anisocoria .
2)Shape – Normally both pupils are circular in shape .
3) Light reflex –When the light is shown in one eye the pupil of that eye constricts .This is the direct light reflex. When the opposite pupil also constricts it is the indirect light reflex.

A stimuli such as bright light shone in one eye will send an afferent impulse along the optic nerve and the efferent impulse pass to the eye through the occulomotor nerve .

1) In optic nerve lesions – Direct light reflex will be abolished ,
2) Occulomotor nerve lesion – No direct light reflex but consensual reflex is present in the affected eye . In normal eye direct light reflex is present but consensual light reflex absent .

Accomodation reflex
This reflex occurs when the patient immediately focuses his vision on a near object.
Test – The patient is asked to fix his eyes on the examiners index finger kept at a meter away and rapidly brought near the patient’s nose.

The 3 “ C” of accommodation
1) Convergence of eye .
2) Contraction of ciliary muscle .
3) Constriction of pupil.

Ciliospinal reflex
When the skin over the neck is pinched , pupil on the same side dilate reflexively . This results from the stimulation of the sympathetic nerves which supply the dialator pupillae muscles . Ciliospinal reflex is abolished in lesions of cervical sympathetic nerves , affection of upper cervical and thoracic segments and medulla oblongata .

Other abnormalities of pupillary reflex
1) Argyll Robertson’s pupil
Pupils are small , irregular in shape , they do not react to light but react to accommodation reflex. This is characteristic of tabes dorsalis & GPI .
This response can also occur in midbrain lesions which are neoplastic, inflammatory , vascular & demylinative .
2)Marcus Gunn pupil
Seen in optic nerve lesions .Light is swung from one eye to another as it falls on affected eye it dialates and on unaffected eye it constricts .
3) Hippus
Rhythmic alternating constriction and dialatation of pupils . It is usually normal but is marked in retrobulbar neuritis and encephaalitie

Trigeminal nerve
Trigeminal nerve is the largest of all cranial nerves. It is a mixed nerve. It has got 4 nuclei.

1) Main sensory nuclei
2) Spinal nuclei
3) Mesencephalic nuclei
4) Motor nuclei

Main sensory nucleus is situated in pons and it extends to the spinal nucleus. The spinal nucleus extends through the whole length of medulla oblongata into spinal cord. Mesencephalic nucleus is in the midbrain and extends to pons and motor nuclei is situated in the pons itself. All these nuclear fibers join to form the trigeminal nerve. Trigeminal nerve comes out from the middle of the pons. As it passes down it divides into 3 branches.
1) Opthalmic
2) Maxillary
3) Mandibular

Proprioceptive fibers terminate in mesencephalic nucleus. Light touch fibers terminate in main sensory nucleus. Pain and temperature fibers terminate in spinal nucleus. Motor fibers arise from motor nucleus.
We can test the sensation over the face. Take a pin and slightly prick it over the three areas of distribution of trigeminal nerve.
Light touch can be appreciated by using a cotton wisp and touching it lightly on face.
Temperature can be tested by using hot and cold tubes.
Look whether the sensory deficit has got a root pattern or an onion peel pattern. Onion peel pattern occurs in lower pontine, medullary and cervical lesions.
The separate location of main sensory and spinal nuclei results in dissociated sensory loss i.e low pontine or medullary lesion will result in loss of pain and temperature with the preservation of light touch.

Corneal reflex
Test the corneal sensation by touching with a wisp of wet cotton wool . A blink response should occur bilaterally. Afferent root is the ophthalmic division of trigeminal nerve and efferent root is the facial nerve .This test is the most sensitive indicator of trigeminal nerve damage.

Motor examination
Ask the patient to clench the jaws and teeth together , feel the temporalis and masseter .Observe for wasting and thinning of temporalis muscle and masseter . look for hollowing out of temporalis fossa .
Ask the patient to open the mouth against resistance . Action of both pterygoid muscles keeps the open jaw in the midline. If pterygoid muscles of one side is paralysed , the jaw is deviated to the paralysed side ( Pterygoid musckes of one side pushes the jaw to the opposite side normally )

Jaw jerk
Ask the patient to relax jaw .Place finger on the chin and tap with a hammer . Slight jerk occurs normally .Increased jerk occurs in bilateral upper motor lesions. Absence of jaw jerk is not significant since in may also occur in normal persons .

Facial nerve
Facial nerve is a mixed nerve . It has three nuclei –motor nuclei, sensory nuclei and parasympathetic nuclei
Sensory nuclei receives fibers from anterior 2/3rd of tongue , floor of the mouth and soft palate . Main motor nuclei is situated deep in pons. Fibers coming from above the nuclei from cerebral hemisphere supplies the lower part of the face on contralateral side . Fibers from below the nuclei supplies the whole half of the same side .In supra nuclear lesion there will be contralateral involmemt of lower face .In infranuclear lesion there will be involvement of upper and lower face on same side .

Facial nerve supplies the facial muscles
frontalis- Ask the patient to wrinkle his fore head by looking upwards . If the frontalis muscle is paralysed he won’t be able to wrinkle the forehead .
2) Orbicularis occuli – Ask the patient to close eyes while examiner attempts to open them . If orbicularis occuli is paralysed patient is not able to close the eyes.
3) Buccinator – Ask the patient to hold water in the mouth .Water
escapes through affected side due to the paralysis of buccinator.
The saliva is found to drool out of mouth .When patient holds
air in cheeks and the affected side is tapped the air escapes .Patient
will not be able to tightly close the lips .
4) Orbicularis oris and levator angili oris
Ask the patient to show the teeth . if there is paralysis ,the affected side won’t move out as the normal side .Angle of mouth will be at a lower level . When he attempts to smile the muscles of normal side pulls the angle of mouth to the normal side . There will be obliteration of nasolabial fold .

On attempting to close the eyes the eyeballs pass upwards reflexively –Bell’s sign.In facial palsy, this reflex is exaggerated & the whole cornea goes under the eyelid . This is called Bell’s phenomenon .
In UMN lesions the lower part of the face on contralateral side is affected . There is no Bell’s phenomenon , closing of eyes is possible , there is no obliteration of wrinkles on forehead .

In LMN all features are seen because half of the face is involved . In bilateral LMN lesion the whole face is involved.

  • Taste sensation in anterior two third of the tounge is affected
  • Ask the patient to protude the tounge and put sugar granules , then rinse the mouth and test with salt, vineager and quinine.
  • Inability to identify correctly or delay in response is abnormal.
  • Aguesia – loss of taste sensation
  • Hypoguesia – decreased taste sensation
  • Paraguesoa is perverted taste sensation.

Vestibulocochlear nerve
Vestibulocochlear or 8th cranial nerves consists of two divisions.

1) Vestibular division – concerned with sense of movement, position and balance
2) Cochlear division – concerned with hearing

Vestibular nerve arises from the utricle, saccule and semicircular canal while cochlear nerve arises from the cornea. Both these nerves enter the brain stem separately at pontomedullary junction

From brain stem cochlear nerve passes to the cochlear nuclei. From there fibers pass to medial geniculate body , inf-colliculus and finally end in auditory cortex in temporal lobe.

Vestibular nerve passes to vestibular nuclei and from there fibers pass to cerebellum, spinal cord and medical longitudinal fasciculus.
Any lesion in the nerve manifests as tinnitus vertigo and deafness.

Tinnitus is the sensation of noise in absence of any external stimuli. Tinnitus takes several forms such as tunning, roaring, whistling, buzzing etc. It is felt mostly during sleep when the environment is silent. It may interfere with normal hearing.

Test for Cochlear nerve
Ask the patient to stand 6meter apart with his ear to be tested facing the examiner . Ask him to plug the other ear with his finger. Whisper a series of letters or numbers and ask him to repeat the same. Give 10 such numbers. Patient should be able to say 9 out of 10 letters.

A conversational voice should normally he heard 3.5m.

Tuning fork
Tunning fork test helps us to differentiate conduction deafness from nerve deafness.

1) Weber’s test
Place the base of the tuning fork on the vertex of the patient and ask the patient in which ear the sound is heard more loudly. Normally the sound is equally heard in both the ears.
In conductive deafness, the deafness is louder in the affected ear since distraction from outside is reduced in that ear.
Nerve deafness – sound is louder in the normal ear.

2) Rinne’s test
Hold the base of tuning fork against mastoid bone. Ask the patient whether he hears the sound. When sound disappears hold the tuning fork near the external meatus. Patient hears the sound again .Normally the air conduction is better than bone conduction.
In conduction deafness bone conduction is better than air conduction.
In nerve deafness both are impaired.

Glossopharngeal nerve
Glassopharyngeal nerve is a mixed nerve with both sensory and motor fibers. It has got 3 nuclei – main motor nucleus, sensory nucleus and parasympathetic nucleus.

The main motor nucleus is situated in medulla oblongata. The sensory nuclei is a part of tractus solitarius . Sensory nucleus it receives fibres from post 1/3rd of tounge post.part of soft palate, tonsils and pharynx.

Afferent for gag reflex is 9th cranial nerve
Efferent for gag reflex is 10th cranial nerve

Inspect the soft palate and pharynx while the patient keeps his mouth wide open. Gently touch both sides of pharyngeal wall one after another with a swab stick. In normal subjects this should evoke a gag reflex i.e contraction of pharynx with elevation of the roof of the tongue and a feeling to vomit. Also verify that he feels the touch sensation equally in both sides. Sometimes even in normal individuals gag reflex may be absent.

3) Test the taste sensation in post 1/3rd of tongue. Technically this is difficult. Other alternate method is to apply a weak electric current to the back of the tongue. Normally this evokes a sour taste.

Vagus nerve
Vagus nerve is a mixed nerve .It arises from medulla oblongata. It sends motor fibers to pharynx and larynx . It receives sensory fibers from tongue , larynx, pharynx , oesophagus , stomach and intestine .

Motor function
Observe the arches of the palate on both sides with the patient holding the mouth wide open . Normaly both sides should be symmetrical .In unilateral palatal paralysis the arch will be at a lower level . Ask the patient to say ‘ah ‘ and observe the movements of the palate .Normally both the arches will lift to the same extent and the base of the uvula will be moving in the midline . In unilateral palatal paralysis only the normal side will rise up while the paralysed side remains immobile. The midline raphe of the palate and base of the uvula will be pulled towards the normal side .
Unilateral palatal weakness causes minimal symptoms but bilateral palatal weakness causes nasal regurgitation and nasal quality for speech .

Ask the patient to swallow a mouthful of water in sitting position , the fluid regurgitates through the nose . In patients who have some paralysis of vagus and who are semiconscious swallowing leads to aspiration of food onto trachea .

Pharyngeal weakness
In unilateral paralysis pharyngeal wall droops on the affected side . In bilateral paralysis there is marked dysphagia and bubbling speech because of pooling of saliva in the pharynx .Patients may develop cough or choking when he attempts to swallow fluids .

Paralysis leads to hoarseness, stridor , breathlessness and bovine cough.

Bilateral vocal cord paralysis leads to bovinecough . When the patient is asked to cough the vocal cord cannot move and close glottis so the explosive stage of
cough is lost . In unilateral vocal cord paralysis with the passage of time the vocal cord on the normal side crosses over the mid line to lie near its fellow and thereby restore the vocal aperture hence in the chronic vocal cord paralysis cough regains its quality . As the patients with the vocal cord paralysis cannot close the glottis and hold the breadth , they run the risk of drowning when immersed in water .

Accessory nerve
The 11thCranial nerve is purely a motor nerve. It has a cranial component and a spinal component . The cranial component arises from medulla oblongata . Spinal component arises from upper five cervical spinal segments .The spinal components emerge and forms a trunk which then passes upwards and meets the cranial trunk , then it leaves through jugular foramen and travels down the neck as spinal accessory nerve. Fibers of the cranial root are distributed along with the pharyngeal and recurrent laryngeal branches of the vagus. Fibers of the spinal root supplies the sternomastoid and trapezius muscles.
Test for sternomastoid muscles
Ask the patient to turn his head to one side while applying resistance to the chin. This movement is mediated by the sternomastoid of the opposite side which can be seen as contracting . Both sides are tested and the strength of the muscles are compared .

Test for trapezius
Stand behind the patent and observe the bulk & symmetry of the muscles on both sides . Ask the patient to lift his shoulders up against resistance applied on the shoulders and compare the strength on both sides.
UMN lesions produce slight weakness while LMN lesions produce paralysis and wasting.

Hypoglossal nerve
Motor nerve arising from lower part of medulla oblongata and ends in the oral cavity . It supplies the intrinsic muscles of the tongue . These muscles help in protruding the tongue and also takes part in bending , twisting movements of the tongue.

1)Deviation of tongue
Ask the patient to open his mouth and put out his tongue .Normally tongue protrudes in the midline. If there is paralysis of one side , the tongue deviates to the affected side because of contraction of muscles of the opposite side ( Hypoglossus, styloglossus , Genioglossus)
2) Ask the patient to move his tongue from side to side and note the rate and range of movements .Ask him to push out the cheek with the tip of the tongue from within , against resistance offered by your finger from outside .Note the strength .
3) Ask the patient to curl his tongue up and down
4)Small twitching moments that occur spontaneously is called fasciculation .
Reduction of the bulk of tongue on one or both sides suggests atrophy .
5) Tone – Palpate tongue if it is soft and flabby ,it suggests atrophy , if it is hard and firm it suggests spasticty

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