Infections of central nervous system, bacterial meningitis ; a homoeopathic perspective

Dr Appu Gopalakrishnan  

 Central nervous system is commonly affected by various infections. The nervous system may be the primary target of  many infections such as herpes simplex encephalitis, rabies or other forms of meningitis. On the other hand, it can also be affected secondary to other systemic infections, in which  the neurological lesions develop as part of the systemic manifestation of other diseases. The clinical presentations of  these infections are unique and identification of the pattern of which helps in diagnosis and proper management . Meningitis usually affects the leptomeninges and  clinically presents with the classical triad of fever, headache and vomiting. Encephalopathy,which is characterized by altered level of sensorium and occurance seizures, where there is the direct involvement of brain substance or parenchyma. Infections  which causes focal structural brain  damage presents with focal neurological deficits such as hemiplegia or aphasia. Infections which affects the spinal cord usually presents with myelopathy.In some other cases CNS infections can also be present with chronic behavioral disturbances and dementia,especially when the parenchyma or  the  cerebral vasculature is involved(1). 

With the emergence and proliferation of multi drug resistant organisms, the prospect of an ‘antimicrobial perfect storm’in the approaching decades has now become an urgent public health concern. The excessive and indiscriminate use of  all these drugs in both human and veterinary practices has led to the emergence and dissemination of  so many resistant organisms(2). In this era of antibiotic resistance, Homoeopathy offers a great hope in the field of medicine for the purpose of treatment as well as prevention of these deadly infectious diseases.

According to WHO,Bacterial meningitis is characterized by acute onset of fever (usually > 38.5 °C rectal or 38.0 °C axillary), headache and one of the following signs: neck stiffness, altered consciousness or other meningeal signs. Hib, meningococcal meningitis and pneumococcal meningitis cannot be differentiated on clinical grounds alone(3).

It is  characterized by inflammatory response to bacterial infection affeting the leptomeninges. Organisms such as Streptococcus pneumoniae, Haemophilus influenzae and Neisseria meningitides accounts for  about 80% of  the cases of acute purulent meningitis. In case of  pre-term and neonate babies group B streptococcous is most common pathogen. Next in frequency includes coliform bacilli especially those having K1 antigen. Other pathogenic organisms include Klebsiella, Enterobacter, Salmonella and Listeria . Tuberculosis, cryptococcosis  and other fungal infections are responsible  for the majority of chronic meningitis.

Neisseria meningitidis (meningococcus) is pathogenic exclusively to man. The clinical syndromes include meningitis, meningococcal septicemia, and sometimes lesions in the joints, ears, eyes, adrenal glands, lungs and heart.

The organisms can be found in the nasopharynx of  about 5-10 perentage of human beings who act as carriers. Before the occurance of epidemics carrier rate among the local population  may goes up above 20% and during an epidemic  about 90% of subjects may carry the organisms. Outbreaks usually occurs in close-knit communities such as inmates of jails, ships, army camps, or dormitories. Sporadic cases may also occur. In India a clear seasonal prevalence is not observed. The organism commonly spreads through droplet infection and also to some extent through fomites. In most of the cases the infection can be asymptomatic. In some persons, the only manifestation may be an upper respiratory tract catarrh(1). In 2000, a heptavalent pneumococcal conjugate vaccine was introduced and has been associated with a significant decline in the incidence of pneumococcal meningitis(4).

The major lesions are cerebrospinal meningitis and meningococcal septicemia. Bacteremia precedes the meningitis. The organism may reach the central nervous system directly along the perineural sheath of the olfactory nerves or through the bloodstream. Bacteremia leads to endothelial damage and the organisms enter the CSF. Serogroups B and C account for the majority of cases in the west. Serogroups W135 and Y account for a smaller proportion. Group C produces more serious disease. Once the CSF is reached further multiplication is rapid

since the humoral defences are absent. Cytokines promote inflammatory processes and increase vascular permeability. Leukocytes adhere to endothelium. Vasogenic cerebral edema occurs which itself may lead to brain herniation. In the central nervous system meningococci produce suppurative lesions of the pia arachnoid. Inflammatory lesions are seen on the surfaces of the brain and spinal cord and the ependymal lining of the ventricles. The whole of CSF becomes turbid and purulent. The base of the brain and the surface of the cerebral hemispheres show thick pus. This exudate may block the foramina leading to internal hydrocephalus and also compress the cranial nerves emerging from the base of the brain. Meningococci may invade the underlying cerebral cortex as well and cause encephalitis. Histologically the lesions show perivascular cuffing with polymorphs. Thrombosis of small blood vessels may occur. In severe cases, subdural effusions containing blood or exudate may occur. Meningococcal septicemia (meningococcemia) is characterized by hemorrhagic manifestations. The organisms can be demonstrated in the small blood vessels from all organs. Vascular damage occurs as an allergic phenomenon (Schwartzman phenomenon) caused by the endotoxin of meningococci. In fulminant meningococcemia, hemorrhage occurs into the adrenal glands leading to adrenal failure and profound shock. Generalized hemorrhagic tendency may develop due to disseminated intravascular coagulation. Metastatic lesions occur in the joints, ears, eyes, and lungs.

A study conducted in Kerala to find out the aetiology and antibiotic susceptibility pattern of acute pyogenic meningitis in children between one month and 12 years in one year in a tertiary care centre(Department of Microbiology, Medical College Hospital, Trivandrum, Department of Paediatrics, SATH, Trivandrum,Christian Medical College, Vellore). CSF samples were processed by doing Gram-staining and culture in appropriate media. Latex agglutination test (LAT) and PCR were done in all cases for the primary pathogens.

Results shows that Streptococcus pneumoniae (62.5%) was the most common aetiological agent for acute bacterial meningitis followed by Klebsiella pneumoniae subspp pneumoniae, Group B haemolytic Streptococci and Elizabethkingia meningosepticum. LAT could pick up one culture negative case of pneumococcal meningitis. Blood culture was positive in 37.5% of CSF culture positive cases(5).

Infection of the leptomeninges by N meningitides leads to meningococcal meningitis. This may occur in epidemic and sporadic forms. The most common age group is from 6 months of life to adolescence. Incubation period varies from 3-5 days and there may be a preceding upper respiratory tract infection. Onset is acute with fever and other constitutional features like severe headache, neck rigidity, vomiting, and photophobia. Fever is usually high grade, intermittent, and associated with rigor and chills. The pulse is slow. Herpes labialis may develop. The patient is irritable and prefers to lie curled in bed. Drowsiness, confusion, delirium, and coma supervene. Convulsions are common at the onset, especially in children. In children, early signs such as leg pain, coldness of the extremities and abnormal skin colour may develop even before the classic signs of meningitis. Recognition of the disease at this stage and institution of specific therapy are more beneficial. In a large proportion features of meningococcal septicemia are seen. These include maculopapular and purpuric skin rashes appearing over the axilla, flanks, wrists, and buttocks, and ecchymosis and peripheral gangrene . Signs of meningeal irritation are evident from an early stage. These include neck rigidity, Kernig’s sign, and Brudzinski’s signs. 

Kernig’s sign
Vladimir Mikhailovich Kernig (1840-1917), a Russian physician, described first meningeal sign, known as Kernig’s sign.To elicit the Kernig’s sign, patient is kept in supine position, hip and knee are flexed to a right angle, and then knee is slowly extended by the examiner. The appearance of resistance or pain during extension of the patient’s knees beyond 135 degrees constitutes a positive Kernig’s sign(6).

Brudzinski’s sign
Josef Brudzinski (1874-1917), a Polish born pediatrician in early nineties, described 4 maneuvers for the clinical diagnosis of meningitis: The obscure cheek sign, symphyseal sign, Brudzinski’s reflex, and the most popular Brudzinski neck sign. A positive cheek sign is elicited by applying pressure on both cheeks inferior to the zygomatic arch that leads to spontaneous flexion of the forearm and arm.A positive symphyseal sign occurs when pressure applied to the pubic symphysis elicits a reflex hip and knee flexion and abduction of the leg. Brudzinski’s contralateral reflex sign consists of reflex flexion of a lower extremity after passive flexion of the opposite extremity .Sometimes, a lower limb first placed in flexion causes a reflex movement of extension after the passive flexion of the other limb, known as reciprocal contralateral reflex of Brudzinski.The most popular maneuver Brudzinski’s neck sign is performed with the patient in the supine position. To elicit this maneuver, the examiner keeps one hand behind the patient’s head and the other on chest in order to prevent the patient from rising. Reflex flexion of the patient’s hips and knees after passive flexion of the neck constitutes a positive Brudzinski sign .It has been proposed that in patients with meningitis, passive flexion of the neck stretches the nerve roots through the inflamed meninges, leading to pain and flexion movements of lower extremities. Forward head flexion exerts traction on the intradural spinal nerve roots, which attain maximal relaxation when both hip and knee are placed in intermediate degrees of flexion(6).

Rise in intracranial tension may lead lo papilledema.  In a small proportion of cases blindness, deafness, and hemiplegia may be found in the acute phase. Some of the patients recover within a month. A toxic encephalopathy may develop in some patients and this is probably due to diffusion of toxins or bacterial invasion. It is characterized by the development of deep coma within a few days of onset. This condition is associated with a mortality up to 50%. The development of subdural effusion, internal hydrocephalus, or brain abscess should be suspected from the development of localizing signs and progressive deterioration, despite adequate therapy. Most of the untreated patients die in a stage of deep coma within days or weeks, but a few may proceed to a chronic phase characterized by progressive emaciation, opisthotonus, paralysis, bedsores, and hydrocephalus(7).

Suspected: Any person with sudden onset of fever (> 38.5 °C rectal or 38.0 °C axillary) and one of the following signs: neck stiffness, altered consciousness or other meningeal sign
Probable: A suspected case with CSF examination showing at least one of the following:
– turbid appearance;
– leukocytosis (> 100 cells/mm3);
– leukocytosis (10-100 cells/ mm3) AND either an elevated protein (> 100 mg/dl) or decreased glucose (< 40=””>
Confirmed: A case that is laboratory-confirmed by growing (i.e. culturing) or identifying (i.e. by Gram stain or antigen detection methods) a bacterial pathogen (Hib, pneumococcus or meningococcus) in the CSF or from the blood in a child with a clinical syndrome consistent with bacterial meningitis(3).

Clinically meningitis is diagnosed when there is fever, severe headache, and signs of meningeal irritation. This has to be distinguished from meningism which is seen in toxic febrile states where the signs of meningeal irritation are present but the CSF is normal. Meningitis has to be distinguished from encephalitis, subarachnoid hemorrhage, and other causes of coma. Meningococcal meningitis has to be distinguished from other causes of purulent meningitis. At the slightest suspicion of meningitis lumbar puncture should be done and the CSF should be examined to establish the diagnosis. Since early diagnosis and institution of specific antibacterial treatment is the most important single factor in determining the outcome, lumbar puncture should not be delayed. Differential diagnosis includes other bacterial meningitis, mainly caused by H. influenzae and pneumococci.

Laboratory diagnosis
Diagnosis of meningitis is confirmed by examination of CSF. Lumbar puncture should be done at the earliest if there are no contra indications. Conditions which resemble meningitis include subdural empyema, brain abscess, or necrotic temporal lobe in Herpes simplex encephalitis. In patients with onset of seizures, signs of raised intracranial tension and moderate or severe impairment of consciousness, CT or MRI should be done to assess the intracranial pathology before performing LP. Repetition of Lumbar puncture is indicated when the progress with treatment is not satisfactory(8).

Rapid diagnosis of acute pyogenic meningitis by a combined PCR dot-blot assay
A multiplex PCR was employed to amplify unique conserved sequences of DNA from the pathogensHaemophilus.influenzae , Neisseria.meningitidis and Streptococcus pneumoniae from cerebrospinal fluid samples of patients suffering from acute pyogenic meningitis. The accurate identification of the PCR amplified product was achieved by hybridizing dot-blots of the PCR products to probes which were specific, biotinylated internal sequences of the amplified target DNA. Detection of the hybrids was done in a colour reaction using streptavidin–alkaline phosphatase conjugate and BCIP/NBT substrates. The entire protocol took only 7 h for the correct identification of the pathogen present in clinical samples of cerebrospinal fluid. The sensitivity and specificity were >95%.(9)

CSF findings  to confirm the diagnosis of meningitis


Table-1  CSF findings  to confirm the diagnosis of meningitis

In patients with persistent elevation of intracranial tension lumbar picture and release of CSF may lead to trans-tentorial herniation of the temporal lobe of the brain and coning of the brainstem which can be fatal if unrecognized. In such cases LP should be done with precaution to monitor the patient and institute life saving measures if coning occurs. Coning of the brain stem leads to drowsiness, coma and slowing of respiration and death. Emergency management consist of intravenous administration of 200 mL of 20% mannitol, elevation of the foot end of the bed and release of supra tentorial pressure by surgical means. If in any case the LP in likely to be delayed and the clinical suspicion is strong, antibiotic therapy should be started straight away, empirically.

Identification of the infecting agent:

  1. Meningococci may be seen in gram stained CSF preparations. This is the most rapid method for diagnosis.
  2. The organism can be cultured from CSF, blood or material taken from skin rashes.
  3. Meningococcal antigen can be identified in CSF by counter immunoelectrophoresis.
  4. Sera of convalescent patients show antibodies to meningococci and these can be demonstrated by complement fixation test, passive hemagglutination, or by radioactive antigen binding tests. These tests are helpful in retrospective diagnosis.
  5. Carrier state is diagnosed by isolating the organisms from material collected from the nasopharynx using a West’s postnasal swab. The swab has to be transported to the laboratory in a special medium (Sturt’s medium).


1. (HSV) encephalitis
Foremost in the differential diagnosis of bacterial meningitis is viral meningoencephalitis, specifically herpes simplex virus (HSV) encephalitis. The clinical presentation of HSV encephalitis includes headache, fever, altered consciousness, focal neurologic deficits (e.g., dysphasia, hemiparesis), and focal or generalized seizures. Features that distinguish herpes encephalitis from bacterial meningitis include the findings onCSFstudies, neuroimaging, and

electroencephalogram (EEG). The classic CSF profile in patients with viralCNSinfections is a lymphocytic pleocytosis with a normal glucose concentration, as contrasted with thePMNpleocytosis and hypoglycorrhachia characteristic of bacterial meningitis.MRIabnormalities other than meningeal enhancement are not seen in uncomplicated bacterial meningitis. Patients with HSV encephalitis frequently have MRI abnormalities, including increased signal within the orbitofrontal and medial temporal lobes and insular cortex on T2-weighted and FLAIR images. There is a distinctive EEG pattern in HSV encephalitis consisting of periodic, stereotyped, sharp-and-slow wave complexes originating in one or both temporal lobes and repeating at regular intervals of 2 to 3 s. The periodic complexes are typically noted between the second and the fifteenth day of the illness and are present in two-thirds of pathologically proven cases of HSV encephalitis.

2. Rickettsial disease
The clinical presentation of encephalitis caused by arthropod-borne viruses  can also resemble that of bacterial meningitis. Another consideration is rickettsial disease . Rocky Mountain spotted fever (RMSF) is transmitted by a tick bite and caused by the bacteria Rickettsia rickettsii. The disease may resemble bacterial meningitis because of its common presentation with high fever, prostration, myalgia, headache, and nausea and vomiting. Most patients develop a characteristic rash within 96 h of the onset of symptoms. The rash is initially a diffuse erythematous maculopapular rash that may be difficult to distinguish from that of meningococcemia. It progresses to a petechial rash, then to a purpuric rash, and, if untreated, to skin necrosis or gangrene. The color of the lesions changes from bright red to very dark red,

then yellowish-green to black. The rash typically begins in the wrist and ankles, and then spreads distally and proximally within a matter of a few hours and involves the palms and soles. Diagnosis is made by immunofluorescent staining of skin biopsy specimens.

3. suppurative CNS infections
Focal suppurative CNS infections , including subdural and epidural empyema and brain abscess, should also be considered. The presence of focal features in a patient with suspected bacterial meningitis should prompt immediate neuroimaging studies;MRI is preferable toCT and is extremely sensitive and specific for diagnosis.

4. Subarachnoid hemorrhage
Among noninfectiousCNSprocesses, subarachnoid hemorrhage  is generally the major consideration. A classic presentation of SAH is the explosive onset of a severe headache or a sudden transient loss of consciousness followed by a severe headache. Nuchal rigidity and vomiting are frequently present and contribute to the resemblance between SAH and meningitis.CT scan is a sensitive indicator of the presence of SAH and usually allows for prompt diagnosis, although occasional patients with suspected SAH have a normal CT scan. In these patients a lumbar puncture is indicated, and the presence of grossly bloody CSF allows SAH to be immediately distinguished from bacterial meningitis(10).

As early as possible, specific treatment should be started .The goal is to begin antibiotic therapy within 60 min of a patient’s arrival in the emergency room. Penicillin G is the antibiotic of choice and should be administered intravenously in a dose of 24 million units daily in divided doses. In children the dose is 16 million units/m2. Dexamethasone 10 mg IV should be started with the first dose of antibiotic and repeated 6 h for 4 days. Dexamethasone exerts its beneficial effect by inhibiting the synthesis of IL-1 and TNF at the level of mRNA, decreasingCSFoutflowresistance, and stabilizing the blood-brain barrier . Further doses should be determined, based on the patient’s progress. Addition of glucocorticoids early in treatment favours prompt recovery and prevents complications considerably(4).

Increased Intracranial Pressure
Emergency treatment of increasedICPincludes elevation of the patient’s head to 30 to 45°, intubation and hyperventilation (PaCO225 to 30 mmHg), and mannitol. Patients with increased ICP should be managed in an intensive care unit. In these patients, accurate ICP measurements are best obtained with an ICP monitoring device(10)

In a study conducted  in 2017 by Rajeev seth et al. to know the rapid and accurate diagnosis of acute pyogenic meningitis due to streptococcus pneumoniaeHaemophilus influenzae Type b and Neisseria meningitidis using a multiplex PCR assay found that, Multiplex PCR was more sensitive than culture or antigen detection, and employing this assay can significantly increase the speed and accuracy of identification of the pathogen(9).

Apart from the commonly encountered pathogens, in an article published in The Indian Journal of Pediatrics,says that recurrent meningitis in infant not responding to conventional antibiotic therapy can be caused by Salmonella typhimurium,which is very uncommon(11).

Cranial nerve palsies are well-known complications of basal meningitis, especially in patients with tuberculous meningitis. However, a minority of bacterial meningitis gets complicated with cranial nerve palsies. Although cerebral infarctions are known to occur with acute bacterial meningitis, infarctions occurring in the brainstem are infrequently described. In an article published  in “Case Reports in Neurological Medicine”. Explained  a  case of 46-year-old healthy female who presented with dysarthria with fever, headache, and vomiting and was diagnosed to have acute pyogenic meningitis complicated with a brainstem infarction resulting in bilateral hypoglossal palsy. Her MRI revealed an infarction in the lower part of the medulla oblongata, probably involving the bilateral hypoglossal nuclei. Isolated bilateral hypoglossal nerve palsy is an extremely rare cranial nerve palsy, secondary to pyogenic meningitis(12).

In a study to evaluate the role of CSF C-Reactive protein for rapid diagnosis and differentiation of different forms of meningitis in children it has found that CSF CRP measurement seems to be a valid early diagnostic test for pyogenic meningitis. It also helps in differentiating pyogenic from other forms of meningitis. The cut off value of CSF CRP for both acute bacterial and partially treated meningitis was ≥0.62 mg/dL and ≥0.55 mg/dL, respectively(13).

Another study aimed to investigate the frequency, clinical characteristics, and prognosis associated with pediatric hyponatremia due to bacterial meningitis  concludes that, Hyponatremia occurred in 66.4% of the assessed pediatric bacterial meningitis patients. Moderate and severe hyponatremia affected the severity of pediatric bacterial meningitis. Only severe hyponatremia affected the short-term prognosis of patients with pediatric bacterial meningitis(14). 

Morbidity and mortality of meningitis are driven by an uncontrolled host inflammatory response. This comprehensive update evaluates the role of the complement system in upregulating and maintaining the inflammatory response in bacterial meningitis. Genetic variation studies, complement level measurements in blood and CSF, and experimental work have together led to the identification of anaphylatoxin C5a as a promising treatment target in bacterial meningitis(15).

In a study to evaluate the role of cortisol as a diagnostic and therapeutic marker in acute bacterial meningitis, says that Cortisol levels in CSF are highly elevated in patients with acute bacterial meningitis. This suggests that intrathecalcortisol may serve as a valuable, rapid, relatively inexpensive diagnostic marker in discriminatingbetween bacterial and aseptic meningitis. This helps in earlier institution of appropriate treatment and thereby decreasing morbidity and mortality(16).

Antibiotic-resistant S. pneumoniae strains may cause infections that fail to respond to antimicrobial-therapy. A study conducted to determine the antibiotic susceptibility of S. pneumoniae strains isolated from children in a primary-care setting in the post-13-valent pneumococcal conjugate vaccine (PCV-13) era shows that pneumococcal nasopharyngeal and AOM isolates from children exhibit reduced susceptibility to penicillin, third generation cephalosporin, fluoroquinolone and carbapenem antibiotics. The new strains have a different profile of resistance compared to the pre-PCV-13 era(17).

Since micro organisms are only one of the many causes of disease, the curative remedy for the disease in the individual must correspond to the  combined effects of various causes. Each and every individual disease varies in its cause and conditions and consequently in its symptoms or effects, and for this reason it follows that there can be no common specific remedy for a disease. Susceptibility ,  a pre condition to acquire the infection which enables bacteria to enter the body, should be considered and treated accordingly(18). In this era of antibiotic resistance Homoeopathy offers a great platform for the treatment of aute infectious diseases like meningitis.

Miasmatic basis
The concept of miasms always appears to be a controversy in Homoeopathy. It was based on Hahnemann’s observations and influenced by the limited pathological knowledge of his time. In Hahnemann’s time very little was known about the etiology and pathogenesis of any disease, including acute infectious diseases. Although scientific world was aware of the existence of microorganisms, their relation with diseases was not fully appreciated. But because of their uniform clinical presentation the acute infectious diseases were recognized as distinct clinical entities even before the discovery of their exact causative factors. Hahnemann used the term ‘acute miasm’ for all such acute infectious diseases(19).

In aphorism 73 of the Organon (6th edition) he mentions acute miasm as recurring in the same manner and hence known by some traditional name. To explain the mechanism of spread of these acute miasms among people he wrote, explaining the term ‘dynamic influence’ in the footnote to the 11th aphorism of the Organon(20).

 Miasmatic basis of Bacterial meningitis
After the entry of the organism in our body, the miasmatic evolution can be explained with the pathogenesis. The organisms at first colonize in the nasopharynx and those people with more susceptibility will allow the entry of which through the ciliated columnar cells and enters the circulation. From there it enters the CSF by passing through the blood brain barrier. All these initial pathologies can be attributed to psora. Upto this stage patient will not feel any symptoms except mild weakness and sore throat. After the bacterial toxins are released, the immune system becomes over stimulated and constitutional symptoms becomes evident. Inflammation of leptomeninges and resulting classical symptoms of meningitis can still be considered as that of psoric in nature. 

As the infalammatory process continues and more and more pro inflammatory mediators are released into the body, cerebral oedema develops which is sycotic in nature. In this stage CSF pressure increases and hydrocephalus may develop. Sub arachanoid fibrosis,cerebritis,ventriculitis can also be attributed to sycosis.

If the infectious process is still not met by the treatment, the bacteria can be disseminated through the circulation to the entire organ system and starts producing damages to the organs such as endocarditis, pyogenic arthritis, adrenal gland haemorrhage and adrenal failure. Further reduced oxygen supply to brain along with thrombosis of small vessels produces brain infarction. All these indicates the miasmatic predominance as syphilitic.

Reportorial approach

1.Shroyen’s synthesis repertory(21).

acon. aesc-g. agar. am-c. Apis arg-n. Arn. ars. bapt. BELL. Bry. bufo cadm-s. Calc. Calc-p. canth. carb-ac. cic. Cimic. Cina Cocc. cor-r. Cupr. diph. dulc. echi. Gels. Glon. HELL. helo-s. Hipp. Hippoz. Hyos. hyper. ign. influ. iodof. ip. Kali-br. Lach. lachn. leptos-ih. lyc. mag-p. med. meningoc. Merc. merc-d. Nat-m. nat-s. Op. oreo. Ox-ac. parathyr. Phos. phys. Plb. pyrog. Rhus-t. sec. Sil. sol-ni. staphycoc. STRAM. Sulph. syc. toxo-g. tub. tub-a. verat. verat-v. ZINC. zinc-cy.

acon. aeth. agar. am-c. ant-t. APIS Arg-n. arn. ars. bapt. BELL. bry. cact. Calc. camph. canth. Carb-v. Cic. Cimic. cocc. crot-h. cupr. cupr-act. dig. GELS. glon. hell. hydr-ac. hyos. Ign. lyc. Nat-m. NAT-S. Nux-v. OP. Phos. phys. plb. psor. pyrog. RHUS-R. Rhus-t. sal-ac. Sil. sol-ni. stram. Sulph. tarent. verat. VERAT-V. Zinc.

abrot. Acon. APIS, BELL. Bry. Calc. Cic. Cimic. cocc. crot-h. cupr. cyt-l. dulc. echi. GELS. helo-s. Hyos. hyper. Ip. kali-i. merc. Nat-m. Nat-s. nux-v. Op. oreo. ox-ac. Plb. Rhus-t. sec. tub. verat-v. Zinc.

GENERALS – CONVULSIONS – meningitis, in cerebrospinal
ail. Ant-t. Apis Arg-n. cic. Crot-h. cupr. ferr-p. Glon. Hell. ip. nat-s. Tarent. Verat. verat-v. zinc.

GENERALS – NEUROLOGICAL complaints – meningitis; from

MIND – DELIRIUM – meningitis cerebrospinalis
Apis Chr-ac. Hell. naja Nat-s. Sulph. Verat. verat-v. zinc.

EAR – INFLAMMATION – Media – followed by – meningitis

2. Homoeopathic Medical Repertory by Robin Murphy(22).

Diseases – MENINGITIS, brain
acon. aeth. Agar. ail. APIS apoc. arg-n. Arn. ars. atro. bapt. BELL. Bry. Calc. calc-br. Calc-p. camph. canth. carb-ac. chin. chinin-s. chr-o. Cic. cimic. Cina Cocc. crot-c. crot-h. Cupr. Cupr-act. Cupr-m. dig. echi. Gels. Glon. HELL. Hippoz. Hydr-ac. Hyos. hyper. iod. iodof. ip. Kali-br. kali-i. kreos. Lach. med. Merc. merc-c. merc-d. mosch. Nat-m. nat-s. Op. oreo. ox-ac. Phos. phys. Plb. Rhus-t. Sil. sol-ni. STRAM. Sulph. Tub. verat-v. vip. ZINC. Zinc-c. Zinc-m. 

Diseases – MENINGITIS, brain – basilar
carb-ac. CIC. tub. verat-v.

Diseases – MENINGITIS, brain – children, of
ACON. APIS apoc. arn. BELL. calc-p. con. gels.

Diseases – MENINGITIS, brain – chronic
PHOS. plb. sep.

Diseases – MENINGITIS, brain – chronic – effusion of serum into cavity of arachnoid, with

Diseases – MENINGITIS, brain – delirium, with
apis BELL. cic. STRAM.

Diseases – MENINGITIS, brain – eruption, after suppressed
APIS stram.

Diseases – MENINGITIS, brain – exanthematous fevers

Diseases – MENINGITIS, brain – eyes inflamed, wild, staring, pupils dilated, shrinking look as if from fear

Diseases – MENINGITIS, brain – head from pillow, frequently lifts

Diseases – MENINGITIS, brain – paralytic symptoms, with
crot-h. hell.

Diseases – MENINGITIS, brain – sun, from exposure to, after having hair cut

Diseases – MENINGITIS, brain – suppressed ear discharge, from

Diseases – MENINGITIS, brain – traumatic
ARN. Hyper. op.

Diseases – MENINGITIS, brain – tubercular
APIS atro. calc. Calc-p. lyc. spong. Tub.

Diseases – MENINGITIS, brain – violent disposition to strike, bite, or injure others
bell. Stram.

Diseases – MENINGITIS, brain – vomit, inclination to

Diseases – MENINGITIS, brain – wet, after getting

Diseases – MENINGITIS, brain – meningitis, cerbro-spinal
acon. aeth. agar. am-c. ant-t. APIS Arg-n. arn. ars. bapt. BELL. bry. cact. camph. canth. Cic. Cimic. cocc. crot-h. cupr. dig. GELS. glon. hell. hydr-ac. hyos. Ign. lyc. Nat-m. NAT-S. Nux-v. OP. Phos. plb. Rhus-t. sol-ni. tarent. verat. verat-v. Zinc.

Diseases – MENINGITIS, brain – meningitis, spinal
Acon. APIS BELL. Bry. Calc. Calc-p. Cic. Cimic. cocc. crot-h. cupr. dulc. GELS. Hyos. hyper. Ip. kali-i. merc. Nat-m. Nat-s. nux-v. Op. ox-ac. Plb. Rhus-t. sec. verat-v. Zinc.

Diseases – MENINGITIS, brain – meningitis, spinal – bony structures, involving

3. Concise Repertory of Homoeopathic Medicines by S.R Phatak(23)

C – Cerebro-spinal axis – fever
Apis arn. Bell. bry. cupr. Gels. hell. merc-d. nat-s. stram. sulph. verat-v. zinc.

C – Cerebro-spinal axis – fever – basilar

C – Cerebro-spinal axis – fever – suppressed discharges, from

C – Cerebro-spinal axis – fever – urine; with clear, pale
bell. hyos. lach. phos.

4. A Synoptic Key to the Materia Medica By Cyrus Maxwell Boger(24)

HEAD – Meningitis
Apis arn. Bell. bry. cupr. Gels. hell. merc-d. stram. sulph. Zinc.

5. Boericke’s repertory(25)

HEAD – Brain – Inflammation – cerebral, acute and chronic
acon. aeth. Apis apoc. arn. ars. bapt. Bell. Bry. calc. calc-br. calc-p. camph. carb-ac. chin. chinin-s. chr-o. Cic. cimic. crot-h. Cupr. Cupr-act. dig. gels. glon. Hell. hydr-ac. hyper. iod. iodof. kali-i. kreos. lach. merc-c. merc-d. mosch. Op. ox-ac. phos. phys. plb. rhus-t. Sil. sol-ni. Stram. Sulph. Tub. verat-v. vip. Zinc.

HEAD – Brain – Inflammation – basilar
Cupr-cy. dig. hell. iod. sec. tub. Verat-v.

HEAD – Brain – Inflammation – cerebrospinal
Agar. ail. Apis arg-n. atro. Bell. bry. Cic. Cimic. cocc. Crot-h. Cupr-act. cyt-l. echi. Gels. glon. Hell. hyos. ip. kali-i. nat-s. op. oreo. phys. sil. stram. sulph. verat-v. zinc. Zinc-cy.

HEAD – Brain – Inflammation – traumatic
acon. Arn. bell. Hyper. nat-s. sil.

HEAD – Brain – Inflammation – tubercular
Apis Bac. bell. bry. calc. Calc-p. cocc. Cupr-cy. dig. glon. Hell. hyos. iod. Iodof. kali-i. op. stram. Sulph. tub. Verat-v. zinc. zinc-o.

6. The Complete Repertory,  Roger Van Zandvoort(26)

HEAD – INFLAMMATION – meninges, meningitis
achy. acon. AETH. aether agar. ail. am-br. ant-t. aphis APIS apisin. apoc. arg-n. ARN. ARS. atro-pur. bac. BAPT. BELL. BRY. cadm-s. CALC. calc-br. calc-hp. CALC-P. CAMPH. cann-s. canth. CARB-AC. cham. CHIN. chinin-s. chlol. CHR-AC. cic. cimic. CINA cob-n. COCC. con. cor-r. crot-h. cryp. CUPR. CUPR-ACT. cupr-cy. cyt-l. daph. desm-g. DIG. diph-t-tpt. dor. echi. ferr. ferr-p. flav. GELS. GLON. HELL. hep. hippoz. hoit. hydr-ac. HYOS. HYPER. iod. iodof. ip. KALI-BR. kali-hp. kali-i. kali-m. kreos. LACH. lachn. lyc. med. MERC. merc-c. merc-cy. mosch. NAT-M. nat-s. nux-v. oena. OP. oreo. OX-AC. phos. PHYS. PLB. prot. PULS. ran-b. RHUS-T. SIL. SOL-NI. STRAM. stry-xyz. SULPH. syc. thuj. toxo-g. tub. VERAT-V. vip. ZINC. zinc-cy. zinc-o. zinc-val.

HEAD – INFLAMMATION – meninges, meningitis – children, in
ACON. APIS apisin. APOC. ARN. CON. cor-r. ferr. flav. gels. GLON. HELL. HEP. med. prot. STRAM. thuj. toxo-g. zinc.

HEAD – INFLAMMATION – meninges, meningitis – children, in – sycotic or syphilitic background, with

HEAD – INFLAMMATION – meninges, meningitis – fear, from –OP.

HEAD – INFLAMMATION – meninges, meningitis – grief, from OP.

HEAD – INFLAMMATION – meninges, meningitis – injury, after ARN.

HEAD – INFLAMMATION – meninges, meningitis – opisthotonos, with cic.

HEAD – INFLAMMATION – brain – delivery, parturition, in insufficient gels.

HEAD – INFLAMMATION – brain – cerebro-spinal
AGAR. ail. am-br. ant-t. APIS arg-n. atro-pur. BELL. bry. cedr. chlol. CIC. CIMIC. cocc. crot-h. CUPR-ACT. cupr-ar. cyt-l. echi. GELS. glon. HELL. helo. hyos. ip. kali-i. nat-s. op. oreo. phys. ran-s. sil. stram. sulph. tarent. verat. verat-v. zinc. ZINC-CY.

HEAD – INFLAMMATION – exsudativa, meninges HELL.

HEAD – INFLAMMATION – tetanic, meninges phys.


1.The Twelve Tissue Remedies of Schüssler,William Boericke(27)
Ferrum phosphoricum First stage of meningitis, high fever, quick pulse, delirium, etc. Kalium muriaticum The second remedy, when effusion takes place. Calcarea phosphorica The chief remedy in hydrocephalus, acute and chronic.Hydrocephaloid conditions, open  fontanelles, flat, depressed, etc. Prevents hydrocephalus in families predisposed thereto.  Give a powder of the second trituration morning and evening. When already developed, alternate with Argent. nit. 6. (Grauvogl.) Natrium sulphuricum Violent head-pains, especially at base of brain and back of neck.  Crushing pain, as if base of brain were crushed in a vise, or something gnawing there.  After injuries to the head.

2.  The Prescriber, J.H Clarke (28)

Arn. 1, 1h.When caused by a blow, at the beginning. 

Aco. 3, 1h.

When fever comes on, with restlessness, anxiety, fearfulness, dry skin,thirst. 

Bell. 3, 1h. 

When there is delirium, patient tries to escape, flushed face, dilated pupils.  

Bry. 3, 1h.

 If there is little delirium, but much pain, white tongue, nausea; wheneffusion appears to have taken place, depression and stupor coming on.  

Hell.n.  3, 1/2h. 

Great depression, much pain in the back of the head and neck. 

Apis 3x, 1h. Shrill cries in sleep, nervous fidgetiness. 

Sul. 6, 1h.

After Apis and other medicines, hot head, cold feet in thosesubject to eruptions. 

Arn. 1, 2h. 

When the fever has subsided, if the original cause has been concussion,and after Apis or Bry. has been given.  

Zinc. met. 6, 2h.

After the fever, when Bell. or Helleb. has been given. 

3. Practical Homoeopathic Therapeutics  ,W. A. Dewey(29)

Belladonna  Belladonna corresponds to the initial stages, where there is intense heat of body, strong pulse, bright red face and delirium, where the cerebral irritation is marked by intense pain in the head, starting out of sleep crying out, grinding teeth. For simple meningitis, not the tubercular form, when everything is acute and intense; when effusion commences, however, it ceases to be the remedy. Aconitum napellus  Meningitis from heat of the sun’s rays after long exposure thereto, or cerebral congestions from anger. It is only useful at the onset. Fear is a marked symptom.  Veratrum viride  Intense cerebral congestion, rapid pulse, tendency to convulsions, followed by prostration. Elliot considers Veratrum viride in the lower potencies our best remedy in acute meningitis. Coldness of the surface, loss of consciousness, dilated pupils, labored, slow, irregular pulse.  Gelsemium sempervirens  Is hardly homoeopathic to pain as its action is wholly motor, but it may be indicated in meningitis by its general symptoms. It is less often indicated and hence less valuable than Belladonna. Yet Spalding has used the remedy as a basic one in the cerebro-spinal variety with uniform success, losing but one case.  Bryonia alba  Suits well cerebral effusions with a benumbed sensorium. The following will be useful indications upon which to prescribe Bryonia. Constant chewing motion with the mouth; when moved screams with pain; child stupid, abdomen distended; tongue white, pains are most sharp and stitching, and the patient drinks greedily; there is a livid flushed face, high temperature, copious sweats. Thus it is seen that Bryonia produces a characteristic image of meningitis and suits especially cases caused by suppressed eruptions.  Apis mellifica

Here nervous agitation predominates; there are shrill cries, stabbing pains; the child puts its hand to its head and screams. There is an oedematous face, scanty urine, and the patient is thirstless, it suits especially infantile cases and especially the tubercular form due to an undeveloped eruption.  Cicuta virosa  Cicuta is useful in the irritative stage when there are general convulsions, twitching in fingers and unconsciousness. It also markedly controls the effusion. The head is spasmodically drawn back with stiff neck. Violent jerks in any part of the body. Strangles on drinking, dilated pupils and staring look, trismus; one of our best remedies, having a fine clinical record.  Helleborus niger  Mental torpor marks this drug; a sensorial apathy, there is want of reaction. It corresponds to a later stage of the disease, when effusion has taken place; then symptoms such as wrinkling the forehead, dilated pupils and automatic movements of one arm and one leg are indicative of Helleborus. There are shooting pains in the head, sudden crying out, screaming, boring head into the pillow. The cries have a most pitiful sound.  Camphora officinalis  In the fulminant variety where the poison falls on the patient like a thunderbolt and collapse approaches speedily. The patient is cold, pale and pulseless, eyes sunken, face livid. Patient cold, but does not want to be covered.  Iodoformium  Iodoform 6x has proved useful in O’Connor’s hands, and some remarkable cases were reported in the North American Journal of Homoeopathy a few years ago as having been cured by inunctions of Iodoform cerate into the scalp. Some very hopeless cases were thus cured. Dr. Martin, of Pittsburgh, used the 2x with success. It is also endorsed by Boericke and Clarke.

Zincum metallicum  This remedy corresponds to the sub acute form, especially if tubercular and due to suppressed eruptions. Febrile disturbance is absent or slight, there are marked twitchings, jerkings and hyperaesthesia of all the senses and skin, and tremulousness of the feet. At the beginning there are sharp lancinating pains and great exhaustion of nerve force. The 6x trituration is recommended.  Sulphur  Sulphur is useful in tubercular meningitis; the child lies in a stupor with cold sweat on forehead, jerking of limbs, spasms, and suppressed urine. Retrocessed eruptions may be the cause.  Tuberculinum bovinum kent  Tuberculinum and Calcarea carbonica may prove useful remedies. They correspond to a basic or psoric taint which favors the development of the disease. Clarke advises Bacillinum 100th, which he claims is very prompt in its action.  Calcarea carbonica  Tuberculinum and Calcarea carbonica may prove useful remedies. They correspond to a basic or psoric taint which favors the development of the disease. Clarke advises Bacillinum 100th, which he claims is very prompt in its action.  Cuprum metallicum  Cuprum suits cases marked with violent convulsions, thumbs clenched, loud screaming, face pale with blue lips. No remedy equals it in these conditions, but it is of more use in the later stages.

Exact diagnosis of the organism is the main stay in the antibiotic therapy advocated in the management of Bacterial meningitis. Most  of the patients treated as bacterial meningitis did not receive a proper diagnostic workup. The choice of antibiotic was not tailored to the specific clinical condition of the patient. Such an approach may result in poor treatment outcomes and lead to antibiotic resistance(30). The excessive and indiscriminate use of  all these drugs in both human and veterinary practices has led to the emergence and dissemination of  so many resistant organisms. In this era of antibiotic resistance, Homoeopathy offers a great hope in the field of medicine for the purpose of treatment as well as prevention of these deadly infectious diseases. According to the principles of Homoeopathy, the Homoeopathic medicines will bring the immunity of the patient to a higher level. Apart from the acute life threatening stages of these infections,where the patient needs various basic life supports, Homoeopathic medicines can be employed in the convalescent stages inorder to prevent the further progress and complications. As the literature evidences are few , it is necessary to do more studies in this regard to promote the scope of Homoeopathy in the management of various infections of central nervous system.


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Dr.Appu Gopalakrishnan MD(Scholar)
Dept. of Organon of Medicine
Govt.Homoeopathic Medical College,Calicut

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