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Meningitis & Encephalitis



Definition– It is an infection of pia – arachnoid and the CSF of the arachnoid space.


  1. >20years- S. pneumoniae                   
  2. 2 to 20 years-N. meningitides
  3. Neonates-Streptococcus agalactiae               
  4. 2 to 12 months-H. influenzae
  5. <1mth, pregnant,>60years old, immunocompromised, organ transplant (LQ 2012) -Listeria monocytogenes

Clinical FeaturesTriad of symptom –

  1. Fever,
  2. Headache,
  3. Neck stiffness.
  1. Meningeal signs -
    1. Neck rigidity                                        
    2. Kernig’s sign                                
    3. Brudzinski’s sign
  2. Raised ICP signs -
    1. Bradycardia                                
    2. Irregular respiration            
    3. Hypertension        
    4. Decerebrate rigidity             
    5. Papilledema                 
    6. VI Nerve palsy
  3. Seizures
    1. Due to Focal arterial ischemia                     
    2. Focal edema
    3. Cortical venous thrombosis with haemg.        
    4. Fever
  4. Hyponatremia (SIADH)
  5. Cerebral oedema
  6. Rash of meningococcemia

Complications of Meningitis

  1. Raised ICP           
  2. Cranial nerve palsy              
  3. Vasculitis              
  4. Focal deficit
  5. Seizure                
  6. Hydrocephalus                      
  7. SIADH                 
  8. Brain abscess
  9. Mental retardation         
  10. Sub dural effusion (Common in children with H. influenza meningitis)
  11. Altered sensorium
  12. Death
Important Points:

Cerebral hamartoma is not a complication.

Causes of altered sensorium in a patient on treatment for meningitis:

  1. Hyponatremia due to SIADH
  2. Hydrocephalus
  3. End arteritis / brain infarction
  4. TB encephalopathy
  5. Hemorrhagic – Leukoencephalopathy
  6. Ventriculitis / arachnoiditis
  7. Iatrogenic drug induced hepatitis

Investigation need to be done in such cases are (AIIMS Nov 2012)

  1. MRI             
  2. NCCT           
  3. Liver function tests



CSF analysis (AIPG 2007)



Cells /ml





0 – 5

2/3 of Plasma

15 – 45mg%



Highly raised, mainly polys

Highly reduced

1 – 2g%


Fibrin web

raised, mainly Lympho


2 – 5 g%

Aseptic (viral)


50 – 1500 Lympho





Malignant cells


Normal/ increased


Extra edge: CSF abnormalities in bacterial meningitis. (Ref. Hari. 18th ed., Pg- 3414)


1. Opening pressure


>180 mmH2O

2. CSF/serum glucose



3. Latex agglutination


May be positive in patients with meningitis due to S. pneumoniae,
N. meningitidis, H. influenzae type b, E. coli, group B streptococci

4. Limulus lysate


Positive in cases of gram-negative meningitis

5. PCR


Detects bacterial DNA

6. Gram's stain


Positive in >60%

7. Culture


Positive in >80%

Important Points:

Elevated CSF protein and decreased sugar and chloride levels along with characteristic clinical features of meningitis suggest a diagnosis of Tubercular meningitis.

Typical CSF features of Tubercular Meningitis are: (LQ 2012)

  1. Cells: Mononuclear cells (except early infection when PMN cells are seen)
  2. Protein: Increased above 40 mg/100ml. 
  3. Sugar: Usually reduced to less than 2/3rd of blood sugar.
  4. Chloride level: usually reduced.

Important points about TBM:

  1. In TBM, the exudate is mainly basal (basal brain is involved)
  2. Subarachnoid space is involved-by the exudate (i.e. subarachnoiditis is present) 
  3. Involvement is mainly of the Leptomeninges i.e. Pia-arachnoid. (Duramater is usually spared.)

Protein Level in CSF


Low CSF protein levels can occur in conditions such as

  1. Repeated lumbar puncture or a chronic leak,
  2. Seen in some children between the ages of six months and two years,
  3. In acute water intoxication
  4. In a minority of patients with idiopathic intracranial hypertension.

Extra Edge: CSF protein levels do not fall in hypoproteinemia.

Treatment – 
(Ref. Hari. 18th ed., Table 381.3 Pg- 3416)


1. Empirical therapy

Third generation cephalosporin and vancomycin

2. N. Meningitidis (7 days)

Penicillin G/Ampicillin, ceftriaxone/cefotaxime

3. Str. Pneumoniae (14 days)

Penicillin G, Vancomycin + ceftriaxone

4. Gm negative (21days)


5. Pseudomonas


6. Staphylococci

Nafcillin, Vancomycin

7. Listeria (21 day)


8. H. influenza


Important Points Role of: I/V Dexamethasone -
  1. Used in Meningitis due to H. influenza and str. pneumonia in children (0.6mg/kg/d) for 2 – 4 days
  2. It decrease meningeal inflammation
  3. Decrease Neurological sequelae like hearing loss.

Important Points: Treatment of Raised ICT
  1. Elevation of head to 30 – 450
  2. Hyper ventilation
  3. Mannitol

Treatment of Cryptococcosis:

Neural (Meningo-encephalitis)

Amphotericin B ± Flucytosine for 2 weeks, followed by Fluconazole (oral) OD


Amphotericin B ± Flucytosine


Important Points:

Amphotericin B is the drug of choice for Cryptococcosis.


Extra Edge: Neoplastic Meningitis: (Ref. Hari. 18th ed., Pg- 2271)

  1. Tumor involving the leptomeninges is a complication of both primary CNS tumors and tumors that metastasize to the CNS.
  2. Melanoma, breast and lung cancer, lymphoma (including AIDS-associated), and acute leukemia are the most common causes.
  3. Diagnosis is made by demonstrating malignant cells in the CSF; (Up to 40% of patients may have false-negative CSF cytology).
  4. An elevated CSF protein level is nearly always present (except in HTLV-1–associated adult T cell leukemia).
  5. MRI findings suggestive of neoplastic meningitis include leptomeningeal, subependymal, dural, or cranial nerve enhancement; superficial cerebral lesions; and communicating hydrocephalus.

Chronic Meningitis
(Ref. Hari. 18th ed., Pg- 3435)

  1. Chronic inflammation of the meninges can produce profound neurologic disability and may be fatal if not successfully treated.
  2. The condition is most commonly diagnosed when a characteristic neurologic syndrome exists for >4 weeks and is associated with a persistent inflammatory response in the CSF (white blood cell count >5/mL).
  3. Five categories of disease account for most cases of chronic meningitis:
    1. Meningeal infections,
    2. Malignancy,
    3. Noninfectious inflammatory disorders,
    4. Chemical meningitis
    5. Parameningeal infections.
  4. Spread from the subarachnoid space into brain parenchyma may occur via the arachnoid cuffs that surround blood vessels that penetrate brain tissue (Virchow-Robin spaces).


Viruses causing encephalitis.

1. The most common cause of sporadic viral encephalitis


2. The most common cause of epidemic viral encephalitis


3. The most common cause of viral meningitis is


Important Points:
  1. Japanese encephalitis virus is an arbovirus and is one of the most common causes of encephalitis outbreaks.
  2. Nipah virus: is a new member of the paramyxo virus family.
  3. HSV type 2 is a common cause of aseptic meningitis but it is not a cause of encephalitis.
  4. Focal findings in a patient with encephalitis should always raise the possibility of HSV encephalitis.

Clinical manifestations common to all viral encephalitis

  1. Fever, Altered consciousness/confusional state, Headache
  2. Focal findings
    1. Focal seizures          
    2. Focal deficit (weakness)   
    3. Frontoparietal hyper intense lesion on MRI

Examples of focal findings include:


Areas of increased signal intensity in the frontotemporal, cingulate or insular region of brain on MRI


Temporoparietal areas of low absorption, mass effect and contrast enhancement


Periodic temporal lobe spikes on a background of slow or low amplitude activity on EEG

Important Points:


MRI findings in other condition


MRI findings


Multiple cystic lesions with enhancement of MRI

Acute pyogenic meningitis

Diffuse meningeal enhancement on MRI

Carcinoma meningitis

Nodular tumor deposits in the meninges or diffuse meningeal enhancement on MRI

The drug of choice in Herplex Simplex encephalitis is Acyclovir.



Drug of choice

1. Herpes simplex Encephalitis

2. Neonatal herpes simplex

3. Herpes simplex Keratitis

4. Herpes simplex Oro-labialis



Trifluridine / Vidarabine


Herpes Virus Encephalitis

  1. HSE result from primary HSV-1 infection, predominantly occurring under the age of 18; or over 50 years of age.
  2. HSE is thought to be caused by the retrograde transmission of virus from a peripheral site on the face following HSV-1 reactivation, along a nerve axon, to the brain.  
  3. The virus lies dormant in the ganglion of the trigeminal cranial nerve, The olfactory nerve may also be involved in HSE, which may explain its predilection for the temporal lobes of the brain, as the olfactory nerve sends branches there.
  4. Without treatment, HSE results in rapid death in approximately 70% of cases. 
  5. MRI shows frontal and temporal lobe enhancement. (AIIMS May 2008)


  1. Most common central nervous system parasitic infection Neurocysticercosis.
  2. Commonest presentation of neurocysticercosis is Seizures
  3. These is wide variety of presentation of Neurocysticercosis depending on the intensity of the infestation, the localization of cysticerci and the degree of inflammatory reaction.
  4. Cysticercosis is infection with the larval stage (cysticercus cellulosae) of T. solum(beef tape –worm).
  5. The lesion of neurocysticercosis is readily visualized by MRI or CT Scan.
  6. Parenchymal brain calcifications are the most common findings on NCCT.

These cysts are located in order of frequency in:

  1. CNS (Neurological manifestations are the most common) - Harrison's 15th/1249
  2. Subcutaneous tissue             
  3. Striated muscle    
  4. Globe of the eye
  1. Brain Parenchyma is the most common site of neurocysticercosis. 'The ventricular system is the second most common site of neurocysticercosis.
  2. Most common sites of Neurocysticercosis:
    Parenchymatous> interventricular > subarachnoid> spinal> orbital.


  1. Niclosamide is ineffective for neurocysticercosis
  2. Albendazole and praziquantel are both effective in treatment
  3. Albendazole is preferred. (DOC is albendazole)
  4. Anticonvulsants (antiepileptics) should be given during drug treatment and probably for an indefinite time afterwards.
  5. Corticosteroids are used during the acute phase of cysticercotic encephalitis, if intracranial hypertension is present. (it is used for the prevention of development of hydrocephalus, and does not have much role once hydrocephalus is already present.)

Granulomatous amoebic encephalitis

  1. Granulomatous amoebic encephalitis ("GAE") is a central nervous system disease caused by certain species, especially species of Acanthamoeba and Balamuthia mandrillaris.
  2. Clinical Features
    1. GAE can present with: focal paralysis, seizures, brainstem symptoms, and other neurological problems, some of which may mimic glioma (especially brainstem glioma), or other brain diseases, which may hamper timely  diagnosis.
    2. These symptoms are caused by inflammatory necrosis of brain tissue brought on by amoebic infiltrates.
  3. Appearance on Biopsy
    1. A brain biopsy will reveal the presence of infection by pathogenic amoebas.
    2. In GAE, these present as general inflammation and sparse granules.
    3. On microscopic examination, infiltrates of amoebic cysts and/or trophozoites will be visible.
  4. Treatment
    Even with treatment, the condition is often fatal

Slow virus diseases


  1. Subacute Sclerosing Panencephalitis (SSPE)
    1. SSPE is a chronic complication of measles with a delayed onset and an outcome that is nearly always fatal
    2. This is considered a 'slow virus infection' and is believed to result from persistent infection with an altered measles virus that is harboured intracellularly in CNS for several years.
    3. Progressive disorder characterized by demyelination of CNS
    4. Associated with a chronic infection of brain tissue with measles virus. 

Note: Stage II of SSPE - Massive Myoclonus Is Characteristic - Nelson 18h /1335.

Important Points:
  1. CNS manifestation of CMV include meningoencephalitis and retinitis.
  2. Hemorrhagic infarctions is not a feature of CMV retinitis.
  1. Progressive Multifocal Leukoencephalopathy (PML)
    1. PML is a rare demyelinating CNS disorder caused by the reactivation of JC virus.
    2. The virus stays latent in the kidneys and lymphoid organs until reactivation.
    3. PML mainly occurs in adults with impaired cell-mediated immunity, especially AIDS patients but also in those with lymphoproliferative and myeloproliferative disorders.  Decreasing immunosuppression in non-AIDS patents with PML (eg. Transplant patients).
    4. JCV causes lytic infection of oligodendrocytes in the white matter. (AIPG 2011)
    5. Symptoms include altered mental status, aphasia, ataxia, hemiparesis or hemiplegia and visual filed disturbances, Seizures.
    6. Treatment: Risperidone and mirtazapine.
Important Points:

Oligodendrocyte inclusion bodies are seen in PML (AIIMS Nov 2010).

  1. Prion Diseases
    1. Prion (PrPSC) is an altered form of normal protein (PrPC) (AIIMS Nov 2012) that can transform other normal protein into prion protein hence infectivity.
    2. Prion are highly resistant to common sterilization procedure. (AIIMS Nov 2012)
    3. They are not immunogenic (AIIMS Nov 2012)
    4. Prion disease have a long incubation period. (AIIMS Nov 2012)

Prion Diseases are (Ref. Hari. 18th ed., Pg- 3441)

  1. Creutzfeldt- Jakob disease                   
  2. Kuru      
  3. Gerstmann Sträussler-Scheinker syndrome  
  4. Fatal familial insomnia

Creutzfeldt- Jakob disease. (AIPG 2008)

  1. The unique feature of this disease is that it can be transmitted as infectious, congenital or degenerative
  2. 10 – 12 % cases are familial. 
  3. On light microscopy, the pathologic hallmarks of CJD are spongiform degeneration (Tiny cavities in the brain) and astrocytic gliosis.
  4. The lack of an inflammatory response in CJD and other prion diseases is an important pathologic feature of these degenerative disorders.
  5. The gene for the prion protein is on chromosome 20; approximately 10% of cases are hereditary.
    Illness can develop because of infection or somatic and germ cell mutations. The CSF 14-3-3 protein is a marker for Creutzfeldt - Jakob disease.
  6. It can be transmitted by corneal transplant also. (LQ 2012)
  7. Patients has severe dementia with cerebellar ataxia and diffuse myoclonic jerks.
  8. Cortical blindness can occurs
  9. The EEG often demonstrates periodic discharges and an abnormal background rhythm.
  10. Death usually occurs within several months of the onset of the disease.

Extra Edge: EEG characteristic in diseases other than epilepsy:

  1. Subacute sclerosing panencephalitis (SSPE)
    Characteristic periodic pattern with bursts every 3 to 8 seconds of high voltage, sharp slow waves followed by periods of  attenuated (falt) background) (Burst Suppression)
  2. Creutzfeldt Jacob disease (CJD)
    (Repetitive high voltage, triphasic and polyphasic sharp discharges are seen in most advanced cases)      
  3. Hepatic encephalopathy
    Characteristic Symmetric high voltage triphasic slow wave in frontal region.
  4. HSV
    Periodic lateralizing epileptiform discharges (PLEDs)

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