EMERGENCY:Fever + confusion + seizure = possible encephalitis —call040-46324365immediately — 24 hours, 7 days— 24/7
Expert assessment of Japanese encephalitis, herpes simplex encephalitis, dengue and scrub typhus encephalitis, and NMDA- receptor autoimmune encephalitis — with same-hour MRI brain, lumbar puncture with viral PCR and autoimmune antibody panels, EEG, empirical IV acyclovir from admission, and immunotherapy for autoimmune cases at KIMS Neuroscience, Secunderabad, Hyderabad.
Encephalitis is inflammation of the brain parenchyma (the brain tissue itself), distinguished from meningitis (which affects the covering membranes) by the presence of brain dysfunction: altered consciousness, personality and behaviour change, seizures, or focal deficits. Causes in India include Japanese encephalitis (JEV; endemic in Telangana, July–November, 20–30% CFR, mosquito-borne), herpes simplex encephalitis (most common treatable cause), dengue encephalitis, scrub typhus encephalitis (underdiagnosed; the eschar is pathognomonic), enteroviral encephalitis, and autoimmune encephalitis (NMDA-receptor encephalitis is treatable and often associated with an ovarian teratoma in young women). At KIMS, empirical IV acyclovir is started in ALL encephalitis presentations while investigation proceeds, because delayed HSV encephalitis treatment is permanently destructive. Autoimmune encephalitis must be excluded before a primary psychiatric diagnosis is accepted.
| Fact | Details |
|---|---|
| Definition | Brain parenchyma inflammation (not meninges) · Fever + altered consciousness + seizures + behaviour change · Distinguished from meningitis by brain dysfunction |
| India causes | JEV (Telangana endemic, Jul–Nov) · HSV (treatable) · Enteroviral (faecal-oral) · Dengue · Scrub typhus (underdiagnosed) · NMDA-R autoimmune (treatable) |
| JEV | Culex mosquito · Rice paddies · 20–30% CFR · 50–70% neuropsychiatric sequelae in survivors · Thalamic butterfly sign on MRI · Parkinsonian + dystonic features · No antiviral: supportive only |
| Scrub typhus eschar | Painless black crusted mite bite lesion · Pathognomonic · Look in: axillae, groin, behind ears, genitals · Doxycycline dramatically effective |
| NMDA-R encephalitis | Psychiatric features first · Anti-NMDAR antibody in CSF · Ovarian teratoma ~50% of young women · Treatable: steroids + IVIg + teratoma removal · Delta brush on EEG |
| KIMS protocol | Empirical acyclovir ALL presentations · MRI brain + LP (viral PCR + autoimmune panel) · EEG · Autoimmune antibody panel (NMDAR, LGI1, CASPR2, GABA-B, AMPAR, DPPX) · Pelvic MRI in young women |
| Autoimmune encephalitis stopping rule | Autoimmune encephalitis must be excluded before primary psychiatric diagnosis is accepted · Young woman + new-onset psychosis + movement abnormalities + seizures = NMDAR antibody test first |
The essential facts that shape how encephalitis is recognised, triaged, and treated at KIMS — from the brain-parenchyma definition that distinguishes it from meningitis through the India-specific epidemic and endemic causes to the autoimmune encephalitides that mimic acute psychiatric illness but are fully treatable when caught early.
Encephalitis is inflammation of the brain parenchyma (the brain tissue itself), distinguished from meningitis (inflammation of the covering membranes) by the presence of brain dysfunction: altered consciousness, personality and behaviour change, cognitive impairment, or focal neurological deficits. In practice, meningo-encephalitis (both membranes and brain involved) is common. Encephalitis can be infectious (viral, bacterial, parasitic) or immune-mediated (autoimmune encephalitis — the brain attacked by the immune system rather than a pathogen directly).
Japanese encephalitis (JEV) is the most significant epidemic viral encephalitis in India, with large endemic zones in Telangana, Andhra Pradesh, Uttar Pradesh, Bihar, and Assam. It is mosquito-borne (Culex mosquitoes, which breed in rice paddies), seasonal (July–November, peak post-monsoon), with case fatality rates of 20–30% and neuropsychiatric sequelae in 50–70% of survivors. Dengue encephalitis, scrub typhus encephalitis, and enteroviral encephalitis are important additional causes in Hyderabad and Telangana.
Anti-NMDA receptor encephalitis and other autoimmune encephalitides present with psychiatric features (psychosis, agitation, personality change) followed by seizures, autonomic instability, and coma. They can initially be mistaken for acute psychiatric illness. They are not caused by a pathogen — the brain is attacked by the patient’s own antibodies. They are treatable with immunotherapy (steroids, IVIg, plasma exchange) and outcome is excellent when treated promptly. The diagnosis is made by detecting specific antibodies in CSF or serum. NMDA-R encephalitis is the most common autoimmune encephalitis and is seen across India including in Hyderabad.
Any person with fever and any change in consciousness (confusion, unusual behaviour, drowsiness, personality change) or new-onset seizures has possible encephalitis until proven otherwise. Do not attribute confusion to dehydration, heatstroke, or stress without neurological assessment. Call 040-46324365.
040-46324365
040-44885000
A 26-year-old woman in Hyderabad develops fever on a Monday. By Wednesday, her family notices she is behaving strangely — agitated, saying things that do not make sense, laughing at nothing. By Thursday morning, she has a generalised tonic-clonic seizure. By Thursday afternoon, she is admitted to KIMS in an altered state of consciousness, GCS 11.
This is not a simple fever. The progression from fever to psychiatric symptoms to seizures to impaired consciousness over 4 days is the hallmark of encephalitis — inflammation of the brain parenchyma itself. At KIMS, the assessment is urgent. MRI brain shows T2/FLAIR signal change in the bilateral temporal lobes and orbitofrontal cortex. CSF shows mild lymphocytic pleocytosis. HSV PCR is sent. Anti-NMDA receptor antibody in CSF and serum is sent. EEG shows diffuse slowing with right temporal sharp waves. IV acyclovir 10 mg/kg three times daily is started immediately (because HSV encephalitis cannot be excluded and cannot wait for the CSF PCR result). IV methylprednisolone is also started for the possibility of autoimmune encephalitis.
The CSF HSV PCR returns negative at 48 hours. Anti-NMDA receptor antibody returns strongly positive. The diagnosis is NMDA-receptor autoimmune encephalitis — not an infection, but her own immune system attacking her brain. Acyclovir is stopped. Immunotherapy is escalated: IV methylprednisolone →1g for 5 days, IVIg 2g/kg over 5 days. A pelvic MRI and CT chest reveal an ovarian teratoma (the most common tumour trigger for NMDA-R encephalitis in young women). The teratoma is removed laparoscopically.
At 6 weeks, she is walking, talking, and beginning to return to normal. Full recovery takes 6 months. This outcome — complete recovery from a condition that looked like acute psychosis and could easily have been managed on a psychiatric ward — is what happens when encephalitis is correctly diagnosed and treated promptly.
Fever + confusion, fever + seizure, or fever + behaviour change requires emergency neurological assessment — not reassurance and paracetamol. KIMS Neuroscience runs an immediate triage pathway with same-hour MRI, LP, EEG, empirical acyclovir, and the autoimmune antibody panel for any suspected encephalitis.
040-44885000Appointment line: 040-44885000The six causes below summarise what the KIMS encephalitis pathway is built around — JEV as the most significant epidemic viral encephalitis in India; HSV as the most common treatable sporadic cause; enteroviral, dengue, and scrub typhus as endemic infectious differentials in Hyderabad and Telangana; and NMDA-R autoimmune encephalitis as the great imitator that demands an antibody panel before a primary psychiatric diagnosis is accepted.
Key clinical features: Acute fever, altered sensorium, movement disorders (tremor, Parkinsonism), seizures.
Diagnostic test: Serology (IgM ELISA in CSF/blood).
Case fatality: 20–30%.
Sequelae: 50–70% of survivors develop neuropsychiatric sequelae.
Key clinical features: Fever, headache, personality change, temporal lobe seizures, aphasia.
Diagnostic test: CSF HSV PCR.
Case fatality: <30% with acyclovir; >70% without.
Sequelae: Memory loss, personality change, epilepsy.
Key clinical features: Fever, encephalitis, hand-foot-mouth (EV71), rhombencephalitis.
Diagnostic test: CSF/stool PCR.
Case fatality: 5–25% (EV71).
Sequelae: Neurological deficits in survivors.
Key clinical features: Fever, rash, altered consciousness, seizures.
Diagnostic test: NS1 antigen, dengue IgM/IgG.
Case fatality: <5% with encephalitis.
Sequelae: Usually good.
Key clinical features: Fever, eschar (painless black skin lesion), encephalitis, multi-organ failure.
Diagnostic test: Weil-Felix, specific IgM ELISA.
Case fatality: 7–15%.
Sequelae: Variable.
Key clinical features: Psychiatric features first, then seizures, catatonia, autonomic instability, coma.
Diagnostic test: Anti-NMDAR antibody in CSF.
Case fatality: <5% with treatment.
Sequelae: Excellent with immunotherapy if treated promptly.
Encephalitis presents with a combination of fever, altered consciousness, seizures, psychiatric features, characteristic movement disorders (in JEV), and pathognomonic skin findings (the eschar of scrub typhus) — each of which is specifically assessed and acted on at KIMS.
Present in most infectious encephalitis. Fever may be absent or mild in some autoimmune encephalitides (particularly NMDA-R encephalitis). Headache is common but not as defining as in meningitis. The absence of fever does not exclude encephalitis.
The key feature distinguishing encephalitis from meningitis: impaired consciousness, confusion, disorientation, or marked personality and behaviour change. Ranges from subtle cognitive changes to coma. Any altered consciousness with fever is encephalitis until proven otherwise. GCS scoring at KIMS documents baseline and tracks progression.
Seizures occur in approximately 60–80% of encephalitis cases. They may be focal (jerking of one limb, eye deviation) or generalised. Status epilepticus (prolonged or repeated seizures) is a common complication of severe encephalitis and is managed with IV antiseizure medications at KIMS (levetiracetam, valproate, phenobarbitone, with IV lorazepam or diazepam for active seizures).
Autoimmune encephalitis (particularly NMDA-R) typically begins with prominent psychiatric features: acute psychosis, agitation, visual or auditory hallucinations, personality change, or catatonia. These occur before or alongside mild fever. Young women with new-onset acute psychosis, particularly when accompanied by movement abnormalities (orofacial dyskinesia, abnormal eye movements), autonomic instability (variable heart rate and blood pressure), or seizures, should have autoimmune encephalitis specifically investigated at KIMS before a primary psychiatric diagnosis is confirmed.
JEV encephalitis produces a characteristic movement disorder profile: parkinsonian features (rigidity, tremor, mask-like face), dystonia, and myoclonus — reflecting damage to the basal ganglia, thalamus, and brainstem. This profile in a patient from an endemic area during the July–November season is highly suggestive of JEV encephalitis. Contrast MRI typically shows T2 signal change in the thalami and substantia nigra (the “thalamic butterfly sign”).
Scrub typhus encephalitis from Orientia tsutsugamushi (transmitted by mite bites) is significantly underdiagnosed in India, including Telangana. The eschar — a painless black, crusted lesion at the mite bite site — is pathognomonic. It is typically found in concealed locations: axillae, groin, behind the ears, around the genitals. Many patients and doctors do not look for it. Any encephalitis with fever, particularly in rural or periurban patients, should prompt a systematic skin examination for eschar at KIMS.
Encephalitis diagnosis at KIMS combines emergency clinical assessment with same-hour MRI brain, simultaneous lumbar puncture with a full viral PCR plus autoimmune antibody panel, EEG for seizure and pattern detection, and an autoimmune-specific antibody panel from both serum and CSF with a tumour search where indicated — all begun before empirical IV acyclovir is delayed.
Immediate clinical assessment: fever, GCS, seizure history, focal neurological signs, meningism. Blood tests: CBC, metabolic panel, liver function, blood cultures, dengue NS1 and IgM/IgG, scrub typhus IgM ELISA, malaria antigen if appropriate. ECG (cardiac arrhythmias in NMDA-R encephalitis). Continuous EEG monitoring if seizures have occurred.
MRI brain with gadolinium, specifically: FLAIR and DWI sequences for cortical signal change; T2 for basal ganglia and thalamic changes (JEV, autoimmune); temporal lobe signal changes (HSV); leptomeningeal enhancement (meningo-encephalitis). Normal MRI does not exclude encephalitis. MRI is performed within hours at KIMS in acute encephalitis.
CSF for: cell count, glucose, protein; bacterial culture; AFB and TB PCR; viral PCR panel (HSV-1/2, VZV, CMV, EBV, Enterovirus, JEV); anti-NMDA-R antibody and other autoimmune encephalitis antibodies; India ink and cryptococcal antigen. Opening pressure measured (raised in meningitis and some encephalitides with cerebral oedema).
Routine or continuous video-EEG for seizure identification and monitoring. Delta brush pattern is characteristic of NMDA-R encephalitis. Periodic lateralised epileptiform discharges (PLEDs) in the temporal lobe are characteristic of HSV encephalitis. EEG guides antiseizure medication dosing and identifies subclinical seizures.
In any encephalitis without a clear infectious cause, or with prominent psychiatric features, a full autoimmune encephalitis antibody panel is sent from both serum and CSF: anti-NMDAR, anti-LGI1, anti-CASPR2, anti-GABA-B, anti-AMPAR, anti-DPPX. Ovarian teratoma ultrasound/MRI in young women with NMDA-R encephalitis (present in approximately 50%). Chest CT for thymoma in older patients with thymoma-associated encephalitis.
The KIMS encephalitis protocol: IV acyclovir 10 mg/kg every 8 hours is started in ALL encephalitis presentations while awaiting CSF HSV PCR — even if HSV is not the most likely diagnosis.
The reason: HSV encephalitis is the most common treatable cause of severe sporadic encephalitis, and the consequences of a 24–48 hour delay in treatment (while waiting for PCR results) are permanent and catastrophic.
Acyclovir is safe, and the cost of an unnecessary course is trivial compared to the cost of a preventable death or permanent disability from untreated HSE.
No specific antiviral therapy for JEV exists. Treatment is entirely supportive: airway management and ventilatory support; seizure control with IV antiseizure medications; cerebral oedema management (hypertonic saline or mannitol for raised ICP); fever control; fluid and electrolyte management; nutritional support via nasogastric tube; prevention of complications (aspiration pneumonia, pressure sores, deep vein thrombosis).
Intensive neurorehabilitation at KIMS is begun as soon as the patient is medically stable — the Parkinsonian and movement disorder features of JEV often respond partially to physiotherapy and levodopa.
Doxycycline 100mg twice daily for 7–14 days — dramatically effective when started promptly. Alternative: azithromycin.
Empirical doxycycline should be given to any encephalitis presentation with eschar or from a rural setting where scrub typhus is clinically suspected, even before serology results return.
First-line immunotherapy: IV methylprednisolone 1g/day for 5 days, and/or IVIg 2g/kg over 5 days, and/or plasma exchange (plasmapheresis) for 5 sessions.
Second-line: rituximab or mycophenolate mofetil for patients who do not respond to first-line.
If an underlying tumour is identified (ovarian teratoma, thymoma), urgent removal is the most important treatment — the encephalitis often improves dramatically after tumour removal.
Levetiracetam IV 500–1,500mg twice daily is first-line at KIMS for encephalitis-associated seizures. Valproate IV is added if levetiracetam is insufficient.
Status epilepticus is managed with IV lorazepam → phenobarbitone → intubation + midazolam infusion if refractory.
Related Conditions
Encephalitis belongs to the family of infectious and post-infectious neurological disorders evaluated and managed at KIMS Neuroscience:
Fever + confusion. Fever + seizure. Fever + behaving strangely. These are not symptoms to monitor at home.
At KIMS Neuroscience, Secunderabad, Hyderabad, every encephalitis presentation receives MRI brain, CSF viral and autoimmune panel, EEG, and empirical acyclovir from admission. The treatable causes — HSV, scrub typhus, autoimmune — are specifically identified and treated. Emergency: 040-46324365.
International enquiries: info@kimsneurosciences.com