Encephalitis: Understanding the Affected Body Parts and Causes

Encephalitis: Brain Inflammation Explained

Encephalitis is inflammation of the brain parenchyma. It differs from meningitis (meningeal inflammation) though they often coexist (meningoencephalitis).

Primary Affected Structure

The brain—specifically neurons, glia, and supporting tissues. Inflammation disrupts neural function, causing edema, cellular injury, and circuit dysfunction.

Common Causes

Category	Examples
Viral (most common)	HSV-1, VZV, enteroviruses, arboviruses (WNV, JEV, EEE), rabies, CMV, EBV, HIV
Bacterial	Often secondary to meningitis (S. pneumoniae, N. meningitidis), or direct extension (otitis, sinusitis); Listeria, Mycobacterium
Fungal	Cryptococcus, Histoplasma, Coccidioides, Aspergillus (immunocompromised)
Parasitic	Naegleria fowleri (PAM), Acanthamoeba (GAE), Toxoplasma (immunocompromised)
Autoimmune	Anti-NMDA receptor, LGI1, CASPR2, GAD65 antibodies; ADEM; paraneoplastic
Other	Drug reactions, post-vaccinal (rare), metabolic toxins

Key Clinical Features

• Fever, headache, altered mental status (confusion to coma)
• Seizures (30–50%)
• Focal neurologic deficits (aphasia, hemiparesis, cranial nerve palsies)
• Behavioral/personality changes
• Movement disorders (chorea, dystonia in autoimmune)

Diagnostic Cornerstones

• MRI brain with contrast (T2/FLAIR hyperintensities in temporal lobes for HSV)
• CSF: lymphocytic pleocytosis, elevated protein, normal glucose, PCR for viruses
• EEG: periodic lateralized epileptiform discharges (PLEDs) in HSV
• Serum/CSF autoantibody panels for autoimmune encephalitis

Treatment Principles

• Empiric acyclovir immediately for suspected HSV (reduces mortality from 70% to 20%)
• Targeted antimicrobials per etiology
• Immunotherapy (steroids, IVIG, PLEX, rituximab) for autoimmune
• Supportive: ICP management, antiepileptics, ventilation, nutrition

Early recognition and etiology-directed therapy are critical for survival and neurologic recovery.