Neurology · MU Sofia

47. Primary acute viral panencephalitis

Explains primary acute viral panencephalitis as widespread brain inflammation during a primary viral infection, naming the main causative viruses with HSV-1 singled out as the most important. It then covers pathogenesis, general, CNS, behavioural and focal clinical features, and the temporal-limbic pattern of HSV encephalitis. Examination findings, CSF changes with the red blood cell clue, MRI findings, five differentials, prognosis and treatment with acyclovir and intensive supportive care close the note.

Inside: 1 section · 1 labelled picture · 15 flashcards · 2 min

Topic 47 of 88 in the MU Sofia syllabus for Neurology (Medicine, Year 4). The free AceMed note covers it in 1 section, about 290 words (2 min of reading), with 15 flashcards.

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  1. Primary acute viral panencephalitis

Primary acute viral panencephalitis

Definition: Primary acute viral panencephalitis is a severe viral infection involving widespread inflammation of the entire brain (gray + white matter), occurring during primary viral infection, not due to immune memory or reactivation.

  • It is often rapidly progressive and life-threatening.

Etiology

  • Main viruses: Herpes simplex virus (HSV-1) (most important). Enteroviruses.Arboviruses (mosquito-borne encephalitis viruses). Rabies virus (can produce panencephalitic picture)

Pathogenesis

  • Primary viral invasion of CNS
  • Diffuse neuronal injury + necrosis
  • Widespread inflammation of: Cortex. Basal ganglia.Brainstem. White matter (variable)

Clinical Features

A. General Symptoms: High fever. Severe headache. Malaise. Vomiting

B. CNS Dysfunction (Key Triad)

  • Altered consciousness (confusion → coma)
  • Seizures (often early and severe)
  • Focal neurological deficits

C. Behavioral & Cognitive Changes: Personality changes. Memory loss. Psychosis / hallucinations

D. Focal Signs: Hemiparesis. Aphasia. Cranial nerve deficits

Important Clinical Variant: HSV Encephalitis

  • Typical involvement: Temporal lobe + limbic system
  • Features: Aphasia. Memory impairment. Behavioral changes. Seizures (temporal lobe focus)

Examination Findings

  • General: Fever. Reduced consciousness
  • Neurological exam: UMN signs (hyperreflexia, Babinski).Focal deficits (depending on affected area). Possible meningeal irritation signs

CSF Findings: ↑ opening pressure (mild–moderate). Clear or slightly turbid CSF.↑ lymphocytes.Mild ↑ protein. Normal glucose

  • Special clue: HSV → RBCs in CSF (hemorrhagic necrosis)

Neuroimaging

  • MRI (best modality): Temporal lobe hyperintensity (HSV). Diffuse edema. Necrotic areas

Differential Diagnosis

1. Acute bacterial meningitis: Neutrophils in CSF. Severe meningeal signs. No focal cortical deficits early

2. Tuberculous meningitis: Subacute course.Basal enhancement. Low glucose

3. Brain abscess: Focal lesion. Ring-enhancing on imaging

4. Stroke: Sudden onset. No fever. No CSF inflammation

5. Metabolic encephalopathy: No focal signs. Normal CSF

Prognosis: Often severe and rapidly progressive

  • HSV encephalitis: high mortality if untreated
  • Early treatment improves outcome significantly

Treatment

  • Antiviral therapy: Acyclovir (HSV)
  • ICU supportive care: Control seizures. Reduce intracranial pressure.Management of complications

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