Brain (CNS)
Viral Encephalitis
바이러스성뇌염
Inflammation of brain parenchyma (HSV-1 is most common sporadic cause)
- How common
- ~5-10 per 100,000/yr
- Typical age
- All ages (HSV in children/adults)
What is it?
Neurotropic virus invades brain → neuronal infection → inflammation/necrosis → preferential temporal/limbic involvement (HSV).
Commonly affected: Temporal/limbic (HSV), basal ganglia (some arboviruses)
How it develops
- Viral entryOlfactory/peripheral nerves → CNS
- Neuronal infectionViral replication, neuronal death
- InflammationLymphocytic infiltrate, microglial activation
- Edema/necrosisTemporal hemorrhagic necrosis in HSV
Symptoms
- Altered mental statusConfusion, hallucinations, memory loss
- Seizures50%+ in HSV encephalitis
- Fever/headacheOften as prodrome
- Focal deficitsAphasia, hemiparesis
- Behavior/personality changeLimbic involvement
How it is examined
- Neuro examFocal deficits, LOC, post-ictal state
- Skin examLook for VZV vesicles
- Immune statusHIV, transplant, immunosuppression
Imaging
CT often normal early or shows temporal hypodensity.
- Often normal early
- Temporal edema (HSV)
- Possible hemorrhage
MRI is standard - temporal T2/FLAIR hyperintensity.
- Bilateral temporal T2/FLAIR hyperintensity
- Limbic involvement
- Hemorrhagic necrosis
Non-surgical care
- IV acyclovir immediately10 mg/kg q8h x 14-21 days (empiric for HSV)
- CSF HSV PCRConfirm dx; continue acyclovir even if negative early
- Antiseizure medsLevetiracetam
- ICP controlHead elevation, mannitol
- Supportive careFluids, electrolytes, nutrition
Conservative options are generally tried first. Medications listed here can have side effects — discuss them with your prescriber.
When surgery is considered
Severe edema or impending herniation
Procedures that may be discussed
- Decompressive craniectomy for malignant edema
- EVD for hydrocephalus
- Brain biopsy if diagnosis unclear
Outlook
Untreated HSV encephalitis mortality >70%; with prompt acyclovir, mortality 10-20%, sequelae ~50%.