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Herpes Simplex Virus (HSV) encephalitis

Summary

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  • Acute necrotizing encephalitis caused by HSV-1 or HSV-2
  • Typically affects temporal and frontal lobes
  • Characterised by fever, altered mental status, and focal neurological deficits

Pathophysiology

  • HSV-1 is the most common cause in adults (90% of cases)
  • HSV-2 more common in neonates and immunocompromised individuals
  • Virus enters via olfactory or trigeminal nerve pathways
  • Causes cytotoxic and vasogenic oedema, haemorrhage, and necrosis
  • Predilection for limbic structures, particularly temporal lobes

Demographics

  • Incidence: 2-4 cases per million per year
  • Bimodal age distribution:
    • Peak in young adults (20-30 years)
    • Second peak in older adults (>50 years)
  • No gender predilection
  • Can occur in all age groups, including neonates

Diagnosis

  • Clinical presentation:
    • Fever, headache, altered mental status
    • Focal neurological deficits (e.g., aphasia, hemiparesis)
    • Seizures (70% of cases)
  • Laboratory findings:
    • CSF analysis: pleocytosis, elevated protein, normal glucose
    • PCR detection of HSV DNA in CSF (sensitivity >95%, specificity >99%)
  • EEG: periodic lateralized epileptiform discharges (PLEDs)

Imaging

  • CT findings:
    • Early: normal or subtle low attenuation in affected areas
    • Late: haemorrhage, contrast enhancement, mass effect
  • MRI findings (more sensitive than CT):
    • T2/FLAIR: hyperintense signal in affected regions
    • DWI: restricted diffusion in acute phase
    • T1 post-contrast: gyral enhancement
    • SWI: petechial haemorrhages
  • Typical distribution:
    • Asymmetric involvement of temporal lobes (95% of cases)
    • Frontal lobe involvement (80% of cases)
    • Insular cortex, cingulate gyrus may be affected
    • Sparing of basal ganglia

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  • 50-year-old patient presented with headache and confusion.
  • CT showed swelling and low attenuation in the anterior and mesial left temporal lobe and in the right hippocampus.
  • The parenchymal low attenuation gave the impression of a hyperdense vessel (Mach effect) but infarction was not likely as both MCA nad PCA territories were involved.
  • There was high T2, FLAIR and DWI signal (without clear diffusion restriction) but no enhancement.

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  • 40-year-old patient presented with 2 day history of confusion and reduced GCS, headache and fever.
  • MRI showed hyperintensity and swelling of the right mesial temporal lobe and diffusion restriction extending up to the right parietal lobe.

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  • 70-year-old patient presented with dysphasia and right-sided weakness and seizures. HSV was identified in CSF.
  • MRI showed diffusion restriction in the cortex of left cerebral hemisphere as well as the right insula. There was swelling and subtle cortical enhancement.

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  • 60-year-old patient presented with expressive dysphasia.
  • MRI showed diffuse patchy cortical, white matter and ganglionic hyperintensity.
  • On follow-up, hyperintensity involving most of the left temporal lobe resolved while marked hyperintensity developed in the right temporal lobe.
  • Despite being repeatly negative on CSF, brain biopsy reavealed an HSV encephalitis.

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  • 75-year-old patient presented with dysphasia and right sided weakness.
  • MRI showed cortical DWI hyperintensity in the left frontal, parietal, temporal lobes and insular cortex bilaterally.
  • Initially concerned about an acute infarct, the widespread and exclusively cortical involvement and a normal CTA, made HSV encephalitis more likely (which was confirmed on CSF analysis).

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  • A 45-year-old patient presented with right sided weakness and a fever.
  • CT showed a haematoma in the left paramedian frontal lobe.
  • MRI showed oedema around the haematoma as well as subtle high FLAIR signal in the cortex of the left frontal lobe and the right cingulate.
  • On follow-up imaging, the FLAIR hyperintensity (and diffusion restriction) had extended through the limbic system.
  • CSF HSV-1 PCR was positive.

Treatment

  • Antiviral therapy:
    • Acyclovir 10 mg/kg IV every 8 hours for 14-21 days
    • Early initiation crucial for improved outcomes
  • Supportive care:
    • Management of increased intracranial pressure
    • Seizure control with antiepileptic drugs
    • Monitoring for syndrome of inappropriate antidiuretic hormone secretion (SIADH)
  • Prognosis:
    • Mortality rate: 70% if untreated, 20-30% with treatment
    • Significant neurological sequelae in survivors (memory deficits, personality changes, epilepsy)
    • Early diagnosis and treatment associated with better outcomes

Differential diagnosis

Differential Diagnosis Differentiating Feature
Autoimmune limbic encephalitis Bilateral mesial temporal FLAIR hyperintensity without haemorrhage; typically no cortical ribboning on DWI; may enhance
MCA infarction Confined to MCA vascular territory; involves basal ganglia; no involvement of contralateral mesial temporal lobe
Gliomatosis cerebri / low-grade glioma Infiltrative T2 signal without swelling or DWI restriction; no cortical haemorrhage or gyral enhancement
Neurosyphilis Mesiotemporal T2 hyperintensity similar to HSV; leptomeningeal and cortical enhancement; infarcts from vasculitis
Other viral encephalitides (HHV-6, VZV, EBV) Similar mesiotemporal involvement; indistinguishable on imaging alone