Makindo Medical Notes.com

Related Subjects: |Herpes Varicella-Zoster (Shingles) Infection |Chickenpox Varicella Infection |Varicella Cerebral Vasculopathy |Herpes Viruses |Herpes Zoster Ophthalmicus (HZO) Shingles |MonkeyPox |Mumps |Measles |Rubella (German Measles) |Epstein-Barr Virus infection |Cytomegalovirus (CMV) infections |CMV retinitis infections |Toxoplasmosis

Treat with IV Aciclovir if this is in the differential. Can cause a focal neurological deficit and appear identical to an MCA infarct in a patient who is otherwise well. Clues - fever, cold sore, MRI changes, seizure, confusion, clouding of consciousness and progression. If the presentation is identical to stroke then as it occurs approximately in a ratio to 1 in 3000 strokes then the diagnosis is often delayed. A typical stroke unit may see one case as a stroke mimic every 5-10 years.

About

• Most serious form is Herpes simplex encephalitis
• Other causes include West Nile virus

Epidemiology

• There are approximately 1 cases per million per year
• 50-100 per annum in UK.
• Half over 50 so that is 25-50 over 50 in UK
• Many present late with coma and with florid findings
• Others present clinical like stroke that then deteriorates
• Assume half are stroke like
• This is 12-25 which present on a background of 100,000 strokes PA in UK

Virology

• HSV-1 encephalitis is more common in adults
• HSV-2 infection is more common in neonates

Aetiology

• 90% of normal people are seropositive for HSV-1 indicating past exposure to the virus
• HSV infects nasopharyngeal cells into the sensory branch of lingual nerve then ascends to trigeminal ganglion and remains latent for a lifetime.
• Reactivation may occur due to immunosuppression, trauma, or other stresses
• There can also be secondary reinfection
• HSV-1 has a predilection for the temporal lobes and less so frontal
• Invades brain parenchyma and may cause haemorrhagic necrosis
• Can even cause a fulminant haemorrhagic necrotising encephalitis.
• There is involvement of limbic systems with bilateral but asymmetric involvement.

Reactivation Causes: May see cold sores

• Trauma
• Sunlight (recent Sun holiday ??)
• Immunosuppression
• X-ray irradiation
• Stress - physical or psychological
• Pneumococcal infection
• Meningococcal infection
• Menstruation

Pathology

• There is haemorrhagic necrosis of the inferiomedial portion of the temporal lobe
• Disease begins unilaterally, then spreads to the contralateral temporal lobe

Clinical

• Headache, Fever, Focal seizures and generalised seizures
• Cold sores on lips or mouth
• Altered consciousness, and abnormalities of speech and behaviour
• Hyperreflexia, coma, hemiparesis

Investigations

• FBC: elevated WCC may be present
• U&E: Hyponatraemia may be seen in 50% but occurs in 35% of strokes
• CT/MRI to exclude abscess will show lesions in the temporal lobes. May be necrosis and haemorrhage
• CSF - raised lymphocytes and elevated protein. Bloody CSF can result in a falsely negative PCR as the porphyrins can interfere with the assay
• HSV: also check enteroviral PCR or WNV (West Nile virus) if suspected.
• MRI - asymmetrical temporal lobe changes with HSV with inflammation, swelling and even necrosis. There is restricted diffusion is common due to cytotoxic oedema restricted diffusion is less intense compared to infarction
• EEG - slowing and periodic discharges
• Brain Biopsy - HSV encephalitis may show neuronal inclusion bodies called Cowdry Type A found in the nucleus

Poor prognostic indicators

• Age > 30, Coma at presentation, Bilateral EEG abnormalities
• High CNS viral load, Treatment delayed (4 days), abnormal CT

Differential

• Immunosuppressed consider CMV infection which may need Ganciclovir

Management

• If you have any suspicion of the diagnosis at all then treat with IV Aciclovir even if it turns out to be wrong. Untreated HSV is a tragedy.
• Treatment threshold must be very low initially. Studies show that Mortality was significantly reduced in Aciclovir-treated patients (28 per cent versus 54 per cent) however even with early treatment mortality is 30% and long term neurological injury is common.
• IV Aciclovir 10 mg/kg TDS is given for 2-3 weeks.
• Monitor renal function, hydration and NG feeding as required.
• Often initially managed in HDU setting. Of those who survive there is a high risk of ongoing neurological deficits.
• There is no evidence base for steroids. Treat any seizures.
• For the most severe cases hemicraniectomy may be needed for decompression

Late complications

• Long term sequelae are seen in half of those treated such as poor memory, emotional lability, poor concentration, irritability, depression

References

• Herpes simplex encephalitis
• Herpes encephalitis : a stroke mimicker
• HSV Virology Online

Patient Information

• Patient site on Encephalitis"