|Herpes Varicella-Zoster (Shingles) Infection
|Chickenpox Varicella Infection
|Varicella Cerebral Vasculopathy
|Herpes Zoster Ophthalmicus (HZO) Shingles
|Rubella (German Measles)
|Epstein-Barr Virus infection
| Cytomegalovirus (CMV) infections
| CMV retinitis infections
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.
- Most serious form is Herpes simplex encephalitis
- Other causes include West Nile virus
- 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
- HSV-1 encephalitis is more common in adults
- HSV-2 infection is more common in neonates
- 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
- Sunlight (recent Sun holiday ??)
- X-ray irradiation
- Stress - physical or psychological
- Pneumococcal infection
- Meningococcal infection
- There is haemorrhagic necrosis of the inferiomedial portion of the temporal lobe
- Disease begins unilaterally, then spreads to the contralateral temporal lobe
- Headache, Fever, Focal seizures and generalised seizures
- Cold sores on lips or mouth
- Altered consciousness, and abnormalities of speech and behaviour
- Hyperreflexia, coma, hemiparesis
- 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
- Immunosuppressed consider CMV infection which may need Ganciclovir
- 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
- Long term sequelae are seen in half of those treated such as poor memory, emotional lability, poor concentration, irritability, depression