A

NeurovascularMedicine.com
The contents are under continuing development and improvements and may contain errors of omission or fact. The official launch will be at the end of 2018. Feedback vital and always welcome at drokane at gmail.com. This is not to be used for the assessment, diagnosis or management of patients. It should not be regarded as medical advice. It is only for educational purposes. Please adhere to your local protocols. If you are unwell please seek healthcare advice from your doctor. This does not replace senior or specialist advice. If you do not accept this then please do not use the website.

Encephalitis


Learning objectives

  • Presentation of encephalitis as a stroke mimic
  • Appropriate investigations
  • Managing the patient with suspected encephalitis

Introduction

  • Encephalitis is an inflammatory process involving the brain parenchyma
  • Associated with clinical or laboratory evidence of neurological dysfunction
  • May mimic stroke particularly if affects dominant temporal lobe with dysphasia

Cause

  • Herpes simplex virus types 1 and 2, Varicella zoster virus, CMV
  • Enteroviruses, Adenovirus, Parechovirus, measles virus, HIV
  • St Louis encephalitis, West Nile encephalitis (WNE): Extreme lethargy
  • Autoimmune (main tumour associations in brackets) see below
  • Acute disseminated encephalomyelitis, Bickerstaff's encephalitis

Clinical

  • Confusion/Delirium,change in personality or behaviour
  • Coma. seizures, obtunded, cold sores, lethargy
  • Headache, altered speech, amnesia, temporal lobe seizures

Differential

  • Infectious processes
  • Encephalopathy
  • Autoimmune processes such as ADEM or autoimmune encephalitis

Investigation

  • FBC: Raised WCC, U&E, Raised CRP, Low Na
  • CSF: >5 white cells x 10 9 /L predominantly lymphocytes with normal or moderately raised protein and glucose is normal.
  • CSF PCR for HSV highly sensitive and specific in immunocompetent adults
  • HIV test in all
  • EEG findings suggestive of encephalitis
  • CT head: may show hypoattenuation and oedema and even hydrocephalus
  • MRI: T2 and FLAIR signal hyperintensities abnormal in 90% of cases of HSV encephalitis involving medial temporal lobes. Temporal lobe and limbic abnormalities are seen in HSV and HHV-6 encephalitis
  • Antibodies: NMDAR antibody encephalitis and LGI-1 antibody
  • Antibodies against neuronal surface antigens: NMDAR antibody encephalitis (ovarian teratoma)
  • Antibodies to LGI-1 encephalitis (thymoma)
  • Antibodies against intracellular antigens: anti-Hu (small cell lung tumour), anti-Ma (testicular tumours), anti-GAD

Management

  • ABC and airways management if low GCS. Supportive care. May need a period of ITU and support.
  • With recovery there may be long terms cognitive and amnestic and other issues
  • Aciclovir is a time-critical life-saving treatment for HSV encephalitis and should be commenced if diagnosis suspected before lumbar puncture if this is delayed. Aciclovir treatment for 14 days then repeat LP to ensure PCR negative.
  • Autoimmune encephalitis: corticosteroids intravenously or orally. Intravenous Ig or plasma exchange are often also used, especially in those failing to improve

References

Note: The plan is to keep the website free through donations and advertisers that do not present any conflicts of interest. I am keen to advertise courses and conferences. If you have found the site useful or have any constructive comments please write to me at drokane (at) gmail.com. I keep a list of patrons to whom I am indebted who have contributed. If you would like to advertise a course or conference then please contact me directly for costs and to discuss a sponsored link from this site.

free web counter