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Subcortical type cognitive impairment in herpes zoster encephalitis
L Hokkanen1, J Launes, E Poutiainen
1Department of Neurology, University of Helsinki, Finland.
Journal of Neurology
|April 1, 1997
Summary
Herpes zoster encephalitis (HZE) can cause cognitive decline, particularly affecting memory and processing speed. Brain imaging reveals hypoperfusion, suggesting subcortical dysfunction in HZE patients.
Area of Science:
- Neurology
- Neurovirology
- Infectious Diseases
Background:
- Herpes zoster encephalitis (HZE) is a rare but serious neurological complication of varicella-zoster virus reactivation.
- Understanding the neuroimaging and neuropsychological sequelae of HZE is crucial for patient management.
Purpose of the Study:
- To investigate the neurological, neuroimaging, and neuropsychological characteristics of acute herpes zoster encephalitis.
- To compare the outcomes of HZE patients treated with acyclovir to healthy controls.
Main Methods:
- Neurological and neuropsychological assessments were performed on nine immunocompetent HZE patients treated with acyclovir.
- Computed tomography (CT) and single photon emission computed tomography (SPECT) were used for neuroimaging.
- Neuropsychological performance was compared with 16 healthy controls.
Main Results:
- CT revealed infarct-like lesions in two patients.
- SPECT showed hypoperfusion in the frontal areas of six of seven examined patients.
- Neuropsychological testing indicated a decline in memory and cognitive processing speed, with behavioral and mood changes observed in most patients.
Conclusions:
- Herpes zoster encephalitis is associated with subcortical dysfunction, as evidenced by brain perfusion patterns and neuropsychological profiles.
- While most patients recover well, cognitive deficits, particularly in memory and processing speed, can persist.
- HZE-related memory impairment is generally less severe than that seen in herpes simplex encephalitis.