Cognitive Outcome from Herpes simplex Encephalitis
December 1, 1997 3 minutes read
Cognitive Outcome from Herpes simplex Encephalitis
ABSTRACTS & COMMENTARY
Source: Hokkanen L, Launes J. Cognitive recovery instead of decline after acute encephalitis: A prospective follow up study. J Neurol Neurosurg Psychiatry 1997;63:222-227; McGrath N, et al. Herpes simplex encephalitis treated with acyclovir: Diagnosis and long-term outcome. J Neurol Neurosurg Psychiatry 1997;63:321-326.
Encephalitis, herpes simplex and otherwise, is widely considered to leave a high incidence of chronic neurological disability. In an earlier report of outcomes from a variety of encephalitides (J Neurol Neurosurg Psychiatry 1996;61:478-484; Neuro Alert 1997;15:34-35), Hokkanen et al found immediate cognitive impairment in four of their eight HSE patients and 21 of 37 non-HSV encephalitic cases. The present report provides follow-up data of the total group of patients between 16 and 45 months after onset.
Included cases were: HSE, 8; H. zoster, 7; other defined encephalitides, 9; cause unknown, 21. All patients had initial neuropsychologic appraisals at a mean of 26.5 days after onset of illness. Thirty-three of the 45, including four of the HSE patients, performed normally in the first test. The damaged 12 were retested at a mean of 36.6 months after onset. Of these, eight had measurably improved, and four had not. Five of the 12 patients remained with severe cognitive impairments, while four suffered from intractable epilepsy. Of the remaining 33, 11 were not working, but among these, four were beyond retirement age. As to HSV outcomes, only two had persistent mental disability. One had deteriorated.
McGrath et al describe early and late outcomes in 42 patients (27 females, 15 males) with confirmed HSE. Most common initial symptoms included headache (74%), confusion (67%), nausea-vomiting (60%), fever, and seizures (each 50%). Principal onset signs included fever (98%), abnormal mental state (90%), and meningism (55%). Somatic neurologic changes were less common but included hemiparesis (33%), dysphasia (28%), and mild motor signs (19%). Laboratory findings included 100% accuracy for HSV DNA (36/36) or HSV antibody (16/21) in CSF; CSF pleocytosis (90%); an abnormal EEG (93%) and abnormal CT (66%). Time of treatment after first symptom had no general relationship to outcome, but onset of stupor or coma before starting treatment greatly increased the risk of poor outcome, as did older age.
Eight neurologically devastated patitents died within one year. Of the remaining 34, only one became neurologically normal. Nineteen were able to resume their pre-illness everyday activities, but most had poor memory. Nine others became independent but handicapped, and five others remained severely disabled with memory loss, behavioral-emotional disorders, and epilepsy. Overall employment was not described.
COMMENTARY
The total numbers of these two outcome reports of acyclovir-treated HSE differ somewhat, possibly reflecting differences in numbers and, perhaps, time of acyclovir administration. The Hokkanen and Launes report somewhat glosses over the emotional instability of their patients, whereas the McGrath et al survey may reflect longer treatment delays. McGrath et al emphasize that their results show improvement over earlier years prior to the availability of effective antiviral agents. What’s needed, of course, is better records of outcomes in patients treated within the first few hours after symptoms appear. Acyclovir is minimally toxic, and HSE remains devastatingly dangerous if treatment is delayed. Neurology Alert recommends that all patients who present with unexplained headache, fever, and CSF pleocytosis be tested for HSV DNA in the CSF and be instantly started on acyclovir while awaiting specific or alternate diagnoses. fp
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