Herpes simplex encephalitis treated with acyclovir: diagnosis and long term outcome

N McGrath, N E Anderson, M C Croxson, K F Powell, N McGrath, N E Anderson, M C Croxson, K F Powell

Abstract

Objectives: The frequency and characteristics of the long term sequelae of herpes simplex encephalitis were assessed after treatment with acyclovir.

Methods: Patients were included if they were treated with acyclovir and the diagnosis of herpes simplex encephalitis was confirmed by culture of herpes simplex virus (HSV) from the brain, an increase in the CSF HSV antibody titre, or detection of HSV deoxyribonucleic acid in the CSF. Each patient's medical records were reviewed and surviving patients were interviewed and examined.

Results: A diagnosis of herpes simplex encephalitis was confirmed in 42 patients. Five patients (12%) died in the first month. Three patients (7%) had severe neurological sequelae and died after a longer interval. All but one of the 34 surviving patients had neurological symptoms, an abnormal neurological examination, or both. Twenty patients (48%) performed everyday activities as well as before herpes simplex encephalitis; nine patients (21%) were living independently, but were functioning at a lower level than before the illness; and five patients (12%) had a severe neurological deficit. Twenty nine of the 34 survivors were assessed six months to 11 years after herpes simplex encephalitis. The most common long term symptoms were memory impairment (69%), personality and behavioural abnormalities (45%), and epilepsy (24%). Short term memory impairment (70%), anosmia (65%), and dysphasia (41%) were the most common signs.

Conclusions: Although acyclovir has reduced the mortality of herpes simplex encephalitis, 30% of this group of patients either died or had a severe neurological deficit. The other 70% of the patients regained independence in activities of daily living, but most of these people had persistent neurological symptoms, signs, or both.

References

    1. N Engl J Med. 1967 Dec 14;277(24):1271-7
    1. J Neurol Sci. 1982 May;54(2):209-26
    1. Lancet. 1972 Apr 1;1(7753):718-21
    1. J R Coll Physicians Lond. 1972 Oct;7(1):34-44
    1. Neurology. 1973 Jan;23(1):42-7
    1. Arch Neurol. 1973 Oct;29(4):268-73
    1. Arch Neurol. 1975 Jan;32(1):39-43
    1. Lancet. 1975 Mar 1;1(7905):480-4
    1. J Psychiatr Res. 1975 Nov;12(3):189-98
    1. Acta Paediatr Scand. 1977 Mar;66(2):243-6
    1. N Engl J Med. 1977 Aug 11;297(6):289-94
    1. Psychol Med. 1978 Feb;8(1):21-42
    1. Radiology. 1978 Nov;129(2):409-17
    1. Neurology. 1978 Nov;28(11):1193-6
    1. J Neurol Neurosurg Psychiatry. 1981 Apr;44(4):285-93
    1. Acta Neurol Scand. 1982 Oct;66(4):462-71
    1. J Neurol Neurosurg Psychiatry. 1983 Sep;46(9):809-17
    1. Lancet. 1984 Sep 29;2(8405):707-11
    1. N Engl J Med. 1986 Jan 16;314(3):144-9
    1. South Med J. 1986 Nov;79(11):1376-8
    1. J Clin Neurophysiol. 1988 Jan;5(1):87-103
    1. Q J Med. 1988 Jul;68(255):533-40
    1. Arch Neurol. 1990 Jun;47(6):646-7
    1. Electroencephalogr Clin Neurophysiol. 1990 Jul;76(1):86-9
    1. Lancet. 1991 Jan 26;337(8735):189-92
    1. J Clin Microbiol. 1991 Nov;29(11):2412-7
    1. J Clin Exp Neuropsychol. 1992 Mar;14(2):159-78
    1. J Neurol Neurosurg Psychiatry. 1993 May;56(5):520-5
    1. AJR Am J Roentgenol. 1993 Jul;161(1):167-76
    1. J Neurol Neurosurg Psychiatry. 1994 Nov;57(11):1334-42
    1. J Infect Dis. 1995 Apr;171(4):857-63
    1. J Neurol Neurosurg Psychiatry. 1996 Oct;61(4):339-45
    1. Brain. 1960;83:195-212
    1. Arch Neurol. 1962 Jul;7:45-63
    1. Arch Neurol. 1982 Feb;39(2):99-102
    1. Neurology. 1969 Jul;19(7):679-90

Source: PubMed

3
Abonnere