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1/117. herpes simplex virus encephalitis in pregnancy.

    BACKGROUND: Although polymerase chain reaction (PCR) can detect herpes simplex virus (HSV) in the cerebrospinal fluid (CSF), HSV encephalitis remains a significant cause of neurologic impairment in pregnant women. Assessment of fetal contamination also remains a problem. CASES: We report two cases in which HSV encephalitis initially was not suspected and led to significant maternal neurologic impairment. In both cases, HSV PCR of CSF confirmed the diagnosis. In one case, fetal serum HSV PCR excluded fetal contamination. CONCLUSION: As soon as encephalitis in pregnancy is suspected, a combination of acyclovir and penicillin is recommended because the potential benefits far outweigh the risks. Using the HSV PCR, HSV infection in the fetus can be diagnosed. ( info)

2/117. Cognitive outcome after emergent treatment of acute herpes simplex encephalitis with acyclovir.

    Longitudinally designed case studies, reporting cognitive and psychosocial outcome of herpes simplex virus encephalitis (HSVE), were conducted prior to current antiviral medication usage and primarily in persons with either left hemispheric or bilateral temporal lobe involvement. The current study demonstrated relatively better outcome (cognitive recovery and functional independence for activities of daily life) in an individual treated with IV acyclovir within hours of initial symptoms and whose CT scans showed right hemispheric involvement. In contrast with earlier case reports, no semantic specific categories of memory impairment were noted on serial assessment. The time from first symptoms to antiviral medical treatment appears to be the best predictor of outcome from HSVE. Historical case studies with relatively poorer outcome and differing deficits suggest survivors of HSVE are a heterogenous group. Variability in anatomic lesions and time to treatment contribute to outcome. ( info)

3/117. Disproportionate retrograde amnesia in a patient with herpes simplex encephalitis.

    We describe a patient who developed a severe but temporally limited retrograde amnesia coupled with a relatively mild anterograde amnesia following herpes simplex encephalitis. The patient showed a profound retrograde amnesia for autobiographical events extending for about 10 years prior to the disease onset. Her knowledge about public events and famous persons was also impaired for this period. An MRI and SPECT demonstrated bilateral medial temporal pathology. This case represents a further instance of a relatively focal retrograde amnesia following brain damage. We review other reported cases with focal retrograde amnesia and consider theoretical and neuroanatomical accounts for the present case. Two factors may account for her amnesic patterns: a partial disruption of the store for premorbid binding codes (i.e., information that multimodal feature representations occurred synchronously); along with a relative preservation of the encoding process required to develop new synchronous codes. ( info)

4/117. Use of oral valaciclovir in a 12-year-old boy with herpes simplex encephalitis.

    We report on a 12-year-old boy with herpes simplex encephalitis, in whom a severe localised skin reaction developed following the infusion of intravenous acyclovir. Oral valaciclovir was given as continuation therapy to complete the 3-week course of antiviral treatment and resulted in complete recovery without side effects. This report illustrates the advantage of using the polymerase chain reaction to diagnose herpes simplex encephalitis and the potential use of newer antiviral agents, such as valaciclovir, as continuation therapy in the management of the infection. The higher oral bioavailability of newer antiviral agents allows part of the extended treatment period of patients with herpes simplex encephalitis to be carried out as an ambulatory oral regimen. ( info)

5/117. Cerebral malakoplakia associated with escherichia coli infection.

    Malakoplakia is an unusual chronic inflammatory disease occurring predominantly in the bladder and only rarely affecting other organs. For the urinary tract, its aetiology has been ascribed to the presence of escherichia coli, while the very few cases of cerebral malakoplakia which have been reported so far, have mostly occurred in infants in the clinical setting of neonatal herpes virus infection or otherwise in adults in areas of cerebral infarction. We here report a case of E. coli-associated malakoplakia of the brain. It occurred in a 53-year-old man who had undergone long-term corticosteroid therapy and had previously been operated on a cerebral E. coli-associated abscess. This case indicates that malakoplakia of the brain might also be a histiocytic reaction against bacterial antigens of the E. coli family. ( info)

6/117. A componential analysis of visual object recognition deficits in patients with herpes simplex virus encephalitis.

    Five patients with a diagnosis of herpes simplex Virus Encephalitis (HSVE) underwent neuropsychological assessment to explore the integrity of their visual perceptual abilities. Selective deficits affecting different levels of the recognition processing were found; impaired recognition abilities were also influenced by selective task requirements, which resulted either in facilitatory or constraining effects on patients' performance. A theoretical model of object recognition (Humphreys & Riddoch, 1987) was taken into account to explain patients' performance. Further, the role of specific components of visual processing was evidenced in explaining the performance of patients affected by HSVE. ( info)

7/117. Immunocytochemical characterization of long-term persistent immune activation in human brain after herpes simplex encephalitis.

    The clinical, virological and immunocytochemical features of three children who recovered from acute herpes simplex encephalitis (HSE) before the age of 2 years, and who developed secondary severe focal epilepsy after a symptom-free period, leading to neurosurgery 3-10 years later are described. In one child, relapse of HSE occurred immediately after surgery. In all three patients, brain sample biopsies showed abundant CD3-positive T lymphocytes with a majority of CD8 cells, and abundant activated macrophage-microglial cells, a pattern similar to that found in acute HSE. herpes simplex virus dna was retrieved from the tissue biopsy in one case. The long-term persistent cerebral inflammatory process observed after HSE differed from that observed in another chronic viral disease, subacute sclerosing panencephalitis. This inflammatory reaction may be a result either of low-grade viral expression or self-induced immune activation. The role of inflammation in triggering epilepsy remains hypothetical. Solving these issues should have major therapeutic implications. herpes simplex virus dna latency in brain may be the source of replicative HSE relapse. ( info)

8/117. association of herpes simplex virus encephalitis and paraneoplastic encephalitis - a clinico-pathological study.

    A 57 year-old woman developed acute limbic encephalitis and brainstem dysfunction. Anti-HU antibodies were repeatedly detected in serum and CSF. Postmortem examination showed necrotic and hemorrhagic lesions in the temporal lobes characteristic of herpes simplex virus encephalitis, which was confirmed by immunocytochemistry, and Purkinje cell loss with proliferation of Bergman glia and myelin loss in the external aspect of the dentate nuclei characteristic of paraneoplastic encephalitis. PCR-assay performed on temporal tissue extracts was positive for HSV-1. There was no identifiable neoplasm. This unusual association raises the possibility of a link between the two diseases. ( info)

9/117. Profound amnesia after damage to the medial temporal lobe: A neuroanatomical and neuropsychological profile of patient E. P.

    E. P. became profoundly amnesic in 1992 after viral encephalitis, which damaged his medial temporal lobe bilaterally. Because of the rarity of such patients, we have performed a detailed neuroanatomical analysis of E. P.'s lesion using magnetic resonance imaging, and we have assessed his cognitive abilities with a wide range of neuropsychological tests. Finally, we have compared and contrasted the findings for E. P. with the noted amnesic patient H.M, whose surgical lesion is strikingly similar to E. P.'s lesion. ( info)

10/117. Long-term follow-up of auditory agnosia as a sequel of herpes encephalitis in a child.

    We report a pediatric patient with auditory agnosia as a sequel of herpes encephalitis. His early development was completely normal. He uttered three words at 12 months old. disease onset was 1 year and 2 months of age. He was discharged from the hospital seemingly with no sequel; however, he could not recover his intelligible words even at age 2 years. He was diagnosed as having auditory agnosia caused by bilateral temporal lobe injury. We began to train him at once, individually and intensively. adult patients with pure auditory agnosia followed by two episodes of temporal lobe infarction have impairment in central hearing but not inner language. Therefore, they can communicate by reading and writing. Moreover, impairment in hearing is not always severe and is often transient. However, despite long-term (more than 15 years) energetic education and almost normal intellectual ability (Performance IQ of Wechsler intelligence Scale for Children-Revised was 91), our patient's language ability was extremely poor. Cerebral plasticity could not work fully on our patient, whose bilateral temporal lobe was severely injured in early childhood. The establishment of a systematic training method in such patients is an urgent objective in this field. ( info)
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