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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe the pathological findings and report the detection of herpes simplex virus 1 (HSV1) in the brain in three patients who presented with intractable seizures. All three patients had a previous history of HSV1 encephalitis and went on to develop a medically refractory seizure disorder necessitating surgical intervention. HSV1 encephalitis was clinically diagnosed and treated at 6 months, 3 years, and 7 months and surgical resection was done at 8.5 years, 6 years, and 3 years, in cases 1, 2 and 3, respectively. Pathological examination revealed chronic encephalitis in all three cases, with microglial nodules, intraparenchymal, perivascular and meningeal lymphocytic infiltrates, and gliosis. While immunohistochemical and ultrastructural studies were negative for viral pathogens, polymerase chain reaction (PCR) analysis revealed HSV1 genome. These cases represent examples of chronic herpes encephalitis and seizure disorder with presence of viral genome in the brain long after the initial episode of treated herpes encephalitis.
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PMID:Intractable seizure disorder associated with chronic herpes infection. HSV1 detection in tissue by the polymerase chain reaction. 954 34

In herpes simplex encephalitis (HSE), simultaneous electro-encephalogram (EEG) and evoked potential studies have not been reported, although EEG changes have been described. In this communication, EEG, somatosensory and motor evoked potentials have been reported in 9 patients with HSE. The patients' age ranged between 2 and 70 years and 3 were females. Seven patients had seizures, CT scan was abnormal in 6 and MRI in remaining 3 patients. Seven patients received acyclovir therapy; one patient died and 6 had poor outcome. The initial EEG was carried out within 5 days of ictus and was abnormal in all the patients. The EEG abnormalities included frontotemporal delta slowing in 5, periodic lateralised epileptiform discharge in 3, runs of spike and periodic activity in one patient each. At 3 months, EEG was normal in 6 patients but it did not correlate with clinical recovery. Central motor conduction time (CMCT) to upper limb and median somatosensory evoked potential (SEP) were normal in all. CMCT to lower limbs and tibial SEPs were unrecordable in one patient who had wide spread herpes simplex virus (HSV-1) infection associated with AIDS, and died on 18th day of illness. From this study, we conclude that EEG although is frequently abnormal and may provide useful diagnostic information in a setting of encephalitis but evoked potential changes are infrequent; and if present an association of HIV infection should be considered.
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PMID:Neurophysiological studies in herpes simplex encephalitis. 963 44

Acute herpes simplex encephalitis (HSE) carries significant morbidity and mortality even after early treatment with antiviral agents (7). As well as causing acute neurological disease, Herpes viruses are associated with relapsing--remitting (Varicella--Zoster, Epstein-Barr) and chronic (Rasmussen encephalitis) disease processes (1). A two-year-old girl developed acute HSE which was followed by a 10-year neurologic illness characterised by asymmetric spastic tetraparesis, pseudobulbar palsy, the opercular syndrome of Foix-Chavany-Marie (4) and seizures. The neurological signs remained static until the child died suddenly 12 years after disease onset. Neuropathologic examination demonstrated active chronic encephalitis. Herpes simplex virus (HSV) DNA was recovered from formalin-fixed paraffin-embedded brain tissue. This case provides additional evidence for the development of chronic neurological disease attributable to persistence of herpes simplex virus type 1.
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PMID:Chronic active destructive herpes simplex encephalitis with recovery of viral DNA 12 years after disease onset. 970 20

Brain areas damaged by stroke and seizures express high levels of the 72-kd heat shock protein (HSP72). Whether HSP72 represents merely a marker of stress or plays a role in improving neuron survival in these cases has been debated. Some induced tolerance experiments have provided correlative evidence for a neuroprotective effect, and others have documented neuroprotection in the absence of HSP72 synthesis. We report that gene transfer therapy with defective herpes simplex virus vectors overexpressing hsp72 improves neuron survival against focal cerebral ischemia and systemic kainic acid administration. HSP72 overexpression improved striatal neuron survival from 62.3 to 95.4% in rats subjected to 1 hour of middle cerebral artery occlusion, and improved survival of hippocampal dentate gyrus neurons after systemic kainic acid administration, from 21.9 to 64.4%. We conclude that HSP72 may participate in processes that enhance neuron survival during transient focal cerebral ischemia and excitotoxin-induced seizures.
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PMID:Gene therapy with HSP72 is neuroprotective in rat models of stroke and epilepsy. 977 55

EEG has been used widely in diagnosing encephalitis, as it demonstrates rather typical abnormalities, especially in herpes simplex virus encephalitis (HSVE). We analysed 204 EEG recordings from 98 consecutive acyclovir-treated patients with acute encephalitis between 1984 and 1994. Periodic complexes (PC) in the acute phase predicted poor outcome (Kendall tau 0.40, P < 0.001). However, unlike in many other diseases, e.g. stroke and intracerebral haemorrhage, the diffuse slowing of the background activity at acute phase did not predict outcome (Kendall tau -0.6, P = 0.35). At follow-up, the emergence of diffuse slow background activity was significantly associated with a less favourable outcome (Kendall tau 0.33, P = 0.0016). Among clinical variables, only epileptic seizures early during the course of the disease correlated significantly with outcome. EEG does have value as a prognostic indicator in acute encephalitides, but it seems that diffuse slowing of background activity or irritative features acutely are not as important as previously thought, based on the experiences of the pre-acyclovir era.
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PMID:Is EEG useful in assessing patients with acute encephalitis treated with acyclovir? 987 47

The role of nitric oxide (NO) in the pathogenesis of viral encephalitis was investigated by using an experimental model of herpes simplex virus type 1 (HSV-1) encephalitis in Lewis rats. The expression of inducible NO synthase (iNOS) mRNA determined by Northern blotting was observed first in the olfactory bulb and the brain stem on day 5 after intranasal inoculation of HSV-1, and thereafter iNOS mRNA was detected in other brain regions, i.e., cerebrum and cerebellum. In various parts of the brain, excessive NO production was identified by electron spin resonance spectroscopy. The temporal and spatial patterns of iNOS expression coincided with those of viral propagation, as demonstrated by polymerase chain reaction for HSV-1 gene expression as well as by the plaque-forming assay. Immunohistochemical study determined that iNOS was localized mainly in monocyte-derived macrophages. Treatment of virus-infected animals with the NOS inhibitor Nomega-monomethyl-l-arginine (l-NMMA), but not Nomega-monomethyl-d-arginine, significantly ameliorated not only clinical symptoms such as paralysis and seizures but also mortality. Virus yield from brain tissue was not affected by l-NMMA treatment. It is of interest that increased expression of the antioxidant enzyme heme oxygenase-1 was observed in the HSV-1-infected brain; this increased expression was strongly inhibited by l-NMMA treatment. These data suggest that the high level of NO produced by iNOS is a pathogenic factor in HSV-1-induced encephalitis in rats.
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PMID:Role of nitric oxide in pathogenesis of herpes simplex virus encephalitis in rats. 1019 Nov 85

Inbred rabbits of the B/Jas strain are highly susceptible to herpes simplex virus type-1 (HSV-1) encephalitis, developing seizures of encephalitis after intravenous injection of the KOS strain of the virus. Anti-viral interferon activity became detectable in the serum just prior to or at the onset of seizures, its level being lower in the serum than in the cerebrospinal fluid. The activity was of gamma interferon, as suggested by the acid instability and the inability of Mx protein induction. An immunohistochemical analysis of the brain tissues of encephalitic rabbits showed that MHC class I antigen was expressed on the microglia cells of inflamed lesions but not on these cells in uninflamed areas. These findings were discussed in correlation with the pathogenesis of herpetic encephalitis in the inbred rabbits.
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PMID:Overproduction of gamma interferon in B/Jas inbred rabbits with herpes simplex virus encephalitis. 1038 3

The frequency was studied with which human herpesviruses types 6 and 7 (HHV-6 and HHV-7) occur in the cerebrospinal fluid (CSF) of patients with febrile seizures and matched control patients. CSF samples were prospectively collected from a case series of patients with febrile seizures and from age-, sex-, and race-matched control patients without febrile seizures, all of whom were evaluated in the emergency department of an urban, tertiary care, pediatric medical center. Using polymerase chain reaction, the samples were examined for the presence of viral DNA from HHV-6, HHV-7, herpes simplex viruses types 1 and 2 (HSV-1 and HSV-2), and cytomegalovirus (CMV). CSF from a subset of both groups was also examined for RNA from enteroviruses. During the 7-month, 2-week collection period, a total of 174 patients were evaluated for fever and seizures. Of these, 23 (13.2%) met the study criteria. Their mean age was 1.4 +/- 0.7 years. Sixteen (70%) of the 23 were male. The 23 patients were matched to 21 control subjects. None of the samples from the patients or control subjects had polymerase chain reaction evidence of HHV-6, HHV-7, HSV-1, or HSV-2. All samples from the patients were negative for CMV. One control subject was positive for CMV. The 10 patients and seven control subjects tested for enteroviral RNA were negative. Neither HHV-6 nor HHV-7 appears to be present in the CSF of patients with febrile seizures. What role, if any, they have in the pathogenesis of febrile seizures merits further study.
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PMID:Human herpesviruses types 6 and 7 and febrile seizures. 1058 Aug 81

Viral encephalitis presents with fever, headache, focal and generalized neurologic symptoms and signs, seizures, and CSF pleocytosis. Herpes simplex Virus (HSV) 1 and arboviruses (flaviruses) are the most common causes of encephalitis in Switzerland. The initial work-up in a suspected encephalitis includes CSF analysis, EEG, and brain CT or MRI. The identification of the responsible agent usually occurs with polymerase chain reaction or serology. The differential diagnosis to other infectious and non-infectious acute CNS-disorders may initially be arduous. A specific treatment is possible only in encephalitis caused by viruses of the herpes group. Active immunization should be considered in subjects at high risk for tick-borne encephalitis. With early treatment the prognosis may be satisfactory also in HSV encephalitis.
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PMID:[Viral encephalitis]. 1059 77

Virusencephalitis is characterised by clinical symptoms of a parenchymatous inflammation. In addition, early mental status changes often occur as a result of virusencephalitis, beside focal neurological deficiencies, epileptic seizures, cerebral compression, even coma. Other pathological manifestations of virusencephalitis are disturbances of the neurohumoral and the endocrine system, which are often recognised and treated too late. This case report describes symptoms, treatment, and complications of a 76 year old female in-patient, who was diagnosed with virusencephalitis. The number of lymphocytes in the cerebrospinal fluid was increased to 30 cells per microliter, liquor albumin was 1705 mg/l, liquor sugar was 53 mg/dl and liquor lactat was 1.9 mmol/l. IgM antibodies against herpes viruses were found in the cerebrospinal fluid and distinct contrasting foci were found near the mammillary bodies, hypothalamus, tractus opticus, hypophyseal stalk and right parahippocampal in the magnetic resonance imaging of the head, indicating a focal herpes simplex encephalitis. Within seven days, the following symptoms developed: akinetic parkinsonian syndrome, central diabetes insipidus with hypernatremia and polyuria (6 l/die), hypothyreosis, adrenal insufficiency with adynamia, sopor, hypotension and even hypophyseal coma. Panhypopituitarism was diagnosed after measuring the basal hormone levels (ACTH, TSH, FT3, FT4, Cortisol, Prolactin, LH, FSH, ADH) and conducting the pituitary stimulation test. The severeness of all symptoms was slightly improved after substitution with antidiuretic hormone at 0.4 microgram/die and administration of hydrocortisone at 50 mg/die. Administration of amantadine sulphate at 0.6 g/die and L-dopa at 187.5 mg/die for 14 days resulted in a complete regression of the parkinsonism. After administration of aciclovir at 2.25 g/die for 21 days a complete regression of the clinical symptoms could be reached in connection with a decrease of 90% in number and size of cerebral contrasting foci in the magnetic resonance imaging of the head. Three month after therapy, clinical examination and blood serum analysis revealed persistent panhypopituitarism. The present case report is the first description of a viral infection on of the central nervous system (CNS) in combination with parkinsonism, diabetes insipidus, persistent panhypopituitarism and hyperprolactinemia. Early treatment of viral infections of the brain can improve a patient's prognosis dramatically. Early determination and early treatment of a patient's neurohumoral parameters is therefore critical to prevent or reverse early mental status changes like attention disturbances, alterations of personality and behavior, apathy, and slowed cognition.
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PMID:[Virus encephalitis with symptomatic Parkinson syndrome, diabetes insipidus and panhypopituitarism]. 1059 69


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