Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 1991 to 1997 at the I Clinic of Infectious Diseases of Silesian Medical Academy in Bytom 123 patients with purulent, bacterial meningoencephalitis were treated. Mortality in the analysed group was 28.5% (35 cases). In the course of disease various complications were observed: seizures (43.1% cases), ischaemic stroke (2.4% cases), brain abscess (4.1%). Permanent consequences subsequent to the disease were found in 16.3% cases: deafness and partial deafness, psychic disorders, paresis and paralysis, epilepsy and cranial nerves paralysis. Bacterial infections of the central nervous system are still danger diseases producing high lethality, complications and subsequent neurological sequelae.
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PMID:[Complications and sequelae of the purulent, bacterial meningoencephalitis in the material from the 1st Clinic of Infectious Diseases of Silesian Medical Academy in Bytom in the years 1991-1997]. 1032 Oct 93

A 5.5-year-old French bulldog was presented with acute neck pain and a short history of central vestibular syndrome. A marked neutrophilic pleocytosis and numerous gram-positive cocci were evident on cerebrospinal fluid (CSF) cytology. Streptococcus pneumoniae, a pathogen of humans, was isolated upon CSF microbiological culture. Treatment consisted of intravenous antibiotics, supportive care, and anticonvulsants for the generalized seizures which developed shortly after admission. The dog responded to therapy and two years later exhibited only a mild, residual head tilt. The pathogenesis and treatment of bacterial meningoencephalitis in dogs are reviewed.
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PMID:Streptococcal meningoencephalitis in a dog. 1049 18

Neurocysticercosis, prevalent wherever pigs are raised in the presence of poor sanitation, is the most common identifiable cause of new-onset epilepsy throughout the developing world. As immigration patterns have changed, children with neurocysticercosis are seen throughout the United States. Acute cysticercosis, the most common manifestation in children, reflects the host response to the dying parasite. Children typically present with seizures and have an excellent prognosis. Neuroimaging demonstrates a single ring or nodular enhancing lesion surrounded by edema. Short-term anticonvulsant therapy is indicated, but treatment with antiparasitic agents is not required. Other forms, such as active cysts (intact organism), intraventricular or subarachnoid racemous cysticercosis, and cysticercal meningoencephalitis, are less common manifestations of parasitic infection. Toxoplasmosis, caused by the parasite Toxoplasma gondii, can be acquired by ingestion of infected undercooked meat or from oocytes shed in cat feces. Acquired cerebral toxoplasmosis, due to primary or reactivated infections, rarely occurs in immunocompetent children. In children who are immunodeficient as the result of AIDS, chemotherapy, tissue transplantation, or congenital immunodeficiency, toxoplasmosis may be difficult to distinguish from cerebral lymphoma. A variety of techniques, including neuroimaging, Thallium-201 SPECT, polymerase chain reaction analysis of CSF, and special histological methods, may be used to diagnose acquired toxoplasmosis. Antiparasitic therapy, using pyrimethamine and sulfadiazine, and serial neuroimaging often enable clinicians to differentiate toxoplasmosis from other central nervous system lesions. Toxoplasmosis may respond to other antimicrobials, including macrolide antibiotics, dapsone, clinidamycin, and atovaquone. Suppressive treatment is generally required for life in immunodeficient patients. Immunodeficient children with acquired toxoplasmosis have high rates of mortality and neurological sequelae.
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PMID:Neurocysticercosis and acquired cerebral toxoplasmosis in children. 1064 35

We investigated the clinical features of the patients whose body temperature exceeded 38 degrees C, in 0.5-6 hours after an afebrile seizure (prefebrile seizure). Patients with meningoencephalitis and epilepsy were excluded from this study. From May 1995 to April 1997, seven cases of prefebrile seizures admitted to PL hospital. Three of the 7 had a status and one had a cluster of seizures. Five patients had had several febrile seizures prior to the onset of prefebrile seizures. One developed epilepsy during the follow-up period. We speculate that prefebrile seizures have several factors of complex febrile seizures and require a careful follow-up.
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PMID:[Apparently unprovoked seizures precipitated by prefebrile condition]. 1065 46

A 24-month-old female pug, which had previously been treated for visual hemifield loss, was referred with generalised seizures and other neurological disorders. A diagnosis of necrotising meningoencephalitis was suggested from the clinical signs together with the results of computed tomography and cerebrospinal fluid examination. This was confirmed seven months later by histological examination of the brain following euthanasia. Typical histopathological lesions of the disease were found in various areas of both cerebral hemispheres, including the visual striated cortex of the right cerebrum.
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PMID:Homonymous hemianopia in a pug with necrotising meningoencephalitis. 1081 45

Two children are described who presented with fever and generalized seizures, days 50 and 200, respectively, after matched unrelated donor-bone marrow transplantation. Upon antiepileptic treatment the seizures vanished but somnolence and fever remained. Magnetic resonance imaging (MRI) of the brain was performed and revealed transient asymmetric multifocal hyperintense lesions. Seizures were considered related to infection, and the cyclosporin A (CsA) treatment was not interrupted. Enterovirus was detected by reverse transcriptase-polymerase chain reaction in the spinal fluid of one patient and in the sputum of the other. Both children recovered completely within the next weeks without neurological sequel. This report shows that enteroviral meningoencephalitis can present with seizures during the post-transplant period. It highlights the importance of MRI for neuroimaging and of viral infections as differential diagnosis to CsA neurotoxicity.
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PMID:Enteroviral meningoencephalitis in immunocompromised children after matched unrelated donor-bone marrow transplantation. 1091 50

Fourteen children with Epstein-Barr virus (EBV) encephalitis admitted to our pediatric department during the period 1988 to 1998 were collected and reviewed to characterize the clinical, laboratory and neuroradiological findings. There were 7 boys and 7 girls. The age of onset ranged from 10 months to 14 years. Among them, 5 patients belonged to Alice in Wonderland syndrome, 5 were diagnosed as acute viral encephalitis, 1 presented with acute meningoencephalitis followed by cerebellitis, the remaining 3 cases attributed to acute disseminated encephalomyelitis. The main symptoms were fever (43%), seizure (36%), bizarre behavior (31%), headache (21%) and metamorphopsia (36%). The presenting signs included altered consciousness (50%), meningeal sign (14%), bulbar sign (14%), cerebellar sign (7%), and cranial nerve palsy (7%). Classic findings of infectious mononucleosis were obscure. The laboratory data showed the existence of atypical lymphocyte in only one case but positive serology for EBV infection in all patients. Pleocytosis was found in 3 (30%) of 10 patients examined. Eight (67%) of 12 patients had nonspecific electroencephalographic changes in the acute stage. Computed tomography (CT) scans were abnormal in 2 (40%) of 5 patients tested; while magnetic resonance image (MRI) disclosed lesions in 5 (56%) of 9 patients, with abnormal signals in various parts of the brain. Single photon emission computed tomography (SPECT) brain scan showed abnormal perfusion lesions in 3 (75%) of 4 patients studied. The results demonstrate the diversity of neurological manifestations of EBV encephalitis. EBV should be considered in any acute neurological illness of uncertain etiology in the pediatric population. While MRI remains the image of choice in EBV encephalitis, SPECT detects the abnormal perfusion more precisely in a substantial number of patients.
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PMID:Epstein-Barr virus encephalitis in children. 1092 May 47

Balamuthia mandrillaris is a newly described pathogen that causes granulomatous amebic encephalitis, an extremely rare clinical entity that usually occurs in immunosuppressed individuals. We report a case of pathologically proven Balamuthia encephalitis with unusual laboratory and radiologic findings. A 52-year-old woman with idiopathic seizures and a 2-year history of chronic neutropenia of unknown cause had a subacute illness with progressive lethargy, headaches, and coma and died 3 months after the onset of symptoms. Cerebrospinal fluid (CSF) glucose concentrations were extremely low or unmeasurable, a feature not previously described (to our knowledge). Cranial magnetic resonance imaging scans showed a single large temporal lobe nodule, followed 6 weeks later by the appearance of 18 ring-enhancing lesions in the cerebral hemispheres that disappeared after treatment with antibiotics and high-dose corticosteroids. The initial brain biopsy specimen and analysis of CSF samples did not demonstate amebae, but a second biopsy specimen and the postmortem pathologic examination showed Balamuthia trophozoites surrounded by widespread granulomatous inflammation and vasculitis. The patient's neutropenia and antibiotic use may have caused susceptibility to this organism. Amebic meningoencephalitis should be considered in cases of subacute meningoencephalitis with greatly depressed CSF glucose concentrations and multiple nodular lesions on cerebral imaging. Arch Neurol. 2000;57:1210-1212
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PMID:A case of Balamuthia mandrillaris meningoencephalitis. 1092 4

Herpesvirus glycoprotein C (gC) is one of the major virus attachment proteins. Bovine herpesvirus type 1 (BHV-1) causes respiratory and genital diseases in cattle, whereas BHV-5 causes acute meningoencephalitis in calves. The gC gene sequence of these two viruses are substantially different. To determine the contribution of the BHV-5 glycoprotein gC (gC5) to the neuropathogenesis of BHV-5, we have constructed two BHV-5 recombinants: gC-deleted BHV-5 (BHV-5gCDelta) and BHV-5 expressing BHV1 gC (BHV-5gC1). Neurovirulence properties of these viruses were analyzed using a rabbit seizure model that distinguishes BHV-1 and -5 based on their differential neuropathogeneses. Intranasal inoculations of BHV-5gCDelta and BHV-5gC1 viruses produced neurological signs in 30% and 40% of the infected rabbits, respectively. Immuno-histochemistry results showed that the number of infected neurons was 2 - 4-fold less with the gC-deleted BHV-5 than with the wild-type BHV-5. The gC-deleted BHV-5 did not invade the hippocampus but invaded additional sites not invaded by wild-type BHV-5. Similarly, the BHV-5gC1 virus failed to invade the hippocampus, but it did not invade the additional sites. Virus isolation results suggest that these recombinants replicate less efficiently in the brain than the wild-type and gC-revertant viruses. However, compared to the gC-deleted BHV-5, the gC-exchanged BHV-5gC1 replicated better within the CNS. These results indicate that gC regulates BHV-5 neurotropism in some areas of the olfactory pathway. Additionally, gC is important for BHV-5 neurovirulence in the olfactory pathway but it is not essential.
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PMID:Neurovirulence of glycoprotein C(gC)-deleted bovine herpesvirus type-5 (BHV-5) and BHV-5 expressing BHV-1 gC in a rabbit seizure model. 1095 52

Mycobacterium tuberculosis is one of the most common infectious agents in the world. It causes an insidious form of meningitis characterized by headache, low-grade fever, stiff neck and cranial nerve palsies, and an acute meningoencephalitis characterized by coma, raised intracranial pressure, seizures, and focal neurological deficits. This review focuses on the diagnosis and therapy of the insidious form of tuberculous meningitis and discusses the differential diagnosis of infectious and noninfectious etiologies of the aseptic meningitis syndrome.
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PMID:Mycobacterium tuberculosis meningitis and other etiologies of the aseptic meningitis syndrome. 1105 Dec 97


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