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)

A 2-month-old girl had focal tonic convulsions. Brain CT showed no abnormalities on admission. Three weeks later she got a severe epileptic status. T 1-weighted MRI demonstrated low intensity areas in the right occipital and left frontal regions, and enhanced CT demonstrated low density areas in the same region. An increase of CMV antibody titer in serum suspected CMV infection associated with brain infarction. Then gamma-globulin was given in addition to PB, CBZ, and VPA, resulting in suppression of seizures. At 9 months of age, she had right tonic hemiconvulsions. An increase of CMV IgM antibody titer showed reactivation of CMV infection. Acyclovir and gamma-globulin were given, and her seizures were controlled. However, she showed progressive motor disability with spastic muscle tonus. CT and MRI showed a severe progressive atrophy of the cerebrum and brain stem.
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PMID:[A case of perinatal cytomegalovirus infection with severe progressive brain atrophy]. 838 Jan 11

A serendipitous discovery during early AIDS investigations was human herpes virus type 6 (HHV-6). Two years later (1988) it was shown that HHV-6 and later on also HHV-7 are the causes of exanthema subitum, a childhood disease with previously unknown causation. HHV-6 and HHV-7 are the main cause of febrile seizures. It is assumed that 90% of children are infected before they are three years old. The viruses are also found in adults; HHV-6 may cause mononucleosis and hepatitis. HHV-6 and HHV-7 infect CD4+ cells and may influence the course of HIV infection. In AIDS patients HHV-6 and cytomegalovirus are often isolated together from the lungs, possibly because they activate each other. Another possibility is that the circumstances in the lungs are favourable to both. HHV-6 and HHV-7 infection may be serologically diagnosed. There is little experience with antiviral treatment.
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PMID:[Human herpes viruses type 6 and 7; causative agents of, among others, exanthema subitum]. 861 28

Amplification of viral nucleic acids from the cerebrospinal fluid (CSF) has considerably improved the diagnosis of several acute, subacute and chronic viral infections of the nervous system. In herpes simplex virus (HSV) encephalitis (HSE) the polymerase chain reaction (PCR) has become the method of choice for the rapid, non invasive diagnosis. Other herpes virus associated diseases which can now be reliably diagnosed are encephalitis, ventriculoencephalitis, polymyeloradiculitis, myelitis and an inflammatory polyradiculoneuropathy caused by cytomegalovirus (CMV), HSV, varicella-zoster virus (VZV) or Epstein-Barr virus (EBV), EBV associated primary B-cell-lymphoma of the brain, acute aseptic meningitis in young adults allied with VZV, and meningoencephalitis with recurrent seizures due to human herpes virus type 6 (HHV-6). In AIDS patients, PCR has helped to differentiate lesions either due to the human immunodeficiency virus (HIV) itself or to opportunistic infections such as progressive multifocal leukoencephalopathy (PML) caused by JC virus (JCV) or CMV related complications. HIV can be detected early in the course of infection in the CSF and the amount of proviral DNA in CSF cells seems to be correlated with the severity and/or progression of neurological signs and symptoms. Acute epidemic aseptic meningitis caused by enterovirus infections can now be reliably diagnosed and typed by reverse transcriptase PCR (RT-PCR). Meningitis cases caused by vaccination with the Jeryl Lynn and Urabe vaccine strain of mumps virus have been identified using RT-PCR and sequencing of the amplified products (amplicon).
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PMID:Clinical implications of nucleic acid amplification methods for the diagnosis of viral infections of the nervous system. 879 10

Since cytomegalovirus (CMV) has been implicated in the pathogenesis of Rasmussen's syndrome, we treated four patients with ganciclovir, a potent anti-CMV drug. A 7-year-old girl with seizures escalating to 60/day over 3 months despite triple antiepileptic drug therapy became seizure-free 5 days after initiation of treatment with no recurrence at 1.5 years follow-up. Focal neurologic signs, cognitive function, and the EEG returned to normal. Two patients treated 34 and 72 months after disease onset in association with epilepsy surgery had a reduction in seizures and one had no response. CMV genome was detected in the brains of two of the three patients in whom it was assessed. The response to antiviral therapy supports a viral etiology for chronic encephalitis of Rasmussen. If the disease is suspected, treatment with ganciclovir should be considered as early as possible.
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PMID:Treatment of Rasmussen's syndrome with ganciclovir. 885 20

The murine monoclonal antibody muromonab CD3 (OKT3) is directed against the CD3 antigen on peripheral human T cells and effectively blocks all T cell function. Prophylaxis with muromonab CD3 (5mg intravenously once daily for 10 to 14 days) as induction therapy together with corticosteroids, azathioprine and delayed cyclosporin (sequential therapy) optimises early graft function by delaying the potentially nephrotoxic and hepatotoxic effects of cyclosporin until graft function is established. Although clinical data are limited (by inconsistencies in trial design and trial size), prophylactic muromonab CD3-based sequential therapy is significantly more effective than standard triple therapy in the prophylaxis of allograft rejection in renal and hepatic, but not cardiac, transplant recipients. Benefits are particularly notable in patients with delayed graft function. No significant between-treatment differences in patient survival have been observed. The overall efficacy of muromonab CD3- and polyclonal-based prophylactic regimens appears to be similar, although results vary between investigators and confirmation is needed. An anti-interleukin-2 monoclonal antibody-based prophylactic regimen improved graft and patient survival compared with muromonab CD3-based prophylaxis in hepatic transplant recipients. Antimuromonab CD3 antibodies may develop; however, muromonab CD3 may be successfully reused in patients with low titres. Preliminary pharmacoeconomic data suggest that mean drug costs are greater with quadruple immunosuppressive regimens containing muromonab CD3, antithymocyte globulin (ATG) or antilymphocyte globulin (ALG) than with triple therapy. Drug costs with prophylactic muromonab CD3-based regimens were similar or greater than those with polyclonal-based protocols. The first doses of muromonab CD3 are associated with the 'cytokine-release syndrome'. More severe first-dose events include aseptic meningitis, intragraft thromboses, seizures and potentially fatal pulmonary oedema. The incidence and/or severity of cytomegalovirus infection with prophylactic muromonab CD3 based immunosuppression is similar to or greater than that with triple therapy and ATG- or ALG-based regimens. However, the risk of infection and also the observed increase in lymphoproliferative disorders appears to be related to the degree of immunosuppression rather than to the drug itself Thus, sequential muromonab CD3-based therapy is more effective than standard triple therapy (in renal and hepatic transplant recipients) and appears to be similar to that of polyclonal-based regimens in the prophylaxis of transplant rejection. Although the routine use of prophylactic muromonab CD3 in low-risk patients with primary graft function does not appear to be justified, prophylactic muromonab CD3-based therapy has a role in patients at high risk of rejection.
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PMID:Muromonab CD3: a reappraisal of its pharmacology and use as prophylaxis of solid organ transplant rejection. 886 51

A ten-months-old girl was evaluated for developmental delay, increased muscle tone and seizures. CT and MRI revealed un uncommon combination of two different manifestations of neuronal migration disturbance: agyria/pachygyria and subcortical laminar heterotopia ("double cortex" syndrome). The occurrence of these two manifestations of neuronal migration dosorders in the same individual is quite unusual. The possible pathogenesis of such a complex disorder could probably be established only by histologic examination of the brain. A positive serologic reaction for cytomegalovirus in the infant at the age of 11 months and in the mother suggested but did not prove the cytomegalovirus infection in early gestation as the cause of the disorder.
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PMID:Complex disorder of neuronal migration in an infant with possible congenital cytomegalovirus infection. 889 May 34

We report the extraordinary association of hemimegalencephaly with chronic encephalitis and cytomegalovirus (CMV) positivity in a 5-month-old infant with intractable seizures and a left hemisphere resection. Microscopy revealed a severe neuronal migration disorder (NMD) with fusion of gyri, marked disarray of neuronal lamination, neuronal gigantism and extensive neuronal heterotopias. Also widespread were microglial nodules, gliosis and nodular calcifications and some foci of frank necrosis with calcification. Occasional perivascular and leptomentingeal lymphocytic infiltrates were present. No viral inclusions were identifiable. Polymerase chain reaction on multiple specimens showed unequivocal CMV positivity. In intrauterine CMV infection. NMDs such as polymicrogyria are well recognized, but the association of hemimegalencephaly with CMV infection has not previously been described. Our finding of chronic encephalitis with CMV positivity and hemimegalencephaly in the same patient raises questions about the role of CMV in the etiopathogenesis of the NMD.
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PMID:Coexistence of hemimegalencephaly and chronic encephalitis. Detection of cytomegalovirus by the polymerase chain reaction. 908

This article suggests ways to manage the dose-limiting adverse reactions caused by foscarnet so that this agent may be used with confidence as first-line therapy in patients with cytomegalovirus (CMV) disease. Foscarnet (trisodium phosphonoformate) has been used for the treatment of CMV disease in patients who are infected with HIV. Some physicians who treat patients with CMV infection are reluctant to use foscarnet because of the serious adverse effects that may occur, especially during the induction period. The most frequently reported serious adverse effects are nephrotoxicity, electrolyte disturbances, nausea, penile ulcerations and seizures. The nephrotoxicity associated with foscarnet is attributable to renal tubular damage, and may be minimised by calculating and infusing the appropriate dose after hydrating the patient. Monitoring serum electrolyte levels and replacing electrolytes before symptoms occur may limit the development of dosage-limiting toxicities. Nausea occurring during foscarnet infusions may be ameliorated by using antiemetics and slowing the infusion rate. Seizures associated with the use of this agent are mostly a result of the simultaneous presence of other CNS pathologies. Penile ulcers are best managed by stopping the infusion until the ulcers heal; they may be prevented by paying careful attention to personal hygiene.
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PMID:Minimising the dosage-limiting toxicities of foscarnet induction therapy. 911 93

In the inferior colliculus, adeno-associated virus (AAV) vectors are capable of gene transfer and stable, long-term expression, but it remained to be shown if this in vivo gene transfer could alter focal seizure sensitivity in the inferior colliculus. Because GABA receptors directly modulate inferior collicular seizures, AAV vectors were constructed with a cytomegalovirus (CMV) promoter and a truncated, human GABA(A) alpha1 cDNA in both the sense and antisense orientations. Seven days after collicular microinjection of the sense vectors (1 microl; 3 x 10(9) particles/microl), neurons exhibited GABA(A) alpha-like immunoreactivity in amounts far exceeding endogenous concentrations. Unilateral or bilateral sense vector infusion had no effect on inferior collicular seizure parameters or on [3H]zolpidem binding. In contrast, bilateral infusion of the antisense AAV-GABA(A) alpha1 vector (1 microl; 3 x 10(8) particles/microl) caused a 137% increase in the seizure duration. Moreover, unilateral antisense vector infusion produced a localized, 48% decrease in [3H]zolpidem binding. Thus, in the inferior colliculus, antisense AAV-CMV vectors can reduce a specific receptor subunit protein and change receptor function that directly influences in vivo seizure sensitivity.
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PMID:Adeno-associated virus (AAV) vector antisense gene transfer in vivo decreases GABA(A) alpha1 containing receptors and increases inferior collicular seizure sensitivity. 918 16

In this review, we discuss the important pathological lesions observed in temporal lobectomies and neocortical resections performed for medically refractory seizures in children. A higher percentage of pediatric cases appear to be "lesional" with computed tomography (CT) and magnetic resonance imaging (MRI) and abnormalities and "dual pathology" lesions appear to be more common than pure mesial temporal sclerosis. Almost a third of cases appear to be neuronal migration disorders and low-grade gliomas with some lesions harboring both neoplastic and malformative components. Our experience suggests a role for cytomegalovirus in some cases of Rasmussen's encephalitis.
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PMID:Surgical pathology of epilepsy resections in childhood. 942 50


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