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

This is a report of a 31-year-old woman with non-herpetic acute limbic encephalitis following a type-2 adenovirus infection. The patient was admitted to a hospital with high fever, severe liver dysfunction, and thrombocytopenia. Six days after admission, she became afebrile, and her liver dysfunction was normalized by conservative therapy. However, the patient started to experience generalized seizures that developed into status epileptics. The patient was then transferred to a referred hospital. Brain MR images revealed faint high-signal intensity in the bilateral limbic systems on FLAIR images. A CSF examination indicated mild pleocytosis. These findings suggested acute limbic encephalitis, which may have been mediated by an autoimmune reaction following some viral infection. Thus, steroid pulse therapy was started on the day of admission. The patient's condition, including the seizures and disturbances involving consciousness, improved gradually. The patient was discharged from the hospital in one month while still experiencing mild memory disturbances. Three months after onset of the illness, a T1-weighted MR image showed a linear high-signal intensity in the hippocampi, which indicated focal necrosis. Six months after onset, the patient's memory disturbance had been improved (her MMSE score was 28/30 points). We investigated the titers of many viruses that are known to cause liver dysfunction and found that a titer of the type-2 adenovirus was significantly elevated within three weeks. Although the anti-voltage-gated potassium channel (VGKC) antibody was not detected in the patient's serum, it seems that the autoimmune reaction after the type-2 adenovirus infection may have caused the acute limbic encephalitis.
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PMID:[A case of non-herpetic acute limbic encephalitis associated with a type-2 adenovirus infection]. 1688 98

The role of viral infection in the etiology of febrile seizures is a relatively neglected field of neurologic research. A National Institutes of Health Consensus Conference (1981) omitted reference to causes of infections and the role of fever in febrile seizures, and emphasized outcome and anticonvulsant treatment. In an earlier review of the world literature (1924-1964), except for roseola infantum, viral infections as a cause of febrile seizures were rarely diagnosed. The present review includes reports of viruses most commonly associated with febrile seizures in the last decade, especially human herpesvirus-6 and influenza. The specificity and neurotropic properties of some viruses in the febrile seizure mechanism, a possible encephalitic or encephalopathic pathology, and the essential role of fever and height of the body temperature as a measure of the febrile seizure threshold are discussed. Cytokine and immune response to infection, and a genetic susceptibility to febrile seizures are additional etiologic factors. Future research should emphasize early detection of causative viruses, the nature of viral neurotropism, and the role of cytokines in fever induction. Trials of antiviral agents and vaccines, with attention to safety concerns, and more effective antipyretics would address the febrile seizure mechanism more specifically than anticonvulsant therapies.
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PMID:Role of viral infections in the etiology of febrile seizures. 1693 54

EBV infection in tumor cells is generally restricted to the latent forms of viral infection. Switching the latent form of viral infection into the lytic form may induce tumor cell death. We have previously reported that certain chemotherapy agents can increase the amount of lytic viral gene expression in EBV-positive tumor cells. In this report, we have explored the potential utility of valproic acid (VPA), an anti-seizure drug that also has strong histone deacetylase inhibitory activity, for activating lytic viral gene expression in EBV-positive tumors. Although VPA treatment alone induced only a modest increase in the level of lytic viral gene expression, it strongly enhanced the ability of chemotherapeutic agents to induce lytic EBV gene expression in EBV-positive epithelial and lymphoid cells in vitro. Furthermore, VPA enhanced cell killing in vitro by chemotherapeutic agents in lymphoblastoid cells and gastric cells (AGS) containing wild-type EBV. In contrast, VPA did not enhance the cytotoxicity of chemotherapy in lymphoblastoid cells containing a lytic-defective (BZLF1-knockout) form of EBV or in EBV-negative AGS cells. Finally, we found that the combination of VPA and chemotherapy was significantly more effective in inhibiting EBV-driven lymphoproliferative disease in severe combined immunodeficient mice than chemotherapy alone. These results suggest that VPA could potentiate the efficacy of chemotherapy for EBV-positive tumors in patients.
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PMID:Valproic acid enhances the efficacy of chemotherapy in EBV-positive tumors by increasing lytic viral gene expression. 1695 Nov 92

The body temperature is influenced among other things by time of day or age and exhibits a Gaussian inter-individual distribution. If measured orally, normal values vary between 35.6 degrees C and 38.2 degrees C. Temperature exceeding the 99th percentile (> 37.7 degrees C) can therefore be interpreted as fever. Nevertheless, an universally accepted definition of fever does not exist. Viral infection is the most frequent cause of acute fever in infants, even in the absence of a source. Bacterial infections are by far a rarer reason. Nevertheless, below the age of 3 years, acute fever is a ticklish issue because of the higher risk for rapidly evolving life-threatening invasive bacterial infections. Following introduction of vaccination against Haemophilus influenzae type b (Hib), Streptococcus pneumoniae has advanced to the most frequent cause of invasive bacterial infections in infants. Fever is rarely seen in newborns (age 1-28 days), but when present, it is more frequently serious. Around 12% of these newborns show an invasive bacterial infection. Therefore, a full workup for sepsis is strongly indicated. This includes cultures of blood,urine and cerebrospinal fluid plus a chest radiography. In addition, immediate start of an empirical intravenous antibiotic therapy and monitoring in a hospital setting are necessary. Apart from this exception, primary antibiotic therapy is rarely necessary in fever without a detectable focus and source. Also, routine prescription of antipyretics is not indicated. Though paracetamol may improve well-being and drinking behavior of infants, it does neither shorten the duration of fever duration, nor prevent febrile seizures.
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PMID:[Acute fever in infants]. 1704 85

Immunosuppressive monoclonal antibodies directed to immune system cells may reduce rejection and graft versus host disease (GvHD) after allogeneic stem cell transplantation (SCT), but can increase the risks of viral infection. Here, we report human herpes virus-6 (HHV-6) encephalitis despite antiviral prophylaxis in 5 of 43 (11.6%) patients receiving alemtuzumab supported conditioning. Encephalitis occurred at 41-103 days (median 60 days) presenting with confusion in all patients, combined with amnesia (n=3) or seizures (n=2). MRI revealed non-specific white matter changes in two and a non-enhancing medial temporal lobe lesion in three patients. Cerebrospinal fluid (CSF) PCR amplification for HHV-6 was positive in all five patients, (600-2 25 000 (median 4700) copies/ml CSF), while analysis of peripheral blood revealed 100-22 500 (median 1200) viral copies/ml plasma. CSF protein was elevated in four patients, with minimal CSF pleocytosis. Intravenous foscarnet produced neurological improvement at 8-13 (median 11) days and negative plasma PCR at 30-66 (median 50) days. Four patients had complete neurological recovery, but one patient with persistent viral DNA in the CSF succumbed to progressive encephalopathy. Given this high incidence of HHV-6 and the possibility of successful outcome with prompt treatment, a high index of suspicion of this disorder is required in recipients of monoclonal antibody supported allografts.
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PMID:Human herpesvirus-6 encephalitis following allogeneic hematopoietic stem cell transplantation. 1740 92

Three independent complex segregation analyses found that the cause of Attention Deficit/Hyperactivity Disorder (ADHD) was the presence of major genes interacting with environmental influences. In order to identify potential environmental risk factors for ADHD in the Paisa community--a very well described, genetically isolated group--we randomly selected a sample of 486 children between 6 and 11 years of age. This group included 200 children with ADHD (149 males and 51 females) and 286 healthy controls (135 males and 151 females). The ADHD DSM-IV diagnosis was obtained using the DICA and BASC evaluation instruments, and the children's mothers or grandmothers filled out a questionnaire on each child's exposure to prenatal, neonatal, and early childhood risk factors. The data were analyzed using cross tabulation and stepwise logistic multiple-regression analyses. Cross tabulation associated ADHD with a variety of factors, including miscarriage symptoms, premature delivery symptoms, maternal respiratory viral infection, moderate to severe physical illness in the mother during gestation, prenatal cigarette and alcohol exposure, neonatal seizures, asphyxia or anoxia, severe neonatal illness, mild speech retardation, moderate brain injury, and febrile seizures (odds ratio >or= 2, P < 0.05). Stepwise logistic multiple-regression analysis also uncovered a block of variables, including male gender, maternal illnesses, prenatal alcohol exposure, mild speech retardation, febrile seizures, and moderate brain injury (odds ratio >or= 2.0, P < 0.05). Future studies on the risk of developing ADHD must include these environmental factors as covariates.
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PMID:Environmental influences that affect attention deficit/hyperactivity disorder: study of a genetic isolate. 1748 41

A 9-year-old boy was diagnosed as non-herpetic acute limbic encephalitis (NHALE). Four days after the gastrointestinal infection, he developed a generalized seizure accompanied with delirium and psychiatric change, which evolved into intractable seizures. These seizures were complex partial seizures or generalized tonic clonic seizures, and were highly resistant to many anticonvulsants. Magnetic resonance imaging of the brain demonstrated reversible symmetrical high-intensity lesions in the claustra on the diffusion-weighted image. Laboratory findings did not suggest herpes simplex virus infection. Further, the clinical findings were consistent with those in acute encephalitis with refractory repetitive partial seizures (AERRPS). We assume that a part of AERRPS belongs to the category of parainfectious limbic encephalitis with repetitive seizures.
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PMID:[A case of non-herpetic acute limbic encephalitis in childhood--comparison with acute encephalitis with refractory repetitive partial seizures (AERRPS)]. 1751 38

Six members of the herpesvirus family cause well-described neurologic disease in children: herpes simplex virus-1 (HSV-1), herpes simplex virus-2 (HSV-2), varicella-zoster (VZV), Epstein-Barr (EBV), cytomegalovirus (CMV), and human herpes virus-6 (HHV-6). When herpesviruses infect the central nervous system (CNS), the clinical presentation is non-specific and often confounding. The clinical urgency is often underscored by progressive neurologic deficits, seizures, or even death, and prompt diagnosis and treatment rely heavily on neuroimaging. This review focuses on the spectrum of cerebral manifestations caused by these viruses, particularly on non-congenital presentations. Recent advances in our understanding of these viruses are discussed, including new polymerase chain reaction techniques that allow parallel detection, which has improved our recognition that the herpesviruses are neurotropic and involve the CNS more often than previously thought. Evolving knowledge has also better elucidated viral neuropathology, particularly the role of VZV vasculitis in the brain, HHV-6 in febrile seizures, and herpesvirus reactivation in immunosuppressed patients. The virology, clinical course, and CNS manifestations of each virus are reviewed, followed by descriptions of neuroimaging findings when these agents infect the brain. Characteristic but often subtle imaging findings are discussed, as well as technical pearls covering appropriate use of MRI and MRI adjuncts to help differentiate viral infection from mimics.
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PMID:Neuroimaging of herpesvirus infections in children. 1823 87

Febrile seizures are the most common form of childhood seizures, affecting 2-5% of all children and usually appearing between 3 months and 5 years of age. Despite its predominantly benign nature, a febrile seizure (FS) is a terrifying experience for most parents. The condition is perhaps one of the most prevalent causes of admittance to pediatric emergency wards worldwide. FS, defined as either simple or complex, may be provoked by any febrile bacterial or (more usually) viral illness. No specific level of fever is required to diagnose FS. It is essential to exclude underlying meningitis in all children with FS, either clinically or, if any doubt remains, by lumbar puncture. There is no evidence, however, to support routine lumbar puncture in all children admitted with simple FS, especially when typical clinical signs of meningitis are lacking. The risk of epilepsy following FS is 1-6%. The association, however small, between FS and epilepsy may demonstrate a genetic link between FS and epilepsy rather than a cause and effect relationship. The effectiveness of prophylactic treatment with medication remains controversial. There is no evidence of the effectiveness of antipyretics in preventing future FS. Prophylactic use of paracetamol, ibuprofen or a combination of both in FS, is thus a questionable practice. There is reason to believe that children who have experienced a simple FS are over-investigated and over-treated. This review aims to provide physicians with adequate knowledge to make rational assessments of children with febrile seizures.
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PMID:Assessment of febrile seizures in children. 1957 74

In Europe infection with Puumala or Dobrava viruses causes hemorrhagic fever with renal syndrome (HFRS). In the course of HFRS, mild neurological symptoms such as headache, vertigo, and nausea are common. However, the data about the occurrence of severe, potentially life-threatening neurological manifestations are rather scarce. Here, we present a case of HFRS with serologically proven Dobrava virus infection complicated by epileptic seizures and hemiparesis due to focal encephalitis.
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PMID:Case report: severe neurological manifestation of Dobrava hantavirus infection. 1793 68


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