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

Viral encephalitis affects approximately 7.5 people/100 000 and carries a high rate of morbidity and mortality. Most patients with viral encephalitis will develop some form of seizure during the infectious process, and of those who survive encephalitic disease, approximately 4-20% will develop epilepsy. Arthropod-borne (arbo)viruses are the leading cause of viral encephalitis in the world today, with between 10% and 35% of patients infected with these viruses displaying some form of seizure. Several neurotropic DNA viruses, including Herpes and cytomegalovirus also commonly cause seizures in infected patients. In the clinical setting, the cause of seizures seen during viral encephalitis is usually attributed to acute febrile responses. However, it has become apparent that the mechanisms behind seizure generation during viral encephalitis are likely to be much more complicated. For example, CD4(+) and CD8(+) T cells possibly through their secretion of interferon-gamma, appear to play an important role in determining neuronal responses when challenged with kainic acid. In addition, the ability of the human immunodeficiency virus, transactivating protein to modulate NMDA signaling possibly triggering seizures, highlights the fact that elements of the antiviral response and even virally derived proteins are capable of directly manipulating neuronal function. Understanding the complex relationships between the CNS, the immune system, and invading pathogens is a critical step in understanding the pathogenesis of seizures seen during viral infections and informing the development of novel therapies.
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PMID:Viruses and the immune system: their roles in seizure cascade development. 1820 51

A number of gene therapy approaches have been developed for protecting neurons from necrotic neurological insults. Such therapies are limited by the need for transcription and translation of the protective protein, delaying therapeutic impact. As an alternative, we explore the neuroprotective potential of protein therapy, using a fusion protein comprised of the death-suppressing BH4 domain of the Bcl-xL protein and the protein transduction domain of the human immunodeficiency virus Tat protein. This fusion protein decreased neurotoxicity caused by the excitotoxins glutamate and kainic acid in primary hippocampal cultures, and decreased hippocampal damage in vivo in an excitotoxic seizure model.
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PMID:Anti-apoptotic therapy with a Tat fusion protein protects against excitotoxic insults in vitro and in vivo. 1820 42

The authors describe a patient with known human immunodeficiency virus (HIV)-1 infection who presented with two generalized seizures and was found to have extensive white matter disease and a left/bilateral temporo-occipital focal slowing on electroencephalography (EEG). There were no magnetic resonance imaging (MRI) or cerebrospinal fluid (CSF) indications for opportunistic infection. Plasma viremia was controlled, whereas viral replication was uncontrolled in CSF. CSF-specific genotype-guided adaptation of the antiretroviral therapy in order to optimize central nervous system (CNS) penetration resulted in clinical improvement and normalization of MRI and EEG. Our case report illustrates the importance of individualized antiretroviral therapy in HIV infected patients with neurological complications.
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PMID:Adaptation of antiretroviral therapy in human immunodeficiency virus infection with central nervous system involvement. 1830 78

Patients living with human immunodeficiency virus represent a growing population, and an increased number of central nervous system presentations can be expected over the next decade. Emerging data suggests that both HIV-seropositive patients and cocaine-abusing patients may be at special risk of seizure phenomena. This case report discusses the risks of new-onset seizure activity when these two risk factors converge, which is a common occurrence in this population. Data from the fields of neuroanatomy and neurovirology are presented to explain the heightened risk of this patient population and provide the practitioner with an improved understanding of the central nervous system complexities in HIV.
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PMID:Comorbid HIV encephalopathy and cocaine use as a risk factor for new-onset seizure disorders. 1832 57

Severe congenital neutropenia (SCN) is a rare, heterogeneous, primary immunodeficiency disorder characterized by early onset of severe bacterial infections. We here describe a case of SCN associating neutropenia and neurodevelopmental delay. The girl was well until the age of 9 months, when she suffered from an episode of convulsion. Subsequently, she developed several episodes of superficial abscesses, oral ulcers and otitis media. Further work-up revealed severe congenital neutropenia caused by a homozygous mutation (R86X) in the antiapoptotic molecule HAX1. She also suffered from psychomotor retardation and recurrent seizures. This case illustrates that HAX1 deficiency may be associated with a neurological phenotype.
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PMID:Association of HAX1 deficiency with neurological disorder. 1833 Aug 43

This case of microsporidiosis manifested as mutiple intracranial lesions separated in space and time, and neurological and radiological findings were improved with albendazole administration. A 33-year-old man presented with headache, fever, and dysphasia. His consciousness was clear. Neurological examination revealed acalculia, agraphia, and homonymous hemianopsia. He had a past history of febrile convulsive seizures of unknown cause until 14-years-old, but no history of immunodeficiency. T1-weighted magnetic resonance (MR) imaging showed a hypointense lesion with a hyperintense part, and ring-like enhancement with gadolinium-diethylenetriaminepenta-acetic acid (Gd-DTPA), in the left temporal lobe. T2-weighted and diffusion-weighted MR imaging showed the lesion surrounded by moderate hyperintense areas. He underwent gross total resection of the lesion. Histological examination demonstrated intracellular clusters of small basophilic spore-like bodies in the astrocytes, suggestive of microsporidia-infected astrocytes. However, immunohistochemical, polymerase chain reaction, and serological analyses failed to confirm the definitive diagnosis of microsporidiosis, so that he received no further treatment. Three years later, he presented with sensory disturbance in the left side of his face and left cerebellar ataxia, followed by fever, abnormal sensation in the left side of his face, and aggravated ataxia of the left upper and lower extremities on day 10 after admission. T1-weighted MR imaging with Gd-DTPA showed an enhanced lesion with irregular margin in the left cerebellar peduncle. T2-weighted MR imaging showed a diffuse hyperintense region around the lesion. Cerebrospinal fluid culture, serological analysis for autoimmune disease, and thoracic, abdominal, and pelvic computed tomography and 18F-fluorodeoxyglucose-positron emission tomography detected no abnormalities such as cancers or other lesions in the extracranial organs. No definitive diagnosis was obtained, but recurrence of microsporidiosis was the most probable cause. Administration of albendazole (600 mg/day) was started on day 15, because of rapid neurological and radiological deterioration. This treatment resulted in clinical improvement and disappearance of the lesion on MR imaging after daily administration for 4 weeks. He was discharged on foot with moderate sensory disturbance in the left side of the face and ataxia. Based on the clinical course and negative findings, the final diagnosis was microsporidiosis. This case suggests that microsporidiosis in the central nervous system can persist even in immunocompetent patients without involvement of any other organs, and that albendazole administration is likely to be effective.
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PMID:[Multiple intracerebral enhanced lesions strongly suspected to be microsporidiosis. A case report]. 1863 8

Seizures are not uncommon in patients with human immunodeficiency virus (HIV) infection, and with the upsurge in HIV infection this may be an important cause for acute symptomatic seizures. Seizures may rarely be the presenting manifestation of HIV infection. Opportunistic infections such as toxoplasmosis, tuberculosis, progressive multifocal leucoencephalopathy (PML), cryptococcal meningitis and polymicrobial infections, metabolic and electrolyte disturbances, and drugs are common causes of new-onset seizures in HIV-seropositive individuals. In the absence of any cause, primary HIV infection may be considered responsible for seizures. Because seizures tend to recur in and because they are a poor prognostic indicator in HIV infection, treatment with antiepileptic drugs (AEDs) is the norm. The treatment of HIV-infected individuals with seizures comprises of the administration of AEDs, specific treatment of the underlying conditions, and antiretroviral drugs. Clinicians must consider both therapy-compromising drug-drug and drug-disease interactions while choosing appropriate AEDs. The ideal AED in this setting is one that does not affect viral replication, have limited protein binding, and have no effects on the hepatic cytochrome P450 enzyme system. The risks for AED-induced allergic skin rash appears to be high in HIV-seropositive individuals.
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PMID:Seizures in HIV-seropositive individuals: NIMHANS experience and review. 1875 59

Disseminated cryptocococcosis is a rare and often fatal disease. Here in we report an unusual fatal case of disseminated cryptococcosis. The patient presented with a past history of postmenopausal bleeding with loss of consciousness, altered mental status, few seizures and a low grade fever. Lumbar puncture revealed elevated pressure, lymphocytic pleocytosis, elevated protein and markedly reduced glucose level. Cryptococcus neoformans was isolated from cerebrospinal fluid and blood. Serological assay revealed the presence of human immunodeficiency virus. The patient was treated with antifungal agents intravenously without any signs of improvement and the patient passed away after two weeks of therapy. This is the first case report of disseminated cryptococcosis in an AIDS patient suffering from cryptoccoccal vaginitis.
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PMID:Disseminated cryptococcosis in an AIDS patient with unusual clinical presentation. 1878 90

Extracellular nucleotides and nucleosides act as signaling molecules involved in a wide spectrum of biological effects. Their levels are controlled by a complex cell surface-located group of enzymes called ectonucleotidases. There are four major families of ectonucleotidases, nucleoside triphosphate diphosphohydrolases (NTPDases/CD39), ectonucleotide pyrophosphatase/phosphodiesterases (E-NPPs), alkaline phosphatases and ecto-5'-nucleotidase. In the last few years, substantial progress has been made toward the molecular identification of members of the ectonucleotidase families and their enzyme structures and functions. In this review, there is an emphasis on the involvement of NTPDase and 5'-nucleotidase activities in disease processes in several tissues and cell types. Brief background information is given about the general characteristics of these enzymes, followed by a discussion of their roles in thromboregulatory events in diabetes, hypertension, hypercholesterolemia and cancer, as well as in pathological conditions where platelets are less responsive, such as in chronic renal failure. In addition, immunomodulation and cell-cell interactions involving these enzymes are considered, as well as ATP and ADP hydrolysis under different clinical conditions related with alterations in the immune system, such as acute lymphoblastic leukemia (ALL), B-chronic lymphocytic leukemia (B-CLL) and infections associated with human immunodeficiency virus (HIV). Finally, changes in ATP, ADP and AMP hydrolysis induced by inborn errors of metabolism, seizures and epilepsy are discussed in order to highlight the importance of these enzymes in the control of neuronal activity in pathological conditions. Despite advances made toward understanding the molecular structure of ectonucleotidases, much more investigation will be necessary to entirely grasp their role in physiological and pathological conditions.
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PMID:NTPDase and 5'-nucleotidase activities in physiological and disease conditions: new perspectives for human health. 1880 12

A variety of autoantibodies have been identified with complex neurological disorders including limbic encephalitis. The underlying trigger for the immune-mediated process and the role of autoantibodies in the pathogenesis of limbic encephalitis remain to be clarified. Here, we report a 16-year-old female who was diagnosed with acute-onset non-neoplastic limbic encephalitis. The initial treatment with pulse doses of i.v. methylprednisolone improved the neurological symptoms. During the next 12 months, progressive decline was reported in her academic functioning and seizure control. Additional diagnostic evaluation revealed no evidence of malignancy or central nervous system infection but circulating anti-GAD antibodies were present in the serum and cerebrospinal fluid. Intravenous gammaglobulin infusion was initiated and continued monthly. Intravenous and oral steroids were added to the intravenous immunoglobulin treatment because of the worsening course and seizures, despite treatment with antiepileptic medications. Screening for quantitative immunoglobulins demonstrated hypogammaglobulinaemia with low immunoglobulin M and G in addition to low immunoglobulin A levels. There was a lack of protective pneumococcal antibody titers before and after immunization. Therefore, common variable immunodeficiency was suspected despite there being no history of recurrent infections. To our knowledge, this is the first report describing a possible link between immune-mediated limbic encephalitis and immune deficiency.
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PMID:Limbic encephalitis associated with anti-GAD antibody and common variable immune deficiency. 1953 23


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