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)

We report 2 cases of teenagers who were poisoned with Jimson weed (Datura stramonium) and presented to the emergency department with a severe acute anticholinergic toxidrome after ingestion of several hundred seeds. The patients presented with visual hallucinations, disorientation, incomprehensible and nonsensical speech, and dilated sluggish pupils. Both patients required restraints for combativeness until adequate sedation with lorazepam and haloperidol was achieved. Jimson weed is found in southern Canada and the United States and can cause acute anticholinergic poisoning and death in humans and animals. The treatment of choice for anticholinergic poisoning is mainly supportive care and gastrointestinal decontamination with activated charcoal. Jimson weed intoxication should be considered in cases of patients presenting with unexplained peripheral and central anticholinergic symptoms including delirium, agitation and seizures, especially among younger patients and partygoers. It is important that health care professionals recognize that Jimson weed is a toxic, indigenous, "wild" growing plant, subject to misuse and potentially serious intoxication requiring hospitalization.
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PMID:Teenagers with Jimson weed (Datura stramonium) poisoning. 1807 95

A 37-year-old woman developed memory disturbance and seizures preceded by headache and high fever. Physical examination revealed persistent high fever, confusion, neck stiffness, anterograde and retrograde amnesia and disorientation. CSF showed pleocytosis and normal glucose level, and negative herpes simplex virus DNA on PCR. The fluid attenuated inversion recovery (FLAIR) MRI of the brain demonstrated nearly symmetric high signal intensity areas in the bilateral mesial temporal lobes. The tentative clinical diagnosis was non-herpetic acute limbic encephalitis (NHALE), and administration of methylprednisolone improved her conditions. Laboratory tests revealed mild hypothyroidism with high titers of serum antibodies against TPO and thyroglobulin, consistent with Hashimoto's disease. In addition, antibodies against amino terminal of alpha-enolase in the serum and those against glutamate receptor (GluR) epsilon2 in the serum and CSF were positive. A final diagnosis of Hashimoto's encephalopathy associated with GluRepsilon2 antibody was made. The present case suggests that NHALE-like clinical manifestation can be produced by autoimmune-mediated encephalopathies.
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PMID:[Non-herpetic acute limbic encephalitis-like manifestation in a case of Hashimoto's encephalopathy with positive autoantibodies against ionotropic glutamate receptor epsilon2]. 1809 94

La Crosse virus encephalitis is the most common mosquito-borne virus in children in the United States. La Crosse virus encephalitis has emerged as a significant health concern due to its potential for acute morbidity, including seizures, alterations in mental status, and, in rare cases, death, as well as the potential for chronic morbidity, including, epilepsy and cognitive and behavioral disorders. The aim of this study is to provide a clinical description of the largest series of children reported with periodic lateralizing epileptiform discharges (PLEDS) associated with La Cross virus encephalitis with reference to their clinical course, seizure type, electroencephalogram (EEG) patterns, and 2- and 10-year long-term neurologic outcome. In addition, to evaluate whether this subset of children may indeed have more severe disease than children with La Crosse virus encephalitis without PLEDS, comparisons are made between the 2 groups on specific variables. All patients presented with fever and disorientation; 6 of the 9 (66%) presented with seizures. PLEDS localized to the temporal lobe in 7 patients (77%). The children with PLEDS had longer intensive care unit stays (6.5 +/- 2.4 vs 3.2 +/- 1.9; P < .0001), a higher rate of intubation (88% vs 20%; P < .001), and a higher rate of cerebral herniation (1%; P < .05) than children with La Crosse virus encephalitis without PLEDS. Follow-up data on the subset with PLEDS also suggest a relatively high rate of epilepsy and behavioral difficulties with hyperactivity symptoms, memory deficits, and school difficulties. The implications for recognition, management, and follow-up of this worrisome subset of patients with La Crosse virus encephalitis are discussed.
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PMID:Periodic lateralized epileptiform discharges in La Crosse encephalitis, a worrisome subgroup: clinical presentation, electroencephalogram (EEG) patterns, and long-term neurologic outcome. 1816 May 48

Voltage-gated potassium channel antibody (VGKC-Ab)-associated limbic encephalitis (LE) is a recently described syndrome that broadens the spectrum of immunotherapy-responsive central nervous system disorders. Limbic encephalitis is typically characterised by a sub-acute onset of disorientation, amnesia and seizures, but the clinical spectrum is not yet fully defined and the syndrome could be under-diagnosed. We here describe the clinical profile of four patients with VGKC-Ab-associated LE who had intermittent, episodic hypothermia. One of the patients also described a prodrome of severe neuropathic pain preceding the development of limbic symptoms. Both of these novel symptoms responded well to immunosuppressive therapy, with concurrent amelioration of amnesia/seizures.
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PMID:Hypothermia in VGKC antibody-associated limbic encephalitis. 1820 10

A 34-year-old man with astrocytoma in the left parietal lobe had symptomatic partial epilepsy, and he presented transient episodes of acalculia, agraphia and finger agnosia. Occasionally he had difficulty in finding appropriate letters when making an e-mail, and difficulty in writing and calculation. Neurological examinations revealed ictal symptoms of Gerstmann's syndrome without right to left disorientation. No other higher cortical dysfunction or neurological deficits were noted. Scalp EEGs showed frequent, regional ictal discharges in the left parietal area lasting for 60-240 seconds. These clinico-electrographical observations strongly support that epileptic seizures produced a loss of cortical higher function manifesting Gerstmann's syndrome.
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PMID:[Ictal Gerstmann's syndrome in a patient with symptomatic parietal lobe epilepsy]. 1840 43

A 54-year-old woman had an episode of sudden oral bleeding and generalized petechiae 1 week after a sore throat and diarrhea. On admission, the platelet count was 0.1 x 10(4)/microl, and the platelet-associated IgG level was elevated. Hyperplasia of megakaryocytes in a bone marrow specimen and aberrant Epstein-Barr virus (EBV) antibody patterns led to a diagnosis of EBV-associated idiopathic thrombocytopenic purpura (ITP). Prednisolone (PSL) promptly restored her platelet count; however, she developed disorientation and affective lability soon after PSL was tapered. Subsequently, she ran a high fever and developed convulsive seizures. T2-weighted MRI demonstrated a high signal area in the subcortical white matter, and no abnormal findings were found on examination of the cerebrospinal fluid. The diagnosis of acute disseminated encephalomyelitis (ADEM) was made and steroid pulse therapy was started, which resulted in remission of the symptoms without recurrence in the following months. This is the first reported case of ADEM following EBV infection during treatment for ITP. Administration of PSL for ITP might mask the presenting clinical picture of ADEM. The possibility of ADEM should be investigated in patients of ITP following viral infection who develop acute encephalopathy.
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PMID:[Acute disseminated encephalomyelitis during treatment for idiopathic thrombocytopenic purpura]. 1870 83

The clinical, neuropathologic, and magnetic resonance (MR) imaging features in four cats with necrosis of the hippocampus and piriform lobe are described. All cats had acute generalized seizures and behavioral changes including aggression, salivation, polyphagia, and disorientation. Routine hematologic, serum chemistry, and cerebrospinal fluid analyses were normal. MR imaging abnormalities were restricted to the area of the hippocampus and piriform lobe. The lesions were T2-hyperintense, T1-hypointense, and were characterized by various degrees of contrast enhancement. Lesions were consistent with necrotizing encephalitis. Two cats were euthanized and underwent postmortem examination within a week after MR imaging due to the lack of response to antiepileptic drug therapy and progressive encephalopathy [corrected] The remaining two cats lived for about four months and were then euthanized because of persistent behavioral and neurologic signs; only one of these cats underwent postmortem examination with histopathologic examination. Histopathological findings were typical of severe, diffuse, bilateral symmetric necrosis, and degeneration of neurons in the hippocampus and piriform lobe, but an etiologic agent was not apparent. This apparently unique feline syndrome, now reported in Switzerland and Italy, has no known cause at this time.
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PMID:Magnetic resonance imaging of feline hippocampal necrosis. 1872 Jul 64

We compared clinical characteristics and autoantibodies against GluRepsilon2 between 95 patients with nonparaneoplastic non-herpetic acute limbic encephalitis (NPNHALE) and 19 patients with non-herpetic acute encephalitis accompanying ovarian teratoma (NHAE-OT). Onset age (mean +/- SD) was 27.7 +/- 18.6 years old in NPNHALE, 27.5 +/- 6.5 in NHALE-OT. Preceding factors were found in 63.8% of patients with NPNHALE and 89.5% of patients with NHALE-OT (Fisher's exact test, p = 0.025), and major preceding factors were upper respiratory infections or fever in both groups. Symptoms at the onset were disorder of behavior and talk > seizures > impairment of consciousness in NPNHALE, and disorder of behavior and talk > seizures > disorientation in NHALE-OT. Symptoms at the acute stage were similar between NPNHALE and NHAE-OT, but duration of hospital stay was longer in NHAE-OT (209.0 days) than NPNHALE (87.5 days) (Mann Whitney test, p<0.0001). At the onset, cell counts in CSF were 51.6 +/- 66.4/mm3 and protein levels were 35.4 +/- 14.7 mg/dl, and IgG levels were 6.6 +/- 4.2 mg/dl in NHAE-OT, and these data were not significantly different between NPNHALE and NHAE-OT. In acute stage, autoantibodies against whole molecule of GluRepsilon2 in CSF were detected in 51.8% (29/56) of adult NPNHALE, and 40% (6/15) of NHAE-OT patients by immunoblot. These autoantibodies in both groups included epitopes to n-terminal of GluRepsilon2. Antibodies against NMDAR complex (Dalmau's method) in CSF were detected in 90.9% (10/11) of NHAE-OT patients.
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PMID:[Acute limbic encephalitis and NMDA type-glutamate receptor]. 1919 20

Alzheimer disease (AD) is associated with cognitive decline and increased incidence of seizures. Seizure activity in AD has been widely interpreted as a secondary process resulting from advanced stages of neurodegeneration, perhaps in combination with other age-related factors. However, recent findings in animal models of AD have challenged this notion, raising the possibility that aberrant excitatory neuronal activity represents a primary upstream mechanism that may contribute to cognitive deficits in these models. The following observations suggest that such activity may play a similar role in humans with AD: (1) patients with sporadic AD have an increased incidence of seizures that appears to be independent of disease stage and highest in cases with early onset; (2) seizures are part of the natural history of many pedigrees with autosomal dominant early-onset AD, including those with mutations in presenilin-1, presenilin-2, or the amyloid precursor protein, or with duplications of wild-type amyloid precursor protein; (3) inheritance of the major known genetic risk factor for AD, apolipoprotein E4, is associated with subclinical epileptiform activity in carriers without dementia; and (4) some cases of episodic amnestic wandering and disorientation in AD are associated with epileptiform activity and can be prevented with antiepileptic drugs. Here we review recent experimental data demonstrating that high levels of beta-amyloid in the brain can cause epileptiform activity and cognitive deficits in transgenic mouse models of AD. We conclude that beta-amyloid peptides may contribute to cognitive decline in AD by eliciting similar aberrant neuronal activity in humans and discuss potential clinical and therapeutic implications of this hypothesis.
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PMID:Epilepsy and cognitive impairments in Alzheimer disease. 1920 49

Autoimmune limbic encephalitis (LE) can arise both by paraneoplastic and non-paraneoplastic mechanisms. Patients with LE usually have a subacute onset of memory impairment, disorientation and agitation, but can also develop seizures, hallucinations and sleep disturbance. The following investigations may aid the diagnosis: analysis of cerebrospinal fluid (CSF), electroencephalography, magnetic resonance imaging, fluorodeoxyglucose positron emission tomography and neuronal antibodies in the serum and CSF. Neuronal antibodies are sometimes, but not always, pathogenic. Autoimmune LE may respond to corticosteroids, intravenous IgG (IVIG) or plasma exchange. The cornerstone of paraneoplastic LE therapy is resection of the tumour and/or oncological treatment. Several differential diagnoses must be excluded, among them herpes simplex encephalitis.
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PMID:Autoimmune limbic encephalitis. 1956 2


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