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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alzheimer's disease is a known risk factor for seizures, and age older than 60 years is a recognized risk factor for poor outcome from convulsive and nonconvulsive status epilepticus. The authors suspect that there may be a causal relationship between dementia pathology and the development and maintenance of refractory seizures. They report two selected patients with complex partial status epilepticus whose presentation and clinical course provide partial support for this hypothesis. Their methods include case reports with clinical, EEG, imaging, and pathologic correlations. The patients were 70 and 85 years of age. Both had central and peripheral brain atrophy on imaging studies (with some regions that were affected more than others), left temporal seizure foci corresponding to areas of greatest cortical atrophy, and early presentation with inhibitory epileptic symptoms (aphasia), with evolution to complex partial status epilepticus. Pathologic confirmation of Alzheimer's disease was obtained in one patient who had not been diagnosed previously. It involved maximally the cortex underlying the seizure focus. A diagnosis of probable Alzheimer's disease was established in the other patient. Alzheimer's disease may be causal in some cases of complex partial status epilepticus. Additional observations in support of this hypothesis are needed.
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PMID:Alzheimer's disease underlies some cases of complex partial status epilepticus. 1108 55

L-Deprenyl (Selegeline) introduced for use in parkinson's disease, is implicated to show beneficial effects in epilepsy, alzheimer's disease, cognition, depression and other age related neurological diseases. In this study, we investigated the CNS effects of L-deprenyl with special reference to epilepsy, anxiety and cognition and memory in mice. L-deprenyl (10, 20 and 40 mg/kg) showed a significant anticonvulsant activity against pentylenetetrazole (PTZ)-induced convulsions. Combination of L-deprenyl (10 mg/kg) with the sub-protective dose of diazepam (1 mg/kg) showed potentiation of the anticonvulsant effect. In the maximal-electroshock (MES)-induced convulsions, L-deprenyl (10 mg/kg) significantly delayed the onset and decreased the duration of extensor phase. Its combination with the lower dose of phenytoin (10 mg/kg) showed potentiation in response compared to the per se effect of both the drugs. However, L-deprenyl did not show any protective effect in lithium-pilocarpine induced status epilepticus. Acute treatment with L-deprenyl had no effect on learning and memory. In chronic treatment, L-deprenyl per se showed no effect on learning and memory but did improve the condition in mice with scopolamine induced memory deficit. L-Deprenyl per se was anxiogenic though in combination with diazepam (1 mg/kg) it potentiated the antianxiety effect of the latter. The above observations suggest that in epilepsy, L-deprenyl might be acting partially by influencing the GABAA/benzodiazepine mechanism in the brain (similar to diazepam and phenytoin), and in cognition enhancing effect, the cholinergic system might be playing a role. Thus, L-deprenyl could prove to be an adjuvant in the antiepileptic therapy and beneficial in dementia associated with epilepsy.
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PMID:Studies on anticonvulsant actions of L-deprenyl. 1121 8

This study included 341 subjects aged over 60 years, 174 females and 167 males, (mean age 72-years), who experienced their first epileptic seizure and fulfilled all inclusion criteria over an 8-year period. Data were available from the physical examination, EEG, laboratory tests and CT scan or MRI for all patients. The international classification of epileptic seizures was applied, 41 p.cent of the seizures were generalized and 59 p.cent were partial. Status epilepticus occurred in 8 p.cent of the patients. The EEG recording was contributive to diagnosis or helpful for localizing the epileptic focus in 55 p.cent of the patients. Normal brain imaging was observed in 40 p.cent of the patients. The main etiology was cerebrovascular disease (33 p.cent), acute stroke (27 patients), or more often postvascular epilepsy (87 patients). Other etiologies were degenerative cortical dementia in 7 p.cent of the patients, metabolic and toxic disorders in 11 p.cent, and benign or malignant brain tumors in 6.5 p.cent. Thirty-two percent of the seizures were of unknown origin (cryptogenic seizures). No correlation was found between sex, age, and etiology. An antiepileptic drug treatment was initiated in 77 p.cent of the patients who were given either valproate (43 p.cent), carbamazepine (26 p.cent) or barbiturates (7 p.cent). These findings are in agreement with those reported in the reviewed literature.
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PMID:[First epileptic seizure in the elderly: electroclinical and etiological data in 341 patients]. 1245 41

A 64-year-old man developed progressive dementia and altered consciousness with myoclonus over 2 months. Neurological examination revealed mild dysphagia and negative myoclonus of both hands. Electroencephalography (EEG) showed continuous periodic synchronous discharge (PSD) of 1 Hz, although his EEG abnormality was not similar to that usually observed in Creutzfeldt-Jakob disease (CJD). Magnetic resonance imaging (MRI) of the brain revealed only few lacunes. Laboratory data were also normal. Since his consciousness level fluctuated and the PSD were spiky, we came to a diagnosis of nonconvulsive status epilepticus (NCSE). After administering the valproic acid, his symptoms and EEG finding improved. Nine months after the onset, despite his continued valproic acid, the patient had recurrent NCSE and PSD of 1 Hz. Diffusion-weighted MRI showed a T2-hyperintense lesion in the right parietal lobe, where SPECT scans showed hyperperfusion. After adding zonisamide, he improved slowly. The follow-up MRI and SPECT showed a disappearance of the previous lesion. Now CT scans of the abdomen showed enlarged periaortic lymph node and endoscopic ultrasonography disclosed a submucosal tumor of the stomach. Biopsy of the periaortic lymph node by laparotomy revealed undifferentiated adenocarcinoma with its origin being unclear. Chemotherapy didn't work well for the tumor and the patient underwent a downhill course, although his mental and neurological manifestation were mostly unremarkable. Two years and four months after the onset, he died in emaciation. Autopsy confirmed small cell carcinoma originating in the stomach and metastases in the liver and lungs. Neuropathological examination revealed only mild scattered gliosis. This case was unique in the prolonged CJD-like manifestations, which turned out to be due to NCSE. Despite anti-neuronal antibodies were not detected, we suspect yet another paraneoplastic brain syndrome in this patient.
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PMID:[An autopsy case of encephalopathy associated with small cell carcinoma of the stomach with nonconvulsive status epilepticus resembling Creutzfeldt-Jakob disease]. 1283 85

The electroencephalogram (EEG) is a long-used tool assisting health care providers with the diagnosis, management, and treatment of various neurological disorders. This article highlights several scenarios in which a consultant may utilize the routine EEG in managing specific neurological cases. Eight case scenarios from a tertiary referral hospital are presented for the reader's consideration. Scenarios selected are new-onset seizures, encephalopathy, syncope, dementia, brain death, hypoxic-ischemic encephalopathy, status epilepticus, and migraine. A history in each condition is presented and is followed by a discussion of how useful an EEG may be in these specific situations. These eight cases highlight specific learning points where the EEG may be useful and how it can be practically incorporated into care of patients. Understanding how the EEG may be useful in the presented cases will allow the efficient and effective use of the EEG in similar clinical scenarios.
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PMID:Using EEG in a consultative role. 1472 25

We report on a 50-year-old man with mental retardation and right-sided hemi-paresis. He seemed to be cured from epilepsy. In a short time a mental and physical deterioration developed which looked like a dementia, which was suggested by vascular risk factors. The EEG showed marked epileptic activity characterized by spikes appearing every 10 seconds over the left temporal lobe. After introduction of carbamazepine, a fast and long-term improvement of symptoms was noticed resulting in self sufficiency. The fast and marked effect of an antiepileptic drug being given to the patient with an non-typical reactivation of epilepsy in which the dementia-syndrome was caused by a transitory cognitive impairment due to sub-clinic electric seizures or non-convulsive status epilepticus.
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PMID:[Atypical epilepsy symptomatology as cause of a dementia like state in a mentally and physically retarded patient]. 1499 95

We present a 43-year-old man with recurrent episodes of Hashimoto's encephalopathy who was diagnosed with autoimmune thyroiditis in childhood. Encephalopathy started with subacute dementia followed by extrapyramidal and psychiatric symptoms of insidious onset. He had also status epilepticus which occurred within the first year of the disease. The patient was in euthyreosis, but increased levels of antithyroid antibodies were found. MRI of the brain was normal. Electroencephalography was initially normal and later showed diffuse slowing with generalized theta/delta activity. The cerebrospinal fluid examination revealed a high level of protein which decreased when remission of the disease was achieved. After other etiology was excluded Hashimoto's encephalopathy was diagnosed. Almost complete clinical recovery after steroid administration was observed. Attempts of prednisone withdrawal led to recurrence of neurological and psychiatric symptoms. The diagnosis of Hashimoto's encephalopathy should be considered in each case with subacute encephalopathy associated with high levels of antithyroid antibodies (despite normal thyroid function) and in the absence of other brain diseases.
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PMID:[Hashimoto's encephalopathy. Case report and literature review]. 1504 70

Creutzfeldt-Jakob disease (CJD) is a rare prion disease characterized by a spongiform encephalopathy in humans. Although the characteristic triad of myoclonus, dementia, and periodic EEG activity is easy to recognize, unusual manifestations of the disease may be challenging and create a diagnostic dilemma. We report a case of CJD that occurred in a 26-year-old patient who presented with a receptive (Wernicke's) aphasia secondary to nonconvulsive status epilepticus.
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PMID:Sporadic Creutzfeldt-Jakob disease presenting with nonconvulsive status epilepticus. 1538 Jan 38

We report two patients of status epilepticus, in which detailed brain magnetic resonance image (MRI) studies were performed. In one patient apparent diffusion coefficient (ADC) increased in the right temporopareital regions in the acute phase. This patient finally has good clinical course without neurological deficits, and abnormal findings on MRI also disappeared. In another patient ADC increased in the similar regions in the acute phase, and an MRI demonstrated cortical laminar necrosis on T1-weighted scans in the same regions in the posticteric phase about 3 months later. The patient had a poorer prognosis with moderate dementia. It has been demonstrated that increased ADC reflects extracellular edema, while decreased ADC indicates cytotoxic edema. ADC mapping appears to be useful for predicting the reversibility of brain damages due to status epilepticus.
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PMID:[Early detection of brain damages in status epilepticus using apparent diffusion coefficient mapping]. 1551 5

Neuropathologically, Alzheimer-type abnormalities are demonstrated in patients with Down syndrome (DS), both demented and nondemented and more than a half of patients with DS above 50 years develop Alzheimer's disease (AD). The apolipoprotein E epsilon4 allele, oestrogen deficiency, high levels of Abeta1-42 peptide, elevated expression of BACE2, and valine polymorphism of prion protein gene are associated with earlier onset of dementia in DS individuals. Advanced AD alone may be an important risk factor for new-onset seizures in older adults and age above 60 years is a recognized risk factor for poor outcome from convulsive and nonconvulsive status epilepticus. DS patients aged over 45 years are significantly more likely to develop Alzheimer's disease than those less than 45 years and up to 84% demented individuals with DS develop seizures. Late-onset epilepsy in DS is associated with AD, while early-onset epilepsy is associated with an absence of dementia. In AD patients with a younger age of dementia onset are particularly susceptible to seizures. DS adults with epilepsy score significantly higher overall on the adaptive behaviour profile. Language function declined significantly more rapidly in AD patients with seizures and there is a good correlation between the severity of EEG abnormalities and cognitive impairment whereas in DS slowing of the dominant occipital rhythm is related to AD and the frequency of the dominant occipital activity decreases at the onset of cognitive deterioration.
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PMID:Down syndrome, Alzheimer's disease and seizures. 1586 85


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