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 14-year-old female with tuberous sclerosis and history of seizures was found dead in bed at home 3 days after she had been assessed as doing well at a routine neurology clinic appointment. She had been treated with an antiepileptic drug, felbamate, for 36 months and had been seizure-free except for one seizure episode 5 months before death. Postmortem examination revealed cerebral edema, with uncal and tonsillar herniation, and pulmonary edema, consistent with seizure-induced apnea. Multiple microglial nodules with mature perivascular lymphocytic cuffing and diffuse infiltrates were identified around subependymal tuberous sclerosis giant cell nodules. Immunostaining and electron microscopy revealed human herpesvirus-6-infected macrophages, astrocytes, lymphocytes, and endothelial cells in the subependymal tuberous sclerosis lesions and choroid plexus. Subacute human herpesvirus-6 encephalitis is postulated to have precipitated a seizure and thus sudden unexpected death in epilepsy in this otherwise stable adolescent patient.
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PMID:Sudden unexpected death associated with HHV-6 in an adolescent with tuberous sclerosis. 1042 36

Autonomic dysreflexia (AD) may complicate spinal cord injured (SCI) subjects with a lesion level above the sixth thoracic level. There are several ways to remove triggering factors and, furthermore, new trigger mechanisms may be added by the introduction of new treatments. New data about the pathogenic mechanisms have been suggested in recent years as well as signs of metabolic effects associated with the reaction. This review of the syndrome includes clinical aspects of the AD reaction; the known pathogenic mechanisms, the incidence and prevalence and triggering factors. AD is associated with some cases of severe morbidity, including cerebral haemorrhage, seizures and pulmonary oedema. Symptomatic as well as specific treatments are discussed. Finally, some further questions are raised by the necessity of a proper definition of the syndrome, the revealing of the underlying pathophysiology, and new investigations concerning incidence and prevalence.
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PMID:Autonomic dysreflexia. 1062 49

The coverage of large surface areas of the brain for electrographic monitoring purposes necessitates a craniotomy to achieve comprehensive sampling. We undertook a review and prospective analysis over 3 years of 38 patients undergoing craniotomy for electrode implantation. The indication for invasive monitoring was to determine candidacy for resective surgery in patients whose seizure focus was not well localized by scalp electroencephalography and other noninvasive testing. Prophylactic cultures from the epidural space were obtained at electrode removal. There were five positive epidural cultures. All five patients went on to seizure-free status. Two positive cultures occurred in patients without obvious infection and who were not treated with antibiotics. Other complications included individual cases of atrial fibrillation, pulmonary edema, postoperative fever, and epidural hematoma. There was no mortality or permanent neurologic morbidity related to craniotomy for electrode placement. There was a 7.9% rate of clinical infection per patient and a 5.7% rate per craniotomy side. This study has identified several factors that significantly correlate with positive epidural culture results: > 100 electrodes, more than ten cables, more than 14 days of implantation, and more than one cable exit site.
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PMID:Morbidity and infection in combined subdural grid and strip electrode investigation for intractable epilepsy. 1051 77

In summary, SUDEP accounts for death in approximately 8% of the young epileptic population. It is commoner in young male epileptics with a long history of generalised seizures, who have a history of head trauma and alcohol excess, and who are taking more than one antiepileptic drug. Most deaths are unwitnessed and occur at home, usually in bed and presumably overnight. Subtherapeutic AED levels do not necessarily imply non compliance, and may simply reflect drug degradation in the plasma after death. Many victims have pulmonary oedema on postmortem examination, and some show ischaemic damage of the heart despite normal coronary arteries. This possibly arises as a result of repeated episodes of vasoconstriction from seizure related catecholamine bursts. Animal studies have demonstrated the occurrence of central apnoea and also support the theory of acute fatal cardiac failure. Possible association with the daily level of geomagnetic activity is reported. The precise reason for a particular seizure being fatal in an otherwise healthy individual is as yet undetermined.
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PMID:Sudden unexpected deaths in epileptics--a literature review. 1062 8

Eclampsia is defined as the occurrence of seizures in pregnancy or within 10 days of delivery, accompanied by at least two of the following features documented within 24 hours of the seizure: hypertension, proteinuria, thrombocytopenia or raised aspartate amino transferase. Eclampsia complicates approximately one in 2,000 pregnancies in the United Kingdom and it remains one of the main causes of maternal death. Up to 38% of cases of eclampsia can occur without premonitory signs or symptoms of pre-eclampsia-that is, hypertension, proteinuria, and oedema. Only 38% of eclamptic seizures occur antepartum; 18% occur during labour and a further 44% occur postpartum. Rare cases of eclampsia have occurred over a week after delivery. Outcome is poor for mother and child. Almost one in 50 women suffering eclamptic seizures die, 23% will require ventilation and 35% will have at least one major complication including pulmonary oedema, renal failure, disseminated intravascular coagulation, HELLP syndrome, acute respiratory distress syndrome, stroke, or cardiac arrest. Stillbirth or neonatal death occurs in approximately one in 14 cases of eclampsia. Up to one third of eclamptic seizures occur out of hospital. For this reason, initial management may involve accident and emergency departments. Early involvement of senior obstetric staff is crucial. Optimal emergency management of seizures, hypertension, fluid balance and subsequent safe transfer is essential to minimise morbidity and mortality.
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PMID:Management of eclampsia in the accident and emergency department. 1065 82

Status epilepticus is common and associated with significant mortality and complications. It affects approximately 50 patients per 100,000 population annually and recurs in >13%. History of epilepsy is the strongest single risk factor for generalized convulsive status epilepticus. More than 15% of patients with epilepsy have at least one episode of status epilepticus and low antiepileptic drug levels are a potentially modifiable risk factor. Other risks include young age, genetic predisposition, and acquired brain insults. Fever is a very common risk in children, as is stroke in adults. Mortality rates are 15% to 20% in adults and 3% to 15% in children. Acute complications result from hyperthermia, pulmonary edema, cardiac arrhythmias, and cardiovascular collapse. Long-term complications include epilepsy (20% to 40%), encephalopathy (6% to 15%), and focal neurologic deficits (9% to 11%). Neuronal injury leading to temporal lobe epilepsy is probably mediated by excess excitation via activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors and consequent elevated intracellular calcium that causes acute necrosis and delayed apoptotic cell death. Some forms of nonconvulsive status epilepticus may also lead to neuronal injury by this mechanism, but others may not. Based on clinical and experimental observations, complex partial status epilepticus is more likely to result in neuronal injury similar to generalized convulsive status epilepticus. Absence status epilepticus is much less likely to result in neuronal injury, and complications because it may be mediated primarily through excess inhibition. Future research strategies to prevent complications of status epilepticus include the study of new drugs (including NMDA antagonists, new drug delivery systems, and drug combinations) to stop seizure activity and prevent acute and delayed neuronal injury that leads to the development of epilepsy.
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PMID:Status epilepticus: risk factors and complications. 1088 37

From April through June 1997, 29 previously healthy children aged <6 years (median, 1.5 years) in Sarawak, Malaysia, died of rapidly progressive cardiorespiratory failure during an outbreak of hand, foot, and mouth disease caused primarily by enterovirus 71 (EV71). The case children were hospitalized after a short illness (median duration, 2 days) that usually included fever (in 100% of case children), oral ulcers (66%), and extremity rashes (62%). The illness rapidly progressed to include seizures (28%), flaccid limb weakness (17%), or cardiopulmonary symptoms (of 24 children, 17 had chest radiographs showing pulmonary edema, and 24 had echocardiograms showing left ventricular dysfunction), resulting in cardiopulmonary arrest soon after hospitalization (median time, 9 h). Cardiac tissue from 10 patients showed normal myocardium, but central nervous system tissue from 5 patients showed inflammatory changes. Brain-stem specimens from 2 patients were available, and both specimens showed extensive neuronal degeneration, inflammation, and necrosis, suggesting that a central nervous system infection was responsible for the disease, with the cardiopulmonary dysfunction being neurogenic in origin. EV71 and possibly an adenovirus, other enteroviruses, or unknown cofactors are likely responsible for this rapidly fatal disease.
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PMID:Deaths of children during an outbreak of hand, foot, and mouth disease in sarawak, malaysia: clinical and pathological characteristics of the disease. For the Outbreak Study Group. 1101 15

While undergoing video-EEG monitoring, a 20-year-old woman had a 56-second convulsive seizure, after which she developed persistent apnea. The rhythm of the electrocardiogram complexes was unimpaired for approximately 10 seconds, after which it gradually and progressively slowed until it stopped 57 seconds later. Evaluation after successful cardio-respiratory resuscitation showed no evidence of airway obstruction or pulmonary edema. The patient had a previous cardio-respiratory arrest after a complex partial seizure without secondary generalization. Although epileptic seizures are known to be potentially arrhythmogenic to the heart, our observations strongly suggest that one probable mechanism of sudden unexplained death in epilepsy is the marked central suppression of respiratory activity after seizures.
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PMID:Postictal central apnea as a cause of SUDEP: evidence from near-SUDEP incident. 1107 66

Sudden death is an "electrical accident" caused by fatal cardiac arrhythmias. While brain-heart control has physiological advantages, cerebrogenic sudden death and nonfatal cardiovascular disturbances can complicate stroke of all types, seizures and epilepsy, head injury, other neurological conditions, neurosurgical procedures, and intense emotional states. Cerebrogenic cardiovascular and autonomic disturbances include electrocardiographic changes, elevation of cardiac enzymes, cardiac arrhythmias, disturbances of blood pressure regulation, and cerebrogenic pulmonary edema. Evidence from experimental studies and clinical observations indicates a crucial role of the insula in cerebrogenic cardiovascular disturbances and sudden death. Future studies should focus on identification of at-risk patients, confirmation of a vulnerable period of cerebrogenic sudden death in those with different neurological conditions and intense emotional states, and clarification of the neurochemical mediators.
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PMID:The insula and cerebrogenic sudden death. 1111 33

Pulmonary oedema with severe, dramatic course following CNS injury was termed neurogenic pulmonary oedema (NPO). NPO was mainly described as a consequence of grand mal seizures, subarachnoid bleeding, intracranial bleeding or head injury. However, the pathogenesis of NPO is not entirely clear yet. In the majority of cases, early or classic symptoms of pulmonary oedema are evident from several minutes up to several hours after CNS damage. Dyspnoea, chest pain, bloody expectoration are observed shortly after consciousness disorders, although NPO may occasionally be diagnosed on the basis of chest x-ray in patients with no clinical symptoms. Tachypnoea, tachycardia, rales without any changes in cardiac system are usually observed during physical examination. The ailments withdraw quickly in the majority of patients, who may require oxygen therapy at most. NPO has been well-known in adults, but our knowledge of its occurrence in children is still rather sparse. The current work presents a case of a 13-year-old boy with pulmonary oedema as a post-seizure complication.
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PMID:Neurogenic pulmonary oedema in a 13-year-old boy in the course of symptomatic epilepsy--case report. 1120 46


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