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)

This study was a 13-month prospective, descriptive case series of risperidone overdose reported by telephone to a regional poison control center (PCC) serving Philadelphia, PA. Patients were seen in local Philadelphia-area emergency departments. The variables examined were medical history, therapeutic use of risperidone, time postingestion, reported coingestants, clinical findings, decontamination and treatment, electrocardiograph results, laboratory data, standard toxicologic screen results, and length of time in hospital. Thirty-one patients (29 adult/adolescent, 2 pediatric) with reported risperidone overdose were identified. Risperidone was the sole ingestant in 15 cases (1 mg to 180 mg). The major observed effects in this group included lethargy (7), spasm/dystonia (3), hypotension (2), tachycardia (6), and dysrhythmia (1). Sixteen cases involved coingestants, including benzodiazepines, selective serotonin reuptake inhibitors, ethanol, tricyclic antidepressants, lithium, anticonvulsants, diphenhydramine, ibuprofen, and anticholinergic agents. Major effects in these patients included lethargy (10), coma (1), seizure (1), tachycardia (7), bradycardia (1), hypotension (4), and a syndrome of muscle spasms, diaphoresis, and fever. Treatment provided for patients in this study included antiarrhythmics (1), diphenhydramine (2), anticonvulsant (1), vasopressor agent (1), endotracheal intubation/assisted ventilation (5), and supportive care. One patient who coingested imipramine died of medical complications. In the remaining patients, symptoms resolved with 24 hours in the majority, with all patients asymptomatic at 72 hours postingestion. These data show that risperidone toxicity manifests primarily as mild central nervous system effects and reversible neuromuscular and cardiovascular effects.
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PMID:Effects of risperidone in overdose. 972 65

Cerebral palsy is the result of an injury to the developing brain during the antenatal, perinatal or postnatal period. Clinical manifestations relate to the area affected. Some of the conditions associated with cerebral palsy require surgical intervention. Problems during the peri-operative period may include hypothermia, nausea and vomiting and muscle spasm. Peri-operative seizure control, respiratory function and gastro-oesophageal reflux also require consideration. Intellectual disability is common and, in those affected, may range from mild to severe. These children should be handled with sensitivity as communication disorders and sensory deficits may mask mild or normal intellect. They should be accompanied by their carers at induction and in the recovery room as they usually know how best to communicate with them. Postoperative pain management and the prevention of muscle spasm is important and some of the drugs used in the management of spasm such as baclofen and botulinum toxin are discussed. Epidural analgesia is particularly valuable when major orthopaedic procedures are performed.
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PMID:Anaesthesia and pain management in cerebral palsy. 1079 81

Vigabatrin (VGB) has demonstrated high efficacy in infantile spasms (IS) due to tuberous sclerosis. Our first objective was to evaluate the cognitive long term effect outcome of children whose refractory spasms definitely disappeared when VGB was given as an add on drug. Our second objective was to determine the response of generalized epilepsy (infantile spasms) compared to partial epilepsy on cognitive impairment. A non selected series of 13 children underwent psychometric and behavioural evaluation before VGB initiation at a mean of 3 years on VGB treatment. Eight of them could perform detailed neuropsychological tests at follow-up. Seven had infantile spasms (Group I), they all were spasm free before 2 years of age and five remained with rare partial seizures (mean age, 5.5 years). Six others had partial epilepsy without spasms (Group II) and five remained with rare seizures (mean age, 7.5 years). Patients of Group I experienced dramatic changes. Developmental quotient (DQ) significantly rose in six out of seven by ten to more than 45 points (P = 0.03) and autistic behaviour disappeared in five out of the six who presented with. The four tested children had normal verbal level after 5 years and could integrate at school but they remained with marked visuospatial disabilities. By contrast, patients of Group II remained with an unchanged DQ of about 60 so that both groups had similar DQ levels on follow-up. The cessation of spasms with VGB is therefore associated with significant improvement of cognition and behaviour in children with tuberous sclerosis. Controlling secondary generalization induced by infantile spasms seems to be a key factor for mental development.
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PMID:Mental and behavioural outcome of infantile epilepsy treated by vigabatrin in tuberous sclerosis patients. 1064 43

The International Classification of Epileptic Syndromes considers epileptic spasms to be typical seizures of West syndrome. Literature reports show that spasms are present in epileptic syndromes other than West syndrome but there are few data on their characteristics in adults. We describe ictal, clinical and video-polygraphic findings in three patients (aged 21, 32 and 57 years) with epileptic spasms and with diffuse (case 2), focal right fronto-parietal (case 1) and bi-opercular (case 3) pachygyria. Spasms had been present since the ages of 1 month, 11 and 27 years respectively. Only one patient is mentally retarded. Two of our patients (cases 2 and 3) have partial seizures. Ictal polygraphic studies showed a positive, diffuse, high amplitude slow wave activity during spasms, with superimposed fast activity, followed by a diffuse flattening in all cases with a typical muscle pattern. Epileptic spasms, as typically described in West syndrome, can maintain the same semeiological and electroencephalographic features during adulthood in certain patients with cortical dysplasia.
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PMID:Clinical and video-polygraphic features of epileptic spasms in adults with cortical migration disorder. 1093 29

A child with Goldenhar's syndrome presented at about one week of age with stereotyped, repetitive paroxysmal episodes of hemifacial contraction, suggestive of partial seizures or hemifacial spasm. Later in life he also developed independent, permanent abnormal eye and chin movements identical in rhythm to those seen in myorhythmias, suggesting involvement of the dentato-olivary pathway. MRI demonstrated a hamartomatous lesion at the level of the pontomedullary junction. We speculate that the nature of the lesion could be responsible for the partial seizures mimicking hemifacial spasm and that because of its location, this same lesion could also be implicated in the genesis of myorhythmias. The presence of a hamartomatous lesion in a region affected by the abnormal development of the first and second branchial arches is not fortuitous.
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PMID:Hemifacial spasm or subcortical epilepsy? 1093 42

A case of early infantile epileptic encephalopathy with suppression-bursts (EIEE or Ohtahara syndrome) with an excellent response to zonisamide is reported. Tonic spasms began immediately after birth and increased in number, such that they formed a series of several dozen spasms lasting for 5 to 15 minutes. When the patient was 1 month old, a partial clonic seizure emerged predominantly on the right side of her face and extremities. It was often followed by tonic spasms and later continued after the beginning of the spasm series. Interictal electroencephalography demonstrated an atypical suppression-burst pattern and focal paroxysmal discharges. Detailed hematologic tests, magnetic resonance imaging, single-photon emission computed tomography, and auditory brainstem response did not reveal any metabolic or structural abnormalities. Oral administration of zonisamide first controlled the partial seizures and, subsequently, the tonic spasms in a dose-dependent fashion. The mode of response to zonisamide and the findings on electroencephalography indicate that EIEE may be caused by multiple independent brain lesions and that EIEE is a heterogeneous disorder. It is suggested that zonisamide may be useful in the treatment of EIEE.
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PMID:Zonisamide treatment of early infantile epileptic encephalopathy. 1106 68

This is a multicenter, open-label, add-on trial, investigating the safety and efficacy of ganaxolone (GNX) in a population of children with refractory infantile spasms, or with continuing seizures after a prior history of infantile spasms. A total of 20 children aged 7 months to 7 years were enrolled in this dose-escalation study, after baseline seizure frequencies were established. Concomitant antiepilepsy drugs were maintained throughout the study period. The dose of GNX was progressively increased to 36 mg/kg/d (or to the maximally tolerated dose) over a period of 4 weeks, then maintained for 8 weeks before tapering and discontinuation. Seizure diaries were maintained by the families, and spasm frequency was compared with the baseline period. The occurrence of adverse events was clinically monitored, and global evaluations of seizure severity and response to treatment were obtained. A total of 16 of the 20 subjects completed the study, 15 of whom had refractory infantile spasms at the time of study enrollment. Spasm frequency was reduced by at least 50% in 33% of these subjects, with an additional 33% experiencing some improvement (25-50% reduction in spasm frequency). Ganaxolone was well tolerated, and adverse events attributed to GNX were generally mild. Ganaxolone was safe and effective in treating this group of refractory infantile spasms patients in an open-label, add-on trial. Further investigation with randomized, controlled study design is warranted.
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PMID:Ganaxolone for treating intractable infantile spasms: a multicenter, open-label, add-on trial. 1107 86

To determine the occurrence, outcome, and prognostic factors of West syndrome (WS), we performed a retrospective epidemiological study of WS occurred in 47 children (26 boys and 21 girls) in Nagasaki prefecture during a recent 10-year period from 1989 to 1998. The incidence of WS was 3.1/10,000 live births. The mean age at onset of spasm is 6.3 months (range: 2 to 12 months). Thirty-nine patients (83%) had symptomatic WS, in which the prenatal causes (patients) were most frequent, followed by low-birth weight infants (patients), perinatal (patients) and postnatal (patients). The brain CT was performed in 37 patients, and revealed congenital brain malformations (9 patients), destructive brain disorders (12 patients), and no structural abnormalities (16 patients). The seizure outcome was worse in the symptomatic WS than in the cryptogenic WS; seizure/disappeared in 39% of the former and in 75% of the latter/developmental delay before the onset of WS, relapse of WS and persistence of seizures were associated with poor seizure outcomes. Among the remaining seizures at the time of this surveillance, a tonic seizure was most frequently observed, followed by the partial seizures. Lennox-Gastaut syndrome was observed in 2 patients only. Epileptic discharge in the latest interictal EEG were diffuse in 4.3%, focal or multifocal in 60.7%, and absent in 35%, suggesting that many patients with WS had cortical epileptogenic foci. The developmental outcome was very poor in both the symptomatic and cryptogenic WS. The mean DQ in all the patients was 25, and only 4 patients (11%) had a normal DQ (> 75). DQ was lower in patients with congenital brain malformations than in those with destructive brain disorders.
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PMID:[Epidemiological and clinical study of West syndrome in Nagasaki Prefecture, Japan]. 1119 88

Knowledge concerning the relationship between multiple sclerosis and epilepsy is reviewed. Epidemiological studies have established that epileptic seizures are more frequent in multiple sclerosis than predicted by chance. Partial epilepsies with focal seizures often with atypical symptoms and with or without secondary generalisation are the usual pattern. In the survey special emphasis is laid on the direct correlation between paroxysmal phenomena and plaques now demonstrable by modern imaging techniques. These images have shown that epileptic seizures can be caused by cortical and subcortical lesions and by their accompanying oedema. We extend the review to non-epileptic paroxysmal symptoms, such as tonic spasm, which may be confused with epileptic seizures. As far as they are supported by data, recommendations for diagnosis and therapy are given. Open questions are identified and issues for further research are suggested.
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PMID:Epileptic and non-epileptic seizures in multiple sclerosis. 1126 15

Hyperekplexia (startle disease) is a rare non-epileptic disorder characterised by an exaggerated persistent startle reaction to unexpected auditory, somatosensory and visual stimuli, generalised muscular rigidity, and nocturnal myoclonus. The genetic basis is a mutation usually of the arginine residue 271 leading to neuronal hyperexcitability by impairing glycinergic inhibition. Hyperekplexia is usually familial, most often autosomal dominant with complete penetrance and variable expression. It can present in fetal life as abnormal intrauterine movements, or later at any time from the neonatal period to adulthood. Early manifestations include abnormal responses to unexpected auditory, visual, and somatosensory stimuli such as sustained tonic spasm, exaggerated startle response, and fetal posture with clenched fists and anxious stare. The tonic spasms may mimic generalised tonic seizures, leading to apnoea and death. Consistent generalised flexor spasm in response to tapping of the nasal bridge (without habituation) is the clinical hallmark of hyperekplexia. Electroencephalography may show fast spikes initially during the tonic spasms, followed by slowing of background activity with eventual flattening corresponding to the phase of apnoea bradycardia and cyanosis. Electromyography shows a characteristic almost permanent muscular activity with periods of electrical quietness. Nerve conduction velocity is normal. No specific computed tomography findings have been reported yet. Clonazepam, a gamma aminobutyric acid (GABA) receptor agonist, is the treatment of choice for hypertonia and apnoeic episodes. It, however, may not influence the degree of stiffness significantly. A simple manoeuvre like forced flexion of the head and legs towards the trunk is known to be life saving when prolonged stiffness impedes respiration.
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PMID:Hyperekplexia in neonates. 1152 14


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