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Tonic-clonic Seizures (tonic-clonic + seizures)
Kinds of Tonic-clonic Seizures Selected AbstractsParental psychopathology and self-rated quality of life in adolescents with epilepsy in NigeriaDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 7 2006Abiodun O Adewuya MBChB This study sought to investigate the relationship between parental psychopathology and health-related quality of life in a group of Nigerian adolescents with epilepsy. The participants were 86 adolescents with epilepsy (50 males, 36 females; mean age 14y 5mo [SD 2y 1mo]; age range 12,18y). There were 54 (62.8%) adolescents with complex partial seizures, six (7.0%) with simple partial seizures, 14 (16.3%) with generalized tonic-clonic seizures, four (4.7%) with absence seizures, and eight (9.2%) with other types of seizure. They completed the Quality of Life in Epilepsy Inventory for Adolescents (QOLIE-AD-48). Parents also completed the General Health Questionnaire, Zung's Self-Rating Anxiety Scale, and Zung's Self-Rating Depressive Scale as measures of their psychopathology. Factors correlating with poor overall quality of life in the adolescents include longer duration of illness, large number of antiepileptic drugs, more severe medication toxicity, and psychopathology in the parents. General psychopathology in parents is significantly associated with QOLIE-AD-48 subscales of Epilepsy Impact (r= 0.527, p < 0.001), Attitude (r= 0.214, p= 0.047), Physical Function (r= 0.417, p < 0.001), Stigma (r= 0.305, p= 0.004), Social Support (r= 0.365, p= 0.001), and School Behaviour (r= 0.220, p= 0.042). There is a possibility of a cross-cultural difference on the effect of epilepsy on the quality of life of adolescents. Psychopathology in parents is significantly associated with poorer quality of life of these adolescents. Physicians should consider this, therefore, when planning intervention strategies in improving the quality of life in adolescents with epilepsy. [source] Evidence-based Treatment of Idiopathic Generalized Epilepsies with Older Antiepileptic DrugsEPILEPSIA, Issue 2005Nikolas Hitiris Summary:, Older antiepileptic drugs continue to play a major role in the treatment of the idiopathic generalized epilepsies. Comparative studies of ethosuximide and valproate have demonstrated equivalence in the treatment of childhood absence epilepsy. Valproate can be regarded as the recommended first-line treatment for juvenile myoclonic epilepsy based on case series reports. Studies in patients with generalized tonic-clonic seizures have not separated out idiopathic from secondary generalized events. Treatment for the other idiopathic generalized epilepsy syndromes lacks evidence other than a few case reports and diverse expert opinion. Further randomized controlled trials of older antiepileptic drugs are recommended to solidify the evidence-based treatment of the idiopathic generalized epilepsies. [source] Anticonvulsant Action of Topiramate Against Motor Seizures in Developing RatsEPILEPSIA, Issue 10 2000Renata Haugvicová Summary Purpose: To study the anticonvulsant action of topiramate (TPM) in developing rats. Methods: Motor seizures were elicited by administering pentylenetetrazol (100 mg/kg subcutaneously) in five age groups of Wistar rats (7, 12, 18, 25, and 90 days old). TPM was administered intraperitoneally in doses from 10 to 640 mg/kg 2 hours before pentylenetetrazol. The time course of TPM action was studied in 12- and 25-day-oId rats up to 24 hours after the 160-mg/kg dose, and the incidence and pattern of seizures were evaluated. Results: TPM did not influence minimal seizures (clonus of forelimb and head muscles with preserved righting ability). Generalized tonic-clonic seizures, however, were reliably changed at all developmental stages studied. The tonic phase was suppressed so that the majority of animals exhibited generalized clonic seizures (with a loss of righting reflexes). In addition, the incidence of generalized seizures was decreased after the 20-, 40-, and 80-mg/kg doses in the 7-day-old rat pups. The specific suppression of the tonic phase of generalized seizures was observed up to 12 hours in the 12-day-old rat pups. The same result was obtained over 6 hours after TPM administration in the 25-day-old animals, and with longer intervals the incidence of generalized seizures decreased in this age group. Conclusions: TPM exhibits stable anticonvulsant action against the tonic phase of generalized tonic-clonic seizures throughout development. In addition, it suppresses all phases of generalized seizures in 7-day-old rats. The anticonvulsant action of TPM lasted longer in 25-day-old than in 12-day-old rats. The two actions of TPM might be ascribed to two different mechanisms of action. [source] Epilepsy Can Be Diagnosed When the First Two Seizures Occur on the Same DayEPILEPSIA, Issue 9 2000Peter Camfield Summary: Purpose: Experts have suggested that when the first two (or more) unprovoked seizures occur on the same day, they should be considered as a single event and the diagnosis of epilepsy await a further seizure. We have studied the subsequent clinical course of children with their first two seizures on the same day ("same day" group) compared with children with their first two seizures separated by more than one day ("different day" group). Method: The Nova Scotia childhood epilepsy database documented all newly diagnosed children with epilepsy from 1977 to 1985 with follow-up in 1990 and 1991. Epilepsy was defined as two or more unprovoked seizures regardless of the interval between seizures provided that consciousness fully returned between seizures. All patients had their first seizure between the ages of 1 month and 16 years. Seizure types were restricted to partial, generalized tonic-clonic, and partial with secondary generalization. Results: Of the 490 children with partial or generalized tonic-clonic seizures and follow-up of more than 2 years, 70 had their first two or more seizures on the same day and 420 had their first two seizures on different days. Eighty percent (56 of 70) of the "same day" group subsequently had one or more further seizures with (n = 14) or without (n = 42) medication; 80.9% (340 of 420) of the "different day" group had one or more further seizures with (n = 115) or without (n = 225) medication. Seizure types were nearly identical. Cause was the same (except for fewer idiopathic "genetic" cases in the "same day" group: 1 of 70 vs. 42 of 420; p = 0.02). Rates of mental handicap and previous febrile seizures were the same. Children in the "same day" group were younger on average (60 vs. 84 months; p = 0.001) and were somewhat more likely to have neurological impairment. Outcome after 7 years average follow-up was the same: 58% of the "same day" group and 56% of the "different day" group were in remission. Conclusion: If two or more unprovoked seizures (with normal consciousness between) occur on the same day, the child appears to have epilepsy and will have a clinical course identical to that of the child with a longer time interval between the first two seizures. [source] Movement-Induced Focal Motor Seizures and Choreoathetosis As- sociated with Nonketotic Hyperglycemia: A Case ReportEPILEPSIA, Issue 2000Hisashi Tanaka Case Report: We report the case of a diabetic woman who developed right-sided reflex seizures and bilateral choreoathetosis during an episode of nonketotic hyperglycemia. The patient was a 67-year-old woman with a 14-year history of HCV-related liver cirrhosis who experienced polydipsia and polyuria in January 1998. She began to have episodes of abnormal hyperkinetic movements of the right upper extremity and tonic-clonic seizures in the right arm triggered by voluntary movements of right or bilateral arms in the beginning of March 1998. The seizures increased in frequency and consequently left her disabled. She was admitted to our hospital with complaints of these abnormal motor phenomena on March 9, 1998. Neurological examinations revealed that she was alert, well-oriented, and that cranial nerve functions were normal. Slight motor weakness of the right upper limb and deep tendon hyporeflexes were observed in all extremities. Sensations and cerebellar functions were intact. Choreic or athetotic involuntary movements were seen in the bilateral upper limbs and neck. These involuntary movements were increased by voluntary movement or posturing of the upper limbs. The focal tonic-clonic seizures were easily triggered by voluntary movements such as knotting a cord. This seizure suddenly began by tonic movements in the right upper limb and gradually progressed to the right hemi-face and neck without loss of consciousness. The average duration of seizures was about one minute. The laboratory data demonstrated mild leukocytopenia, thrombocytopenia, hepatic dysfunction, and hyperglycemia without ketosis. Fasting blood glucose was 41 I mg/dl, and HbAlc was 14.5%. Blood ammonia was within normal levels. Cranial CT revealed no abnormalities. Brain MRI on T I-weighted images demonstrated bilateral high signal intensity in the putamen. An interictal EEG revealed a symmetrical slow background activity of 7,8 Hz. An ictal EEG recording showed a 2.5 4 Hz irregular sharp and slow wave discharge in the bilateral frontal-central regions. Treatment with carbamazepine was ineffective for the seizures. However, the seizures completely disappeared after the administration of insulin on March 17. Under good control of the hyperglycemia, the abnormal involuntary movements decreased gradually and then completely disappeared; the patient became neurologically asymptomatic by March 30. The follow-tip EEG demonstrated 9-Hz alpha background activity without any epileptic discharges. Conclusions: Nonketotic hyperglycemia has been rarely reported to cause stimulus-induced seizures or hyperkinetic involuntary movements such as hemichorea-ballism. To our knowledge, this is the first reported case of both induced seizures and involuntary movements simultaneously caused by hyperglycemia. Movement-induced seizures and choreoathetoid movements in this patient can be considered to result from transiently-increased activity in the basal ganglia and/or cerebral cortex associated with metaholic disorders. [source] Effect of Ganaxolone on Flurothyl Seizures in Developing RatsEPILEPSIA, Issue 7 2000a Liptáková Summary: Purpose: To determine the effects of a newly synthesized epalon, ganaxolone (GNX), on primarily generalized seizures in rats of various ages during development. Epalons are classified as neuroactive steroids that interact at unique site of the GABAA receptor-Cl, channel complex in the central nervous system. Methods: Sprague-Dawley male rats were used at 9, 15, 30, and 60 postnatal days (PN). GNX dissolved in 2-hydroxypropyl-,-cyclodextrine was administered intraperitoneally in different doses at various time points before flurothyl testing. The incidence and threshold of clonic and tonic-clonic flurothyl seizures were evaluated. Behavioral changes were also assessed. Results: In all age groups, the effects of GNX were dose dependent and more prominent 10 min after its administration. In PN 60 and PN 30 rats, GNX had dose-dependent anticon-vulsant effects; tonic-clonic seizures were more sensitive to GNX treatment than clonic seizures. In PN 15 and PN 9 rats, GNX demonstrated dose- and time-dependent anticonvulsant effects against both types of flurothyl-induced seizures. GNX was more effective in PN 15 rats than in other age groups, but at doses that altered motor behavior. Conclusions: GNX has anticonvulsant effects against flurothyl-induced seizures in all age groups tested. Its effects are more prominent in the two younger age groups, especially in PN 15 rats, but are associated with motor side effects. [source] Isolated vitamin E deficiency with demyelinating neuropathyMUSCLE AND NERVE, Issue 2 2005Vinod Puri MD Abstract A 22-year-old man, with a past history of generalized tonic-clonic seizures treated with phenobarbital, presented with spinocerebellar ataxia. The electrophysiological studies revealed a demyelinating motor-sensory neuropathy. The serum vitamin E level was low. Sural nerve biopsy revealed loss of large myelinated fibers with evidence of remyelination. Vitamin E supplementation led to clinical and electrophysiological recovery of sensory conduction and evoked potentials. Motor nerve conduction, however, showed only partial recovery. Vitamin E deficiency leading to a demyelinating neuropathy, as in the present case, suggests that the full spectrum of the disease entity is not fully defined. Muscle Nerve, 2005 [source] Seizures associated with poisoning in children: tricyclic antidepressant intoxicationPEDIATRICS INTERNATIONAL, Issue 6 2006AGOP ÇITAK Abstract Background: The aim of this study was to examine the characteristics of seizure due to poisoning. Methods: This was a retrospective analysis, throughout 4 years of hospital admissions for poisoning. Data of patients with seizures due to poisoning were evaluated with respect to the causes, frequencies and complications of seizures. Results: Among the 1561 admissions due to intoxication during the review period, seizures developed in 26 cases (1.6%). Tricyclic antidepressant overdose (n = 11, 42%) was the leading cause of seizure due to poisoning. Generalized tonic-clonic seizures were observed in 24 patients. Status epilepticus developed in six patients (23%). Mechanical ventilation was applied in 12 (46%) patients. Cardiac complications were observed in 11 (42%) patients with seizures. Two patients who had cardiac arrest due to acepromazin maleat and imipramine intoxication died. Conclusion: One of the causes of seizures in pediatric age group is intoxication. Seizures due to intoxications may cause serious clinical conditions. Intoxications should be thought when a patient is admitted with the diagnosis of afebrile seizure even if there is no history of drug intake. [source] Disproportionately High Rate of Epileptic Seizure in Patients Abusing DextropropoxypheneTHE AMERICAN JOURNAL ON ADDICTIONS, Issue 5 2009Debasish Basu MD Dextropropoxyphene (DPP), a weak opioid, is often abused as a psychoactive substance. In this retrospective chart review to document, characterize and put in perspective the often-obtained history of epileptic seizures in patients with DPP abuse, we analyzed the case files of all patients with DPP abuse registered in our center (a tertiary-care drug de-addiction clinic in north India) from May 1, 2001 until April 30, 2007 and those with use of other opioids during the same period. Non-drug-related seizures were excluded from analysis. Out of 312 patients with DPP abuse, 63 (20.2%) had epileptic seizures related to DPP use, in contrast to 0.4% ,4.2% of other opioid users. The seizures were mostly characterized as generalized tonic-clonic seizures (87.3%), occurring around two hours following a higher-than-usual dose of DPP. Those with seizures had significantly greater duration of DPP use and higher rates of medical comorbidity compared to patients without seizure. Age, duration of use and medical comorbidity were better predictors of seizure than dosage of drug or use of multiple drugs. Thus, DPP-induced epileptic seizures are common (one in five), and much more frequent than seizures in patients using other opioids. The awareness of this phenomenon has implications for diagnosis and management, as well as for drug regulation policy. [source] Murine succinate semialdehyde dehydrogenase deficiencyANNALS OF NEUROLOGY, Issue S6 2003Maneesh Gupta MBBS Inherited succinic semialdehyde dehydrogenase (SSADH) deficiency (,-hydroxybutyric aciduria) is one of the few neurogenetic disorders of GABA metabolism, and one in which tonic-clonic seizures associate with increased central nervous system GABA and ,-hydroxybutyrate (GHB). To explore pathomechanisms and develop new preclinical treatment approaches, we developed a murine knockout model of SSADH deficiency. In the absence of intervention, SSADH,/, mice suffer 100% mortality at week 3 to 4 of life from generalized tonic-clonic seizures. In this report, we summarize earlier studies indicating disruption of the GABA/glutamine axis in SSADH,/, mouse brain, effective pharmacotherapeutic approaches, preliminary gene-therapy results, and electrophysiological analyses of mutant mice. We also present new evidence for oxidative stress in SSADH,/, mice, significant alterations of dopamine metabolism, and abnormal neurosteroid levels in brain, potentially implicating the GABAA receptor in pathogenesis. In SSADH deficiency, the accumulation of two neuroactive species, GABA and GHB, is significant because GABA is one of the earliest transmitters expressed in mammals, with key roles in synaptogenesis and myelination, whereas GHB displays a vast array of pharmacological actions. The SSADH,/, mouse may represent a useful model in which to explore the effect of GABA and GHB accumulation on central nervous system development and function. Ann Neurol 2003;54 (suppl 6):S81,S90 [source] Mortality in epilepsy in the first 11 to 14 years after diagnosis: Multivariate analysis of a long-term, prospective, population-based cohortANNALS OF NEUROLOGY, Issue 3 2001Samden D. Lhatoo MRCP The United Kingdom National General Practice Study of Epilepsy is a prospective, population-based study of newly diagnosed epilepsy. A cohort of 792 patients has now been followed for up to 14 years (median follow-up [25th, 75th percentiles] 11.8 years, range 10.6,11.7 years), a total of 11,400 person-years. These data are sufficient for a detailed analysis of mortality in this early phase of epilepsy. Over 70% of patients in this cohort have developed lasting remission from seizures, although the mortality rate in the long term was still twice that of the general population. The standardized mortality ratio (SMR), the number of observed deaths per number of expected deaths, was 2.1 (95% confidence interval [CI] = 1.8, 2.4). Patients with acute symptomatic epilepsy (SMR 3.0; 95% CI = 2.0, 4.3), remote symptomatic epilepsy (SMR 3.7; 95% CI = 2.9, 4.6), and epilepsy due to congenital neurological deficits (SMR 25; 95% CI = 5.1, 73.1) had significantly increased long-term mortality rates, whereas patients with idiopathic epilepsy did not (SMR 1.3; 95% CI = 0.9, 1.9). This increase in mortality rate was noted particularly in the first few years after diagnosis. Multivariate Cox regression and time-dependent co-variate analyses were utilized for the first time in a prospective study of mortality in epilepsy. The former showed that patients with generalized tonic-clonic seizures had an increased risk of mortality. The hazard ratio (HR), or risk of mortality in a particular group with a particular risk factor compared to another group without that particular risk factor, was 6.2 (95% CI = 1.4, 27.7; p = 0.049). Cerebrovascular disease (HR 2.4; 95% CI = 1.7, 3.4; p < 0.0001), central nervous system tumor (HR 12.0; 95% CI = 7.9, 18.2; p < 0.0001), alcohol (HR 2.9; 95% CI = 1.5, 5.7; p = 0.004), and congenital neurological deficits (HR 10.9; 95% CI = 3.2, 36.1; p = 0.003) as causes for epilepsy and older age at index seizure (HR 1.9; 95% CI = 1.7,2.0; p < 0.0001) were also associated with significantly increased mortality rates. These hazard ratios suggest that epilepsy due to congenital neurological deficits may carry almost the same risk of mortality as epilepsy due to central nervous system tumors and that epileptic seizures subsequent to alcohol abuse may carry almost the same risk of mortality as epilepsy due to cerebrovascular disease. The occurrence of one or more seizures before the index seizure (the seizure that led to the diagnosis of epilepsy and enrolment in the study) was associated with a significantly reduced mortality rate (HR 0.57; 95% CI = 0.42, 0.76; p = 0.00001). Time-dependent co-variate analysis was used to examine the influence of ongoing factors, such as seizure recurrence, remission, and antiepileptic drug use, on mortality rates in the cohort. Seizure recurrence (HR 1.30; 95% CI = 0.84, 2.01) and antiepileptic drug treatment (HR 0.97; 95% CI = 0.67, 1.38) did not influence mortality rate. There were only 5 epilepsy-related deaths (1 each of sudden unexpected death in epilepsy, status epilepticus, burns, drowning, and cervical fracture), suggesting that death directly due to epileptic seizures is uncommon in a population-based cohort with epilepsy. Ann Neurol 2001;49:336,344 [source] Focal clinical and electroencephalographic features in patients with juvenile myoclonic epilepsyACTA NEUROLOGICA SCANDINAVICA, Issue 2 2010S. S. Jayalakshmi Jayalakshmi SS, Srinivasa Rao B, Sailaja S. Focal clinical and electroencephalographic features in patients with juvenile myoclonic epilepsy. Acta Neurol Scand: 2010: 122: 115,123. © 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Objective,,, To identify prevalence and factors associated with occurrence of focal clinical and electroencephalogram (EEG) abnormalities in patients with juvenile myoclonic epilepsy (JME). Materials and methods,,, Clinical asymmetries in the seizures and focal EEG abnormalities were analyzed in 266 patients with JME. Results,,, All the patients had myoclonic jerks (MJ) and generalized tonic-clonic seizures (GTCS); 56 (21%) had absence seizures. Asymmetry in clinical seizures was reported in 45 (16.9%) and focal EEG abnormalities were noted in 92 (45.5%) patients. Amplitude asymmetry or focal onset of generalized discharges was noted in 41 (44.6%) and independent focal EEG abnormalities in 30 (32.6%) patients. A statistically significant association was seen with the presence of GTCS and MJ (P = 0.007), a family history of epilepsy (P = 0.001) and drug resistance (P = 0.04) and the occurrence of focal EEG abnormalities. Conclusion,,, Patients with JME showed focal clinical and EEG features. These features should not be misinterpreted as indicative of partial epilepsy. [source] | ||||||||||