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At least 19 recordsLinked to original sources
PubMed2004

The coexistence of idiopathic generalized epilepsy and partial epilepsy.

PURPOSE: To describe the clinical, EEG, and imaging data of a series of patients with features of both idiopathic generalized epilepsy (IGE) and partial epilepsy. METHODS: A computerized database of all patients attending the regional epilepsy clinic was used to identify all patients with IGE. Case notes were reviewed, and cases with clinical evidence of co-existing partial epilepsy identified. RESULTS: Nine cases with clinical features of a partial and generalized-onset epilepsy and with electrophysiological evidence of IGE are presented. This represented <1% of the overall IGE population in the clinic. Five (55.6%) patients are currently in remission, with successful epilepsy surgery in one patient. CONCLUSIONS: The coexistence of IGE and partial epilepsy is uncommon, and if appropriate treatment with a broad-spectrum antiepileptic drug is given, then the prognosis can be good. Surgery should be considered for those cases with medically intractable partial-onset seizures as part of this syndrome.

Adult↗
PubMed1999

Observations on the misdiagnosis of generalized epilepsy as partial epilepsy: causes and consequences.

More therapeutic options (surgical and pharmacologic) are available for partial than for generalized epilepsies. This report describes and analyzes a possible bias to diagnose focal epilepsies. Data were prospectively collected on patients who underwent noninvasive prolonged EEG-video monitoring over a 2-year period at an epilepsy program. Cases where the diagnosis of 'partial seizures' (after monitoring) was questionable were identified and the data reviewed. Sixteen cases were identified. (a) Six had an idiopathic generalized epilepsy. All had generalized tonic-clonic (GTC) seizures, two had myoclonic seizures, and three had typical absences. All patients had generalized spikes and spike-wave complexes. All had normal IQs and normal brain imaging. One patient underwent invasive EEG. (b) Ten patients had a symptomatic or cryptogenic generalized epilepsy. IQs ranged from 49 to 74 (mean: 63). All patients had diffuse EEG slowing, and generalized ictal EEG patterns. Interictal EEG showed generalized spike-wave complexes in nine, and multifocal spikes in five. Seizures included GTC in all, generalized tonic in four, and atypical absences in two. Two of the 10 patients underwent invasive EEG. The misdiagnosis of generalized epilepsy as partial epilepsy occurs for both idiopathic and cryptogenic or symptomatic generalized epilepsies, more often in the latter case. Risk factors may include: asymmetry in EEG or seizure semeiology, the eagerness to enroll in drug studies or surgical programs, and the lack of team thinking involving several epileptologists. This problem is almost certainly under-reported and may occasionally result in unwarranted invasive procedures.

Adolescent↗
PubMed1987

[Idiopathic partial epilepsies in children (benign or primary partial epilepsies)].

The concept of idiopathic partial epilepsies in childhood is not yet accepted by all neurologists. We review the diagnostic criteria of these syndromes and stress both wake and sleep EEG characteristics. Different clinical entities have been individualized among other forms: benign partial epilepsy with centro-temporal spikes, benign epilepsy with occipital paroxysms, benign psychomotor epilepsy.

Adolescent↗
PubMed1998

Familial partial epilepsy with variable foci: a new partial epilepsy syndrome with suggestion of linkage to chromosome 2.

Familial partial epilepsy with variable foci (FPEVF) joins the recently recognized group of inherited partial epilepsies. We describe an Australian family with 10 individuals with partial seizures over four generations. Detailed electroclinical studies were performed on all affected and 17 clinically unaffected family members. The striking finding was that the clinical features of the seizures and interictal electroencephalographic foci differed among family members and included frontal, temporal, occipital, and centroparietal seizures. Mean age of seizure onset was 13 years (range, 0.75-43 years). Two individuals without seizures had epileptiform abnormalities on electroencephalographic studies. Penetrance of seizures was 62%. A genome-wide search failed to demonstrate definitive linkage, but a suggestion of linkage was found on chromosome 2q with a LOD score of 2.74 at recombination fraction of zero with the marker D2S133. FPEVF differs from the other inherited partial epilepsies where partial seizures in different family members are clinically similar. The inherited nature of this new syndrome may be overlooked because of relatively low penetrance and because of the variability in age at onset and electroclinical features between affected family members.

Adult↗
PubMed2000

Zonisamide for drug-resistant partial epilepsy.

BACKGROUND: The majority of epileptic patients have a good prognosis and their seizures can be well controlled with the use of a single antiepileptic agent, but up to 30% develop refractory epilepsy, especially those with partial seizures. In this review we summarise the current evidence regarding a new antiepileptic drug, zonisamide, when used as an add-on treatment for drug-resistant partial epilepsy. OBJECTIVES: To evaluate the efficacy and tolerability of zonisamide when used as an add-on treatment for patients with drug -resistant partial epilepsy. SEARCH STRATEGY: We searched the Cochrane Epilepsy Group trial register, the Cochrane Controlled Trials Register (Cochrane Library Issue 4, 1999). In addition, we contacted Dianippon and Elan Pharma (makers and licensees of zonisamide) and experts in the field to seek any ongoing studies or unpublished studies. SELECTION CRITERIA: Randomized placebo controlled add-on trials of zonisamide in patients with drug-resistant partial epilepsy. DATA COLLECTION AND ANALYSIS: Two reviewers independently selected trials for inclusion and extracted relevant data. The following outcomes were assessed: (a) 50% or greater reduction in total seizure frequency; (b) treatment withdrawal (any reason); (c) adverse events. Primary analyses were intention to treat. Sensitivity best and worst case analyses were also undertaken. Summary odds ratios (ORs) were estimated for each outcome. MAIN RESULTS: Three trials were included with 499 patients randomized. EFFICACY: Overall odds ratio (OR, 95% CI) for 50% reduction in seizure frequency compared to placebo was 2.07 (1.36,3.15) for a 400mg/day dose of zonisamide. When the full treatment period of 12 weeks was considered for all three trials including varied rates of titration to 400mg/day the OR compared to placebo was 2.72 (1.74,4. 25). There was insufficient evidence to support a dose response relationship between dose and responder rate. Tolerability: Treatment withdrawal OR compared to placebo was 1.74 (1.03,2.95). Adverse events: ataxia 3.94 (1.23,12.57), somnolence 2.11 (1.11, 3. 98), agitation 3.52 (1.26,9.68), agitation and irritability 2.43(1. 04,5.66) and anorexia 2.98(1.38,6.42) were significantly associated with zonisamide. REVIEWER'S CONCLUSIONS: Zonisamide has efficacy as an add-on treatment in patients with drug-resistant partial epilepsy. Minimum effective and maximum tolerated doses cannot be identified. The trials reviewed were of 12 week duration and results cannot be used to conform longer periods of effectiveness in seizure control. The results cannot be extrapolated to monotherapy or to patients with other seizure types or epilepsy syndromes.

Anticonvulsants↗
PubMed2000

Gabapentin for drug-resistant partial epilepsy.

BACKGROUND: The majority of epileptic patients have a good prognosis and their seizures can be well controlled with the use of a single antiepileptic agent, but up to 30% develop refractory epilepsy, especially those with partial seizures. In this review we summarise the current evidence regarding a new antiepileptic drug, gabapentin, when used as an add-on treatment for drug-resistant partial epilepsy OBJECTIVES: To evaluate the efficacy and tolerability of gabapentin when used as an add-on treatment for patients with drug-resistant partial epilepsy. SEARCH STRATEGY: We searched the Cochrane Epilepsy Group trial register, the Cochrane Controlled Trials Register of The Cochrane Library Issue 4, 1998. In addition, we contacted Parke Davis (manufacturers of gabapentin) and experts in the field to seek any ongoing studies or unpublished studies. SELECTION CRITERIA: Randomized placebo controlled double blind add-on trials of gabapentin in patients with drug-resistant partial epilepsy. DATA COLLECTION AND ANALYSIS: Two reviewers independently selected trials for inclusion and extracted the relevant data. The following outcomes were assessed: (a) 50% or greater reduction in seizure frequency; (b) treatment withdrawal (any reason); (c) side effects. Primary analyses were intention to treat. Sensitivity best and worst case analyses were also undertaken. Summary odds ratios were estimated for each outcome. Dose response was evaluated in regression models, and Number Needed to Treat (NNTs) were calculated for individual doses. MAIN RESULTS: Four trials were included representing 750 randomized patients. EFFICACY: Overall odds ratio (OR) (95% Confidence Interval (CI)) for 50% or greater reduction in seizure frequency compared to placebo 2.22 (1.49 - 3.32). Dose regression analysis shows increasing efficacy with increasing dose, with 28.5% (21.5 - 36.7) of patients responding to 1800mg of gabapentin compared to placebo, NNT 6.7 (3.0 - 10.5). Global effectiveness: treatment withdrawal OR (95% CI) compared to placebo 1.40 (0.76 - 2.55); Side effects: OR (99% CI) compared to placebo. dizziness 2.26 (1.28 - 3.99); fatigue 2.29 (1.11 - 4.74); somnolence 2.04 (1.21 - 3.45) were significanty associated with gabapentin. REVIEWER'S CONCLUSIONS: Gabapentin has efficacy as an add-on treatment in patients with drug-resistant partial epilepsy. However, trials reviewed were of relatively short duration, and provide no evidence for the long term efficacy of gabapentin. Results cannot be extrapolated to monotherapy or patients with other epilepsy types.

Acetates↗
PubMed2000

Topiramate for drug-resistant partial epilepsy.

BACKGROUND: The majority of epileptic patients have a good prognosis and their seizures can be well controlled with the use of a single antiepileptic agent, but up to 30% develop refractory epilepsy, especially those with partial seizures. In this review we summarize the current evidence regarding a new antiepileptic drug, topiramate, when used as an add-on treatment for drug-resistant partial epilepsy. OBJECTIVES: To evaluate the efficacy and tolerability of topiramate when used as an add-on treatment in patients with drug resistant partial epilepsy. SEARCH STRATEGY: (a) The Cochrane Library (1999 Issue 1); (b) The controlled trial register of the Cochrane Epilepsy Group; (c) Johnson and Johnson, makers of topiramate; (d) Experts in the field. SELECTION CRITERIA: Randomized placebo controlled add-on trials of topiramate in patients with drug resistant epilepsy. DATA COLLECTION AND ANALYSIS: Two reviewers independently selected trials for inclusion and extracted the relevant data. The following outcomes were assessed: (a) 50% or greater reduction in seizure frequency; (b) treatment withdrawal (any reason); (c) side effects. Primary analyses were intention to treat. Summary odds ratios (OR) were estimated for each outcome. Dose response was evaluated in regression models. MAIN RESULTS: Six trials were included representing 743 randomized patients. EFFICACY: Overall OR (95% CIs) for 50% or greater reduction in seizure frequency compared to placebo 4.06 (2.86-5.78). Dose regression analysis shows increasing efficacy with increasing dose, but found no advantage for doses over 400 mg per day. Global effectiveness: treatment withdrawal OR (95% CIs) compared to placebo 2.57 (1.65-4.00). Side effects: OR (99% CIs)compared to placebo, dizziness 1.99 (1.20-3.29); fatigue 2.52 (1. 47-4.32); nausea 2.84 (1.36-5.93); somnolence 2.89 (1.72-4.85) and 'thinking abnormally' 3.71 (2.02-6.80) were significantly associated with topiramate. REVIEWER'S CONCLUSIONS: Topiramate has efficacy as an add-on treatment in patients with drug resistant partial epilepsy. However, trials reviewed were of relatively short duration, and provide no evidence for the long term efficacy of topiramate. Results cannot be extrapolated to monotherapy or patients with other epilepsy types.

Anticonvulsants↗
PubMed1983

[Benign partial epilepsies: 11 cases of frontal partial epilepsy with favorable prognosis].

The authors report a retrospective study of 11 observations of partial frontal epilepsy. Cases have been selected on the basis of a complete lack of any associated neurological or psychiatric sign and a disappearance of seizures with normalization of the EEG trace for more than 5 years. This peculiar type of focal epilepsy characterized by an EEG frontal spike focus is first shown to share clinical and electroencephalographic signs with other forms of benign epilepsy of childhood and adolescence. Then the predictive value of some electro-clinical criteria to indicate a favourable outcome is examined.

Adolescent↗
PubMed2002

[Idiopathic generalized epilepsies misdiagnosed as partial epilepsies].

Idiopathic generalized epilepsy (IGE) is often not recognized with serious consequences on the sufferers. We examined factors contributing to the missed diagnosis of IGE in 41 adults attending our epilepsy clinic with diagnosis of partial epilepsy who had semiology or EEG findings suggesting a possible differential diagnosis. After careful re-evaluation, the diagnosis of IGE was established in 25 patients: 22 (88%) with JME, one with juvenile absence, one with perioral myoclonia with absences, one with eyelid myoclonia with typical absences. Myoclonic jerks, the hallmark of the JME and other IGE, were not usually reported by patients or misdiagnosed as focal motor seizures. Brief and infrequent absence seizures and focal EEG abnormalities were other factors contributing to not recognizing JME. All 25 patients did not achieve seizure control before re-evaluation of diagnosis. After appropriate diagnosis of IGE and change of AED to valproate or valproic acid, 19 (76%) became seizure free and six (24%) had a significant improvement on seizure control. Association with lamotrigine provided further improvement in three of these patients. An appropriate questioning to identify myoclonic and absence seizures and a proper interpretation in the context of whole clinical constellation are essential for a correct seizure classification and diagnosis of IGE in adults.

Adolescent↗
PubMed2000

Lamotrigine add-on for drug-resistant partial epilepsy.

BACKGROUND: Epilepsy is a common neurological disorder, affecting almost 0.5 to 1% of the population. Nearly 30% of patients with epilepsy are refractory to currently available drugs. Lamotrigine is one of the newer antiepileptic drugs and is the topic of this review. OBJECTIVES: To examine the effects of lamotrigine on seizures, side effects, cognition and quality of life, when used as an add-on treatment for patients with drug-resistant partial epilepsy. SEARCH STRATEGY: We searched the Cochrane Epilepsy Group trials register, the Cochrane Controlled Trials Register (Cochrane Library Issue 1, 2000), MEDLINE (January 1966 to December 1999) and reference lists of articles. We also contacted the manufacturers of lamotrigine (Glaxo-Wellcome). SELECTION CRITERIA: Randomized placebo controlled trials, of patients with drug-resistant partial epilepsy of any age, in which an adequate method of concealment of randomization was used. The studies may be double, single or unblinded. For crossover studies, the first treatment period was treated as a parallel trial. DATA COLLECTION AND ANALYSIS: Two reviewers independently assessed the trials for inclusion and extracted data. Primary analyses were by intention to treat. Outcomes included 50% or greater reduction in seizure frequency, treatment withdrawal (any reason), side effects, effects on cognition, and quality of life. MAIN RESULTS: We found three parallel add-on studies and eight cross-over studies, which included 1243 patients (199 children and 1044 adults). The overall Peto's Odds Ratio (OR) and 95% confidence intervals (CIs) across all studies for 50% or greater reduction in seizure frequency was 2.71 (1.87, 3.91) indicating that lamotrigine is significantly more effective than placebo in reducing seizure frequency. The overall OR (95%CI) for treatment withdrawal (for any reason) is 1.12 (0.78, 1. 61). The 99% CIs for ataxia, dizziness, nausea, and diplopia do not include unity, indicating that they are significantly associated with lamotrigine. The limited data available preclude any conclusions about effects on cognition and quality of life, though there may be minor benefits in affect balance (happiness) and mastery. REVIEWER'S CONCLUSIONS: Lamotrigine add-on therapy is effective in reducing the seizure frequency, in patients with drug-resistant partial epilepsy. Further trials are needed to assess the long term effects of lamotrigine, and to compare it with other add-on drugs.

Anticonvulsants↗
PubMed2005

LGI1 gene mutation screening in sporadic partial epilepsy with auditory features.

Partial epilepsy with auditory features occasionally segregates in families as an autosomal dominant trait. In some families mutations in the leucine-rich glioma inactivated (LGI1) gene have been identified. Sporadic cases might harbour either denovo or low-penetrant LGI1 mutations, which will substantially alter the family risk for epilepsy. We selected sixteen sporadic patients with cryptogenic temporal lobe epilepsy and partial seizures with auditory features. We compared clinical features of these patients with those of published autosomal dominant family cases. We screened these patients for LGI1 mutations. Comparing the sporadic patients with the published familial cases no difference in either the primary auditory features or in the other associated epileptic manifestations was identified. Sequence analysis of the whole LGI1 gene coding regions in sporadic patients did not reveal changes in the LGI1 gene. The genetic analysis demonstrates that LGI1 is not a major gene for sporadic cases of partial epilepsy with auditory features at least in the Italian population. Screening of sporadic patients for LGI1 mutations appears not useful in genetic counselling of these patients.

Adult↗
PubMed1989

Indications of radiological explorations in partial epilepsy of childhood.

In partial epilepsy of childhood the decision to request radiological exploration rests on a good knowledge of the disease. The authors summarize the electrical and clinical features of the various types of partial epilepsy. Most of these types, and in particular benign partial epilepsy with rolandic paroxysms, require no exploration. In contrast, symptomatic partial epilepsy must be investigated in search of a brain lesion. In such cases CT is indispensable. The more accurate and more sensitive MRI may be performed either initially or after a negative CT scanning in children with partial epilepsy which does not respond to medical treatment.

Child↗
PubMed2000

Benign partial epilepsies in infancy.

Benign partial epilepsies are not rare in infancy and comprise two forms, although both are closely related. One is partial epilepsy with complex partial seizures (CPS) and the other one with secondarily generalized seizures (SGS). The most frequent site of seizure origin was in the temporal area in the former and central, parietal or occipital area in the latter. The former has not been well recognized because of subtle seizure manifestations and a favorable outcome. Its unique characteristics should be emphasized because it may be difficult to diagnose it unless we know its presence. Benign convulsions are also common in infancy. Most of them may belong to partial epilepsy with SGS, although confirmation with ictal EEG recording is necessary for accurate diagnosis. Some are familial and many of them seem to show an autosomal dominant pattern, but some seem to have autosomal recessive inheritance.

Age of Onset↗
PubMed2002

Partial epilepsy with pericentral spikes: a new familial epilepsy syndrome with evidence for linkage to chromosome 4p15.

The genetic analysis of simple Mendelian epilepsies remains a key strategy in advancing our understanding of epilepsy. In this article, we describe a new family epilepsy syndrome, partial epilepsy with pericentral spikes, which we map to chromosome 4p15. We distinguish it clinically, electrophysiologically, and genetically from previously described Mendelian epilepsies. The family described is a large Brazilian kindred of Portuguese extraction in which affected family members manifest a variety of seizure types, including hemiclonic, hemitonic, generalized tonic-clonic, simple partial (stereotyped episodes of epigastric pain), and complex partial seizures consistent with temporal lobe epilepsy. The syndrome is benign, either requiring no treatment or responding to a single antiepileptic medication. Seizure onset is in the first or second decades of life, with seizures in individuals up to the age of 71 years and documented encephalogram changes up to the age of 30 years. A key feature of partial epilepsy with pericentral spikes is a characteristic encephalogram abnormality of spikes or sharp waves in the pericentral region (centroparietal, centrofrontal, or centrotemporal). This distinctive encephalogram abnormality of pericentral spikes unites these several seizure types into a discrete family epilepsy syndrome. As with other familial epilepsies, the inherited nature of this new syndrome may be overlooked because of the variability in penetrance and seizure types among affected family members.

Adolescent↗
PubMed2004

Basic mechanisms of partial epilepsies.

PURPOSE OF REVIEW: Partial epilepsies are characterized by cell loss with consequences for neuronal organization, excitability, mnestic and cognitive functions and present with pharmaco-resistance and difficulties in clinical management. While mesial temporal lobe epilepsies present frequently with cell loss and neuronal reorganization, neocortical epilepsies frequently involve developmental alterations. RECENT FINDINGS: There is increasing evidence that nerve cells in epileptic tissue become more vulnerable to excitotoxic cell death due to impairment of mitochondrial functions and that free radical formation is critically involved in these processes. Whether and to what extent such alterations contribute to pharmaco-resistance is unclear. However, at least three mechanisms may contribute to pharmaco-resistance: changes in target molecules for antiepileptic drugs, upregulation of drug transporters, and potentially reorganization processes in inhibitory networks. Upregulation of drug transporters also seems to be involved in pharmaco-resistance of developmental alterations underlying focal epilepsies. Recent data from the literature suggest that transgenic models for disturbances of cortical development may be useful models for the study of these variable forms of partial epilepsies. SUMMARY: The data suggest that improvement of therapy could result from free radical scavenging and from manipulation of drug transport into the affected tissue. New models of developmental epilepsies may help us to understand mechanisms underlying increased vulnerability to seizures as well as improving strategies for treatment.

Anticonvulsants↗
PubMed2000

Long-term open multicentre, add-on trial of vigabatrin in adult resistant partial epilepsy. The Canadian Vigabatrin Study Group.

Vigabatrin (VGB) has been shown in a number of clinical trials with varying designs to be effective and well-tolerated as both add-on therapy and monotherapy in epilepsy with partial seizures with or without secondary generalization as well as in infantile spasms. The present study is an open, long-term (1 year) extension of a randomized double-blind placebo-controlled multicentre Canadian trial of VGB in resistant partial adult epilepsy. The present study was designed to examine the safety and long-term efficacy of VGB. Completers of the preceding double-blind study had their dose of VGB titrated to 4 g/day over 3 weeks. Patients were evaluated every 2-4 weeks and at week 14 were allowed to continue only if they achieved a 50% seizure reduction compared with pre-VGB baseline. In addition to neurological and physical examinations, safety was assessed by a cognitive psychosocial test battery, visual and somatosensory evoked potentials and MRI scans. Ninety-seven of 100 eligible patients entered the study, 53 of whom completed the 52 weeks. Fifty-eight percent of the patients had a greater than 50% seizure reduction in seizures vs. pre-VGB baseline. Seizure reductions of 56% and 45%, respectively, were seen in the VGB and placebo groups from the preceding study. Fifty-four percent of patients were judged by the investigators to have experienced at least a moderate therapeutic effect. Discontinuations were 29% for lack of efficacy and 12% for adverse effects. There was a mean weight gain of 3.7 +/- 0.2 kg by end of study. Neurologica/psychiatric side effects were the most common reason for withdrawal including three behavioral reactions attributed to the drug which required temporary hospitalization. There were no abnormalities on laboratory or special tests and there was a tendency for improvement on most tests of cognitive function and mood. Vigabatrin, as an add-on agent, is well-tolerated and can be of long-term benefit in a substantial proportion of patients with intractable partial epilepsy.

Adolescent↗