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Query: UMLS:C0014547 (focal epilepsy)
1,627 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors studied clinical characteristics in 11 patients with intractable focal epilepsy and preictal headache (PIHA) using a standardized interview. Headache was frontotemporal, ipsilateral to the focus, in nine patients with temporal lobe epilepsy (TLE) and contralateral in one with TLE and in one with frontal seizures. Migrainous features were found in four. After surgery, all seven seizure-free patients and two with rare seizures were free of PIHA. It may be a useful lateralizing sign in patients with TLE.
Neurology 2005 Dec 27
PMID:Preictal headache in partial epilepsy. 1638 Jun 25

Identification of focal cortical dysplasia (FCD) on magnetic resonance (MR) images of young children with refractory focal epilepsy is important, as surgical resection may offer improvement of seizure control and subsequent developmental progress. However, the MR appearances of malformations of cortical development may change during brain maturation. We report 4 children with refractory focal epilepsy, whose MR images in infancy showed localized cortical and subcortical signal abnormalities (hypointense on T(2)-weighted and hyperintense on T(1)-weighted images), suggestive of abnormal cortical development. The visibility of these lesions was significantly reduced on later MR images. Subtle blurring of the gray-white matter junction in these areas was the only indicator of cortical abnormality in 3 patients, which was recognized only after comparison with earlier images. Taylor-type FCD was subsequently confirmed in all patients, following surgical cortical resection of the lesions. MR images performed early within the first year of life in children with epilepsy are important to identify areas of FCD. The appearances of FCD on later scans can be very subtle escaping recognition, and conclusions may be misleading with respect to diagnosis and appropriateness of surgical treatment.
Epilepsia 2005 Dec
PMID:Taylor-type focal cortical dysplasia in infants: some MRI lesions almost disappear with maturation of myelination. 1639 66

Impaired transmission in GABAergic circuits is thought to contribute to the pathogenesis of epilepsy. Although it is well established that major reorganization of GABA(A) receptor subtypes occurs in the hippocampus of patients with medically refractory temporal lobe epilepsy (TLE), it is unclear whether this disorder is also associated with alterations in GABA(A) receptor subtypes in the neocortex. Here we have investigated immunohistochemically the subunit composition and neocortical distribution of three major GABA(A) receptor subtypes using antibodies specifically recognizing the subunits alpha1, alpha2, alpha3, beta2/3 and gamma2. Cortical tissue was obtained at surgery from patients with TLE and hippocampal sclerosis (HS; n = 9), TLE associated with neocortical lesions (non-HS; n = 12) and frontal lobe epilepsy (FLE; n = 5), with post-mortem samples serving as controls (n = 4). A distinct laminar and neuronal expression pattern of the alpha-subunit variants was found across the neocortical regions examined in the temporal and frontal lobes in both control and patient tissue samples. In the five patients with FLE, GABA(A) receptor subunit staining was unchanged as compared to controls. In patients with TLE we observed a marked decrease in alpha3-subunit staining in the superficial neocortical layers (I-III), but no change in the deep layers (V and VI) or in the expression pattern of the alpha1 and alpha2-subunits. Reduced expression in alpha3-containing GABA(A) receptors was detected in six out of nine patients of the HS group and four out of twelve patients of the non-HS group. Histopathological changes were present in eight out of the ten patients with decreased alpha3-subunit staining. The selective reduction in alpha3-containing GABA(A) receptors was confirmed using semiquantitative measurements of optical density (OD). The specific changes unique to alpha3-subunit expression in the superficial neocortical layers of patients with TLE suggest that this subtype is of particular significance in the reorganization of cortical GABAergic systems in focal epilepsy.
Brain 2006 Dec
PMID:Altered expression of alpha3-containing GABAA receptors in the neocortex of patients with focal epilepsy. 1704 56

Epileptic nystagmus is a rare, ictal phenomenon characterized by rapid, repetitive eye movements caused by epileptic activity. We report on a patient with cryptogenic focal epilepsy who presented a long-lasting (>30mn) episode of left head and eyes deviation and left-beating nystagmus not crossing the midline. Interictal EEG showed right temporal abnormalities.[Published with video sequences].
Epileptic Disord 2006 Dec
PMID:Epileptic nystagmus. 1715 Apr 46

The aim of this study was to determine the effects of long-term continuous cerebrocortical electrical stimulation in the treatment of partial epilepsy. The authors review the case of a 44-year-old man with medically intractable postencephalitic localization-related epilepsy with ictal onset in the primary motor cortex. For 5 years he was treated using patterned subthreshold electrical stimulation of the ictal site. This therapy has successfully eliminated the jacksonian march of cortical excitability and secondary generalization and reduced seizure frequency and intensity with an immediate postictal return of motor function. Over time, the seizure frequency subsided by more than 90%, with the patient showing no adverse features resulting from focal stimulation. The results in this case support the hypothesis that effective and safe long-term modulation of focal epilepsy is possible with focal cerebrocortical electrical stimulation.
J Neurosurg 2006 Dec
PMID:Long-term electrical stimulation-induced inhibition of partial epilepsy. Case report. 1740 61

The iron-induced model of post-traumatic chronic focal epilepsy in rats was studied by depth-electrode mapping to investigate the spread of epileptiform activity into subcortical brain structures after its onset in the cortical epileptic focus. Electrical seizure activity was recorded in the hippocampal CA1 and CA3 areas, amygdala and caudate-putamen, in rats with iron-induced chronic cortical focal epilepsy. These experiments showed that the epileptiform activity with its onset in the cortical focus synchronously propagated into the studied subcortical brain areas. Seizure behaviours seemed to increase in correspondence with the spread of the epileptic electrographic activity in subcortical areas. Comparison of the cortical focus electroencephalographic and associated multiple-unit action potential recordings with those from the subcortical structures showed that the occurrence and evolution of the epileptiform activity in the subcortical structures were in parallel with that in the cortical focus. The intracerebral anatomic progression and delineation of seizure spread (mapped by field potential (EEG) and multiple-unit action potentials (MUA) recordings) indicated participation of these regions in the generalization of seizure activity in this model of epilepsy. The seizure-induced activation of the hippocampus appeared to evolve into an epileptic focus independent of the cortical focus. The present study demonstrates the propagation of epileptic activity from the cortical focus into the limbic and basal ganglia regions. Treatment of iron-induced epileptic rats with ethosuximide, an anti-absence drug, resulted in suppression of the epileptiform activity in the cortical focus as well as in the subcortical brain areas.
Seizure 2007 Dec
PMID:Iron-induced experimental cortical seizures: electroencephalographic mapping of seizure spread in the subcortical brain areas. 1762 12

Psychogenic non-epileptic seizures can co-exist with epileptic seizures. Differentiating between the two is central to appropriate management. We report the case of a patient with established focal epilepsy who developed psychogenic non-epileptic seizures in direct response to second-person auditory hallucinations. To our knowledge, this is the first description of such an occurrence. These non-epileptic seizures improved with treatment of the underlying psychosis. The relationship between epilepsy and psychosis is outlined, and the possible causes and nosology of these psychogenic non-epileptic seizures are discussed.
Seizure 2007 Dec
PMID:Development of psychogenic non-epileptic seizures in response to auditory hallucinations. 1768 71

Functional MRI was used to evaluate factors influencing hemispheric dominance for language in 34 children suffering from intractable focal epilepsy due to left hemispheric lesion of pre- (n = 19) or postnatal (n = 15) origin. Nineteen children (56%) exhibited pronounced left-hemispheric language dominance. Significant co-activation of the right hemisphere or a complete language shift to this hemisphere was present in 15 children (44%). Atypical language representation was detected in 6 children (31,6%) with developmental pathology and in 9 patients (60%) with acquired epileptogenic lesion. Younger age at epilepsy onset and longer duration of epilepsy correlated significantly with atypical language presentation (p < 0,017 and p < 0,025). Whereas lesser tendency of prenatal lesions to displace cortical language centers did not reach statistical significance in simple paired tests, multiple logistic regression analysis viewed positive interaction between language shift, etiology and age at epilepsy onset. In conclusion, the language network reorganization was strongly influenced by both, the age at epilepsy onset and duration of epilepsy, and to a lesser degree by the character of the epileptogenic lesion, either developmental or acquired postnatally.
Epileptic Disord 2007 Dec
PMID:Language lateralization in children with pre- and postnatal epileptogenic lesions of the left hemisphere: an fMRI study. 1831 97

We analyzed sexual function in 29 women suffering from focal epilepsy using the Female Sexual Function Index, Beck Depression Inventory, Beck Anxiety Inventory and a battery of laboratory tests were performed to find possible correlations and differences. A total FSFI score lower than the predefined cut-off score was found in 20.7% women and the presence of at least one subtype of sexual dysfunction was found in 51.7% of them. The most frequent dysfunction was lack of lubrication, which occurred in 34.5% of patients. A higher depression score was significantly correlated with a worse total score of Female Sexual Function Index and with decreased score of lubrication, satisfaction and pain. Patients who were seizure-free had better total score of Female Sexual Function Index and score of lubrication, orgasm and pain in comparison to patients who were not seizure-free. A higher anxiety scale was correlated only with lower satisfaction. We found a statistically significant correlation of reduced desire and use of carbamazepine and with lower dehydroepiandrosterone sulphate and free-androgene index. Reduced arousal was also correlated with the use of carbamazepine and lower dehydroepiandrosterone sulphate. Patients with a combination of complex partial and generalized tonic-clonic seizures had a worse total sexual function score and pain score than those with complex partial and generalized tonic-clonic seizures only. Sexual dysfunctions are relatively common problems in epileptic women with focal epilepsy. Prospective studies, including a control group, are needed.
Epileptic Disord 2007 Dec
PMID:Sexual functions in women with focal epilepsy. A preliminary study. 1831 5

Malformations of cortical development (MCD) represent a major cause of developmental disabilities and severe epilepsy. Advances in imaging and genetics have improved the diagnosis and classification of these conditions. Up to now, eight genes have been involved in different types of MCD. Lissencephaly-pachygyria and subcortical band heterotopia (SBH) represent a malformative spectrum resulting from mutations of either LIS1 or DCX genes. LIS1 mutations cause a more severe malformation in the posterior brain regions. DCX mutations usually cause anteriorly predominant lissencephaly in males and SBH in female patients. Additional forms are X-linked lissencephaly with corpus callosum agenesis and ambiguous genitalia associated with mutations of the ARX gene. Lissencephaly with cerebellar hypoplasia (LCH) encompass heterogeneous disorders named LCH type a to d. LCHa are related with mutation in LIS1 or DCX, LCHb with mutation of RELN gene, and LCHd could be related with TUBA1A gene. Polymicrogyria encompass a wide range of clinical, aetiological and histological findings. Among several syndromes, recessive bilateral fronto-parietal polymicrogyria has been associated with mutations of the GPR56 gene. Bilateral perisylvian polymicrogyria showed a linkage to chromosome Xq28 in some pedigrees, and mutations in SRPX2 gene in others conditions. X-linked bilateral periventricular nodular heterotopia (BPNH) consists of BPNH with focal epilepsy in females and prenatal lethality in males. Filamin A (FLNA) mutations have been reported in some families and in sporadic patients. It is possible to infer the most likely causative gene by brain imaging studies and other clinical findings. Based on this experience, a detailed phenotype analysis is needed to develop the most efficient research on MCD in the future.
Rev Neurol (Paris) 2008 Dec
PMID:[Epileptogenic brain malformations: radiological and clinical presentation and indications for genetic testing]. 1880 83


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