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

We studied the excitability of the motor cortex using, transcranial magnetic stimulation (TMS) in patients with temporal and extratemporal epilepsy. We applied single and paired-pulse TMS to 15 patients with temporal (n = 7), extratemporal (n = 6) and focal epilepsy lateralised to one hemisphere (n = 2). Patients had no antiepileptic drugs in the last 48 h and were seizure free for 4 h prior to testing. We determined the threshold for EMG responses at rest (RMT), the cortically evoked silent period (CSSP) and intracortical inhibition (ICI, intervals of 2-4 ms) and facilitation (ICF, 7-15 ms) and compared the results to those obtained in 17 normal controls. ICI and ICF was reduced in both hemispheres (P < 0.01. ANOVA) compared to the controls. In the hemisphere of seizure origin ('abnormal') there was a reduction of ICF (P < 0.01) and normal ICI, in the 'normal' hemisphere there was a reduced ICI (P < 0.01) and a slight reduction of ICF (P < 0.05). ICF on the 'abnormal' side was reduced (P < 0.05) compared to the 'normal' hemisphere. RMT was increased in two patients, but group comparison of RMT and CSSP showed no significant differences between patients and controls. The results suggest a remote effect of epileptic activity onto the motor cortex leading to an alteration of activity in local inhibitory circuits.
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PMID:Motor cortex excitability in patients with focal epilepsy. 1094 Jun 19

It is unclear whether focal epilepsies chronically influence the processing of cortex distant to the epileptogenic zone. Therefore, motor cortex excitability was analysed in patients with temporal and extratemporal epilepsies whose epileptogenic zones did not include the primary motor area. Single and paired-pulse transcranial magnetic stimulation (TMS) was applied to the primary motor cortex in 20 healthy controls and 23 patients with focal epilepsy (39.4 +/- 13.2 years; 12 left, 11 right; 14 temporal, nine extratemporal: six frontal, three parieto-occipital) ipsi- and contralateral to the epileptogenic zone. In all patients, the epileptogenic zone did not include the primary motor cortex. The resting motor threshold (RMT), the cortical silent period (CSP), the intracortical inhibition [ICI; combined interstimulus intervals (ISI) 2 and 3 ms] and the intracortical facilitation (ICF; combined ISI 10 and 15 ms) were determined. The measures obtained ipsilateral to the epileptogenic zone were compared with those elicited in contralateral hemispheres and, in exploratory analyses, with controls using non-parametric tests, including Hodges-Lehmann estimates of median differences (HLE) with 95% confidence intervals (CI). In the patient group, the CSP elicited in the ipsilateral motor cortex (median 162.3 ms) was shortened compared with the contralateral CSP (median 174.6 ms; HLE 15.9 ms; CI 6.2, 27.0 ms; P = 0.002). This interhemispheric difference was more pronounced in extratemporal epilepsies (HLE 23.4 ms; CI -3.2, 67.6 ms) compared with temporal epilepsies (HLE 14.3 ms; CI 4.7, 26.2 ms). Patients with parieto-occipital epilepsies showed the greatest interhemispheric differences in CSP (HLE 33.5 ms) and patients with mesial temporal epilepsies the smallest (HLE 9.9 ms). No significant differences were found between ipsi- and contralateral RMT, ICI or ICF. In analyses of subgroups, the CSP was shorter in epileptic hemispheres of patients with extratemporal epilepsies (141.4 ms) than in controls (173.4 ms; HLE 40.0 ms; CI 3.2, 83.4 ms; P = 0.029). ICF was increased in epileptic hemispheres of extratemporal epilepsies (147.6%) compared with temporal epilepsies (114.6%; HLE 33.0%; CI 4.1, 68.3%; P = 0.038). The results suggest that focal epilepsies influence chronically distant cortex, leading to decreased inhibition and increased facilitation in the ipsilateral motor cortex even when the epileptogenic zone is apart from it. This alteration may be due to synaptic reorganization and appears to be more pronounced in extratemporal and neocortical temporal than in mesial temporal epilepsies. This may have diagnostic implications.
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PMID:Motor cortex excitability in focal epilepsies not including the primary motor area--a TMS study. 1572 58

Intracortical disinhibitory mechanisms play a crucial role in epilepsy. Therefore, the recruitment of motor cortical excitability was evaluated to distinct between focal and generalized epileptic syndromes. Twenty-five untreated patients with epilepsy and 20 controls were enrolled. Classification into focal (FE, n=10) or idiopathic generalized (IGE, n=15) epilepsy was based on seizure semiology, EEG and MRI. The recruitment of motor cortical inhibition and facilitation was measured by varying the stimulus intensity (SI) of the first conditioning stimulus in a paired-pulse transcranial magnetic stimulation (TMS) paradigm producing stimulus-response (S-R) curves of intracortical excitability. S-R curves were then compared with other commonly used TMS measures of cortical excitability [cortical silent period (CSP) and motor threshold (MT)]. In patients with IGE, inhibition occurred only at higher conditioning SIs compared to patients with focal epilepsy and controls. Recruitment of inhibition was unchanged in patients with focal epilepsy compared to controls. Recruitment of facilitation (ICF), CSP duration and MT, were not different between patients with FE or IGE or between patients and controls. These results suggest that the recruitment for motor cortical inhibition in patients with IGE is less effective. This may reflect a disturbed access to or an increased threshold of inhibitory neurons within the motor cortex. Impaired recruitment of inhibition might be a helpful parameter to access cortical excitability in newly diagnosed patients with generalized or focal epilepsy.
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PMID:Recruitment of motor cortex inhibition differentiates between generalized and focal epilepsy. 1928 51