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Results for “JACKSONIAN SEIZURE”

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At least 19 recordsLinked to original sources
PubMed1976

Sensory Jacksonian seizures.

Sensory Jacksonian seizures were analyzed in 42 patients with regard to anatomical and temporal sequences. The origin of sensory Jacksonian seizures, in contrast to motor Jacksonian seizures, often began at peripheral sites with littel cortical representation. The progression of seizure activity across the cerebral cortex followed a course that was neither rectilinear, radiate, nor random; it appeared to preceed in an organized manner to involve functionally coherent units. The patterns analyzed conformed more closely to cortical somatosensory maps reported for the chimpanzee than the sensory sequences presently available for the cortex of man. Complete diagnostic studies are indicated in patients presenting with sensory Jacksonian seizures because of the frequency of related focal pathology.

Arm↗
PubMed1979

Sensory Jacksonian seizures triggered by a frontally-located meningioma.

A patient who presented with sensory Jacksonian seizures and no other clinical symptoms was found to have a meningioma in the premotor area of the frontal lobe. The possibility that brain oedema caused by the tumour encroached on the supplementary motor area and triggered the seizures via cortico-cortical pathways is discussed.

Aged↗
PubMed2000

A case of post-anoxic encephalopathy with initial massive myoclonic status followed by alternating Jacksonian seizures.

To contrast stimulus-sensitive generalized myoclonus with ensuing multifocal localized myoclonus in a patient with post-anoxic coma, we stressed the clinical as well as electroencephalographical differences between his initial generalized and subsequent focal myoclonus. While generalized myoclonus was presumably of extracortical origin and responsive to valproic acid, alternating Jacksonian seizures were definitely cortical and suppressed with phenytoin. These two different types of myoclonus should not be confused in post-anoxic coma.

Aged↗
PubMed1982

[Clinical picture and pathogenesis of Jacksonian seizures in cerebral arteriovenous aneurysms].

The results of combined examinations of 26 patients with arteriovenous aneurysms in the brain are presented. The patients constituted two groups in one of which the aneurysm took a "neoplastic", and in the other a "vascular" course. The morphological and clinical forms of the aneurysm course that depended on the localization and size of the anomaly are described in detail. The brachial and crural types of Jacksonian seizures are specified. In the neoplastic form of the aneurysms (contrary to the vascular one) these seisures were the leading clinical symptom at the disease onset and had a complicated structure that included diverse sensitive phenomena, the tonic constituent of the convulsions and symptoms of transient cerebrovascular insufficiency. In the periods between the seizures the neurological and EEG symptoms were weak. The disturbances of the vestibular system revealed at the trunco-cortical level point to a progressing character of the disease and a high frequency of the paroxysms. The leading links in the pathogenesis of the seizures were circulatory disturbances in the system of the aneurism-carrying vessels in the neoplastic form, and cicatricial-atrophic changes at the sites of the former hemorrhages in the vascular form of the aneurism.

Adult↗
PubMed1996

[Sensory Jacksonian seizures as initial manifestation of sarcoidosis].

A 46-year old patient is reported presenting with somatosensory focal seizures of either arm as the only manifestation of an otherwise clinically inapparent sarcoidosis. MRI showed signs of a granulomatous leptomeningeal affection. Histological examination of a meningeal biopsy proved the diagnosis of sarcoidosis by demonstrating noncaseating granulomas. There was no other clinical manifestation of sarcoidosis. Chest X-ray was normal and the serum level of angiotensin-converting-enzyme was only slightly elevated. The CD4/CD8 ratio in the bronchoalveolar lavage cell population, however, was clearly abnormal, supporting the role of this diagnostic tool in the diagnosis of sarcoidosis.

Biopsy↗
PubMed1978

[Jacksonian seizures in the clinical picture of supratentorial brain tumors].

An analysis of the structure and frequency of Jackson's seizures during the illness in 27 patients with brain tumors displayed correlation of these parameters with a histological type of a neoformation and a degree of the involved mediobasal brain structures. In the process of development of the disease the epileptic activity in the EEG was replaced by a slow activity. The displayed peculiarities of the structure and the course of Jackson's seizures taking into account other clinical manifestations can be used in preoperational diagnosis of a histological nature of a tumor.

Adolescent↗
PubMed1986

[Treatment of epileptic patients with Jacksonian seizures].

The article describes the treatment of patients with Jackson's epilepsy, the latter being variable in the structure and the time of development. The author offers the necessary information and recommendations concerning the characteristics of the action and pharmacokinetics of a number of antiepileptic drugs and preparations of resorptive therapy. The effect of surgery on the epileptic process is outlined.

Anticonvulsants↗
PubMed1995

[Jacksonian seizure model induced by a kainic acid microinjection into unilateral sensori-motor cortex].

Kainic acid microinjection into unilateral sensori-motor cortex induced focal seizure status and secondarily generalized seizure status for about 4 hours. After these seizure status, focal myoclonic jerkings were induced for about 2 days. EEG demonstrated generalized synchronous periodic spikes with these myoclonic jerkings. This phenomenon was very similar to those symptoms of epilepsia partialis continua in man. During focal seizure status, autoradiographic study with 14C-deoxyglucose demonstrated increased local cerebral glucose utilizations in the injected site of the sensori-motor cortex, ipsilateral caudate nucleus, globus pallidus, substantia nigra and thalamic nuclei. The result suggested that subcortical pathways played an important roles in the seizure propagation from the cortical epileptogenic focus.

Animals↗