Clinical Neuroscience

[CONGRESS CALENDAR]

MAY 20, 2007

Clinical Neuroscience - 2007;60(05-06)

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Clinical Neuroscience

[100 years of riddle… X. Jubilee Alzheimer’s disease congress on the 100th anniversary of disease description]

Clinical Neuroscience

[TREATMENT OF SPASTIC UPPER LIMB WITH BOTULINUS TOXIN]

DÉNES Zoltán, FEHÉR Miklós, VÁRKONYI Andrea

[Objective - Examination of the effect of local botulinus toxin treatment on spastic upper limb, on patients with different brain injury. Patients and method - Prospective study in Traumatic Brain Injury Rehabilitation Unit of the National Institute for Medical Rehabilitation in the year 2003 and 2004. Thirteen patients (eight with stroke and five with traumatic brain injury) were treated locally on the spastic upper limb with 100 units botulinus A toxin. Results - Spasticity decreased one or two level on Modified Ashworth Scale, and in nine cases the good result were observed still at the end of 3rd month. No local or other complication was detected. Conclusions - Local treatment with botulinus toxin is an effective and safe method to decrease spasticity on upper limb in patients with different brain injury.]

Clinical Neuroscience

[Determining the term of schizencephaly]

KENÉZ József, LEEL-ŐSSY Lóránt

Clinical Neuroscience

[NOVEL CELL-BIOLOGICAL IDEAS DEDUCIBLE FROM MORPHOLOGICAL OBSERVATIONS ON “DARK” NEURONS REVISITED]

GALLYAS Ferenc

[The origin, nature and fate of ”dark“ (dramatically shrunken and hyperbasophilic) neurons are century-old problems in both human and experimental neuropathology. Until a few years ago, hardly any cell-biological conclusion had been drawn from their histological investigation. On the basis of light and electron microscopic findings in animal experiments performed during the past few years, my research team has put forward novel ideas concerning 1. the nature of ”dark“ neurons (malfunction of an energystoring gel-structure that is ubiquitously present in all intracellular spaces between the ultrastructural elements), 2. the mechanism of their formation (non-programmed initiation of a whole-cell phase-transition in this gel-structure), 3. their capability of recovery (programmed for some physiological purpose), 4. their death mode (neither necrotic nor apoptotic), and 5. their relationship with the apoptotic cell death (the gel structure in question is programmed for the morphological execution of ontogenetic apoptosis). Based on morphological observations, this paper revisits these ideas in order to bring them to the attention of researchers who are in a position to investigate their validity by means of experimental paradigms other than those used here.]

Clinical Neuroscience

[LATE CONTRALATERAL EPILEPTOGENESIS AFTER INCOMPLETE SURGERY IN TEMPORAL LOBE EPILEPSY FOLLOWED ACROSS 18 YEARS]

HALÁSZ Péter, JANSZKY József, KELEMEN Anna, BARSI Péter, RÁSONYI György

[Objectives - To present evidence of changes in seizure semiology suggesting late contralateral epileptogenesis after incomplete surgery in a patient with temporal lobe epilepsy. Methods - The presently 36 year old female patient was followed across 18 years by clinical observation and EEG, and video-EEG monitored before and 18 years after surgery. Results - The patient had complex partial seizures defined by video-EEG which started from the right temporal lobe with an ictal spread to the contralateral (left) temporal lobe. After right amygdalo-hippocampectomy she did not become seizure free. Years after surgery a new type of seizure emerged. Video-EEG monitoring 18 yrs after surgery revealed two seizure types. One started in the right temporal region clinically resembling to the earlier seizures. The new seizure type showed left sided electroclinical pattern. The postoperative MRI detected bilateral hippocampal sclerosis. Side specific memory tasks revealed bilateral hippocampal dysfunctions with subdominant (right) side predominance. Conclusions - The well documented evolution from unilateral to bilateral seizures suggests late contralateral epileptogenesis in which the persisting seizure spread from the primary epileptogenic side and/or the earlier silent contralateral hippocampal sclerosis (HS) may play role. This case show that progressive changes with bilateral involvement may occur during the course of chronic temporal lobe epilepsy.]

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