Clinical Neuroscience

[SLEEP DISORDERS IN PARKINSON SYNDROMES]

SZŰCS Anna1, KOVÁCS Gábor Géza2, NARULA Lalit1, HALÁSZ Péter1

MAY 20, 2007

Clinical Neuroscience - 2007;60(05-06)

[About 90% of neurodegenerative diseases with parkinsonism are associated with sleep disorders including daytime sleepiness, sleep-related breathing disorders and parasomnias. It is hard to define what ratio of insomnia and daytime hypersomnia is caused by the antiparkinsonian tratment, by the somatic and mentalemotional symptoms of the neurodegenerativ disease and by the neurodegenerative brain process itself. Recent research suggests that the latter group is more important than expected. In Parkinson syndromes the structures included in sleep regulation - mainly within the brainstem - are also affected resulting in specific sleep disorders being the primary biological symptoms of these diseases. The recently described parasomnia - REM sleep behavior disorder - has a specific significance in this respect: it may prevent by several years a high ratio of the parkinsonian disorders - especially synucleinopathies - offering the possibility of prevention by identifying the affected individuals. There seems to exist a similar although less clarified association between daytime sleepiness and Parkinson disease. Analysing the behavior of the orexin system in neurodegenerative diseases may help to learn more about this, recently described neurohumoral system and may clear the association of narcolepsy with neurodegeneration. By understanding the associations of parkinsonian disorders and sleep disorders new therapeutical strategies may be invented and may offer new aspects to understand the mechanism of them.]

AFFILIATIONS

  1. Országos Pszichiátriai és Neurológiai Intézet, „A” Neurológiai Osztály, Budapest
  2. Országos Pszichiátriai és Neurológiai Intézet, Neuropatológiai Osztály, Budapest

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[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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