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23-01-2008, 16:30
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חבר מתאריך: 27.02.06
הודעות: 1,132
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מגוון מאמרים מדעיים המוכיחים אחרת
בתגובה להודעה מספר 5 שנכתבה על ידי u-367 שמתחילה ב "אני לא רופא ועדיין אומר שאין קשר בנתיים בין חוסר שינה לפרכוסים"
מצ"ב מבחר מאמרים מ-PUBMED המראים את ההשפעה של חוסר שינה על "השראת" התקף אפליפטי.
חיפוש מקיף יותר יניב מאמרים רבים על הנושא אשר אצל כולם פחות או יותר מסקנה זהה.
עדיין לא ברור אם חוסר בשינה גורם לאדם בריא להיות חולה אפילפטי, אך די ברור שחוסר שינה יכול ואכן גורם להתקף אפילפטי באדם בריא.
Increasing cortical excitability: a possible explanation for the proconvulsant role of sleep deprivation.
Scalise A, Desiato MT, Gigli GL, Romigi A, Tombini M, Marciani MG, Izzi F, Placidi F.
Department of Neurosciences, S. Maria della Misericordia Hospital, Udine, Italy. annascalise@libero.it
STUDY OBJECTIVE: Sleep deprivation (SD) is known to facilitate both seizures and interictal epileptiform abnormalities. For this reason, it is often used in the routine diagnostic workup of epileptic patients as an activating procedure for eliciting epileptiform and/or seizure patterns in their EEGs. In order to evaluate the effects of SD on cortical excitability, we studied the effects of sleep loss on healthy subjects by transcranial magnetic stimulation (TMS). DESIGN AND PARTICIPANTS: Seven normal subjects underwent TMS examination in baseline condition and after total sleep deprivation. The TMS investigation included two protocols: a) the evaluation of motor evoked potential and silent period parameters recorded in response to single-pulse magnetic stimulation; and b) the evaluation of the time course of intracortical motor activity tested with paired-pulse TMS applied at inter-stimulus intervals of 1-6 ms. SETTING: Clinical neurophysiology laboratory in a general hospital. INTERVENTIONS: None. RESULTS: After SD, the principal finding observed using single-pulse TMS was a decrease of the silent period duration, whereas a reduction of the intracortical inhibition, in particular at inter-stimulus intervals 1 and 2 ms, was found, using the paired-pulse TMS. CONCLUSION: Our findings suggest that SD may modify cortical excitability, seen as the balance between inhibitory and excitatory cortical phenomena, which could reduce the epileptic threshold
1: J Neurol Neurosurg Psychiatry. 2001 Dec;71(6):809-12.
[התמונה הבאה מגיעה מקישור שלא מתחיל ב https ולכן לא הוטמעה בדף כדי לשמור על https תקין: http://www.ncbi.nlm.nih.gov/corehtml/query/egifs/http:--highwire.stanford.edu-icons-externalservices-pubmed-standard-jnnp_final_free.gif] Links
Cortical excitability and sleep deprivation: a transcranial magnetic stimulation study.
Civardi C, Boccagni C, Vicentini R, Bolamperti L, Tarletti R, Varrasi C, Monaco F, Cantello R.
Clinica Neurologica, Ospedale Maggiore, Corso Mazzini 18, 28100 Novara, Italy. c_civardi@yahoo.com
The objective was to assess the changes in cortical excitability after sleep deprivation in normal subjects. Sleep deprivation activates EEG epileptiform activity in an unknown way. Transcranial magnetic stimulation (TMS) can inform on the excitability of the primary motor cortex. Eight healthy subjects (four men and four women) were studied. Transcranial magnetic stimulation (single and paired) was performed by a focal coil over the primary motor cortex, at the "hot spot" for the right first dorsal interosseous muscle. The following motor evoked potential features were measured: (a) active and resting threshold to stimulation; (b) duration of the silent period; (c) amount of intracortical inhibition on paired TMS at the interstimulus intervals of 2 and 3 ms and amount of facilitation at interstimulus intervals of 14 and 16 ms. The whole TMS session was repeated after a sleep deprivation of at least 24 hours. After the sleep deprivation, the threshold to stimulation (in the active and resting muscle), as well as the silent period, did not change significantly. By contrast, the paired stimulus study showed a significant (p<0.05) reduction in both intracortical inhibition and facilitation. Thus, TMS showed that sleep deprivation is associated with changes in inhibition-facilitation balance in the primary motor cortex of normal subjects. These changes might have a link with the background factors of the "activating" effects of sleep deprivation.
1: Seizure. 2000 Dec;9(8):580-4.
[התמונה הבאה מגיעה מקישור שלא מתחיל ב https ולכן לא הוטמעה בדף כדי לשמור על https תקין: http://www.ncbi.nlm.nih.gov/corehtml/query/egifs/http:--linkinghub.elsevier.com-ihub-images-PubMedLink.gif] Links
The usefulness of sleep and sleep deprivation as activating methods in electroencephalographic recording: contribution to a long-standing discussion.
Roupakiotis SC, Gatzonis SD, Triantafyllou N, Mantouvalos V, Chioni A, Zournas C, Siafakas A.
Department of Neurology, Athens Medical School, Eginition Hospital, 72 vas.Sofias av., Athens 11528, Greece.
Sedated sleep and sleep deprivation are commonly used methods to increase the diagnostic yield of the electroencephalogram (EEG), especially in the evaluation of people with epilepsy, but the rate of activation achieved by them is controversial, as is the issue of whether it is sleep itself, or sleep deprivation which is responsible for their alleged efficacy. We retrospectively studied the EEGs of epileptic patients, examined in our laboratory, who, after having undergone an inconclusive initial routine recording, had then been examined with a second recording. This was after either: (1) sleep deprivation with evidence of drowsiness in the recordings, (2) sleep deprivation without drowsiness (indicative of the effect which sleep deprivation per se has in eliciting abnormal patterns), or (3) drug-induced sedation. The activation rates found were (1) 22.5%, (2) 24% (22.6% for sleep deprivation collectively, regardless of the presence or not of subsequent drowsiness) and (3) 27% respectively. Only the sleep deprivation rate was statistically different from the 9.6% increased rate of abnormal patterns elicited by the simple repeating of a second routine recording, while the rate of drug-induced sleep was not. Although, sleep deprivation appeared to be more effective as an activating method of EEG compared with sedated sleep, no conclusions could be drawn about which stage of sleep, wakefulness or drowsiness, is primarily responsible for the method's efficacy. Copyright 2000 BEA Trading Ltd.
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