Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Absence of sleep EEG markers in fatal familial insomnia healthy carriers: a spectral analysis study
Autore:
Ferrillo, F; Plazzi, G; Nobili, L; Beelke, M; De Carli, F; Cortelli, P; Tinuper, P; Avoni, P; Vandi, S; Gambetti, P; Lugaresi, E; Montagna, P;
Indirizzi:
Univ Genoa, DISMR, Sleep Disorder Ctr, Genoa, Italy Univ Genoa Genoa Italy v Genoa, DISMR, Sleep Disorder Ctr, Genoa, Italy Univ Bologna, Inst Clin Neurol, Bologna, Italy Univ Bologna Bologna Italy iv Bologna, Inst Clin Neurol, Bologna, Italy CNR, Ctr Cerebral Neurophysiol, Genoa, Italy CNR Genoa ItalyCNR, Ctr Cerebral Neurophysiol, Genoa, Italy Univ Modena & Reggio Emilia, Dept NPS, Modena, Italy Univ Modena & Reggio Emilia Modena Italy milia, Dept NPS, Modena, Italy Case Western Reserve Univ, Inst Pathol, Div Neuropathol, Cleveland, OH 44106 USA Case Western Reserve Univ Cleveland OH USA 44106 Cleveland, OH 44106 USA
Titolo Testata:
CLINICAL NEUROPHYSIOLOGY
fascicolo: 10, volume: 112, anno: 2001,
pagine: 1888 - 1892
SICI:
1388-2457(200110)112:10<1888:AOSEMI>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
PRION PROTEIN GENE; SEX-DIFFERENCES; YOUNG-ADULTS; OSCILLATIONS; FREQUENCIES; AROUSALS; SPINDLE; AGE;
Keywords:
sleep EEG markers; fatal familial insomnia; healthy carriers; spectral analysis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
17
Recensione:
Indirizzi per estratti:
Indirizzo: Ferrillo, F Ctr Med Sonno, Cattedra Neurofisiopatol, Dipartimento Sci Motorie & Riabilitat, Largo Rosanna Benzi 10, I-16132 Genoa, Italy Ctr Med Sonno Largo Rosanna Benzi 10 Genoa Italy I-16132 taly
Citazione:
F. Ferrillo et al., "Absence of sleep EEG markers in fatal familial insomnia healthy carriers: a spectral analysis study", CLIN NEU, 112(10), 2001, pp. 1888-1892

Abstract

Objectives: Fatal familial insomnia (FFI) is linked to a mutation at codon178 (C178) of the prion protein gene (PRNP). FFI is pathologically characterized by selective atrophy of the anteroventral and mediodorsal thalamic nuclei and clinically by loss of sleep, dysautonomia and motor signs. A key early polysomnographic sign of the disease onset is the loss of sleep spindling (sigma activity, SA). In FFI tho loss of SA leads to the spectral representation of a sudden slow wave activity (SWA) increase from an awake state, the reaching of a stable plateau without oscillations, followed by abrupt fall down to REM sleep. We evaluated the presence of differences in the spectral sleep EEG pattern in FFI relatives carriers (C178(pos)) or non-carriers (C178(neg)) of the C178 mutation. Methods: Seventeen healthy relatives of FFI patients, 8 carriers of the C178 FFI mutation in a preclinical condition and 9 non carriers, underwent two-night polysomnography. The absolute and relative EEG power of the 4 main bands (delta: SWA, 0.5-4.0 Hz; theta: TB, 4.5-8 Hz; alpha: AB, 8.5-12 Hz; sigma: SA, 12.5-16 Hz) has been studied for the total sleep time, the periodof delta increase after sleep onset, and the period of delta plateau. Multiple regression has been applied to investigate relations between the powerof the bands studied and 3 parameters: age, the gender of the subjects andthe C178 genotype. Results: Our study could not show evidence of differences in the sleep EEGcomposition between carriers and non-carriers of the C178 FFI mutation. Conclusions: The spectral analysis techniques we used were not able to disclose sleep EEG markers linked to the FFI C178(pos) in the preclinical condition. Key sleep EEG alteration become evident only at the clinical onset of the disease. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 02:19:41