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Titolo:
Receptor test (pupillary dilatation after application of 0.01% tropicamidesolution) and determination of central nervous activation (Fourier analysis of pupillary oscillations) in patients with Alzheimer's disease
Autore:
Grunberger, J; Linzmayer, L; Walter, H; Rainer, M; Masching, A; Pezawas, L; Saletu-Zyhlarz, G; Stohr, H; Grunberger, M;
Indirizzi:
Univ Vienna, Dept Psychiat, A-1090 Vienna, Austria Univ Vienna Vienna Austria A-1090 Dept Psychiat, A-1090 Vienna, Austria SMZ Ost, Dept Psychiat, Vienna, Austria SMZ Ost Vienna AustriaSMZ Ost, Dept Psychiat, Vienna, Austria
Titolo Testata:
NEUROPSYCHOBIOLOGY
fascicolo: 1, volume: 40, anno: 1999,
pagine: 40 - 46
SICI:
0302-282X(1999)40:1<40:RT(DAA>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
GENERALIZED ANXIETY DISORDER; NONORGANIC INSOMNIA; DAYTIME VIGILANCE; SLEEP;
Keywords:
Alzheimer's disease; tropicamide; central nervous activation; Fourier analysis of pupillary oscillations;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
19
Recensione:
Indirizzi per estratti:
Indirizzo: Grunberger, M Univ Vienna, Dept Psychiat, Wahringer Gurtel 18-20, A-1090 Vienna, Austria Univ Vienna Wahringer Gurtel 18-20 Vienna Austria A-1090 ia
Citazione:
J. Grunberger et al., "Receptor test (pupillary dilatation after application of 0.01% tropicamidesolution) and determination of central nervous activation (Fourier analysis of pupillary oscillations) in patients with Alzheimer's disease", NEUROPSYCHB, 40(1), 1999, pp. 40-46

Abstract

Memory loss and severe cognitive deficits in Alzheimer patients are supposed to be related to a reduction of acetylcholine as well as to central nervous deactivation. For the investigation of cholinergic deficits and deactivation, we used computer-assisted pupillometry. Cholinergic deficits caused by a particularly severe loss of cholinergic neurons may be responsible forcognitive and mnemonic performance deficits. The control of the pupillary diameter represents a balance between cholinergic and adrenergic innervation and is influenced directly or indirectly by central and autonomic nervoussystem inputs. Either of these systems could be affected in Alzheimer patients. A reduced innervation of the target muscle through neuronal cell death, axon retraction, reduced release, increased reuptake of altered amounts or function of neurotransmitter receptors seems to affect the pupillary response to cholinergic antagonists in Alzheimer patients. There is, however, no relationship between pupillary diameter and central deactivation, but between central nervous activation and pupillary oscillations which reflect the physiological corticodiencephalic activity, a relationship has to be assumed. Frequencies and amplitudes of pupillary oscillations measured by means of Fourier analysis are modulated corticodiencephalicaIly. Therefore, Alzheimer patients were compared to healthy controls with respect to their pupillary diameters and responses to an acetylcholine antagonist. Twenty-nine patients, aged between 55 and 85 years, suffering from mild to moderate Alzheimer's disease (AD) and 29 normal controls of similar age formed. Times of measurement were: 0 (baseline), 20, 40, 60, 80, and 100 min. After 4 min tropicamide was instilled. Forty min after the instillation of tropicamide into the left eye, the Alzheimer patients showed a pronounced dilatation of41.57%. The dilatation in normal controls was 28.5%. Fourier analysis of pupillary oscillations (sum of frequency bands = power) demonstrated a marked deactivation (low amplitudes in low-frequency bands, but in contrast to our expectations no higher amplitudes in the higher frequency bands) in patients with AD which remained constant at all times of measurement. By means of discriminant analysis of pupillary diameter and pupillary oscillations (frequency band 0.00-1 Hz), 89.7% were correctly predicted to be Alzheimer patients, 89% to be normal controls.(56-85 years) participated in the study. The cholinergic receptors of the pupil were blocked by the acetylcholine antagonist tropicamide. It could be assumed that the larger the pupillary dilatation, the larger the extent of cognitive deficits. Alzheimer patients show abnormal acetylcholine neurotransmission. Changes of pupillary diameterafter instillation of 1 drop of 0.01% tropicamide solution were measured and Fourier analysis of pupillary oscillations was performed. Times of measurement were: 0 (baseline), 20, 40, 60, 80, and 100 min. After 4 min tropicamide was instilled. Forty min after the instillation of tropicamide into the left eye, the Alzheimer patients showed a pronounced dilatation of 41.57%. The dilatation in normal controls was 28.5%. Fourier analysis of pupillary oscillations (sum of frequency bands = power) demonstrated a marked deactivation (low amplitudes in low-frequency bands, but in contrast to our expectations no higher amplitudes in the higher frequency bands) in patients with AD which remained constant at all times of measurement. By means of discriminant analysis of pupillary diameter and pupillary oscillations (frequency band 0.00-1 Hz), 89.7% were correctly predicted to be Alzheimer patients, 89% to be normal controls.

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Documento generato il 12/07/20 alle ore 03:01:59