Differentiating pathologic delta from healthy physiologic delta in patients with Alzheimer disease

被引:24
作者
Crowley, K
Sullivan, EV
Adalsteinsson, E
Pfefferbaum, A
Colrain, IM
机构
[1] Compumed Ltd, Melbourne, Vic, Australia
[2] SRI Int, Human Sleep Res Program, Menlo Pk, CA 94025 USA
[3] Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA
[4] MIT, Dept Elect Engn & Comp Sci, Cambridge, MA 02138 USA
[5] Harvard Univ, MIT, Div Hlth Sci & Technol, Cambridge, MA 02138 USA
[6] SRI Int, Neurosci Program, Menlo Pk, CA 94025 USA
[7] Univ Melbourne, Dept Psychol, Parkville, Vic 3052, Australia
关键词
sleep physiology; electroencephalography; delta; K-complex; Alzheimer disease;
D O I
10.1093/sleep/28.7.865
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Study Objective: In patients with Alzheimer disease, the electroencephalogram during wakefulness shows pathologic signs of abundant, diffuse, large-amplitude delta activity. The carryover of this abnormal delta activity into non-rapid eye movement sleep raises the question of whether the observed delta electroencephalographic activity during sleep in Alzheimer disease in any way reflects normal physiologic delta activity slow-wave sleep. The objective of the study was to compare patients with Alzheimer disease with age-matched controls using an experimentally controlled procedure that can test the capacity of the nervous system to generate physiologic delta-frequency responses during sleep. Setting: Research sleep laboratory. Participants: Seven ambulatory patients with Alzheimer disease (mean age = 70.0 +/- 5.77 years) meeting the National Institute of Neurological and Communicative Diseases and Stroke and Alzheimer's Disease and Related Disorders Association criteria for probable Alzheimer disease and 8 controls (mean age = 69.25 +/- 4.95 years), underwent at least 1 night of evoked-potential recordings. Measurement and Results: Data were collected during stage 2 sleep. Responses to stimuli were classified based on whether they produced a K-complex. Averages of K-complex responses were calculated, latencies and amplitudes of components evaluated, and K-complex incidence was determined. Relative to controls, subjects with Alzheimer disease produced significantly fewer evoked K-complexes (P <.001) and had substantially smaller N550 amplitudes than controls (P <.05). A lower probability of eliciting a K-complex correlated with greater dementia severity, as measured by the Mini Mental State Examination and Dementia Rating Scale. Conclusions: Despite observed increases in pathologic delta-frequency electroencephalographic activity, patients with Alzheimer disease have an impaired capacity to generate normal physiologic delta responses during non-rapid eye movement sleep.
引用
收藏
页码:865 / 870
页数:6
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