Brain morphology and sleep EEG in patients with Huntington's disease

SummaryIn 12 patients with Huntington's disease, the relationship between brain morphology, nocturnal sleep EEG, and clinical variables was studied. Global cerebral atrophy did not significantly correlate with sleep parameters, whereas atrophy of the caudate nuclei was associated with reduced slow wave sleep and increased time spent awake. Several clinical parameters (e.g., anergia and thought disturbance scores of the Brief Psychiatric Rating Scale, illness duration and global clinical assessment) showed significant correlations with global cerebral atrophy. Similar studies in other neuropsychiatric disorders demonstrate associations between sleep alterations and brain morphological changes of different localizations, thus pointing to a complex relationship between both. It can be hypothesized that the caudate nuclei may be involved in sleep regulation; indirect evidence from studies with positron emission tomography (PET) point in the same direction.

[1]  J. Margerison,et al.  The EEG in Huntington's chorea: a clinical and neuropathological study , 1972, Journal of neurology, neurosurgery, and psychiatry.

[2]  T. Neylan,et al.  Decreased slow-wave sleep and enlarged lateral ventricles in schizophrenia. , 1988, Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology.

[3]  A. Rechtschaffen A manual of standardized terminology, techniques and scoring system for sleep of human subjects , 1968 .

[4]  G. Simpson,et al.  A rating scale for tardive dyskinesia , 1979, Psychopharmacology.

[5]  R. Doerr,et al.  Lehrbuch der inneren Medizin , 1934 .

[6]  W. Hacke,et al.  A quantitative approach to measuring the cerebrospinal fluid space with CT , 2004, Neuroradiology.

[7]  M S Buchsbaum,et al.  Regional cerebral glucose metabolic rate in human sleep assessed by positron emission tomography. , 1989, Life sciences.

[8]  I. Shoulson,et al.  Clinical‐pathologic correlation in Huntington's disease , 1989, Neurology.

[9]  M S Buchsbaum,et al.  Frontal cortex and basal ganglia metabolic rates assessed by positron emission tomography with [18F]2-deoxyglucose in affective illness. , 1986, Journal of affective disorders.

[10]  F. Holsboer,et al.  The effect of neuroendocrine secretion on brain morphology and EEG sleep in patients with eating disorders , 2004, European archives of psychiatry and neurological sciences.

[11]  M. Schumacher,et al.  Neuroradiologische Diagnostik bei Huntingtonscher Krankheit , 1988 .

[12]  J. Krieg,et al.  Enlargement of cerebrospinal fluid spaces in long-term benzodiazepine abusers , 1987, Psychological Medicine.

[13]  M. Dose,et al.  Nocturnal sleep in huntington's disease , 1991, Journal of Neurology.

[14]  Y. Nakazawa,et al.  Cerebral atrophy and slow wave sleep of abstinent chronic alcoholics. , 1987, Drug and alcohol dependence.

[15]  J C Mazziotta,et al.  Cerebral metabolic rates for glucose in mood disorders. Studies with positron emission tomography and fluorodeoxyglucose F 18. , 1985, Archives of general psychiatry.

[16]  A. Rechtschaffen,et al.  A manual of standardized terminology, technique and scoring system for sleep stages of human subjects , 1968 .

[17]  P. Hansotia,et al.  Sleep disturbances and severity of Huntington's disease , 1985, Neurology.

[18]  K. Pirke,et al.  Endocrine, metabolic, and cranial computed tomographie findings in anorexia nervosa , 1988, Biological Psychiatry.

[19]  J. Overall,et al.  The Brief Psychiatric Rating Scale , 1962 .