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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was electrophysiological recording of sleep in patients after damage to the right or left cerebral hemisphere after stroke. The studied material comprised 15 patients ages 45 to 75 years, ten of whom had ischaemic stroke in the area of vascularization of the middle cerebral artery as confirmed by CT. In 5 cases the left and in 5 the right hemisphere was damaged. Five patients without organic brain changes served as controls. Sleep study was carried out 4 weeks after stroke, the patients were EEG-monitored during 9 hours of sleep. In stroke patients disruption of the normal pattern of EEG during sleep was found, with absence of sleep cycles and disturbed sequence of these stages. Changes were noted also in the durations of stages N-REM, REM, WASO. In left hemisphere damage the duration of N-REM was shorter, and that of REM was longer than in cases with right hemisphere damage and in controls. After stroke the per cent proportion of the first stage of sleep N-REM was higher mainly in right-sided lesions, while the per cent proportions of stages II and III + IV were lower than in controls. The latency of sleep onset and onset of the first REM was evidently shorter after stroke.
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PMID:[Electrophysiological pattern of sleep after stroke]. 802 2

Paramedian thalamic stroke (PTS) is a cause of organic hypersomnia, which in the absence of systematic sleep-wake studies has been attributed to disruption of ascending activating impulses and considered a "dearoused" state. However, an increasing mount of data suggests a role of the thalamus in sleep regulation and raises the possibility that a sleep disturbance contributes to hypersomnia in PTS. We evaluated 12 patients with magnetic resonance imaging-proven isolated PTS and hypersomnia with 10 to >20 hours of sleep behavior per day. Nocturnal polysomnographic findings paralleled the severity of hypersomnia. All subjects had increased stage 1 NREM sleep, reduced stage 2 NREM sleep, and reduced numbers of sleep spindles. In patients with severe hypersomnia, slow-wave (stages 3-4) NREM sleep was often reduced, but there were no major REM sleep alterations. Daytime sleep behavior was associated mostly with stage 1 sleep by electroencephalogram; there was no correlation between hypersomnia and results of nap tests. We conclude that hypersomnia following PTS is accompanied by deficient arousal during the day and insufficient spindling and slow-wave sleep production at night. These observations support the hypothesis of a dual role of the paramedian thalamus as "final common pathway' for both maintenance of wakefulness and promotion of NREM sleep.
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PMID:Hypersomnia following paramedian thalamic stroke: a report of 12 patients. 861 25

Snoring, a leading symptom of the sleep apnoea syndrome (SAS), has been reported to be one of the risk factors for sleep-related cerebral strokes. Episodes of apnoea are accompanied by hypoxaemia as well as hypercapnia. As CO2 constitute a major regulatory factor controlling cerebral blood flow, it is likely that changes in cerebral perfusion are to be found in patients with SAS, which may be related to nocturnal stroke. A computer-assisted pulsed (2 mHz) Doppler ultrasonography system has been modified for continuous long-term and on-line recording of cerebral haemodynamics together with simultaneous polysomnography, continuous blood pressure recordings, and measurement of the end-expiratory CO2. The dynamics of cerebral blood flow velocity (CBFV) during sleep were measured in the right middle cerebral artery in 10 SAS patients. CBFV showed a characteristic nocturnal pattern with decreases during non-rapid eye movement (NREM) sleep and increases during REM sleep. Changes in sleep stage patterns as well as awakenings from NREM sleep were not regularly accompanied by corresponding changes in CBFV. Dramatic increases in CBFV could be observed during apnoeic episodes, with maximum increases during REM sleep. CO2 reactivity and changes in CBFV related to apnoea duration were markedly increased during sleep compared with the waking state in SAS patients. The dynamic feature of CBFV in relation to sleep patterns reflects quantitative uncoupling between cerebral electrical activity and cerebral perfusion during sleep in SAS patients as has been previously reported for normal subjects (Hajak et al. 1994). It supports a dissociation in the activity of central regulatory mechanisms during human sleep which might cause abnormal cerebral perfusion under certain circumstances. The increased CO2 reactivity during sleep in SAS suggests a 'hypersensitivity' of intracranial vasoactive receptors and/or disturbances in the central autonomic control of cerebrovascular functions. It may be concluded that, under certain conditions, the interaction of decreased cerebral perfusion in SAS patients with sleep-related cerebral perfusion patterns and haemodynamic changes during apnoeic episodes might lead to a critical reduction in cerebral perfusion.
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PMID:Cerebral perfusion during sleep-disordered breathing. 1060 90

Sleep-disordered breathing (SDB) in the form of obstructive sleep apnea is a possible risk factor for stroke. We carried out a cross-sectional survey out in a rehabilitation center among patients with first-ever stroke to further determine the incidence and types of SDB and its relationship to known risk factors for stroke. Full polysomnography was performed in 147 consecutive patients (95 men, 52 women, age 61+/-10 years) admitted to our neurological Rehabilitation Department 46+/-20 days after first-ever stroke. Subjective sleepiness (Epworth Sleepiness Scale), vascular risk factors, anthropometric data, and polysomnographic findings were compared between stroke patients with varying degrees of SDB. With a cutoff point for the respiratory disturbance index (RDI) of 5, 10, 15, or 20 the respective prevalence of SDB was 61%, 44%, 32%, and 22%. The type of SDB was generally obstructive, with dominant central apneas in only 6% of patients. Patients with an RDI of 20 or higher had less REM sleep, thicker necks, and a more central type of obesity. Even in patients with an RDI of 20 or higher subjective sleepiness, although higher than in those without SDB, was not a predominant symptom. Snoring and anthropometric data suggest that obstructive SDB may have existed prior to stroke. The prevalence of hypertension and coronary heart disease were higher among stroke patients with an RDI of 20 or higher than in those without SDB. We conclude that the prevalence of SDB among patients with stroke is high. Examination of stroke should include screening for SDB.
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PMID:Sleep-disordered breathing among patients with first-ever stroke. 1070 96

Background/objective: Since reports of the effects of cerebral hemispheric stroke on sleep architecture are rare and contradictory, we prospectively studied 24 patients with first acute supratentorial, extra-thalamic stroke.Methods: We assessed stroke severity, topography, and volume (on brain MRI). Sleep electroencephalogram recordings were performed a mean of 12 days after stroke onset, and scored for sleep stages over the healthy hemisphere. Sleep spindles and sawtooth waves were analyzed over both hemispheres. Data were compared with those of 17 age and gender-matched patients with normal brain imaging.Results: Compared to controls, stroke patients had lower total sleep time (P<0.01), lower sleep efficiency (P=0.02), and reduced amounts of NREM sleep stages 2-4 (P=0.02). Sleep spindles and sawtooth waves were often bilaterally reduced in patients with stroke volumes >25 ml. Abnormalities of REM sleep were more common in sleep studies performed within 3 days after stroke onset. Compared to patients with poor outcome, those with good outcome had higher sleep efficiency (P<0.01), more sleep time (P=0.02), and more NREM sleep stage 2 (P<0.01).Conclusion: Acute hemispheric stroke is accompanied by sleep EEG changes over the healthy hemisphere that correlate with stroke severity. These findings support the hypothesis that the cerebral hemispheres participate in the control of sleep.
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PMID:Sleep electroencephalogram changes in acute hemispheric stroke. 1131 81

We present a comprehensive review of sleep studies performed in patients with brain lesions complemented by 16 additional personal selected cases and by discussion of the corresponding animal data. The reader is cautioned about the risk of establishing an erroneous correlation between abnormal sleep and a given disorder due to the important inter and intra variability of sleep parameters among individuals. Salient points are stressed: the high frequency of post-stroke sleep breathing disorders is becoming increasingly recognised and may, in the near future, change the way this condition is managed. Meso-diencephalic bilateral infarcts induce a variable degree of damage to both waking and non-REM sleep networks producing and abnormal waking and sometimes a stage 1 hypersomnia reduced by modafinil or bromocriptine, which can be considered as a syndrome of cathecholaminergic deficiency. Central pontine lesions induce REM and non-REM sleep insomnia with bilateral lateral gaze paralysis. Bulbar stroke leads to frequent sleep breathing disorders. Polysomnography can help define the extent of involvement of various degenerative diseases. Fragmented sleep in Parkinson's disease may be preceded by REM sleep behavioural disorders. Multiple system atrophies are characterised by important sleep disorganization. Sleep waking disorganization and a specific ocular REM pattern are often seen in supra-nuclear ophtalmoplegia. In Alzheimer patients, sleep perturbations parallel the mental deterioration and are possibly related to cholinergic deficiency. Fronto-temporal dementia may be associated with an important decrease in REM sleep. Few narcoleptic syndromes are reported to be associated with a tumour of the third ventricle or a multiple sclerosis or to follow a brain trauma; all these cases raise the question whether this is a simple coincidence, a revelation of a latent narcolepsy or, as in non-DR16/DQ5 patients, a genuine symptomatic narcolepsy. Trypanosomiasis and the abnormal prion protein precociously after sleep patterns. Polysomnography is a precious tool for evaluating brain function provided it is realised under optimal conditions in stable patients and interpreted with caution. Several unpublished cases are presented: one case of pseudohypersomnia due to a bilateral thalamic infarct and corrected by modafinil, four probable late-onset autosomal recessive cerebellar ataxias without sleep pattern anomalies, six cases of fronto-temporal dementia with strong reduction in total sleep time and REMS percentage on the first polysomnographic night, one case of periodic hypersomnia associated with a Rathke's cleft cyst and four cases of suspected symptomatic narcolepsy with a DR16-DQ5 haplotype, three of which were post-traumatic without MRI anomalies, and one associated with multiple sclerosis exhibiting pontine hyper signals on MRI.
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PMID:Sleep and brain lesions: a critical review of the literature and additional new cases. 1181 Sep 86

Sleep-disordered breathing seems to play a role in pathogenesis of stroke: for example, it was showed that snoring is a risk factor for stroke. Sleep disorders and sleep-disordered breathing increase the risk for stroke, probably by influencing systemic and cerebral blood circulation, causing hypoxaemia during night. This theory is supported by the fact of higher prevalence of stroke in the morning. During REM sleep there is a higher requirement for oxygen; as most sleep apnoeas occur during REM, it is possible that there is a relative hypoxaemia during this sleep stage. Stroke, including hemispheric stroke, can cause or aggravate the pre-existing sleep-disordered breathing. There are contradictory data in the literature regarding the influence of stroke on sleep architecture. Sleep disorders are associated with poorer stroke outcome, so their detection and treatment can be important in secondary stroke prophylaxis and will improve the patient's functioning and quality of life.
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PMID:[Sleep disorders as a risk factors for stroke]. 1187 95

Wakefulness, NREM sleep, and REM sleep are accompanied by specific changes in breathing control, which arise from the interaction of automatic (metabolic, involuntary) and behavioural (voluntary and involuntary control systems. Considering the complexity in the neuroanatomy and neurophysiology of breathing control, it is not surprising that neurologic disorders are frequently accompanied by sleep disordered breathing. An introduction on pathophysiology, clinical features, diagnosis, and treatment of sleep disordered breathing in such diseases as stroke, epilepsy, dementia, spinal cord disease, polyneuropathies, and myopathies is presented.
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PMID:Sleep disordered breathing in neurologic disorders. 1204 98

Presented here is a clinical case of thalamic stroke which affected mainly non-specific thalamic regions. In acute disease stage, the patient exhibited a prominent psychopathological features, slight hemihypoaesthesia and sleep disturbances. Polysomnography confirmed the disturbances of sleep structure: the increase of sleep onset latency, number of awakenings, waking time and stage 1 duration, decrease of both deep sleep stages (3 and 4) and REM sleep. Visual analysis revealed EEG spindle asymmetry in stage 2 of the first sleep cycle, with sleep spindles predominating in the undamaged hemisphere. Spectral EEG analysis confirmed the presence of power asymmetry not only in the sigma-band but also in the other band ranges. This clinical case allows discussing the role of the thalamus in generation of quiet sleep EEG phenomena.
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PMID:[The case of prominent EEG sleeping activity in thalamic stroke patients]. 1283 May 17

The aim of this work was to study the structure of nocturnal sleep in stroke patients with various lesion. 160 patients and 30 healthy controls were studied. In all cases the diagnosis was confirmed by CT or MRI. Clinical and neurological studies were performed and polygraph traces of nocturnal sleep (electroencephalograms, electrooculograms, electromograms) were recorded. Sleep parameters were analyzed using a program developed at the Sleep Studies Center, I.M. Sechenov Moscow Medical Academy; along with standard parameters, this program involves analysis of segmental structure of sleep. The most prominent sleep disturbances were seen in stroke in the right hemisphere. Frontal lesions cause reduction and derangement of delta-sleep, parieto-temporal stroke affects the second stage and REM-sleep and brainstem stroke in pons affects REM-sleep.
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PMID:[Structure of nocturnal sleep in patients with various locations of stroke]. 1283 May 39


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