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

Validity of regional blood flow (rCBF) measurements recorded over the human posterior fossa after 133Xe inhalation was tested. Recording of counts from both brain stem and cerebellum (BSC) was reproducible and contamination by counts derived from surrounding anatomical structures was low and no greater than that found over hemispheres. BSC values were F1 = 99 +/- 19 ml/100g brain/min, F2 = 17 +/- 4 in reasonable agreement with data reported from experimental animals. BSC flow values showed significant correlation with the state of awareness as judged by clinical and EEG evaluation with lowest F1 values in semicoma and step increases in stupor, non-REM sleep, drowsiness, rest, activation, REM sleep and highest values during focal and generalized epileptic seizures.
Stroke
PMID:Critical appraisal of cerebral blood flow measured from brain stem and cerebellar regions after 133 Xe inhalation in humans. 50 81

We studied polysomnographic recordings using an Oxford Medilog 9000 System in 18 patients with ischemic stroke in the middle cerebral artery territory. All patients underwent neurologic examination and brain CT scan within 5 h after the onset of symptoms. Polysomnographic recordings were started immediately thereafter and went on for three nights. Clinical and polysomnographic follow-up were performed 3 weeks after admission. The number and duration of REM phases were significantly reduced in the acute phase. This reduction correlated with the severity of neurological deficit at outcome and with the anatomical site of the lesion on CT scan. Our data provide evidence that polysomnographic recording is useful to detect symptoms of patients with different clinical outcomes during the acute phase of ischemic stroke.
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PMID:Sleep patterns in acute ischemic stroke. 148 42

The cyclical changes in heart rate and systemic blood pressure that accompany apneic events are predominantly mediated by fluctuations in the activity of the autonomic nervous system. Increased vagal efferent parasympathetic activity is responsible for the cyclical reductions in heart rate during apnea. In contrast, the cyclical elevations in systemic blood pressure are believed to result from recurrent peripheral vasoconstriction mediated by repetitive activation of the sympathetic nervous system. Maximal activation and pressures coincide with apnea termination and brief arousal from sleep. These cyclical elevations in systemic pressure during sleep increase ventricular workload and, thereby, may contribute to the development of ventricular hypertrophy. Systemic hypertension is present during wakefulness in approximately 50% of patients with OSA. Although age and obesity are the predominant risk factors for diurnal hypertension, OSA probably makes an independent contribution in younger obese men. Sinus bradycardia, Mobitz type 1 second-degree heart block, and prolonged sinus arrest have all been documented in association with the apneic events. Increased ventricular ectopy has been observed with oxyhemoglobin desaturations below 60%. Myocardial ischemia, infarction, sudden death, and stroke all demonstrate similar circadian variations in time of onset. Peak frequencies occur between 6 AM and noon, generally within several hours of awakening. Although sleep is associated with decreased frequencies of these adverse cardiovascular events in the general population, evidence exists linking REM sleep to an increased risk of myocardial ischemia. In men who habitually snore, epidemiologic data have detected an increased risk for ischemic heart disease and stroke. Habitual snoring has also been associated with an increased risk of sudden death during sleep. In patients with clinically significant OSA, there is reasonable information indicating excessive mortality in the absence of treatment. This mortality is predominantly cardiovascular and tends to occur during sleep.
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PMID:Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea. 152 12

There are no previous reports on parasomnias (sleep behavior disorders) affecting patients on intensive care units (ICUs). During 8 years of clinical practice, we evaluated over 200 adults with complaints of injurious, sleep-related behaviors, 20 of whom had ICU admissions while their parasomnias had been active and generally undiagnosed/untreated. Mean age during ICU confinement was 62.8 (+/- SD 13.1) years; 85.0% (17/20) were males. Patients underwent comprehensive clinical examinations along with extensive polysomnographic and audiovisual monitoring (electrooculogram, 9 channel EEG with paper speeds of 15 and 30 mm/sec, electromyogram [submental and 4 limbs], EKG, airflow). The polysomnographic studies were diagnostic for the REM sleep behavior disorder (vigorous dream-enactment during rapid eye movement [REM] sleep) in 85.0% (17/20) of patients, and for night terrors/sleepwalking in 15.0% (3/20). Three groups of parasomnia-ICU relationships were identified: i) Parasomnias originating in ICUs, stroke-induced (n = 3); ii) Admission to ICUs resulting from parasomnia-induced injuries: C2 odontoid process fracture and C3 spinous process fracture with severe concussion (n = 2); iii) Parasomnias in patients admitted to ICUs for various other medical problems (n = 15). Physicians should be thus alerted about the possibility of injurious, but usually treatable, parasomnias in ICU patients.
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PMID:Injurious sleep behavior disorders (parasomnias) affecting patients on intensive care units. 174 7

We achieved a unique and timely recording of cerebral activity in a 70 year old woman immediately pre- and post-stroke, while studying the effect of acute cerebral infarction on sleep-electroencephalogram (EEG) patterns. Normal patterns, except for increased wakefulness, were recorded during two pre-infarct polysomnograms. Immediately following cerebral infarction increased delta activity was recorded from the infarcted hemisphere only. Initially, REM sleep could not be recorded from either side; however, on the third post infarct day REM sleep returned. Background EEG levels from both hemispheres became progressively slower, flatter and simpler. In addition, sleep spindles and the distinctive saw-tooth wave forms of sleep almost disappeared. At one year post-stroke sleep-EEG rhythm recordings from both hemispheres became more similar except for persisting delta activity from the left hemisphere. Unexpected deterioration of sleep-EEG pattern recordings from the undamaged hemisphere taken during the patient's clinical recovery remains unexplained. Serial sleep recording may facilitate the study of brain recovery, activity and reorganization following stroke.
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PMID:Clinical recovery and sleep architecture degradation. 220 92

This review summarizes briefly the present knowledge on sleep-related factors in ischaemic heart disease. A marked circadian rhythm in the frequency of onset of acute myocardial infarction has been found, but the exact mechanism is not known. The circadian variation is possibly explained by several mechanisms. The best documented is sleep apnoea syndrome, which seems to be a risk factor for ischaemic heart disease and stroke. Stressful REM-sleep seems to be potentially arrhythmogenic in patients with decreased cardiopulmonary function. The role of coronary spasm, increased thrombocyte aggregation and mental stress in sleep disorders is still poorly understood.
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PMID:Cardiovascular stress and sleep. 331 Aug 37

Vegetative control of the heart was assessed on the basis of cardiac rhythm (CR) and stroke volume parameters in the course of an active orthostatic test and bicycle ergometry in 508 myocardial infarction patients and 30 normal subjects. Central hemodynamic parameters and CR spectrum were examined with respect to phases of sleep in 125 coronary patients and 25 normal subjects. Coronary patients showed a disrupted vegetative CR regulation, which was chiefly parasympathetic (reduced CR response to an active orthostatic position and rationed exercise, and a smaller share of high-frequency constituent of the CR energy spectrum). Disrupted vegetative CR regulation was correlated with low hemodynamic baseline and respective values in active orthostatic position, exercise and REM sleep. Reduced CR response to stress as well as reduced CR spectrum during sleep corresponded to more severe clinical conditions.
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PMID:[Possibilities of the evaluation of autonomic regulation of cardiac activity in patients with ischemic heart disease using non-invasive methods of examination]. 339 65

Sleep in normal individuals is associated with mild alveolar hypoventilation, which results in 2 to 8 mm Hg increases in PaCO2 and 3 to 11 mm Hg reductions in PaO2, which decreases mean arterial oxyhemoglobin saturation by less than 2 per cent. Arterial blood pressure and heart rate consistently decrease during sleep, and cardiac output either decreases or remains unchanged. Greater variability in these hemodynamic variables occurs during REM than during NREM sleep. Cyclical fluctuations in ventilation, blood pressure, and heart rate have been observed in normal subjects, and fewer than five apneas per hour sleep is considered to be normal. In patients with obstructive sleep apnea, reductions in SaO2 that occur with apneas and hypopneas are highly variable within and between individuals. Multiple variables interact to determine the severity of the episodes of oxyhemoglobin desaturation that are associated with cyclical changes in heart rate and systemic blood pressure. The magnitude of the increase in systemic pressure is related to the severity of the oxyhemoglobin desaturation, with mean elevations in systolic and diastolic pressures being on the order of 25 per cent. However, the magnitude of the systemic pressor response to oxygen desaturation varies widely between individuals. Pulmonary artery pressure often increases with sequential apneas to substantially elevated values, and this increase in combination with the large negative intrathoracic pressures generated during obstructive apneas increases ventricular afterload. Alterations in stroke volume and cardiac output in response to the dynamic events that occur with apneas have not been adequately investigated. Reductions in heart rate that occur during apneas are related to the severity of the oxyhemoglobin desaturation and the arterial chemoreceptor-mediated increase in vagal efferent activity. Marked sinus bradycardia, sinus pauses of 2 to 13 seconds' duration, second-degree heart block, and ventricular tachyarrhythmias have all been associated with severe arterial hypoxemia. Sudden death during sleep in obstructive sleep apnea presumably results from a lethal cardiac arrhythmia, but the relative contributions of severe bradyarrhythmias and ventricular tachyarrhythmias are unknown.
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PMID:Gas exchange and hemodynamics during sleep. 390 2

We studied the capacity of stroke patients to report dreams following awakening from REM sleep. Four left-hemisphere aphasia and two right-hemisphere visuospatial deficit patients reported dreams. The expression of ideas in dreams appeared normal despite the patients' waking difficulties. Given their similar rules of grammar, both dream and phonetic language modalities could emanate from common sites.
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PMID:The capacity of stroke patients to report dreams. 402 40

Non-invasive methods are described for estimating local cerebral blood flows (LCBF) and partition coefficients (L lambda) during inhalation of 35% stable xenon gas (Xes) in oxygen during CT scanning. After denitrogenation by 100% oxygen breathing, 35% Xes is breathed for 7-8 minutes to minimize subanesthetic effects. Mean changes in brain Hounsfield units extrapolated to 15 minutes were 7.7 units for white matter and 5.3 units for gray matter. They were measured from volumes 80 cubic mm (10 mm2 area x 8 mm), or larger with an EMI 1010 scanner at 1 minute intervals. These data were used for computing LCBFs and L lambdas. Irradiation measured at the center of brain slices was 1 rad per minute. To calculate L lambdas about 6 exposures are necessary, thereafter, each 1 minute scan provides LCBF measurements for 2 adjacent 8 mm slices. Reproducibility for LCBF was r = 0.85 (P less 0.001). Mean L lambdas were 0.86 +/- 0.08 for gray and 1.34 +/- 0.10 for white matter. Normative mean flows (mls/100 g brain/min) were: basal ganglia = 79.6 +/- 9.3, cortex = 82.3 +/- 8.5, white matter = 29.2 +/- 5.9, midbrain tegmentum = 94.3 +/- 14.8, cerebellar cortex = 80.1 +/- 10.9, dorsal pons = 89.3 +/- 4.7, brachium pontis = 35.0 +/- 4.2. Subject finger exercises produced increases of LCBF in contralateral pre-central and post-central gyri. Eye closure decreased flow values limited to the visual system. Gray matter flow values diffusely decreased in non-REM sleep but increased above normal in REM sleep. Cerebral infarction and hemorrhage resulted in zones of zero flow with borders having reduced lambdas and low flows attributed to edema.
Stroke
PMID:Mapping local blood flow of human brain by CT scanning during stable xenon inhalation. 697 21


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