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

Changes in central respiratory disorders under the effect of hyperbaric oxygenation (HBO) were studied in 29 patients in the acute stage of ischemic stroke. Spirography, tetrapolar rheography, and examination of the blood gas composition were carried out. Before HBO was begun, various disorders of the respiratory function were found (hyperventilation syndrome, periodical rhythms: Cheyne-Stokes respiration, alternating respiration, etc.). It was revealed that HBO session causes a normalizing effect on the respiratory function in central disorders of respiration: the Cheyne-Stokes rhythm was replaced at the end of the session by wave-like respiration which is biologically more adequate, the regimen of hyperventilation changed to normoventilation, etc. There was parallel improvement in the indices of central hemodynamics and the blood gas composition.
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PMID:[Potentials of hyperbaric oxygenation in correcting central respiratory disorders in ischemic stroke]. 46 32

Cyclically fluctuating intracranial pressure (ICP) with periodic breathing was first described by Nils Lundberg in 1960. While Cheyne-Stokes respiration (CSR) frequently accompanies severe cerebrovascular accidents, it is not commonly appreciated that cycles of severe intracranial hypertension can complicate this abnormal ventilation pattern. We recently treated a patient with a hemorrhagic stroke in whom episodes of elevated ICP were synchronously associated with CSR.
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PMID:Fluctuating intracranial hypertension due to Cheyne-Stokes respiration. 55 16

Respiratory rates and patterns were studied in 23 patients with acute brain stem infarction using impedance pneumography. Autopsy was obtained in six of eight fatal cases. Pontine lesions were present in all patients, with coexistent infarction of midbrain in four and of medulla in nine. Respiratory rate and pattern abnormalities observed included Cheyne-Stokes respiration, Cheynb-Stokes variant pattern and tachypnea. Abnormalities of respiratory rate and pattern of varying duration were observed at some time in all patients. All patients in whom prominent Cheyne-Stokes respiration or tachypnea were observed had extensive bilateral pontine lesions involving both basal and tegmental portions. However, not all patients with large pontine infarcts had Cheyne-Stokes respiration or tachypnea. Cheyne-Stokes respiration was prominent in four patients (two fatal, two nonfatal). Cheyne-Stokes variant pattern was present frequently in four patients (one fatal, three nonfatal). Sustained tachypnea developed in five patients, four of whom died. In ten patients (one fatal, nine nonfatal), normal respiratory rate and pattern predominated with only rare or occasional apperance of Cheyne-Stokes respiration or Cheyne-Stokes variant pattern, especially during sleep. The types of respiratory rate and pattern abnormalities in acute brain stem infarction were not specifically related to the level of lesions, but rather to the size and bilaterality of the lesions. Respiratory alkalosis was present in varying degrees in most patients with either tachypnea or prominent CSR.
Stroke
PMID:Respiratory rate and pattern disturbances in acute brain stem infarction. 96 Jan 58

We report a case of familial antithrombin III (AT-III) abnormality accompanied with progressing ischemic stroke. The patient was a 31-year-old female who developed consciousness disturbance and left hemiparesis on December 1 in 1987. She had a history of two transient ischemic attacks and three episodes of thrombophlebitis of the extremities. Cerebral CT scan showed a low density area on the right temporal lobe that had extended to the right parietal and on the left frontal lobe as clinical symptoms worsened. Cerebral angiogram revealed branch occlusions of the right middle cerebral artery and showed no cerebral venous and sinus obstruction. When her symptoms had been progressing to show semi-comatose state, left hemiplegia and transient Cheyne-Stokes respiration, we found her decreased biological activity and normal immunological level of AT-III. The diagnosis of familial AT-III abnormality had been made by familial investigation. As the treatment of AT-III concentrates transfusion was started from the third day, her symptoms gradually recovered and the low density area stopped extending. Further examinations revealed that she was a homozygote of AT-III abnormality presenting no affinity for heparin and that her parents were heterozygotes. It was suggested that the homozygous AT-III abnormality was the main cause of her progressing ischemic stroke.
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PMID:[Familial antithrombin III abnormality accompanied with progressing ischemic stroke]. 269 32

For the purpose of elucidating the mechanisms and/or effects of the cardiovascular changes occurring during Cheyne-Stokes respiration, we utilized Doppler echocardiography to determine intracardiac flow velocity profiles during the changing phases. Left ventricular inflow (LVI) and outflow (LVO) were examined in ten patients, nine with heart failure and one with a cerebrovascular accident. The mean LVI, peak early (E) and late diastolic (A) and LVO velocities were measured at the end of both the hyperpneic and apneic phases. The phasic hemodynamic changes observed during Cheyne-Stokes respiration by Doppler profile could be explained by the development of LV diastolic dysfunction and a decrease in LV stroke volume during the apneic phase of Cheyne-Stokes respiration. Alternatively, an increase in PCO2 during the apneic phase may increase pulmonary vascular resistance lowering preload and stroke volume, whereas during the hyperpneic phase, pulmonary vascular resistance is reduced with resultant increase in left ventricular preload and increase in stroke volume. Both theories are speculative and the precise hemodynamic changes associated with Cheyne-Stokes respiration requires further investigation.
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PMID:Doppler evaluation of changing cardiac dynamics during Cheyne-Stokes respiration. 230 87

We monitored breathing pattern and arterial oxygen saturation in 32 conscious patients with acute ischemic stroke. Seventeen (53%) had Cheyne-Stokes respiration with concomitant drops in oxygen saturation, unrelated to infarct location. The ventilatory disturbance promptly reversed after intravenous theophylline ethylenediamine or oxygen inhalation. The therapy is a simple way of improving arterial oxygenation in a large subgroup of patients with acute ischemic stroke.
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PMID:Cheyne-Stokes respiration in ischemic stroke. 772 77

Because cardiovascular disorders and stroke may induce Cheyne-Stokes respiration, our purpose was to study the interaction among cerebral activity, cerebral circulation, blood pressure, and blood gases during Cheyne-Stokes respiration. Ten patients with heart failure or a previous stroke were investigated during Cheyne-Stokes respiration with recordings of daytime polysomnography, cerebral blood flow velocity, intra-arterial blood pressure, and intra-arterial oxygen saturation with and without oxygen administration. There were simultaneous changes in wakefulness, cerebral blood flow velocity, and respiration with accompanying changes in blood pressure and heart rate approximately 10 s later. Cerebral blood flow velocity, blood pressure, and heart rate had a minimum occurrence in apnea and a maximum occurrence during hyperpnea. The apnea-induced oxygen desaturations were diminished during oxygen administration, but the hemodynamic alterations persisted. Oxygen desaturations were more severe and occurred earlier according to intra-arterial measurements than with finger oximetry. It is not possible to explain Cheyne-Stokes respiration by alterations in blood gases and circulatory time alone. Cheyne-Stokes respiration may be characterized as a state of phase-linked cyclic changes in cerebral, respiratory, and cardiovascular functions probably generated by variations in central nervous activity.
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PMID:Hemodynamics, cerebral circulation, and oxygen saturation in Cheyne-Stokes respiration. 933 27

To investigate the prevalence and behavior of sleep-related breathing disorders (SRBDs) associated with a first-ever stroke or transient ischemic attack (TIA), we prospectively studied 161 consecutive patients admitted to our stroke unit. Complete neurological assessment was performed to determine parenchymatous and vascular localization of the neurological lesion. Stroke subtype was categorized as TIA, ischemic (IS), or hemorrhagic (HS). A portable respiratory recording (PRR) study was performed within 48-72 h after admission (acute phase), and subsequently after 3 mo (stable phase). During the acute phase, 116 patients (71.4%) had an apnea-hypopnea index (AHI) > 10 events/h and 45 (28%) had an AHI > 30. No relationships were found between sleep-related respiratory events and the topographical parenchymatous location of the neurological lesion or vascular involvement. Cheyne-Stokes breathing (CSB) was observed in 42 cases (26.1%). There were no significant differences in SRBD according to the stroke subtype except for the central apnea index (CAI). During the stable phase a second PRR was performed in 86 patients: 53 of 86 had an AHI > 10 and 17 of 86 had an AHI > 30. The AHI and CAI were significantly lower than those in the acute phase (16.9 +/- 13.8 versus 22.4 +/- 17.3 and 3.3 +/- 7.6 versus 6.2 +/- 10.2, respectively) (p < 0.05) while the obstructive apnea index (OAI) remained unchanged. CSB was observed in 6 of 86 patients. The prevalence of SRBD in patients with first-ever stroke or TIA is higher than expected from the available epidemiological data in our country. No correlation was found between neurological location and the presence or type of SRBD. Obstructive events seem to be a condition prior to the neurological disease whereas central events and CSB could be its consequence.
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PMID:Time course of sleep-related breathing disorders in first-ever stroke or transient ischemic attack. 1067 74

Obstructive sleep apnoeas are common among stroke patients and, as different from central apnoeas, they do not decline during stroke rehabilitation. Cerebral and cardiovascular changes display a different pattern during central and obstructive sleep apnoeas. The cerebral blood flow velocity according to transcranial Doppler increases during an obstructive apnoea and decreases after apnoea termination concomitant with changes in arterial pressure. The changes in cerebral circulation during obstructive apnoeas could be an immediate effect of rapid changes in blood pressure because cerebral autoregulation is overridden. Low cerebral blood flow, low arterial pressure and hypoxemia after apnoea termination may predispose to nocturnal cerebral ischaemia. The opposite pattern is seen during a central apnoea, with a decrease in cerebral blood flow velocity during apnoea and an increase after apnoea termination. Changes during obstructive apnoeas are probably hazardous, with adverse cardiovascular effects including stroke. This may not be the case during central apnoeas, as Cheyne-Stokes respiration with central apnoeas is a result of an underlying disorder such as heart failure and stroke and is not a disease entity in itself. It is suggested that obstructive sleep apnoea is a risk factor for stroke as it is common among stroke victims and cerebral hypoperfusion occurs after an obstructive apnoea. The treatment of sleep apnoea should also be taken into account among stroke patients. Large cohort studies, treatment studies and further studies of possible mechanisms for apnoea-induced stroke are, however, essential in order to evaluate whether obstructive sleep apnoea is an independent risk factor for stroke.
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PMID:Cerebral haemodynamics in obstructive sleep apnoea and Cheyne-Stokes respiration. 1250 76

Sleep-disordered breathing (SDB) and sleep-wake disturbances (SWD) are frequent in stroke patients. They deserve attention, because they may significantly influence rehabilitation process and functional outcome. In addition, SDB may increase the risk of stroke recurrence. More than 50% of stroke patients have SDB, mostly obstructive sleep apnea (OSA). In some patients, stroke recovery is accompanied by an improvement of SDB. The treatment of choice for OSA is continuous positive airway pressure. Oxygen, theophylline, and other forms of ventilation may be helpful in patients with other forms of SDB (eg, Cheyne-Stokes breathing). In at least 20% to 40% of stroke patients, SWD are present, mainly in form of increased sleep needs (hypersomnia), excessive daytime sleepiness, or insomnia. Depression, anxiety, SDB, stroke complications (eg, nocturia, dysphagia, and urinary or respiratory infections), and drugs may contribute to SWD and should be addressed first. In patients with SWD of primary neurologic origin, treatment with stimulants or dopaminergic drugs and hypnotics or sedating antidepressants, respectively, can be attempted.
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PMID:Sleep Apnea and Other Sleep-Wake Disorders in Stroke. 1267 Apr 13


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