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1/6. Case control study of cerebrovascular damage defined by magnetic resonance imaging in patients with OSA and normal matched control subjects.

    STUDY OBJECTIVES: To assess whether MRI detectable evidence of silent cerebrovascular disease is more prevalent in patients with obstructive sleep apnea (OSA) when compared to carefully matched control subjects. DESIGN AND SETTING: Case-control study of patients with OSA attending a specialist sleep clinic and matched control subjects drawn from the normal community. PARTICIPANTS: Forty-five sleep clinic patients with moderate to severe OSA and excessive daytime sleepiness, matched to 45 control subjects without excessive sleepiness or evidence of OSA on a sleep study. Matched variables included age, body mass index (BMI), alcohol and cigarette consumption, treated hypertension, and ischaemic heart disease. INTERVENTIONS: N/A MEASUREMENTS AND RESULTS: All subjects underwent 24-hour ambulatory blood pressure recordings (before treatment in OSA patients) and sagittal T1, axial T2, and coronal dual echo cerebral MRI imaging to detect clinically silent abnormalities related to hypertensive cerebrovascular disease; areas of high signal foci in deep white matter (DWM), lacunae, and periventricular hyperintensity. Lacunae/high signal foci in DWM and/or periventricular hyperintensity were present in 15 (33%) OSA subjects and 16 (35%) controls, despite significant increases in mean daytime diastolic blood pressure (4.6mmHg, p<0.05), and both nighttime diastolic (7.2mmHg, p<0.001) and systolic blood pressures (9.2mmHg, p<0.05) in OSA subjects. These data exclude more than a 17% excess prevalence of MRI detected minor cerebrovascular disease in the OSA patients, with 95% confidence. CONCLUSIONS: Sub-clinical cerebrovascular disease is prevalent in both clinic patients with OSA and their matched control subjects. Despite the increased arterial blood pressures, there is, however, no apparent excess of MRI-evident subclinical cerebrovascular disease in patients with OSA compared to appropriately matched control subjects.
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2/6. Excessive daytime sleepiness and levodopa in Parkinson's disease: polygraphic, placebo-controlled monitoring.

    The authors performed 72-hour polysomnography, including a levodopa-placebo-controlled choice reaction time test with continuous monitoring of cardiovascular variables in two patients with Parkinson's disease complaining of excessive daytime sleepiness on levodopa monotherapy. The subacute levodopa challenge was accompanied by physiologic sleep episodes, worsened reaction times, and a reduction in mean blood pressure and heart rate over baseline values, linked temporally to the sleep episodes.
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3/6. Maxillomandibular expansion for the treatment of sleep-disordered breathing: preliminary result.

    OBJECTIVE: To assess the outcomes of maxillomandibular expansion (MME) by distraction osteogenesis (DO) for the treatment of sleep-disordered breathing (SDB). methods: This was a prospective study of six consecutive patients with SDB. All of the patients have maxillary and mandibular constriction and were treated with MME. Variables examined include age, sex, body mass index (BMI), polysomnographic results (PSG), Epworth Sleepiness Scale (ESS), and the extent of the widening of the maxilla and mandible. RESULTS: All six patients (4 males) completed MME for the treatment of SDB. The mean age was 22.2 /- 11.4 years. The mean maxillary expansion was 10.3 /- 3.0 mm, and the mean mandibular expansion was 9.5 /- 2.9 mm. ESS improved from 10.2 /- 1.9 to 5 /- 2.9. The mean apnea/ hypopnea index (AHI) improved from 13.2 /- 15.6 to 4.5 /- 5.8 events per hour, and the mean lowest oxygen saturation (LSAT) improved from 88.2 /- 2.9% to 91.3 /- 3.3%. The mean esophageal pressure improved from -20 /- 11.3 cm H2O to -8 /- 3.6 cm H2O. No complications were encountered, and the follow-up period was 18.1 /- 9.8 months. CONCLUSION:: The result suggests that MME improves SDB in patients with maxillary and mandibular constriction and can be a valid treatment.
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4/6. slit ventricle syndrome presenting with paroxysmal hypersomnia in an adult: case report.

    The slit ventricle syndrome (SVS), defined as intermittent shunt malfunction without substantial ventricular enlargement, is usually observed in shunted children with small, slitlike ventricles. This syndrome has been attributed to recurrent obstruction of the ventricular catheter, which then causes an increase of intracranial pressure. Only rarely has the SVS been reported in adults. We describe a 29-year-old woman whose shunt malfunction presented with long-lasting paroxysmal hypersomnia and was diagnosed with computed tomographic evidence of small lateral ventricles. This episodic hypersomnia presented every 2 to 3 weeks and each episode lasted 1 to 2 weeks. After revision of the ventricular catheter, her symptoms stopped and she remained well.
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5/6. Hypersomnolence with beta-adrenergic blockers.

    An elderly, mildly demented, hypertensive male patient developed hypersomnolence on administration of propranolol for treatment of hypertension; no other cause for hypersomnolence was detected. Upon replacement of propranolol with atenolol, he felt better but continued to be quite somnolent. When atenolol was discontinued, he reported to have lack of sleep. On readministration of subtherapeutic doses of the same beta-adrenergic blocking agents, he once again experienced excessive sleepiness. By discontinuing beta-blocking agents and introducing captopril, he felt much better, became pleasant and talkative, and blood pressure was well controlled. Beta antagonists are important drugs in the management of many cardiovascular problems. propranolol, a lipophilic beta-blocking agent, and atenolol, a hydrophilic beta-blocking agent, are two of the major agents currently used clinically in the united states. Numerous neuropsychiatric side-effects of the beta-adrenergic blocking drugs have been reported, but hypersomnolence is not readily recognized as one of them.
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6/6. Deficient blood pressure regulation in a case of hypersomnia with sleep drunkenness.

    In a 43-year-old man suffering from hypersomnia with sleep drunkenness, a polygraphic sleep study with direct measurement of blood pressure was carried out. The main findings were lack of blood pressure activation with arousals during the sleep period and persistence of sleep levels after morning awakening. This indicates that cardio-vascular responses to the needs of active behaviour are insufficient. Taking into account feedback mechanisms of blood pressure on alertness, this could be a cause for sleep drunkenness and daytime sleepiness. The blood pressure sustaining drug etilefrine seems to alleviate these symptoms.
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