Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with congestive heart failure (CHF) suffer from respiratory muscle weakness which may contribute to dyspnea. Nasal continuous positive airway pressure (NCPAP) can improve left ventricular ejection fraction (LVEF) and reduce dyspnea in patients with CHF and Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) but its effects on respiratory muscle strength are not known. We therefore studied the effects of NCPAP on maximal inspiratory and expiratory pressures (MIP and MEP, respectively), LVEF, dyspnea, and fatigue in patients with chronic CHF and CSR-CSA over 3 mo. Eight patients were randomized to control and nine to nightly NCPAP. There were no significant changes in any of these factors in the control group during the study. In contrast, among the NCPAP group, MIP increased from 79.3 +/- 8.1 to 90.7 +/- 10.4 cm H2O (mean +/- SEM; p < 0.02), LVEF increased from 24.0 +/- 4.0 to 32.6 +/- 6.6% (p < 0.02) and symptoms of dyspnea and fatigue were alleviated. However, MEP did not change. In addition, the number of apneas and hypopneas decreased from 49 +/- 11 to 17 +/- 7 per hour of sleep (p < 0.001) and mean low Sao2 during sleep increased from 87.9 +/- 1.0 to 93.0 +/- 1.0% (p < 0.01). Our data indicate that nightly application of NCPAP in patients with CHF and CSR-CSA improves inspiratory muscle strength and LVEF, and relieves dyspnea and fatigue.
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PMID:CPAP improves inspiratory muscle strength in patients with heart failure and central sleep apnea. 854 29

Two children complaining of sleep apnea presented with brain stem gliomas. In the early stage of their illness, neurological disorders were too subtle to be recognized as significant by the physicians or to be noted by the parents. Case 1 experienced an episode of unsteady gait and weakness in the bilateral arms, at the age of 5. When it recurred after 7 years of remission, the predominant symptom was sleep apnea. Case 2 exhibited nasality of speech as the earliest sign of this illness very early in his life, presumably 5 years before the diagnosis of brain stem glioma. A slight sleep apnea which developed afterwards did not draw attention of the physicians because no neurological signs other than paralyses of the bilateral soft palates were present. MRIs of the both cases revealed diffuse, infiltrating lesions in the pons, the medulla oblongata and the upper cervical spinal cord. Both cases shared some features: (1) diagnostic delay of several years from the first symptom; (2) the main lesion in the medulla oblongata, where important structures for respiratory control are identified; (3) infiltrative growth patterns in the MRI of the tumor, which might account for the uncommon clinical courses.
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PMID:Pediatric brain stem gliomas with the predominant symptom of sleep apnea. 888 7

Patients with obstructive sleep apnea syndrome (OSAS) present upper airway obstruction during sleep which can be documented by electromyography. The cause of weakness in oropharyngeal muscles is still unknown. Lesions of pons and medulla oblongata have to be expected. Brainstem auditory evoked potentials (BAEP) may indicate pathological changes in these regions. Several studies described normal BAEP in OSAS-patients. Moderate forms of OSAS as well as central sleep apnea syndromes were investigated, however. In our study 20 patients (17 men, 3 women, mean age 53.9 +/- 2.1 ys) with severe OSAS (apnea/hypopnea-index: 34.2 +/- 14.1/h, part of O2-saturation < or = 90% during sleep (SaO2 < or = 90%): 13.5 +/- 4.2%, minimal nocturnal O2-saturation: 78.0 +/- 2.5%) before starting nCPAP-therapy were investigated. BAEP were elicited after applying clicks 70 dB above threshold to each ear. Means of single wave latencies as well as interpeak latencies (I-V, I-III, III-V) were delayed significantly compared to normal controls. Main prolongations were seen regarding wave latency I (p < or = 0.001) and-interpeak latency I-V (p < or = 0.001). Prolongation of interpeak latencies (mean +/- 2.5 SD) of one or two sides could be demonstrated in 12 out of 20 patients. Pontomesencephal lesions (9 patients) dominated. There was no connection with respiratory parameters. As against pathological BAEP changes correlated with the duration of the disease. In conclusion pathological BAEP indicating brainstem lesions were seen in 60% of the examined OSAS-patients. Mesencephal lesions dominated, number of lesions increased with duration of disease. Therefore pathological findings have not to be considered as cause but as a result of hypoxemia in OSAS. Pathological BAEP may reveal a higher risk for cerebrovascular stroke. Therefore these patients should be leaded to further cerebrovascular investigation.
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PMID:[Acoustic evoked potentials (AEP) in obstructive sleep apnea syndrome]. 909 89

We studied 134 patients with Steinert's myotonic dystrophy (MD) in order to determine the prevalence of chronic hypercapnia, the level of muscle weakness and forced expiratory volume at which hypercapnic respiratory failure is likely to occur, and how clinical assessment might help predict hypercapnic respiratory failure. Subjects were divided into five classes with a muscular disability rating scale (MDRS): 0 = no clinical impairment (n = 9), I = minimal signs of impairment (n = 11), II = distal weakness (n = 41), III = moderate proximal weakness (n = 62), and IV = nonambulatory (n = 11). The prevalence of hypercapnia (PaCO2 > or = 43 mm Hg) was found to be 0%, 27%, 29%, 45% and 55% for MDRS 0 to 4, respectively (p = 0.03). A multiple regression analysis limited to clinical data showed that daytime hypersomnolence was a significant cofactor with the MDRS (p = 0.01) in predicting PaCO2 (r = 0.40). Among respiratory parameters, FVC, respiratory muscle strength (RMS), and maximal inspiratory pressure against occluded airways (PImax) were found to be predictors of nearly equal strength, explaining 16%, 15%, and 14% of the PaCO2 variance, respectively. In multiple regression analysis, sex, daytime sleepiness, and the expected/observed FVC ratio for a given RMS were found to be significant cofactors with PImax in predicting PaCO2 (r = 0.51). It is concluded that respiratory insufficiency should be suspected in MD patients with proximal weakness or daytime sleepiness. The likelihood of hypercapnia also increases with volume restriction and respiratory muscle weakness. Our study suggests that the combination of inspiratory muscle weakness and loading plays a predominant role in the pathogenesis of chronic alveolar hypoventilation in MD patients. The occurrence of daytime hypersomnolence suggests that other factors, such as low central ventilatory drive or sleep apnea, might play an additional role.
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PMID:Relationship between chronic hypercapnia and inspiratory-muscle weakness in myotonic dystrophy. 923 Jul 37

The paper concerns surgical treatment of rhonchus. 41 patients with rhonchus and sleep apnea were examined and treated. The patients were characterized by obesity, short fat neck, diseases of the upper respiratory tracts (chronic tonsillitis, adenoids, distortion of the nasal septum, deformity of the external nose, weakness of the palatine curtain). After cleansing of the upper respiratory tracts and recovery of nasal breathing all the patients underwent CO2 laser surgery on the soft palate with good effect.
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PMID:[On aspects of surgical treatment of pathological snoring]. 979 29

The aim of the study was to assess the clinical picture of patients with sleep apnea syndrome (SAS). The study group consisted of 54 patients (51 men, 3 women) mean age 49.7 +/- 8.7 years, mean body mass index (BMI) 33.1 +/- 5.8. In all cases polisomnography confirmed the diagnosis of SAS. Mean apnea and hypopnea index (AHI) was 66.6 +/- 30.7 and mean minimum arterial blood oxygen saturation was 67.57 +/- 11.58%. It allowed us to qualify 69.4% of patients to the group with a severe SAS. Snoring (93%), apneas (83%), excessive daytime sleepiness (80%), morning weakness (81%), nycturia (66%) were the most common symptoms. The most frequently accompanying diseases in patients with SAS were overweight (89%), depression (67%), arterial hypertension (51%), impaired glucose tolerance (41%).
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PMID:[Clinical picture in sleep apnea syndrome]. 1054 May 85

Patients with developmental disorders, including adolescents, comprise a large and heterogeneous group of individuals who vary in underlying diagnosis and degree of disability. The largest numbers of patients are those with cerebral palsy and with traumatic brain injury. While these conditions themselves do not directly cause airway or parenchymal lung dysfunction, consequences of neuromuscular dysfunction, especially aspiration and ineffective cough, may lead to lung damage. Poor nutritional status, impairment of airway clearance by muscular weakness or incoordination and poor pulmonary reserve (due to chest wall or spine deformity) increase the risk of significant morbidity and mortality from respiratory infections. Individuals who were premature infants or who had prolonged neonatal courses may also have residual chronic lung disease (bronchopulmonary dysplasia) contributing to their pulmonary problems. This review discusses conditions that have adverse effects on the airway and lung (drooling, feeding problems, gastroesophageal reflux, aspiration, spasticity, scoliosis) and some of the consequences of these insults (disordered airway clearance, pneumonia, sleep apnea). Also discussed are issues important to the prevention or amelioration of respiratory difficulties, including preventive care, the effects of exercise, dental hygiene, and surgical intervention.
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PMID:Respiratory problems in the adolescent with developmental delay. 1106 May 58

A hemimedullary infarction, in which both medial and lateral medullary infarctions occur simultaneously, is a rare cerebrovascular disease. Pontomedullary lesions often cause central respiratory failure, and the majority of central respiratory failures are due to bilateral pontomedullary lesions. We report a 66-year-old man with central respiratory failure due to a hemimedullary infarction detected by magnetic resonance imaging. He was admitted to our hospital on March 7, 1998, because of a sudden onset of dysarthria, and both numbness and weakness on his left side. Soon after arriving at the hospital, his spontaneous respiration ceased. Therefore, he was intubated and artificial ventilation was started. Pertinent neurological abnormalities on admission consisted of dysarthria, dysphagia, right Horner's sign, right gaze evoked horizontal nystagmus, right soft palate palsy, and tongue deviation to the right. In addition, left hemiparesis, left Babinski's sign, sensory impairment on the left side including the face, and central respiratory failure were noted. Although voluntary respiration recovered in 12 days, sleep apnea continued for 5 months, which was considered to be due to the automatic respiratory failure. An important feature of this patient was that the hemimedullary infarction caused the central respiratory failure. To our knowledge, this is the third patient whose central respiratory failure occurred because of a hemimedullary infarction.
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PMID:[A case report of central respiratory failure due to hemimedullary syndrome]. 1118 17

A 49-year-old woman with 6 months history of body weight loss, muscle weakness, and dysarthria, was found with respiratory arrest and resuscitated in the morning of January 1999. An MRI brain scan revealed diffuse swelling and T2/FLAIR high signal intensity with mild Gadolinium enhancement in the lower pons and medulla oblongata. Although the histological diagnosis could not be obtained, glioma (astrocytoma) was suspected. In the morning of July 3rd she presented sweating and cyanosis. Her arterial oxygen saturation was 18%. When we asked her to breathe more, she kept breathing and oxygen saturation was normalized. However, she could not breathe at all when she fell asleep without stimulation. She was kept under respiratory support for 2 months. Her symptoms improved with fluctuating course after 70 Gy of radiation therapy. Ondine curse is one type of sleep apnea syndrome, defined as the selective disturbance of autonomous breathing. Surgical operation and stroke are the reported causes of this syndrome. Brainstem tumor is relatively common cause for children's Ondine curse. On the other hand, it rarely causes adult's Ondine curse as a main symptom.
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PMID:[A case of Ondine curse associated with a medullary tumor]. 1121 2

A sleep apnea syndrome is described by several studies in patients with myasthenia gravis. Apnea and hypopnea are mainly not obstructive and occur predominantly in rapid eye movement (REM) sleep. They are associated with oxygen desaturation. Although the sleep apnea index is not correlated with myasthenia gravis severity, it becomes less important as myasthenia gravis improves. Risk factors for the development of sleep apnea in myasthenia gravis patients are age, restrictive pulmonary syndrome, diaphragmatic weakness and daytime alveolar hypoventilation. Sleep apnea are not related to a central cholinergic effect in myasthenia gravis caused either by anticholinesterase used to treat myasthenia gravis or by antibodies to muscle acetylcholine receptors. Indeed acetylcholine receptors in brain are antigenically distinct from acetylcholine receptors in skeletal muscle. Sleep apneas are more likely caused by peripheral mechanisms. Correlation between sleep apnea and total lung capacity as well as the importance of diaphragmatic weakness in myasthenic patients may explain their predominance in REM sleep and their reduction with clinical improvement in the myasthenia gravis.
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PMID:[Respiratory disorders during sleep and myasthenia]. 1192 28


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