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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The family physician's holistic approach to patients forms the basis of good health care for adults with Down syndrome. Patients with Down syndrome are likely to have a variety of illnesses, including thyroid disease, diabetes, depression, obsessive-compulsive disorder, hearing loss, atlantoaxial subluxation and Alzheimer's disease. In addition to routine health screening, patients with Down syndrome should be screened for sleep apnea, hypothyroidism, signs and symptoms of spinal cord compression and dementia. Patients with Down syndrome may have an unusual presentation of an ordinary illness or condition, and behavior changes or a loss of function may be the only indication of medical illnesses. Plans for long-term living arrangements, estate planning and custody arrangements should be discussed with the parents or guardians. Because of improvements in health care and better education, and because more people with this condition are being raised at home, most adults with Down syndrome can expect to function well enough to live in a group home and hold a meaningful job.
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PMID:Health care management of adults with Down syndrome. 1157 24

Alzheimer's disease (AD) is acknowledged to be at least partially genetic, and one of the key genotypic markers for this condition is the APOE4 allele. Links between sleep apnea and AD have long been suspected because of mental impairment seen in some sleep apnea patients and possible evidence suggesting higher rates of sleep apnea in some dementia patients. The recent demonstration of an association between the APOE4 genotype and sleep apnea has rekindled further interest in this topic, particularly because sleep apnea is characterized by multiple genetic vulnerabilities. We review here evidence related to associations between sleep apnea and dementia, the role of APOE4 as a likely marker for cerebrovascular disease, and discuss treatment considerations relevant to sleep apnea as a potentially reversible cause of dementia.
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PMID:Sleep apnea, APOE4 and Alzheimer's disease 20 years and counting? 1212 69

Often ignored, neurocognitive dysfunction in chronic heart failure represents a daunting morbidity progressing to loss of self-reliance. Although the precise mechanisms arbitrating the development of this disorder remain elusive, microembolization and cerebral hypoperfusion are implicated. Other causes of cognitive decline may include prior cardiac surgery, chronic hypertension, sleep disordered breathing, hyperhomocysteinemia, dementia of aging, and more traditional causes such as Alzheimer's disease. The discovery of neurocognitive defects in heart failure must prompt a well-constructed diagnostic evaluation to search for the underlying causes since this process may be at least partially reversible in many cases.
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PMID:Difficult cases in heart failure: the challenge of neurocognitive dysfunction in severe heart failure. 1214 48

Down syndrome (DS) is an autosomal chromosomal anomaly which results from trisomy of all or part of chromosome 21. It is the single most common genetic cause of mental retardation affecting approximately 1 in 700 live births. Since its first description in 1866 by John Langdon Down, much research has focused on this condition. In the past two decades there has been a significant increase in information about its causes, diagnosis and medical and dental consequences. In this, the first of two articles, we pay tribute to the work of Harvey Brown, and we review the pathogenesis, general and cranio-dental features of Down Syndrome. The cause of DS is usually non-dysjunctive trisomy 21, with 91 percent of cases being maternally derived. Uncommon causes are mosaicism or translocation from other chromosomes. DS patients suffer from congenital cardiopathies, growth retardation, endocrinopathies, sleep apnoea, neoplasias and early-onset Alzheimer's disease. Typically, craniofacial features include midfacial hypoplasia with a resultant flattened face, ocular hypotelorism and mandibular prognathism. The universal characteristic of the DS face is the upward slanting of the palpebral fissures and epicanthic folds. Dental features include tooth size reduction, hypodontia, reduced root lengths, changes in tooth shape and excessive tooth wear.
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PMID:The Down syndrome patient in dental practice, part I: Pathogenesis and general and dental features. 1533 Mar 83

The angiotensin-converting enzyme (ACE) gene insertion/deletion polymorphism influences ACE activity, cardiovascular risk, blood pressure, and possibly the risk of developing Alzheimer's dementia. We explored the association of the insertion/deletion polymorphism with sleep-disordered breathing (SDB) and hypertension in 1,100 subjects of the Wisconsin Sleep Cohort. The polymorphism did not influence body mass index or the occurrence of SDB, but was dose-dependently associated with blood pressure. Interestingly, SDB and the insertion/deletion polymorphism interacted significantly to modulate blood pressure independently of age, sex, ethnicity, and body mass index. Most specifically, the association of the deletion allele with hypertension was most pronounced in subjects with mild to moderate degrees of sleep apnea (5 < or = apnea-hypopnea index < or = 30). We hypothesize that in the absence of SDB the effect of the deletion allele alone may not be sufficient to increase blood pressure. At severe levels of SDB, the effect of sleep apnea on blood pressure overwhelms any association of the deletion allele with hypertension and occurs independent of any ACE gene genotype.
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PMID:Angiotensin-converting enzyme, sleep-disordered breathing, and hypertension. 1544 44

Some piperidine-based nocaine/modafinil hybrid ligands have been designed, synthesized, and found to display an improved potency at all three monoamine transporters and particularly for DAT and/or NET. Some highly active and selective monoamine transporter inhibitors with low nanomolar to subnanomolar potency were identified. Ligands of this type may find important applications as positron emission tomography imaging tools and in the treatment of central nervous system disorders such as depression and sleep apnea.
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PMID:Piperidine-based nocaine/modafinil hybrid ligands as highly potent monoamine transporter inhibitors: efficient drug discovery by rational lead hybridization. 1553 37

Significant progress in the field of VaD resulted from publication of the NINIDS-AIREN Diagnostic Criteria for VaD (G.C. Roman, T.K. Tatemichi, T. Erkinjuntti, et al., Vascular dementia (VaD): diagnostic criteria for research studies. Report of the NINDS-AIREN International Workshop. Neurology 43 (1993) 250-260). Epidemiological studies confirmed the importance of VaD as the second most common cause of dementia in the elderly, representing 15-20% of all cases of dementia. In Europe and North America, Alzheimer's disease (AD) predominates over VaD in a 2:1 ratio; in contrast, in Japan and China VaD accounts for almost 50% of all dementias. Case-control studies have identified risk factors for VaD including ageing, hypertension, diabetes mellitus, hyperlipidemia, recurrent stroke, cardiac disease, smoking, sleep apnea, and more recently, hyperhomocysteinemia, among others. Hypertension treatment may prevent VaD and AD. This finding has enormous importance from the Public Health viewpoint to decrease the future number of patients with dementia in the elderly. Along with advances in the field of VaD came a number of controversies and damaging misconceptions and myths. Myth no. 1--Vascular dementia is a non-entity: The false idea that VaD does not exist is particularly destructive because it creates the perspective that VaD is unworthy of study or research. A condition that either does not exist or represents only a minute proportion of all cases of dementia in the elderly, lacks public health relevance and becomes a low priority for research by funding agencies and industry. In fact, vascular brain lesions are the commonest and most important component of dementia in the elderly. Myth no. 2--Vascular dementia is so difficult to diagnose that only experts can recognize and identify it accurately: VaD does exist and the diagnosis of post-stroke VaD, in particular is straightforward. Most cases fulfill NINDS-AIREN criteria for probable VaD; i.e., (1) there is acute onset of dementia demonstrated by impairment of memory and two other cognitive domains, such as orientation, praxis or executive dysfunction; (2) relevant cerebrovascular lesions are demonstrated by neuroimaging; and (3) a temporal relation between stroke and cognitive loss is evident. In the donepezil trials on VaD, post-stroke dementia represented about 75% of the >1,200 patients enrolled. Myth no. 3--Improvement in clinical trials of cholinergics in VaD is due to underlying AD, not to the vascular lesions. Experimental, clinical and pathological evidence has demonstrated cholinesterase deficits in VaD (independently of any concomitant AD pathology), including low acetylcholine in cerebrospinal fluid, and reduced choline acetyltransferase (ChAT) in the brain.
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PMID:Facts, myths, and controversies in vascular dementia. 1553 19

Ischemic or hemorrhagic cerebrovascular disease (CVD) produces injury of brain regions important for executive function, behavior, and memory leading to decline in cognitive functions and vascular dementia (VaD). Cardiovascular disease may cause VaD from hypoperfusion of susceptible brain areas. CVD may worsen degenerative dementias such as Alzheimer disease (AD). Currently, the global diagnostic category for cognitive impairment of vascular origin is vascular cognitive disorder (VCD). VCD ranges from vascular cognitive impairment (VCI) to VaD. The term VCI is limited to cases of cognitive impairment of vascular etiology, without dementia; VCI is equivalent to vascular mild cognitive impairment (MCI). Risk factors for VaD include age, hypertension, diabetes, smoking, cardiovascular disease (coronary heart disease, congestive heart failure, peripheral vascular disease), atrial fibrillation, left ventricular hypertrophy, hyperhomocysteinemia, orthostatic hypotension, cardiac arrhythmias, hyperfibrinogenemia, sleep apnea, infection, and high C-reactive protein. Research on biomarkers revealed increased CSF-NFL levels in VaD, whereas CSF-tau was normal. CSF-TNF-alpha, VEGF, and TGF-beta were increased in both AD and VaD. VaD shows low CSF acetylcholinesterase levels. This condition responds to acetylcholinesterase inhibitors, confirming the central role of cholinergic deficit in its pathogenesis. Evidence strongly suggests that control of vascular risk factors, in particular hypertension, could prevent VaD.
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PMID:Vascular dementia. Advances in nosology, diagnosis, treatment and prevention. 1587 77

Brain injury from ischemic or hemorrhagic cerebrovascular disease (CVD) produces decline in cognitive functions and vascular dementia (VaD). Likewise, CVD may cause VaD from hypoperfusion of susceptible brain areas. CVD may also worsen degenerative dementias such as Alzheimer's disease. Significant advances have been made in the identification and control of risk factors for stroke and cardiovascular disease. The main risk factors for VaD include age, hypertension and absence of antihypertensive medication, diabetes, cigarette smoking, history of cardiovascular disease (coronary heart disease, congestive heart failure, peripheral vascular disease), atrial fibrillation, left ventricular hypertrophy, hyperhomocysteinemia, orthostatic hypotension, cardiac arrhythmias, hyperfibrinogenemia, and sleep apnea. Recently identified risk factors include chronic infection and elevation of C-reactive protein, particularly in patients with diabetes. Evidence from controlled clinical trials strongly suggests that control of vascular risk factors, in particular hypertension, could prevent the development of dementia.
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PMID:Vascular dementia prevention: a risk factor analysis. 1632 58

Daytime sleepiness and sleep disordered breathing are increased in older compared to middle-aged adults. The cognitive and cardiovascular sequelae associated with obstructive sleep apnea (OSA) have significant implications for the older adult who may already be suffering from chronic illness. Most of the evidence supporting the utilization of continuous positive airway pressure (CPAP) for the treatment of OSA has been generated from studies employing samples consisting predominately of middle-aged adults. To examine the efficacy of CPAP for the treatment of obstructive sleep apnea in older adults with an emphasis on adherence and related treatment outcomes, this paper reviews findings from clinical trials including older individuals as well as those specifically targeting this population. These studies have demonstrated that following CPAP therapy, older adults have increased alertness, improved neurobehavioral outcomes in cognitive processing, memory, and executive function, decreased sleep disruption from nocturia and a positive effect on factors affecting cardiac function, including vascular resistance, platelet coagulability and other aspects of cardiovascular health. Physiological differences in respiratory structure and function between younger and older adults of similar disease severity are believed to result in older individuals requiring titration at lower CPAP levels. Once initiated, CPAP treatment is tolerated by older adults, including those with Alzheimer's disease. Patterns of adherence in older individuals are consistent with that of middle-aged adults.
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PMID:Continuous positive airway pressure treatment for sleep apnea in older adults. 1727 70


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