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)

Hereditary motor and sensory neuropathy (Charcot-Marie-Tooth disease) is characterized by chronic degeneration of peripheral nerves and roots, resulting in distal muscle atrophy, beginning in the feet and legs and later involving the hands. The association of this disease with diaphragmatic dysfunction has not been reported. We studied a patient with hereditary motor and sensory neuropathy type 1 (Charcot-Marie-Tooth disease) and type 2 diabetes mellitus who had severe diaphragmatic impairment. Some of the clinical findings are similar to the sleep apnea syndrome, which could lead to incorrect diagnosis and delay in the administration of appropriate therapy. Transdiaphragmatic pressure studies on the subject's brother, who also has Charcot-Marie-Tooth disease and type 2 diabetes mellitus, revealed subclinical impairment of diaphragmatic function. These findings suggest that phrenic nerve involvement may be part of the spectrum of polyneuropathy in Charcot-Marie-Tooth disease in association with diabetes mellitus.
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PMID:Diaphragmatic dysfunction in siblings with hereditary motor and sensory neuropathy (Charcot-Marie-Tooth disease). 382 50

Chronic hypoxaemia in chronic obstructive pulmonary disease is a well known risk factor for polyneuropathy but the impact of intermittent hypoxaemia on peripheral nerve function has not been established so far. A case-control study was performed to evaluate the prevalence of polyneuropathy in obstructive sleep apnoea (OSA). Out of 24 patients with OSA, 17 (71%) had clinical signs of polyneuropathy versus seven (33%) out of 21 matched controls. The mean amplitude of the sural sensory nerve action potential was smaller in the OSA group than in the control group, indicating axonal nerve damage. The differences were significant and could not be attributed to other known risk factors for polyneuropathy. The severity of axonal damage in patients with OSA correlated with the percentage of the night time with an O(2) saturation below 90%. It is assumed that recurrent intermittent hypoxaemia in OSA is an independent risk factor for axonal damage of peripheral nerves.
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PMID:Axonal polyneuropathy in obstructive sleep apnoea. 1130 69

Severe obesity is associated with multiple comorbidities and is refractory to dietary management with or without behavioral or drug therapies. There are a number of surgical procedures for the treatment of morbid obesity, including purely gastric restrictive, a combination of malabsorption and gastric restriction or primary malabsorption. The purely gastric restrictive procedures, including vertical banded gastroplasty and laparoscopic adjustable silicone gastric banding, do not provide adequate weight loss. African-American patients do especially poorly after the banding procedure with the loss of only 11% of excess weight in one study. Gastric bypass (GBP) is associated with the loss of 66% of excess weight at 1 to 2 years after surgery, 60% at 5 years and 50% at 10 years. For unknown reasons, African-American patients lose significantly less weight than Caucasians after GBP. There is a risk of micronutrient deficiencies after GBP, including iron deficiency anemia in menstruating women, vitamin B12, and calcium deficiencies. Prophylactic supplementation of these nutrients is necessary. Recurrent vomiting after bariatric surgery may be associated with a severe polyneuropathy and must be aggressively treated with endoscopic dilatation before this complication is allowed to develop. The malabsorptive procedures include the partial biliopancreatic bypass (BPD) and BPD with duodenal switch (BPD/DS). The BPD appears to cause severe protein-calorie malnutrition in American patients; the BPD/DS may be associated with less malnutrition. Weight loss failure after GBP does not respond to tightening a dilated gastrojejunal stoma or reducing the size of the gastric pouch. These patients may require conversion to a malabsorptive distal GBP, similar to the BPD. However, because of the risk of severe protein-calorie malnutrition and calcium deficiency BPD should be reserved for patients with severe obesity comorbidity. The risk of death following bariatric surgery is between 1% and 2% in most series but is significantly higher in patients with respiratory insufficiency of obesity. In most patients, surgically induced weight loss will correct hypertension, type II diabetes mellitus, sleep apnea, obesity hypoventilation syndrome, gastroesophageal reflux, venous stasis disease, urinary incontinence, female sexual hormone dysfunction, pseudotumor cerebri, degenerative joint disease pains, as well as improved self-image and employability.
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PMID:Bariatric surgery for severe obesity. 1185 Dec 1

The results of the study of sleep apnea (SA) in different forms of neurological disorders (cerebral stroke, diabetic polyneuropathy, neuromuscular diseases and amyotrophic lateral sclerosis--ALS) are presented. Two hundred and two patients, 103 male and 99 female, aged 17-84 years, have been investigated, using questionnaires and polysomnography. Nocturnal recording of EEG, EMG, electrooculography, oronasal air flow, respiratory thorax and abdomen movements, oxyhemoglobin saturation and breathing sounds has been performed. Clinical features of sleep apnea (SA) were most prominent in patients with neuromuscular diseases (58%) and ALS (54%), however the nocturnal study confirmed the presence of SA in patients with diabetic polyneuropathy (53%, mean RDI 15.7 +/- 18.7 epis./h) and cerebral stroke (41%, mean RDI 12.6 +/- 15.6 epis./h). A comparison of the patient's characteristics and sleep breathing indices revealed that factors of neurological damage contribute most significantly to ALS, but in diabetic neuropathy, age and obesity play a greater role.
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PMID:[Sleep apnea in neurological disorders]. 1507 37

A solvent can be defined as "a liquid that has the ability to dissolve, suspend or extract other materials, without chemical change to the material or solvent". Numerous chemical or technical processes rely on these specific properties of organic solvents in industry. Occupational exposure to solvents is not rare and some activities may cause substantial exposure to these substances in the workforce. Short-term or acute exposures cause a prenarcotic syndrome, and long lasting exposure conditions have been associated with various neurological and neuropsychiatric disorders, e.g., anosmia, hearing loss, colour vision dysfunctions, peripheral polyneuropathy and depression, but most significantly with the gradual development of an irreversible toxic encephalopathy. For the last 3 decades reports and epidemiological studies have been published reporting sleep disturbances among other complaints, related to long-term exposure to these compounds. In addition, the question has been posed if solvents can be the cause of a sleep apnoea syndrome in exposed workers, or on the contrary, if these workers are misdiagnosed and 'common' sleep apnoea syndromes are the cause of their chronic symptoms of fatigue and memory and attentional disturbances.
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PMID:Sleep disturbances and occupational exposure to solvents. 1920 Dec 27

Acute autonomic and sensory neuropathy is a rare disorder that has been only anecdotally reported. We characterized the clinical, electrophysiological, pathological and prognostic features of 21 patients with acute autonomic and sensory neuropathy. An antecedent event, mostly an upper respiratory tract or gastrointestinal tract infection, was reported in two-thirds of patients. Profound autonomic failure with various degrees of sensory impairment characterized the neuropathic features in all patients. The initial symptoms were those related to autonomic disturbance or superficial sensory impairment in all patients, while deep sensory impairment accompanied by sensory ataxia subsequently appeared in 12 patients. The severity of sensory ataxia tended to become worse as the duration from the onset to the peak phase of neuropathy became longer (P<0.001). The distribution of sensory manifestations included the proximal regions of the limbs, face, scalp and trunk in most patients. It tended to be asymmetrical and segmental, rather than presenting as a symmetric polyneuropathy. Pain of the involved region was a common and serious symptom. In addition to autonomic and sensory symptoms, coughing episodes, psychiatric symptoms, sleep apnoea and aspiration, pneumonia made it difficult to manage the clinical condition. Nerve conduction studies revealed the reduction of sensory nerve action potentials in patients with sensory ataxia, while it was relatively preserved in patients without sensory ataxia. Magnetic resonance imaging of the spinal cord revealed a high-intensity area in the posterior column on T(2)*-weighted gradient echo image in patients with sensory ataxia but not in those without it. Sural nerve biopsy revealed small-fibre predominant axonal loss without evidence of nerve regeneration. In an autopsy case with impairment of both superficial and deep sensations, we observed severe neuronal cell loss in the thoracic sympathetic and dorsal root ganglia, and Auerbach's plexus with well preserved anterior hone cells. Myelinated fibres in the anterior spinal root were preserved, while those in the posterior spinal root and the posterior column of the spinal cord were depleted. Although recovery of sensory impairment was poor, autonomic dysfunction was ameliorated to some degree within several months in most patients. In conclusion, an immune-mediated mechanism may be associated with acute autonomic and sensory neuropathy. Small neuronal cells in the autonomic and sensory ganglia may be affected in the initial phase, and subsequently, large neuronal cells in the sensory ganglia are damaged.
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PMID:Clinicopathological features of acute autonomic and sensory neuropathy. 2073 88