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)

Carbaryl, a widely used insecticide, is reputed to have a wide safety margin. It can induce acute cholinesterase poisoning, which is rapidly reversible on discontinuation of exposure. Long-term sequelae from long-term exposure have not previously been described in humans. This report describes the experience of a 75-year-old man who had long-term excessive exposure to carbaryl and in whom a debilitating syndrome, including headaches, memory loss, proximal muscle weakness, muscle fasciculation, muscle cramps, and anorexia with marked weight loss, developed. At the time of diagnosis, serum pseudocholinesterase levels were low, and his major symptoms resolved on termination of exposure. Late clinical features were sleep apnea and progressive development of a peripheral neuropathy. The difficulty in diagnosing the cause of a group of relatively nonspecific symptoms raises the question of whether chronic carbaryl neurotoxicity might be occurring more frequently than previously suspected.
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PMID:Subacute neurotoxicity following long-term exposure to carbaryl. 308 76

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

We report the first case of ocular myasthenia gravis (OMG) in a patient with complete tetraplegia, highlighting diagnostic and management challenges. Spinal multidisciplinary rural clinic and specialised inpatient Spinal Cord Injury Unit, NSW, Australia. A 61-year-old man with established C5 AIS A tetraplegia, presented with sudden onset of diplopia and bilateral ptosis, later diagnosed as OMG, in context of other complex co-morbidities, including a cervical cord syrinx, obstructive sleep apnoea and labile blood pressure. Clinical findings were consistent with fluctuating bilateral partial third and sixth nerve palsies. Acetylcholine receptor antibodies were negative, but electromyography demonstrated muscle fatigue. The ocular signs responded well to pyridostigmine. Medications taken before diagnosis, including solifenacin for neurogenic bladder overactivity, were ceased to avoid attenuating the anti-cholinesterase effect. However, the unopposed anti-cholinesterase activity led to frequent and painful abdominal spasms, associated with uncontrolled detrusor hyperreflexia and worsening autonomic dysreflexia (AD). A trans-vesical phenol block to treat this provided only short-lasting benefit. Pyridostigmine was ceased to avoid provoking his abdominal spasms and his regular medications were recommenced. It was decided that the most appropriate treatment for his distressing diplopia was an eye patch. After discharge home, he continued to experience problems with recurrent urinary tract infections, abdominal spasms, episodic postural hypotension and AD. After 5 months, the patient died from an acute myocardial infarction. This case report contributes new knowledge about the rare presentation of OMG in a person with chronic tetraplegia.
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PMID:Ocular myasthenia gravis in a person with tetraplegia presenting challenges in diagnosis and management. 3126 10