Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Premature declines in function among adults with cerebral palsy (CP) are generally attributed to weakness, spasticity and orthopaedic abnormalities, as well as chronic pain and fatigue. Very little research or clinical attention has been devoted to the confluence and consequences of early muscle wasting and obesity as mediators of secondary comorbidity in this population, and perhaps more importantly, to the role of lifestyle to potentiate these outcomes. At present, there are no national surveillance programmes that monitor chronic health in adults with CP; however, mortality records have demonstrated a greater prevalence of coronary heart disease as compared with the general population. Although by definition, CP is a 'non-progressive' condition, secondary factors such as habitual sedentary behaviour, obesity, and premature sarcoepenia may increase the severity of functional impairment throughout adulthood, and lead to cardiometabolic disease, fragility and/or early mortality. Herein we describe the heightened health risk represented in adults with CP, and discuss the hallmark phenotypic features that coincide with ageing, obesity and cardiometabolic disorders. Moreover, we provide discussion regarding the protective role of habitual physical activity to stimulate anti-inflammatory pathways and to ameliorate global risk. Although physical therapeutic modalities are already widely acknowledged as a vital component to improve movement quality in CP, the purpose of this review was to present a compelling case for the value of lifelong physical activity participation for both function and cardiometabolic health preservation.
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PMID:Chronic disease risk among adults with cerebral palsy: the role of premature sarcopoenia, obesity and sedentary behaviour. 2309 88

Multiple sclerosis affects central nervous system leading to disability. Among other complications the deterioration of body composition is usually neglected and increases the risk for diseases such as coronary heart disease, non-insulin dependent diabetes mellitus, lipid abnormalities and bone loss leading to fractures in this population. Body mass index values, the effect of spasticity, the increased number of drugs used and the relationship between skeletal muscle and bone which interacts with impaired motor function leading to body composition alterations in multiple sclerosis are reviewed.
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PMID:Body composition in multiple sclerosis. 2393 36

Mitochondrial disorders (MIDs) require biochemical or genetic investigations for being diagnosed. In some cases, however, the diagnosis can be suspected upon the syndromic phenotype or upon clinical presentation and family history, as in the following case. The patient was a 74-year-old male admitted for worsening of pre-existing left-sided ptosis and ophthalmoparesis after a birthday party. The history was positive for arterial hypertension, hypertrophic cardiomyopathy with systolic dysfunction, diabetes-type 2, mild renal insufficiency, thyroiditis, and polyneuropathy. Instrumental investigations additionally revealed hepatopathy, hyperlipidemia, hyperuricemia, bifascicular block, white matter lesions, and subacute stroke. Systolic dysfunction resolved upon adequate cardiac treatment. On hospital day 11 the patient suddenly developed asystole. He was successfully resuscitated but died a few hours later from acute myocardial infarction. Surprisingly, a more extensive family history was positive for myopathy (patient, brother, daughter), neuropathy (patient), hypoacusis (patient), Parkinson syndrome (mother), spasticity (son), diabetes (patient, son), renal failure (patient), and generalized atherosclerosis (patient). The individual and family history was strongly suggestive of an MID. In conclusion, individual and family history may strongly suggest MID. Phenotypic variability may be high between family members affected by an MID. MID may be associated with an increasing atherosclerotic risk lastly resulting in coronary heart disease and death.
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PMID:Diagnosing Mitochondrial Disorder without Sophisticated Means. 2661 82