Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the differential diagnosis of intermittent claudication some rare myopathies have to be considered. The most frequent is phosphorylase deficiency (McArdle's disease). Exercise-induced muscular pain, weakness, contractures and occasionally myoglobinuria are the most prominent clinical signs. Serum creatine phosphokinase, aldolase and lactic dehydrogenase may be elevated after exertion. In the ischemic forearm test there is no rise of serum lactic acid. The enzyme deficiency can be demonstrated by histochemical and biochemical examination of a muscle specimen. Further, but more infrequent, enzymatic disturbances of glycolysis are phosphofructokinase deficiency and phosphohexoisomerase inhibitor, which also yield an abnormal ischemic forearm test and must be demonstrated histochemically and biochemically. Apart from muscular signs, myopathy with lactic acidosis is associated with palpitation, dyspnea and exhaustion, and a disproportionate rise in serum lactic acid level after exertion. Histochemically and electronmicroscopically demonstrable fat accumulation in the muscle can be a sign of a disturbance in lipid metabolism. This type of exercise-induced myopathy has been reported only in a few cases with carnitine-pylmityltransferase deficiency, which has to be demonstrated biochemically. Muscular contractures also exercise-induced but painless and reversible within seconds may be due to deficient uptake of sarcoplasmic calcium in the tubular system. Dyskalemic paralysis causes painless paresis within minutes of hours after exertion, which disappears within hours to a few days. Myopathy with tubular aggregates can be differentiated from other exercise-induced myopathies by morphology. Myotonia combined with painful contractures characterizes myopathia myotonica.
 ...
PMID:[Exercise-induced muscular weakness, myalgia and contractures. I. A clinical review]. 13 80

Capillary supply and oxidative and glycolytic enzyme activities were determined in muscle biopsies from the tibialis anterior muscle in six prior polio patients and a control group. The polio patients, who had paresis and atrophy, but were able to walk normally by making maximal use of all remaining anterior tibial motor units, showed type I (slow-twitch) muscle fibre predominance with a mean (SD) of 98 (2%) type I fibres versus 81 (8)% in the controls (p less than 0.01) and muscle fibre hypertrophy, the average type I fibre cross-sectional area being 108% (p less than 0.005) larger than in the controls. The number of capillaries per muscle fibre was not significantly different from that in the control group, but with the increased muscle fibre area in the polio patients, the capillary density was significantly lower. The number of capillaries in contact with type I fibres relative to fibre area was 40% lower in the patients than in the controls (p less than 0.005). The levels of citrate synthase and phosphofructokinase were significantly lower (38% and 33%, respectively, p less than 0.05) in the patients than in the controls, indicating decreased oxidative and glycolytic potentials in the muscle fibres of the polio patients. It is proposed that the abnormal high-frequency activation of all remaining motor units during each step cycle recorded in these patients constitutes a stimulus for type I muscle fibre predominance and hypertrophy but that the overall low muscle usage results in a decreased stimulation of capillary proliferation and mitochondrial enzyme synthesis. The low capillary density and decreased oxidative and glycolytic enzyme potentials might be important factors for the development of muscle weakness, fatigue and muscle pain, which are commonly occurring symptoms in patients with prior poliomyelitis.
 ...
PMID:Prior poliomyelitis-reduced capillary supply and metabolic enzyme content in hypertrophic slow-twitch (type I) muscle fibres. 203 Mar 51