The pattern of muscle activation in walking was studied in a group of 26 hemiparetic patients. Electromyograms were taken with surface electrodes from 6 muscle groups of the paretic leg and analysed after rectification and time averaging. The sagittal rotations in hip, knee and ankle joint were determined with intermittent light photography. The muscle activation pattern of each patient was compared to that in healthy subjects as well as to the movements performed by the patient and to the normal movement pattern. The normal patterns of movement and muscle activation were assessed from compiled data from 10 healthy female volunteers and average values of angular displacements and amplitude of intergrated EMG were determined at each 5 per cent of the gait cycle. Change of muscle length was determined with a length recording transducer. Gait capacity varied highly in the group of patients studied and the movement pattern also varied markedly. Three types of abnormal muscle activation pattern were disclosed in the patients. In 9 patients, the calf muscles were prematurely activated in the stance phase, probably due to enhanced stretch reflexes (Type I). In another 9 patients, EMG activity was abolished or extremely low in 2 or more of the muscles examined (Type II). In 4 patients, there was a pathological coactivation of several or all of the muscles during part of the gait-cycle, thus disrupting the normal sequential shift of activity in antagonistic muscles (Type III). In the remaining 4 patients, the muscle activation pattern was more complex and no common pattern was discerned.
Autologous adrenal medullary tissue was transplanted to the striatum in two patients with severe parkinsonism. The aim was to provide the striatum with a new cellular source of catecholamines. Some rewarding effects were registered. This is the first time that such tissue has been transplanted in the human brain. The results merit further clinical trials.
Abstract.
In a double-blind cross-over study with recombinant methionyl growth hormone (GH) and placebo during 12 weeks, the effect of GH substitution therapy (0.5-0.6 IU · kg−1 · week−1) on physical performance, muscle strength, bone mineral density, and mood and cognitive functions was investigated in 6 GH-deficient adults. During GH substitution serum concentrations of insulin-like growth factor-I and procollagen-III peptide increased in all 6 patients, whereas concentrations of serum urea decreased. Five of the patients identified the GH period and reported improved well-being with increased mental alertness and vitality and improved physical capacity and muscle strength. There was, however, no change of the isokinetic muscle strength during GH substitution therapy, and the working capacity on the bicycle ergometer was just slightly improved in some patients. The bone mineral density was low and unchanged in all patients. Mood and cognitive functions did not change during GH therapy. A reversible fluid retention was observed in one patient during the GH period. In conclusion, short-term GH substitution therapy to GH-deficient adults induced a subjective improvement of general wellbeing. Longer treatment periods will be necessary to establish the effect on physical capacity, muscle strength, bone mineral density, and mood and cognitive functions.
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