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At least 361 records · Page 20Linked to original sources
PubMed1975

Local cooling in myasthenia. Improvement of neuromuscular failure.

Weak myasthenic muscles were tested by nerve stimulation both at normal temperature and after local cooling that was accomplished by exposing the skin to ice bags or cold paraffin oil. Reduction of intramuscular temperature from 35 C to 28 C increased the voltage of the bellytendon electrical response, the force of the tetanus elicited by 10/sec or 20/sec nerve stimulation. The myasthenic decrement of successive muscle responses was less marked after cooling, as were "delayed rundown" and "postactivation exhaustion." All these effects were reversed on rewarming the muscle. The abnormal neuromuscular jitter in motor-unit components was also reduced by local cooling. These observations may explain why diagnostic application of repetitive stimulation may be false-negative; muscle temperature must be controlled.

Adolescent↗
PubMed1996

Acoustic and electrical activities during voluntary isometric contraction of biceps brachii muscles in patients with spastic cerebral palsy.

This study was designed to compare electromyogram (EMG) and acoustic myogram (AMG) recordings of biceps brachii muscles in patients with spastic cerebral palsy (CP). The maximal voluntary contraction (MVC) in the CP group was approximately one half of that of the normal group even after being normalized by the muscle cross-sectional area (CSA) (18.6 - 5.9 kNm/m2 in CP, 37.3 +/- 2.9 kNm/m2 in normal). Both CP and normal groups demonstrated a progressive increase in the root mean squared values per unit muscle CSA in the EMG (RMSEMG/CSA) as well as in the AMG (RMSAMG/CSA) with increasing force up to 50% MVC. The increasing magnitude of the RMSEMG/CSA with force was not significantly different between two subject groups. However, all the levels of force resulted in significantly smaller RMSAMG/CSA in the CP group compared to the normal group. The ratios of RMSAMG to RMSEMG in the CP group (0.75 +/- 0.03 m/s2/mV) were significantly smaller than those in the normal group (1.37 +/- 0.07 m/s2/mV) at force levels above 30% MVC. These results suggest that motor disabilities in CP patients are caused not only by primary neural impairment but also by secondary deterioration in muscular contractile properties, probably resulting from muscle fiber atrophy. This appears to be more selective in fast twitch fibers.

Acoustics↗
PubMed2000

Myosin heavy chain IIX overshoot in human skeletal muscle.

The distribution of myosin heavy chain (MHC) isoforms, fiber type composition, and fiber size of the vastus lateralis muscle were analyzed by sodium dodecylsulfate polymerase gel electrophoresis (SDS-PAGE), ATPase histochemistry, and immunocytochemistry in a group of adult sedentary men before and after 3 months of heavy-load resistance training and, subsequently, after 3 months of detraining. Following the period of resistance training, MHC IIX content decreased from 9.3 +/- 2.1% to 2.0 +/- 0.8% (P < 0.01), with a corresponding increase in MHC IIA (42.4 +/- 3.9% vs. 49.6 +/- 4.0% [P < 0.05]). Following detraining the amount of MHC IIX reached values that were higher than before and after resistance training (17.2 +/- 3.2% [P < 0.01]). Changes in fiber type composition resembled the changes observed in MHC isoform content. Significant hypertrophy was observed for the type II fibers after resistance training. Maximal isometric quadriceps strength increased after resistance training, but returned to pretraining levels after detraining. The present results suggest that heavy-load resistance training decreases the amount of MHC IIX while reciprocally increasing MHC IIA content. Furthermore, detraining following heavy-load resistance training seems to evoke an overshoot in the amount of MHC IIX to values markedly higher than those observed prior to resistance training.

Adenosine Triphosphatases↗
PubMed1989

Distal infantile spinal muscular atrophy associated with paralysis of the diaphragm: a variant of infantile spinal muscular atrophy.

We report the clinical, electrophysiological, and morphological observations of five infants with an unusual form of spinal muscular atrophy (SMA). In these infants muscular weakness and atrophy were initially restricted to the distal limbs and this pattern was associated with paralysis of the diaphragm. The difference between the clinical manifestations of this syndrome and the classical form of infantile spinal muscular atrophy (SMA type 1) as well as other congenital hereditary neuropathies is discussed.

Atrophy↗