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PubMed1981

Electrophysiological studies of gait in spasticity and rigidity. Evidence that altered mechanical properties of muscle contribute to hypertonia.

The surface electromyogram (EMG) of mm. tibialis anterior and triceps surae was recorded in 10 patients with spasticity, 10 patients with rigidity and 20 normal subjects and correlated with the changes in ankle joint angle during the different phases of the gait cycle. While the strength and timing of EMG activity recorded from triceps surae during the stance phase of gait did not differ from that of normal subjects, the EMG of tibialis anterior was significantly stronger during the swing phase in both groups of patients. Although the reciprocally organized innervation pattern of the leg muscles was preserved, spastic patients could hardly lift up the affected foot during the swing phase despite the enhanced activity of tibialis anterior. There was no coactivation of the calf muscles during the hyperactivity of tibialis anterior. Therefore, no electrophysiological explanation could be found for the increased muscle tone in either group of patients. The possibilities of reduced force development by the muscle fibres of tibialis anterior or of some mechanical obstruction in the ankle joint were largely excluded as alternative explanations underlying the impeded elevation of the foot. We suppose that in both diseases the muscle fibres undergo changes which are responsible for increased muscle tone in spasticity and rigidity. The pathophysiological mechanism of these changes remains unknown.

Adolescent↗
PubMed1998

Paresis and unusual electrocardiographic signs in a severely hypomagnesaemic, hypocalcaemic lactating bitch.

A severely hypocalcaemic, hypomagnesaemic lactating bitch exhibited clinical signs of pulmonary oedema, paresis, dementia, gastrointestinal ileus and urinary bladder atony. The total calcium, ionised calcium and magnesium levels were extremely low. The clinical picture was very different from the one typically encountered in canine lactation tetany, and instead resembled bovine postparturient paresis. Muscle tremors, rigidity and seizures were not part of the acute clinical picture, but rather atony, weakness and paresis. General muscle dysfunction probably resulted from the extremely low ionised calcium levels in combination with very low levels of magnesium and possibly potassium. Heart failure and atony of the urinary bladder and intestines were probably a result of the severe hypocalcaemia. The alteration in calcium to magnesium ratio may have depressed neuromuscular transmission, leading to paresis and atony. The unusual electrocardiogram possibly also resulted from abnormal magnesium and calcium cation levels.

Animals↗