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The regulation of muscle tonus takes place at least at six levels of the central nervous system: the spinal cord, vestibular nuclei, the cerebellum, the reticular formation, extrapyramidal system and the motor cortex. A multiple complexity of the connections of these systems in the regulation of muscle tonus is presented, so that therapy can be usefully applied in states of muscle tonus disorders.
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In 19 patients with multiple sclerosis and 1 with subacute sclerosing panencephalitis the mean increase in muscle tonus was found to be 3.1 (range 1--4 according to Burke-Ashwort). In 10 controls with multiple sclerosis the mean spasticity was 2.4. Dantrium was given in doses up to 800 mg for 14--16 days and it caused a greater reduction of spasticity than placebo (p less than 0.05). In 12 patients (60%) varying degrees of muscle tonus reduction was observed. In 11 patients the efect of Dantrium was compared with that of other drugs (Clonazepam, Tetradiazepam, Carisoprodol and Lyoresal). In 6 cases Dantrium was a more effective drug than other muscle relaxants and in 5 cases no difference was observed or other drugs were superior to Dantrium.
The effects of morphine and methionine-enkephalin (met-enkephalin) on the smooth muscle tonus and the contraction induced by transmural stimulation were investigated in the isolated intestinal bulb of carp in vitro. Morphine (30 nM-3 microM) and met-enkephalin (3 nM-5 microM) caused dose-dependent non-sustained contraction. Naloxone (10 nM) inhibited the contraction induced by morphine or met-enkephalin in a competitive manner. Tetrodotoxin (400 nM) or atropine (500 nM) did not inhibit the contraction induced by morphine or met-enkephalin. Cooling of the bath fluid from 20 to 10 degrees C decreased nicotine- and transmural stimulation-induced contraction. But met-enkephalin-induced contraction was not affected. Transmural stimulation-induced contraction (3 Hz) was not affected by pretreatment with morphine, met-enkephalin or naloxone. The results demonstrated that morphine or met-enkephalin caused contraction of the smooth muscle directly through the activation of opiate receptors on the smooth muscle cells and neither morphine nor met-enkephalin regulated the cholinergic neurotransmission presynaptically.
Airway smooth muscle tone is reinforced during the inspiratory phase of the breathing cycle and depends largely from neurogenic motor drive carried by the vagus nerve. This muscle tone seems to be produced mostly by a vago-vagal reflex loop initiated by the tonic discharge of tracheo-bronchial and/or alveolar receptors connected to thin sensory vagal fibres (non-myelinated or C-fibres). Inhibitory influences carried by large myelinated vagal fibres connected to tracheobronchial stretch receptors and also numerous afferents from the upper airways, systemic and pulmonary circulation, digestive tract and skeletal and respiratory muscles participate to the modulation of airway tone. The identification of neurotransmitters specific of the motor or sensory pathways helps to understand the peripheral modulation of airway motor drive and also the central integration of some peripheral informations.
Removal of any component out of a set of biologically active substances augmented the coronary arteries smooth muscle tone. The phenomenon is discussed in respect to participation of intracellular regulatory mechanisms.
On the basis of a summarization of long-term studies of the different types of tonic reactions in normals and patients with different forms of dystonia, the author describes 7 types of such reactions. The paper deals as well as with possible physiological and pathophysiological mechanisms of their occurrence and the significance of these data for the theoretical analysis of the regulation of the human muscular tone.
The results of the examination of the muscle tone by passive movement of the extremity at a low and high rate in patients with spasticity are discussed. In parkinsonism high resistance was noted to passive movements of the extremity at a low rate (with a period of oscillatory movement of 100 s and more) as well as in the first cycles of rapid sinusoidal movement (with a period of 1 s) if the extremity had been at rest for a lengthy period of time. In spasticity of other etiology, there was a gradual increase of the amplitude on the mechanomyogram in high rates of passive movements, which was evidently due to growth of stimulation in the stretch-reflex arc from cycle to cycle as the result of sumation with trace stimulation from the preceding cycles. The shape of the spectromechanomyogram, which is marked by a rise in the region of the high rates, is considered to be a sign of spasticity, whereas the size of this rise is accepted as a quantitative index of the spastic component of the muscle tone.
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The authors noted the high prevalence of facial asymmetry and of unilateral amblyopia in some hundred children suffering from chronic neurological conditions. Unilateral changes in muscle tone are responsible for such asymmetry. Amblyopia in itself may cause a facial asymmetry. The dental arcades are little affected even by severe deformities of their underlying bony supports. Dento-maxillary abnormalities are no more severe in these children than in a normal population.
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