Mechanisms in the pathogenesis of poststroke spasticity

Abstract

Objective: to study the mechanisms of poststroke spasticity and the role of structural and functional impairments of skeletal muscles in its pathogenesis. Patients and methods. Thirty-two patients with prior hemispheric stroke and evolving spastic paresis were examined. Neurophysiological studies of upper and lower motor neuron functions and morphological, histochemical, and immunohistochemical studies of soleus muscle biopsy specimens were conducted. Results. There was diminished excitability of cortical neurons, impaired conduction along the pyramidal tracts, and hyperexcitability of the segmental apparatus of the spinal cord. The muscle exhibited myosin phenotype transformation with a preponderance of fast type II fibers, as well as a higher fiber diameter variability and a lower muscle tissue capillarization. The late periods of spasticity were marked by better conduction along the pyramidal tract, at the same time structural changes tended to increase in skeletal muscle tissue. The time course of the changes suggests that there is partial reversibility in the central nervous system and skeletal muscle, which allows elaboration of approaches to differentiated therapy for the above conditions.

Keywords

• poststroke cerebral spasticity
• pyramidal tract
• segmental apparatus of the spinal cord
• muscle changes
• myosin
• muscle capillarization