Spasticity syndrome in cerebral pathology: evaluation and clinical models

Abstract

Knowing the frequency of spasticity patterns in different muscles allows correcting the botulinum neurotoxin (BoNT) administration schemes and creating spasticity models that could predict the drug consumption and treatment cost.Objective: to develop clinical spasticity models based on the frequencies of the spastic syndrome in the muscles of the extremities in post-stroke patients to optimize BoNT administration.Patients and methods. We examined 129 patients of both sexes aged 61.2±8.0 years with post-stroke spasticity (mean time after the stroke – 4.6±2.2). Twenty-seven muscles were tested for spasticity: shoulder girdle (n=3), upper (n=9) and lower (n=15) extremities. We used the original manual testing methods (MTM) of spasticity and the Tardieu scale (TS).Results and discussion. We observed the following frequencies of spasticity in the arm muscles: pectoralis major, brachioradialis, pronator teres, fl. carpi radialis, fl. digitorum profundus et superfacialis, fl. pollicis long. – over 70%, subscapularis – 61%, brachialis – 56.6%, biceps brachii – 35.8%. Frequencies of spasticity in the leg muscles were: semitendinosus, semimembranosus, fl. digitorum long. – 37.5%, gracilis – 21.4%, cap. med. gastrocnemius – 48%, tibialis post. – 39.2%, soleus – 19.6%, fl. halluces long. – 23%. There was no spasticity in the hip adductors; low spasticity incidence was seen in fl. digitorum brev. et fl. halluces brev. (<10%), tibialis ant., rectus femoris (<5%); biceps femoris, teres major, fl. carpi ulnaris, and cap. lat. gastrocnemius (<2%). Based on the frequency of identified spastic patterns, we created four models of patients with arm spasticity and five models – with leg spasticity with the calculation of the necessary doses of BoNT.Conclusion. We propose several spasticity models, which allow calculating the treatment costs, considering the frequency of involvement of specific muscles in spasticity evaluation, and tracking the rehabilitation follow-up of the patient's transition from one clinical model to another.

Neurointerface with oscillator motifs for inhibitory effect over antagonist muscles

“…The functional rewiring of the nervous system, leading to some compensation of the spastic syndrome, is a process that spreads widely from the spinal level to the supraspinal structures. Clinical symptoms have several phases such as: (1) muscle weakness formation, (2) spastic syndrome formation, and (3) recovery (Kovalenko et al, 2021). The appearing spastic syndrome is a sequential process that goes through all the aforementioned phases at different speeds.…”

Neurointerface with Oscillator Motifs for inhibitory effect over antagonist muscles for compensation of spastical syndrome

“…The functional rewiring of the nervous system leading to some compensation of the spastic syndrome is a widespread process from the spinal level to supraspinal structures. Clinical symptom has several phases: (1) muscle weakness formation, (2) spastic syndrome formation and (3) recovery [4]. Appearing spastic syndrome is a sequential process that goes through all the phases described above with different speeds.…”