Effect of Botulinum Toxin on Sensori-Motor Integration in Movement Disorders: A Scoping Review

Abstract

Background: The primary effect of Botulinum toxin (BoNT) is to cause weakness in the injected muscles by inhibiting the release of acetyl choline from presynaptic nerve terminals. Its effect on sensorimotor integration (SMI) has largely been confined to small studies. The aim of this review is to highlight effect of BoNT on SMI in the context of Parkinson's disease (PD), Cervical dystonia (CD), and Writer's cramp (WC). Methods: Using keywords "Botulinum toxin" and "sensorimotor integration" or "Freezing of gait (FOG)" or 'Tremor"or "Cervical dystonia" or "Parkinson's disease", or "Writer's cramp", PubMed database was searched for relevant articles supporting our view. The abstracts of all resultant articles (case reports, case series, randomized trials, observational studies) were reviewed to look for evidence of effects of botulinum toxin on SMI. The relevant articles were charted in excel sheet for further full text review. Results: In FOG, chronic BoNT injections may alter central motor patterns with inclusion of alternative striatal systems, cerebellum, and its connections. In tremor, the afferent proprioceptive input may be modified with reduction of intracortical facilitation and increment of intracortical inhibition. In CD, BoNT can restore disorganized cortical somatotrophy, the key pathophysiology behind cervical dystonia. Similarly, in WC, both the deficient sensory system and abnormal reorganization of the sensorimotor cortex may be altered following chronic BoNT injections. Conclusions: There is preliminary evidence that BoNT may modulate SMI in PD, CD, and WC by altering inputs from the muscle spindles in short term and modifying circuits/particular anatomic cerebral cortices in the long term. Properly conducted randomized trials comparing BoNT with placebo or prospective large-scale studies to look for effect on various surrogate markers reflective of changes in SMI should be the next step to confirm these findings. Targeting the system of afferents like spindles and golgi tendon organs in muscles may be a better way of injecting BoNT, with lower amounts of toxin needed and potential for lesser side-effects like weakness and atrophy. However, this needs to be proven in controlled trials.

Keywords: basal ganglia; botulinum toxin; sensori-motor integration.

Figure 1

A box diagram showing human motor control with the concept of sensorimotor integration. The boxes in white depict the primary motor pathway, which is modulated by various inputs from the yellow boxes. A defect in any of these multiple levels can have issues with sensori–motor integration. APA: Arcuate Premotor cortex, SSC: Somatosensory cortex, Visual C: Visual cortex, Auditory C: Auditory cortex, Vestibular C: Vestibular cortex, vl-Gpi: Ventrolateral Globus pallidus interna, Caudolateral SNr: Caudolateral substantia nigra pars reticulata, VLo: ventralis lateralis pars oralis, VLm: ventralis lateralis pars medialis.

Figure 2

PRISMA flow diagram of the review “Effect of Botulinum toxin on Sensori–Motor Integration in Movement Disorders-A scoping review”.