Changes in short afferent inhibition during phasic movement in focal dystonia

Abstract

Impaired surround inhibition could account for the abnormal motor control seen in patients with focal hand dystonia, but the neural mechanisms underlying surround inhibition in the motor system are not known. We sought to determine whether an abnormality of the influence of sensory input at short latency could contribute to the deficit of surround inhibition in patients with focal hand dystonia (FHD). To measure digital short afferent inhibition (dSAI), subjects received electrical stimulation at the digit followed after 23 ms by transcranial magnetic stimulation (TMS). Motor evoked potentials (MEPs) were recorded over abductor digiti minimi (ADM) during rest and during voluntary phasic flexion of the second digit. F-waves were also recorded. We studied 13 FHD patients and 17 healthy volunteers. FHD patients had increased homotopic dSAI in ADM during flexion of the second digit, suggesting that this process acts to diminish overflow during movement; this might be a compensatory mechanism. No group differences were observed in first dorsal interosseous. Further, no differences were seen in the F-waves between groups, suggesting that the changes in dSAI are mediated at the cortical level rather than at the spinal cord. Understanding the role of these inhibitory circuits in dystonia may lead to development of therapeutic agents aimed at restoring inhibition.

Modulation of Short-Latency Afferent Inhibition Depends on Digit and Task-Relevance

“…We and others have shown that SAI is reduced during both the onset of muscle activity [6], [8], [9] and during sustained muscle contraction [6], [7]. Specifically, we observed reductions in SAI as early as movement preparation between an auditory “warning” and “go” cue and these reductions are likely cortically or sub-cortically mediated [6].…”

“…First, how is SAI modified when the muscle is involved versus uninvolved in the task? [8], [9]. Second, does the modulation of SAI depend on the specific digit (i.e., digit 2 versus digit 5)?…”

Physiological effects of subthalamic nucleus deep brain stimulation surgery in cervical dystonia

“…In a writer’s cramp study, SAI was observed to increase in the abductor digiti minimi muscle during phasic contraction of Flexor digitorum interrosseous (FDI) muscle, which was speculated to reflect a compensatory mechanism to prevent overflow of dystonia from the index finger to the little finger 11. Similarly an increased SAI in our study during DBS OFF possibly represented a compensatory mechanism in response to worsening of dystonia symptoms.…”

Treatment and Physiology in Parkinson’s Disease and Dystonia: Using Transcranial Magnetic Stimulation to Uncover the Mechanisms of Action

“…At short latencies (less than 40ms) the contralateral S1 and secondary somatosensory cortex (S2) are primarily activated, while at longer latencies (more than 40ms) there is more widespread activation of sensory areas, including S1, bilateral S2, and the contralateral posterior parietal cortex [20,21]. Short latency afferent inhibition (SAI), also exhibits a somatotopic organization [22] such that cortical inhibition due to electrical stimulation of a digit near a target muscle (i.e., homotopic) is stronger than cortical inhibition due to stimulation of a digit distant from a target muscle (i.e., heterotopic)[23]. …”

“…TMS studies found that although SAI and LAI were comparable to healthy controls in focal dystonia patients,[79],[80] there was an increased homotopic digital short afferent inhibition (dSAI), during flexion of the second digit. This suggests that this process was a compensatory act to diminish overflow during movement [23]. Unlike the basal ganglia which receive sensory information indirectly, the cerebellum is a direct recipient of sensory input from the spinal cord [81].…”