Short latency afferent inhibition and facilitation in patients with writer's cramp

Abstract

Patients with writer's cramp (WC) show abnormalities of sensorimotor integration possibly contributing to their motor deficit. We studied sensorimotor integration by determining short-latency afferent inhibition (SAI) in 12 WC patients and 10 age-matched healthy controls. A conditioning electrical median nerve stimulus was followed 14 to 36 msec later by transcranial magnetic stimulation of the contralateral primary motor cortex, and motor evoked potentials (MEP) were recorded from the relaxed or contracting abductor pollicis brevis muscle (APB). SAI was normal in WC but during APB relaxation SAI was followed by abnormal MEP facilitation, which was absent during APB contraction and in the controls. These findings suggest that somatosensory short-latency inhibitory input into the primary motor cortex is normal in WC, whereas a later excitatory input, which very likely reflects the long-latency reflex II, is exaggerated.

Normalization of sensorimotor integration by repetitive transcranial magnetic stimulation in cervical dystonia

“…In line with these clinical findings, application of a sensory alleviating maneuver in CD patients significantly reduced increased intracortical M1 facilitation [8]. Additionally, several studies indicated abnormal processing of somatosensory stimuli in dystonia leading to alterations of sensorimotor integration [9,10]. Previous studies also suggest that somatotopical organization and plasticity of the sensorimotor system are impaired in dystonia [2,3,11,12].…”

“…These divergent findings may either be due to methodological differences, small sample size or different clinical characteristics. Impaired SAI in CD is in contrast to WC patients in whom SAI has been shown to be normal [10,12,13]. Apart from obvious clinical differences between CD and WC in terms of dystonia distribution, onset age and gender [33] one principal group difference relates to the fact that neurophysiological measurements were carried out in a non-dystonic state with the arms at rest in WC but with neck dystonia being present in CD.…”

The Effects of Spinal Manipulation on Central Integration of Dual Somatosensory Input Observed After Motor Training: A Crossover Study

“…However, these alterations may also in some circumstances, such as after an injury or the sustained performance of repetitive muscular activity, become maladaptive plastic changes that are thought to be responsible for initiating and perpetuating certain movement disorders and chronic pain syndromes. 24,[39][40][41][42][43][44][45][46][47][48][49][50][51] Furthermore, joint dysfunction originating from an injury may be a cause of ongoing pain and loss of function due to maladaptive sensorimotor integration from a hyperafferentiation of the CNS from the dysfunctional joints and associated structures. [52][53][54][55][56][57][58] Does Repetitive Muscular Activity and Joint Dysfunction Lead to Maladaptive Plasticity?…”

Evidence for the Specificity of Intracortical Inhibitory Dysfunction in Asymptomatic Concussed Athletes

“…The induced current flow was biphasic with a posterior-anterior direction. Pulses were delivered over the optimal position to elicit a maximal electromyographic (EMG) response of the controlateral abductor pollicis brevis (APB) muscle to conform to afferent inhibition paradigms (Kessler et al, 2005). The EMG signal was amplified using a Powerlab 4/30 system (ADInstruments, Colorado Springs, CO), filtered with a band pass 20-1000 Hz and digitized at a sampling rate of 4 KHz.…”