Abnormal associative plasticity of the human motor cortex in writer's cramp

Abstract

Low-frequency median nerve stimulation, paired with suprathreshold transcranial magnetic stimulation (TMS) over the optimal site for activation of the abductor pollicis brevis (APB) muscle induces a long-lasting increase in the excitability of corticospinal output neurons, if median nerve stimulation is given 25 ms before TMS. Here we employed this protocol of stimulation to assess associative plasticity of the primary motor hand area in 10 patients with writer's cramp and 10 age-matched controls. Motor evoked potentials (MEPs) were recorded from right APB muscle and right first dorsal interosseus (FDI) muscle. Resting and active motor threshold, mean MEP amplitude at rest, short-latency intracortical inhibition (SICI) at an interstimulus interval of 2 ms and the duration of the cortical silent period (CSP) were assessed immediately before and after associative stimulation. In both groups, associative stimulation led to an increase in resting MEP amplitudes which was more pronounced in the right APB muscle. Compared with healthy controls, stimulation-induced facilitation of MEP amplitudes was stronger in patients with writer's cramp. In addition, only patients showed a slight decrease of resting and active motor thresholds after conditioning stimulation. In both groups, associative stimulation induced a prolongation of CSP in the APB and FDI muscles, which was significant only in the APB muscle in healthy controls. Associative stimulation had no effects on SICI in patients and healthy controls. Taken together, in patients with writer's cramp, the motor system exhibited an abnormal increase in corticospinal excitability and an attenuated reinforcement of intracortical inhibitory circuits that generate the CSP in response to associative stimulation. This altered pattern of sensorimotor plasticity may favour maladaptive plasticity during repetitive skilled hand movements and, thus, may be of relevance for the pathophysiology of writer's cramp and other task-specific dystonias.

A comparison of neuroplastic responses to non-invasive brain stimulation protocols and motor learning in healthy adults

“…1). Large response variability has also been reported in the PAS literature with MEP amplitude increases ranging from 32% [7] to 79% [23] and response rates as low as 50% [31]. In the current study, we report a (nonsignificant) 50% increase in MEP amplitude following PAS and a response rate of 67%, a result that falls well within the range of PAS-induced MEP facilitation reported by others.…”

Neuromodulatory Neurotransmitters Influence LTP-Like Plasticity in Human Cortex: A Pharmaco-TMS Study

“…Impaired PAS-induced LTP-like plasticity is typically observed in disorders associated with a dysfunctional dopaminergic system such as Parkinson's disease (Morgante et al, 2006;Ueki et al, 2006;Schwingenschuh et al, 2010) or schizophrenia (Frantseva et al, 2008), or a deficient central cholinergic system such as Alzheimer's disease (Battaglia et al, 2007), whereas exaggerated PASinduced LTP-like plasticity can be observed in states of increased endogenous central cholinergic tone such as dystonia (Quartarone et al, 2003(Quartarone et al, , 2008Weise et al, 2006;Schwingenschuh et al, 2010).…”

Transcranial Magnetic Stimulation to Investigate Motor Cortical Circuitry and Plasticity in Spinal Cord Injury

“…The assumption underlying PAS effects is that nerve stimulation and the TMS pulse both evoke inputs onto a common neuronal population that ultimately demonstrates short-term associative synaptic plasticity due to the repeat pairing of separate inputs. Following PAS protocols in uninjured individuals, increases in MEP amplitude [87] and cSP [90] are observed. PAS-induced increases in corticospinal excitability are mediated by glutamate and are blocked in the presence of NMDA receptor antagonists [89].…”