Short-Latency Afferent Inhibition and Excitation of Primary Motor Cortex in Patients with Focal Hand Dystonia

Sensorimotor integration is abnormal in patients with writer's cramp (WC), and this may contribute to the movement disorder. The earliest somatosensory input to the primary motor cortex (M1) is the short latency afferent inhibition (SAI), a recently described inhibition of the motor evoked potential (MEP) amplitude when the magnetic stimulus is preceded by a conditioning electrical stimulus to the contralateral median nerve applied 20–26 ms earlier. SAI originates through activation of inhibitory interneurones in M1 and is mediated either via thalamo-cortical projections directly into M1 or through a fast relay via primary sensory cortex (S1). We hypothesized that SAI is abnormal in WC patients. SAI was investigated in 12 patients with simple (n=6) or dystonic WC and 10 healthy controls. 12 conditioning-test inter-stimulus intervals (ISIs) were tested from –6 to +16 ms in steps of 2 ms around the individual N20 latency and compared to unconditioned trials. MEPs were recorded in two conditions with the abductor pollicis brevis muscle (APB) either relaxed (resting) or slightly contracted (active). In the resting condition, patients and controls showed a similar SAI magnitude at ISI 0 and +2, i.e., when the median nerve stimulus preceded TMS by the individual N20 latency or 2 ms more. In addition, only in the patient group was a significant facilitation at ISI+10 (p=0.018) found that was significantly more pronounced in the dystonic WC patients (3.2±0.91; n=5) compared to the simple WC patients (1.9±0.26; n=6) (p=0.017; Mann-Whitney test). In the active condition, patients and controls showed similar SAI at ISI 0 and +2, but no significant facilitation at longer intervals. We show that SAI is normal in patients with WC during muscle rest and contraction. The major discriminating finding between WC and healthy controls was an abnormal MEP facilitation during muscle rest in the WC patients at inter-stimulus intervals of 28–34 ms, most likely reflecting an exaggerated long-latency reflex II (LLR II). We conclude that short-latency somatosensory inhibitory input into M1 is normal in WC, whereas the exaggerated MEP facilitation supports the notion of an abnormal sensorimotor integration of fast excitatory inputs into M1, in particular in those with dystonic rather than simple writer's cramp. Supported by the Deutsche Forschungsgemeinschaft, DFG KE487/1–1.