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Plasticity of motor cortex excitability induced by rehabilitation therapy for writing
Ilias Papathanassiou, PhD; Saša R. Filipovic, MD, PhD; Renata Whurr, PhD; and Marjan Jahanshahi, PhD ´

Abstract—The mechanisms of rehabilitation-induced plasticity in the motor system after stroke are not defined. The authors studied seven patients with residual poststroke agraphia,aphasia, and right hemiparesis. After a 40-minute rehabilitation therapy that promoted use of the paretic hand for writing, the authors observed a task-specific increase in recruitment of ipsilateral corticospinal pathways. Rehabilitation aimed to increase the use of the paretic hand may induce recruitment of previously silent ipsilateral corticospinal pathways even in poorly recovered poststrokepatients.
NEUROLOGY 2003;61:977–980

The physiology of acquired disorders of writing and the mechanisms for their recovery are largely unknown. We investigated whether a 40-minute program of writing rehabilitation therapy aimed at the paretic hand could produce changes of the excitability of the corticospinal pathways of the impaired limb in poststroke patients with chronic agraphia accompaniedby aphasia and right hemiparesis (AARH). The therapy program used has already been shown to induce clinical improvements of writing and other motor features in such patients.1 In light of the controversies regarding the roles of the contralateral and ipsilateral hemispheres in the poststroke recovery process,2 their relative contributions in any observed changes were evaluated.
Methods. Westudied seven patients with chronic AARH after a left middle cerebral artery stroke (table). None was taking any medication with CNS effect. Local ethics committee approval and patients’ written consent were obtained. Corticospinal excitability was assessed with transcranial magnetic stimulation (TMS) using Magstim 200 stimulator (Magstim, Whitland, UK) and a focal figure-of-eight coil (external loopdiameters, 9 cm). The coil was held so that the induced current in the brain flowed in the lateroposterior to medioanterior direction. Surface EMG was recorded from three distal and three proximal muscles of the paralyzed limb (figure 1). The stimulation sites (“hot spots”) for each muscle were determined on each hemisphere by varying the position of the coil within a 6-cm-diameter circle centered 1cm anterior to the C3 and C4 EEG sites. The hot spot

was defined as the scalp location where TMS of the lowest intensity was able to elicit a motor evoked potential (MEP) in the EMG from the tested muscle. If a hot spot was found before therapy, it was used for stimulation after therapy as well; otherwise, the procedure for its detection was repeated after therapy. For each muscle hot spot,the motor threshold (MT) was determined, first at rest and then during activation procedures. The activation procedures were arm lifting (a control task, involving proximal muscles only) and writing (a target task in which patients were asked to repeatedly write their own name). Patients were encouraged to try to perform the movements even when no muscle contractions and EMG activity were evident.At rest, MT was determined as the minimum stimulus intensity that produced an MEP of approximately 100 V in at least 50% of six successive trials.4 During the activation procedures, MT was defined as the minimum stimulus intensity that produced an MEP that was more than twice the mean level of background EMG (mean amplitude of the rectified EMG in the 25-ms interval before the TMS pulse) and largerthan other peaks in the background in at least three of the six responses.5 The reciprocal inhibition of H-reflex from the forearm flexor muscles by the antagonist extensor muscle afferents6 was also studied with patients at rest. The disynaptic (interstimulus intervals [ISIs], 2 and 2 ms) and presynaptic (ISIs, 5 to 50 ms) phases of inhibition were analyzed separately. During therapy, patients...
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