Motor cortex excitability after thalamic infarction
Introduction
Normal sensory input is a prerequisite for optimal motor behaviour. Lesion studies in animals (Pavlides et al., 1993) and humans have demonstrated that the loss of sensory discrimination abilities affected motor functions and could impair the success of rehabilitation after stroke (Rose et al., 1994). A loss of sensation usually deteriorates dexterity. Only a few studies have addressed the question of whether the loss of sensory function has direct consequences on motor cortex excitability. Current results suggest that a peripheral sensory nerve block decreases motor excitability of the muscle beneath the anesthetic skin (Liepert et al., 2004, Rossi et al., 1998, Rossini et al., 1996). In contrast, excitability is enhanced in adjacent, non-affected areas (e.g. in the upper arm muscles during an ischemic forearm block) (Brasil-Neto et al., 1992, Ziemann et al., 1998).
Less is known about the consequences of lesions in central somatosensory pathways. A patient with an isolated ischemic lesion in his primary sensory cortex showed an increase of motor cortex excitability as demonstrated by a loss of intracortical inhibition, an increase of intracortical facilitation and a decrease of the duration of the silent period on the affected side (Liepert et al., 2003).
In this paper, we used transcranial magnetic stimulation (TMS) to explore if an impairment of central sensory functions produced by an ischemic thalamic lesion would change motor cortical excitability. In addition, we examined if motor function was impaired. The ventro postero lateral (VPL) nucleus of the thalamus is an important area since sensory afferents are close together. Animal studies have shown that connections originating from ventro-lateral thalamic nuclei project to the primary somatosensory cortex (S1) (Areas 3a and 3b) (Brown and Carman, 1979, Darian-Smith and Darian-Smith, 1993), but also to the primary motor cortex (M1) and the supplementary motor cortex (Darian-Smith et al., 1990, Shindo et al., 1995). A small lesion in the VPL nucleus or the thalamocortical fibers is able to produce hemihypesthesia without affecting the corticospinal tract. We chose patients with thalamic lesions resulting in hemihypesthesia as a model for the understanding of sensory–motor interactions: this type of a subcortical ischemic lesion might induce some functional effect on the motor cortex but does not result in a structural motor cortical lesion as visible in conventional magnetic resonance tomography.
Section snippets
Methods
We studied 8 patients (5 men, mean age: 60.4±13 years; [±SD], range: 33–74 years) with unilateral ischemic thalamic lesion documented by magnetic resonance imaging of the brain (Fig. 1). The results obtained from the affected side were compared with the patients' unaffected side and with an age-matched healthy control group (n=8; 5 men, mean age: 59.2±11.6 years [±SD], range: 40–77 years). It was the first stroke in all patients. In 6 patients, stroke had occurred within 3 weeks prior to the
Results
In the patient group, motor thresholds (MT), central motor conduction times (CMCT) and maximum MEP amplitudes as percentage of the M response (max. MEP) were equal on both sides (Table 1). The results were similar to data obtained in the age-matched control group (control group results: MT: 42±2.3% of maximum stimulator output intensity; CMCT: 4.8±0.6 ms, max. MEP: 56.8±9%; Kruskal-Wallis tests for MT, CMCT and max. MEP: P>0.2).
Paired pulse TMS exhibited enhanced MEP amplitudes in the affected
Discussion
In this study, patients with a hemihypesthesia due to ischemic thalamic lesion exhibited changes of various parameters of motor cortex excitability: an increased M1 excitability was demonstrated by a decrease of intracortical inhibition and an enhancement of intracortical facilitation in the affected hemisphere. At the same time, the prolongation of the silent period indicated an enhanced activity of inhibitory neurons. Performance of the Nine-Hole-Peg Test as an indicator of dexterity was
Acknowledgements
JL and CW were supported by a grant from the Kompetenznetzwerk Schlaganfall. We thank Prof. Dr Zeumer, Department of Neuroradiology, University Hospital Eppendorf, Hamburg, for MRI scans of the patients.
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