Introduction

Motor weakness, isolated or in association with other symptoms or signs, is the commonest problem of stroke patients. In epidemiological stroke studies, motor deficit (paresis/paralysis) is found in 80–90% of all patients (Herman et al., 1982; Bogousslavsky et al., 1988; Libman et al., 1992). There have been attempts to explain this fact using a variety of distinct arguments: (i) motor weakness is easily recorded by the patient, family, or physician; (ii) it can be caused by a stroke anywhere along the corticospinal pathways, from the cerebral cortex to the spinal cord; (iii) the most frequent types of stroke (lacunar, cardioembolic) have a ‘predilection’ for anatomic motor centres or tracts.

Motor-weakness profiles and associated abnormalities can be helpful in predicting stroke subtypes (localization, cause) in the acute phase, which is essential for etiologic diagnostic strategies, for treatment, and for prognosis in individual patients. Motor weakness is also a major element in the rating scales for clinical stroke, because it is important for daily living activities, it is not difficult to evaluate, and its assessment has shown a good interobserver reliability.

Anatomic considerations

The motor cortex is not confined to the large motor cells of Betz in the fifth layer of the precentral gyrus (primary motor cortex), as formulated at the turn of the century. Experimental studies in monkeys have indicated that only 60% of the corticospinal fibres arise from the primary motor cortex and the premotor and supplementary motor areas. The remaining fibres arise mainly from the postcentral gyrus and parietal cortex.