A potential embolic source from the heart or large arteries was the presumed cause in Of the patients with this profile of motor deficit, the majority [ These patients showed a higher prevalence of hypertension than patients with deficits sparing the leg. Cerebral hemorrhages were more common in these patients.
However, cigarette smoking, migraine, and the presence of TIAs were less common in patients with leg involvement when cerebral infarctions were compared. The outcome, the side of stroke, its cause, and localization were also different and are summarized in Table 2 , Table 3 , and Table 4.
Our findings confirm that different brain sites of vascular lesions can lead to a motor deficit sparing the lower limb. However, most were caused by superficial infarcts Table 1. This was the most common motor pattern when lesions involving superficial branches of the MCA were studied. Motor deficits are almost always present after anterior MCA lesions, whereas in posterior MCA lesions, if present, they are generally milder. In anterior MCA infarcts, precentral gyrus ischemia is usually caused by loss of blood supply by the Rolandic central sulcal artery.
In posterior MCA infarcts, the pattern is thought to be secondary involvement of motor pathways coming from the precentral gyrus in the subcortical white matter. The sites of the lesions causing paresis without leg involvement contrast sharply with the locations of those causing paresis with leg involvement, in which deep infarctions were the most common. Although in 1 report 17 predominant leg weakness was often found to be caused by embolic hemispheric lesions, isolated leg weakness represented only 2.
Faciobrachial paresis is also probably common after some classic deep lesions, such as striatocapsular infarcts. The exact topography of the injuries in the internal capsule causing partial hemiparesis is not established. A recent revision of internal capsule anatomy showed that the traditional view of its somatotopic motor representation, with the head and eye in the genu, the upper extremity in the anterior part of the posterior limb, and the lower extremity in the posterior part of the posterior limb, is not well supported by clinical and stereotaxic stimulating studies.
The review suggested that both the corticospinal and corticobulbar fibers lie in a compact bundle in the posterior part of the posterior limb.
Moreover, a large clinical study of lacunar infarcts in the internal capsule did not support its classic anatomical view. Although ACA infarcts usually cause predominantly leg weakness, the presence of so few of these 0. Recently, Chamorro and colleagues 21 suggested that faciobrachial weakness reflects motor neglect caused by damage to medial premotor areas and not by commitment of primary motor pathways.
Usually, a PCA infarct does not cause weakness. Two hypotheses were proposed to explain hemiparesis on the basis of its topography, one being an associated lesion of the corticospinal pathways in the midbrain supplied by perforating branches of the PCA, and the other, involvement of the pyramidal tract in the internal capsule. Brainstem lesions cause typically faciobrachiocrural weakness and, more rarely, brachiocrural paresis.
However, faciobrachial paresis has also been reported 13 and may result from spreading of corticospinal fibers in the pons. The frequency of cerebral hemorrhages was very low 5. Hemorrhages in distinct parts of the brain resulted in paresis without leg involvement. Cerebral hemorrhage can lead to hemiparesis caused by a mass effect and has less localizing value than infarcts. Although the number of deep lesions increased when only pure motor strokes were studied, the most common site of the lesions was still the superficial anterior MCA.
Many studies have considered brachiocrural or faciobrachial paresis 2 of 3 elements as the classic presentation of small-artery disease. This was not true in our sample for faciobrachial paresis and reinforces our assumption that a lacunar cause for pure motor stroke should be applied only to faciobrachiocrural hemiparesis.
We found that large-artery disease and cardioembolism were the main causes of strokes sparing the lower limb. The importance of embolism would have been greater if we had included patients with atherosclerosis without stenosis, in whom embolism from the large arteries arterioarterial embolism was a possible cause.
The frequency of strokes caused by small-artery disease lacune was low. In fact, risk factors for small-artery disease, such as hypertension and diabetes mellitus, were lower than in patients with leg involvement.
In contrast, risk factors for large-artery disease, such as cigarette smoking, were higher. The higher frequency of TIA could be explained by the increased frequency of large-artery disease and atherosclerosis without stenosis in this group.
The frequency of cardioembolism was the same in the 2 groups. Migraine frequency was almost double in patients without leg involvement compared with patients with leg involvement Table 4. Although the relationship between migraine and stroke is disputed, recent epidemiological studies suggest that it is an independent risk factor for strokes in both men 24 and women.
In our study, the frequency of mitral valve prolapse, patent foramen ovale, and arterial dissection did not differ between the 2 groups. Our findings allow us to speculate that migraine is more probably related to involvement of superficial vessels by embolus, vasospasm, or local abnormalities than deep perforating vessels. Patients without leg involvement had a higher frequency of left hemispheric infarcts Table 4.
The same was true for hemorrhage, but the result was not statistically significant, possibly because of the small number of patients with this type of stroke. Left hemispheric strokes are usually accompanied by language problems, whereas cortical signs of right hemispheric lesions are milder.
It can be assumed that fewer patients with right hemispheric lesions seek medical attention, especially when the motor deficits are discrete, sparing the lower limb. In fact, in a study by Norrving and Bogousslavsky, 29 silent infarcts were more often localized to the right hemisphere.
We could speculate that there is a difference in motor representation between the two hemispheres. Mohr and coworkers 30 studied the relationship between convexity infarct and motor patterns of hemiparesis and found that the size of the infarct did not vary between the two sides, but that the location of the lesion differed; a difference in the weakness syndrome for the two sides was suggested.
Another hypothesis is that, because of the asymmetry of the origin of the large vessels from the aortic arch, cardiac emboli may preferentially lodge in the left MCA. Some studies have reported a higher incidence of left MCA involvement in cardioembolic stroke. One study has suggested that cardioembolic stroke may be more common than has been claimed. When selected types of infarcts were studied, faciobrachial paresis was a sign of a better prognosis.
This result might be explained by the fact that most scales available to measure outcome obviously take into account walking as one of the variables. Moreover, fewer complete MCA infarcts were present in this group and, after exclusion of these infarcts from the analysis, mortality was low and equal in the two groups. In summary, our findings suggest that stroke patients in whom the motor deficit spares the leg have 1 a higher frequency of superficial infarcts, 2 increased embolism because of large-artery disease and atherosclerosis without stenosis , 3 a lower frequency of hemorrhage, and 4 more frequent left hemispheric damage than patients with a deficit involving the leg.
Bogousslavsky chuv. Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy Continue. Table 1. View Large Download. Cerebrovasc Dis. Ann Neurol. Foix CLevy M Les ramollissements sylviens. Rev Neurol. Tredici GPizzini GBogliun GTagliabue M The site of motor corticospinal fibres in the internal capsule of man: a computerised tomographic study of restricted lesions.
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J Neurol Neurosurg Psychiatry. The weakness was severe with little improvement. Lesions involving the medial part of the premotor cortex, the supplementary motor area SMA and the rear portion of the medial part of the precentral gyrus caused a contralateral, severe leg-predominant hemiplegia, distally predominant and a less severe proximal weakness of the arm.
Recovery was much better for the arm than for the leg. Lesions affecting the medial part of the premotor cortex, the SMA and sparing the precentral gyrus caused a contralateral hemiparesis predominating on the leg but predominating proximally on both leg and arm. Recovery was good for leg and arm.
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