Carotid Stenosis Determines Impairment of Ipsilateral Dexterity in Stroke
To the Editor:
I read with interest the article by Sunderland et al1 in the May issue of Stroke. This study demonstrated that within 1 month of an infarct involving the parietal and/or posterior frontal lobe, the majority of left hemisphere patients and a smaller proportion of right hemisphere patients have impaired dexterity of the ipsilateral hand. This result was in agreement with prior studies.2 They suggested that ipsilateral sensorimotor losses may contribute to these impairments, but the major factor appeared to be the presence of cognitive deficits, and the nature of these deficits varied with side of brain damage.
A review of the results in light of prior work in our laboratory reveals a rather simpler interaction of handedness, carotid plaque lesion, and apraxia. Since Fisher’s first description of the relationship between stroke risk and extracranial carotid stenosis, several reports have shown that this risk increases with severity of the carotid lesion.3 The relationship between handedness and severity of carotid stenosis has been demonstrated.4 In right-handed persons, the size of the plaque in the right carotid system was greater than in the left (P=0.01). In left-handed persons, there was a tendency for left carotid plaque size to be greater than that of the right. The odds of greater ipsilateral carotid plaque was 9 times, after controlling for the confounding variables.4 In view of these findings, I hereby propose a model that will explain the results of the present study.1 In right-handed patients with right cerebrovascular accidents (RCVA), left hemiplegia will result (see Figure⇓, top panel). This maybe associated with the greater right internal carotid artery (RICA) plaque stenosis. No apraxia is expected on the ipsilateral right hand. This group comprised 13 patients in the study by Sunderland et al.1 Conversely, in right-handed patients with left cerebrovascular accident (LCVA) (probably due to thromboembolus), right hemiplegia developed. However, because the RICA plaque is of greater severity, left apraxia developed ipsilateral to LCVA. This group comprised 15 patients in the study under discussion.1 In left-handed patients (Figure⇓, bottom) with RCVA, left hemiplegia was present. Because the left internal carotid artery (LICA) plaque lesion is of greater severity, right apraxia developed ipsilateral to RCVA. This group comprised 2 patients in the study.1 Conversely, in left-handed patients with LCVA, no apraxia is expected ipsilateral to LCVA. This group was not studied.
The model here described as “carotid plaque apraxia” therefore postulates that ipsilateral apraxia arises mainly if CVA occurs in the hemisphere contralateral to handedness, as a result of significant carotid plaque lesions. This is of immense clinical relevance, because it will help to identify those patients who will require further investigation for carotid artery disease for prevention of a second stroke on the now-ipsilateral side.
Unfortunately, the authors did not present data on the severity of left and right carotid lesions in their sample population to allow further assessment of this postulate. I hope that extracting such data from their database may be possible and will be reported in a future publication with larger sample size.
- Copyright © 2000 by American Heart Association
Sunderland A, Bowers MP, Sluman S-M, Wilcock DJ, Ardron ME. Impaired dexterity of the ipsilateral hand after stroke and the relationship to cognitive deficit. Stroke.. 1999;30:949–955.
Spaulding SJ, McPherson JJ, Strachota E, Kuphal M, Ramponi M. Jebsen hand function test: performance of the uninvolved hand in hemiplegia and right-handed, right and left hemiplegic persons. Arch Phys Med Rehabil.. 1988;69:419–422.
Fisher CM. Occlusion of the internal carotid artery. Arch Neurol Psychiatry.. 1951;65:346–377.
Njemanze PC. Handedness and carotid plaque lesion. Stroke.. 1992;23:1679–1680.
I thank Dr Njemanze for his interest in our article, and I would like to respond on behalf of my colleagues.
An absolutely crucial aspect of our data concerned the distinctive pattern of ipsilateral impairment after left versus right hemisphere stroke. Had we simply found that ipsilateral dexterity was poorer after left hemisphere damage, this could conceivably have arisen from more frequent compromised function of the supposedly intact right hemisphere. In fact, we found that left-hemisphere damage was associated with ipsilateral slowing and postural errors, whereas right-hemisphere damage was associated with visuospatial errors. These patterns of impairment would not be predicted from Dr Njemanze’s simple model, whereas they are exactly what one would predict from lateralization of cognitive function.R1 The model we proposed was therefore that impaired ipsilateral dexterity reflects deficits in cognitive processing within the damaged hemisphere. These will impair performance with either hand, but this tends to be overshadowed by paresis on contralateral side.
To answer the specific points raised, unfortunately there is no detailed data on carotid lesions for the patients in the study. However, I have checked Dr Njemanze’s suggestion that left-handed patients with RCVA should show “right apraxia.” There were 2 such patients in the study. Neither showed any sign of ideomotor apraxia on action imitation, with perfect performance in both cases. One of them showed visual neglect on the cancellation test, and his errors on dexterity tests reflected this (eg, failing initially to pick up objects to his left). This is consistent with our proposal that the pattern of ipsilateral dexterity impairment reflects cognitive deficit.
Kolb B, Whishaw IQ. Fundamentals of Human Neuropsychology. 4th ed. New York, NY: WH Freeman; 1996.