Ideomotor apraxia, visuomotor control and the explicit representation of posture.

Ideomotor apraxia is normally viewed as a disorder of the representation or execution of action. However, the evidence from gesture imitation is that apraxic patients are unable to reproduce the final posture of a gesture but may not show abnormality in movement kinematics. This supports a hypothesis that impaired gesture imitation is due to a deficit in a conceptual representation of body posture rather than indicating a disorder specific to action control. The present study evaluated whether other aspects of apraxic behaviour might also be most consistent with a deficit in the representation of posture. Patients with left hemisphere damage and apraxia on gesture imitation had difficulty in reproducing a series of actions due to failure to adopt the required configuration of the hand whereas there was no consistent reduction in speed of response once the actions had been learned. They also tended to use an abnormal, clumsy grasp when using a spoon but this dissociated from accurate performance on other tests of manual dexterity where there was less scope for variation in configuration of the hand. These data suggest that the most common deficit in ideomotor apraxia is impaired ability to perform tasks where the goal is to reproduce or adopt complex hand configurations and that impaired execution of some types of action is secondary to this problem. This is consistent with a role for the human left parietal lobe in providing an explicit representation of posture which is used to guide some actions and to supplement a more primitive system of direct visuomotor control.

Impaired dexterity of the ipsilateral hand after stroke and the relationship to cognitive deficit.

BACKGROUND AND PURPOSE: Previous research has reported impaired hand function on the "unaffected" side after stroke, but its incidence, origins, and impact on rehabilitation remain unclear. This study investigated whether impairment of ipsilateral dexterity is common early after middle cerebral artery stroke and explored the relationship to cognitive deficit. METHODS: Thirty patients within 1 month of an infarct involving the parietal or posterior frontal lobe (15 left and 15 right hemisphere) used the ipsilateral hand in tests that simulated everyday hand functions. Performance was compared with that of healthy age-matched controls using the same hand. Standardized tests were used to assess apraxia, visuospatial ability, and aphasia. RESULTS: All patients were able to complete the dexterity tests, but video analysis showed that performance was slow and clumsy compared with that of controls (P<0.001). Impairment was most severe after left hemisphere damage, and apraxia was a strong correlate of increased dexterity errors (P<0.01), whereas reduced ipsilateral grip strength correlated with slowing (P<0.05). The pattern of performance was different for patients with right hemisphere damage. Here there was no correlation between grip strength and slowing, while dexterity errors appeared to be due to visuospatial problems. CONCLUSIONS: Subtle impairments in dexterity of the ipsilateral hand are common within 1 month of stroke. Ipsilateral sensorimotor losses may contribute to these impairments, but the major factor appears to be the presence of cognitive deficits affecting perception and control of action. The nature of these deficits varies with side of brain damage. The effect of impaired dexterity on functional outcome is not yet known.

The nature and prevalence of memory disorder late after stroke.

This study aimed to investigate the incidence and nature of memory impairment late after stroke. Out of 193 patients between 12 to 36 months post-cerebrovascular accident contacted in a postal survey, 113 replied that they had experienced memory impairment following the stroke. Seventy of these patients were assessed on an adapted version of the Rivermead Behavioural Memory Test, Warrington's Recognition Memory Test for words and faces, and an every day memory questionnaire. The Token Test and the Benton Facial Recognition Test were also administered as measures of language and visuoperceptual processing. Thirty-five of the patients were impaired on one or more of the memory measures. Of these, 16 showed no evidence of dysphasia or visuoperceptual impairment. The 16 cases of selective memory impairment typically had mild to moderate deficits, and only three were impaired across all three tests. The results suggest that memory impairment following stroke does not necessarily involve general memory impairment. The evidence for material-specific memory deficits was much weaker.

Adaptation to cognitive deficit? An exploration of apparent dissociations between everyday memory and test performance late after stroke.

It is widely believed that spontaneous improvements in functioning late after brain damage are due to processes of adaptation to permanent cognitive deficits. Reports of everyday memory and the pattern of performance on memory tests were investigated in 70 patients more than a year after a stroke. Contrary to the adaptation hypothesis, performance on simulations of everyday tasks (Rivermead Behavioural Memory Test) correlated strongly with performance on a test where there was little scope for compensatory strategies (forced-choice recognition memory for words). In 12 cases, initial assessment with the EMQ20 questionnaire suggested few cognitive failures in everyday life despite poor test performance. However, where further investigation was possible, it seemed that unreliability of measures or subtle everyday effects of non-verbal memory impairment could explain the apparent discrepancies. In addition, patients who did poorly on tests were not reported to make frequent use of memory aids. Adaptation to deficit does not therefore appear to be a major influence on everyday memory performance late after stroke, but it may have subtle effects or may be important in other areas of functioning. Implications for clinical memory assessment are discussed.