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B Macauley

Publications and source records attributed to B Macauley.

6 recordsLinked to original sources

Apraxia differs in corticobasal degeneration and left-parietal stroke: A case study.

Corticobasal degeneration (CBD) is a progressive disorder characterized by both cortical and basal ganglia dysfunction such as asymmetrical apraxia, and akinetic rigidity, involuntary movements, and cortical sensory loss. Although apraxia is a key finding for the differential diagnosis of CBD, it has not been determined whether the features of apraxia seen in subjects with CBD are similar to those features exhibited by subjects with left-hemisphere damage from stroke. Therefore, for both clinical purposes and in order to better understand the brain mechanisms that lead to apraxia in CBD, we studied praxis in a patient with CBD and compared him to patients who are apraxic from left-parietal strokes. We used three-dimensional movement analyses to compare the features of apraxic movement. This subject with CBD was a dentist whose initial complaint had been that he "forgot" how to use his tools in the mouths of his patients. Analyses were performed on the trajectories made when using a knife to actually slice bread, and when repetitively gesturing slicing made to verbal command. Movements of the left hand, wrist, elbow, and shoulder were digitized in 3-D space. Although the CBD subject was clearly apraxic, the features of his apraxia differed markedly from those of the subjects with lesions in the left parietal lobe. For movements to command, the CBD subject showed joint coordination deficits, but his wrist trajectories were produced in the appropriate spatial plane, were correctly restricted to a single plane, and, like control subjects, were linear in path shape. However, when he was actually manipulating the tool and object, all of these aspects of his trajectories became impaired. In contrast, the deficits of the apraxic subjects with left-parietal damage were most pronounced to verbal command with their movements improving slightly although remaining impaired during actual tool and object manipulation. Unlike patients with parietal strokes, patients with CBD have degeneration in several systems and perhaps deficits in these other areas may account for the differences in praxic behavior.

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Apraxia in corticobasal degeneration.

Corticobasal degeneration (CBD) is a degenerative disease that often presents with an asymmetric progressive ideomotor limb apraxia. Some apraxic subjects may fail to perform skilled purposive movements on command because they have lost the memories or representations that specify how these movements should be performed (representational deficit). In contrast, other apraxic subjects may have the movement representations but are unable to utilize the information contained in them to execute skilled purposive movements (production-execution deficit). To learn if the apraxic deficit in CBD is induced by a representational or a production-execution deficit, we tested three nondemented subjects with CBD on tasks requiring production of meaningful or meaningless gestures to command, gesture imitation, gesture discrimination, and novel gesture learning. A fourth subject with incomplete data also is presented. The results suggest that the apraxia associated with CBD is initially induced by a production-execution defect with relative sparing of the movement representations.

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Left hemispheric specialization for learned, skilled, and purposeful action.

Three-dimensional motion analyses were performed on trajectories of repetitive "slicing" gestures by 4 participants with left-hemisphere lesions and limb apraxia, 6 participants with right-hemisphere lesions, and 7 neurologically intact participants. Left hemispheric lesioned participants with apraxia, but not right hemispheric lesioned participants showed impaired coupling of spatial and temporal aspects of wrist trajectories and deficits in interjoint coordination. Both groups of brain-lesioned participants differed from control participants in the 3-D plane of the wrist motion. The deficits of some right hemispheric lesioned participants in controlling the plane of wrist motion may be a consequence of left hemispatial neglect with rightward deviations. In contrast, the deficits of apraxic participants in controlling wrist trajectories and coordinating joint motions seem to reflect a deficit in these participants for the movement plan.

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Visual-imitative dissociation apraxia.

Liepmann posited that, in right handers, the left parietal lobe contains movement formulas or representations. Therefore, performance failures may be induced by degraded representations, a failure of these representations to influence motor systems or a failure of stimuli to fully access these representations. Imitation may help the performance of subjects with degraded representations. However, patients who have impaired visual access to movement representations may perform more poorly with imitation than to verbal command. Trajectories of repetitive 'slicing' gestures made by a previously reported subject (Raymer et al.) with an infarction in the left visual association cortex (left occipital and inferior temporal lobe) that spared the parietal lobe were contrasted with those of three apraxic subjects with lesions that included the left parietal lobe and four non-brain-damaged control subjects. All subjects were asked to produce the gesture to verbal command and to imitation. Movements of the left hand, wrist, elbow and shoulder were digitized from neighboring views, reconstructed in three dimensions, and analysed graphically and numerically. The apraxic subjects with left parietal damage were unable to maintain the proper linearity and spatiotemporal attributes of their wrist motions and showed interjoint coordination deficits. Their deficits were most pronounced to verbal command, with their movements improving though remaining poorly performed when they imitated. The subject with the left occipital and inferior temporal lesion that spared parietal cortex, however, showed an opposite pattern. This subject exhibited close to normal performance when producing the movement to verbal command, but significant deficits when imitating.

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Joint coordination deficits in limb apraxia.

Competing models of the basis of limb apraxia were tested through analysis of joint coordination deficits in three apraxic subjects with lesions that included the left parietal lobe. Three-dimensional shoulder, elbow, wrist and hand trajectories were recorded for repetitive 'slicing' gestures made in a series of conditions in which contextual cues were introduced in a graded fashion. The apraxic subjects showed marked deficits in joint coordination across context conditions. Even when actually manipulating a tool and object, the apraxic subjects failed to show proper joint synchronization, failed to apportion their relative joint amplitudes properly, and failed to produce the correct phase relationships among pairs of arm angles. Thus, apraxic subjects not only have deficits in the spatial plan for the movement, but they also have deficits in translating those plans into the details of the angular motions at the joints, even when actually manipulating a tool and object. These data support a model of apraxia in which apraxia can result from either the destruction of visuo-kinaesthetic motor representations of learned movement, stored in posterior association cortex, or from a separation of these representations from premotor or motor areas.

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Spatial planning deficits in limb apraxia.

Geschwind (1975) proposed a disconnection model in which an apraxic subject is unable to carry out movements to command because the left hemisphere that comprehended the verbal command is disconnected from the right premotor and motor areas which controls the left hand. An alternate model, however, proposes that apraxia results from destruction of spatiotemporal representations of learned movement stored in the left hemisphere (Heilman, 1979). The disconnection hypothesis would predict that apraxic subjects should be able to correctly imitate gestures and correctly use actual tools since these tasks do not require language. The movement representation model predicts that imitation and actual tool use would also be impaired. Motion analyses were performed on the trajectories of repetitive 'slicing' gestures made in a series of conditions in which contextual cues were introduced in a graded fashion. Four cue conditions were presented: no cues (verbal command), object present, tool present and both object and tool present. Positions of the hand, wrist, elbow, and shoulder were digitized from neighbouring views, reconstructed in three dimensions and analysed with respect to specific spatiotemporal features of the trajectories. Three subjects with limb apraxia, who had lesions that included left parietal cortex, and four neurologically intact subjects participated. The apraxic subjects showed disturbances in planning the movement of the hand in space across the cue conditions. For example, they showed deficits in the plane of motion, the shape of the trajectory and in the coupling of hand speed and trajectory shape even when given full contextual cues. These data support the hypothesis that apraxia can result from the destruction of spatiotemporal representations of learned movement, rather than from a disconnection between the receptive language areas in the left hemisphere and the contralateral motor cortices.

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