The previous sections in this chapter have discussed how various cortical areas and descending pathways contribute to voluntary movement in the context of how these areas might provide compensatory control for each other after brain injury. The M1 areas, NPMAs, and descending pathways appear to be a relatively flexible system, controlling movement through parallel, distributed processes. This final section discusses how, in addition to lesion size and location, spared territories and tracts might affect the capacity for functional recovery of movement.
With the development of imaging techniques such as computed tomography (CT) and magnetic resonance (MR), researchers have examined the relationships between lesion size, lesion location, and motor function. The degree of motor impairment and recovery of function cannot be predicted by just lesion size or just lesion location (Chen et al., 2000; Binkofski et al., 2001). Rather, motor impairments and potential for functional recovery can be better predicted by determining what percentage of the corticospinal system is affected (Pineiro et al., 2000). Although we intuitively think that larger lesions will produce more severe motor impairments with less potential for recovery, this relationship is confounded by lesion location and by what territory or tracts are spared. Two lesions of comparable size but in different locations can produce differing degrees of motor impairments and differing prognoses for functional recovery. For example, a small lesion relatively confined to the M1 hand knob results in initial paresis of only the hand and arm (Kim, 2001), yet within a few months, the patient typically can use the hand and arm well except for activities requiring fine independent finger movements, such as typing. In contrast, a lesion of comparable size on one side of the basis pontis, affecting the entire corticospinal tract, results in initial paresis affecting the face, hand, arm, and leg (Fisher, 1982), and although much of the initial deficit typically improves over time, the patient often is left with permanent residual deficits in the hand, arm, and leg. Differences in functional recovery reflect both the structures affected by the lesion and the structures that remain intact. The first lesion damages Ml territory controlling the hand and arm, but compensatory control for functional recovery can arise from both spared M1 territory and the NPMAs, reaching the spinal cord over an otherwise intact corticospinal tract. The latter lesion damages the entire corticospinal tract, so that compensatory control from the intact Ml and NPMAs can reach the spinal cord only through alternate descending pathways. Thus, lesion size, lesion location, and spared territories interact in a complex manner to affect not only motor impairments, but the capacity for plastic reorganization and the resulting recovery of function.
Lesion size and location may also influence which cortical motor areas undergo plastic reorganization after brain injury (Liu and Rouiller, 1999). In the case of very small experimental lesions that affect only a portion of monkey Ml, reorganization was observed primarily in the spared territory within Ml. In the case of small to moderate lesions that affected the entire Ml territory, reorganization occurred primarily in NPMAs in the same hemisphere. And in the case of large lesions that affected Ml and NPMAs, reorganization occurred in the contralateral Ml and NPMAs. Similarly in humans after stroke, better functional recovery is associated with less activation in the NPMAs of the same hemisphere and with less activation in the contralateral Ml and NPMAs (Ward et al., 2003). Patients with more complete recovery were likely to have near normal brain activation patterns, while patients with poor recovery were more likely to activate additional motor areas in the same and in the contralateral hemispheres. Furthermore, the probability of recovery of upper extremity function is greatest after lesions relatively isolated to M1 and decreases progressively with descending lesions affecting the descending corticospinal axons (Shelton and Reding, 2001). Taken together, these data suggest that spared territories and tracts can control voluntary movement in humans after brain injury, but that the spared territories and tracts cannot fully compensate for the highly selective control provided by M1 and the crossed corticospinal system.
In summary, rehabilitation professionals should evaluate what areas and tracts remain intact after each patient's brain injury, as well as assessing lesion location, and size. A better understanding of the anatomy and physiology of the spared components of the nervous system and their capacity for reorganization may improve the ability to design and implement effective individualized rehabilitative strategies, and thus promote greater functional recovery.
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