Localization of Coordination Control and Deficits

Coordination is a prominent part of the examination. Whereas coordination is typically considered to be a test of cerebellar function, coordination deficits can be produced by a wide range of lesions. Coordination depends on the integrity, not only of the brainstem and cerebellum but also of the sensory and motor afferent and efferent pathways and motor and premotor regions.

The location of the first thought of movement is not known. The premotor cortex of the frontal lobe is involved in planning movement and seems to do so by considering movement in the context of prior movements experienced and learned. Then this activates the motor cortex to drive the actual movements. For some movements, especially stabilizing movements, the supplementary motor cortex plays an additional role. The motor cortex projects to the subcortical nuclei, brainstem, and spinal cord. Along the way, there are sensory afferents that indicate how successful the attempts at movement were and aid in adjusting motor effort appropriately at both spinal and cerebral levels. Hence, deficits in coordination can be caused by dysfunction in a wide range of potential locations.

Cerebral cortex lesions usually produce lack of movement if severe and poorly controlled movement if not severe. Reasons for dysfunction include a wide range of pathologies that differ in acuity and hence differ in onset and physiologic compensation for the deficit. Stroke damage is acute, whereas a brain tumor produces slow onset and progression of symptoms.

The basal ganglia participate in control of motor function. The striatum receives afferents from the cortex, thalamus, and substantia nigra, among other regions. There is significant internal processing within the striatum, and output is chiefly to the globus pallidus and substantia nigra. Damage to the basal ganglia produces difficulty with coordination of movement rather than paralysis. This might include excess movement such as dyskinesias or dystonia or impaired movement with tremor and/or ataxia.

The cerebellum is a constellation of structures that serve to coordinate movement. The anatomy and functional physiology of the cerebellum and connections with other motor and sensory systems are complex, but simply, the cerebellar hemispheres coordinate movement of ipsilateral limbs. The cerebellar vermis is predominantly involved in coordination of gait and other midline functions. Cerebellar hemisphere lesions produce dysmetria during finger-nose-finger or heel-knee-shin testing on the side of the lesion. More midline cerebellar lesions produce gait ataxia with impairment in accurate foot placement. Note that vascular causes often affect the brainstem and the cerebellum, so cranial nerve deficits help with that localization.

Clinical Correlations

Differentiating Deficits

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