Motor

Motor System Localization

Identification and description of motor deficits is critical for the understanding of neurologic localization. The assessment of the presence of weakness and other motor deficits provides an excellent basis for approaching the localization of brain lesions.

Elements required for localization of lesions affecting the motor system include:

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  Nature of the deficit

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    Weakness

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    Incoordination

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    Stiffness

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    Tremor

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    Spasms or jerking

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  Location of the motor deficit

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    Generalized

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    Focal

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    Multifocal

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    Shifting location

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  Associated symptoms

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    Sensory loss

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    Visual deficit

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    Speech deficit

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  Examination findings

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    Objective weakness

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    Subjective weakness without objective deficit identified

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    Spasms or clonic movements

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    Tremor

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    Rigidity

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  Associated nonmotor clinical findings

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    Tendon reflex

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    Pathologic reflexes

On the basis of these findings, the deficits can be localized to one of almost innumerable locations. For example, rigidity with hyperreflexia and extensor plantar response indicates a corticospinal tract lesion, and the location of that lesion would be different if there was or was not sensory involvement.

It would be impossible to document the diagnosis with each of the possibilities of these findings, but this chapter will discuss some general principles of how these data are used in diagnosis.

Upper Versus Lower Motor Neuron

The motor system is largely a two-neuron pathway, consisting of an upper motor neuron and a lower motor neuron. The upper motor neuron has its cell body in the cerebral cortex, located in the portion of the cortex according to the somatotopic organization (leg medial, arm superior, face lateral). The upper motor neuron projects through the corona radiata, which coalesces in the internal capsule (in the posterior limb), then continues its descent through the brainstem. Fibers destined for cranial nerves and the innervation of the muscles associated with them will exit this pathway within the brainstem. Fibers destined for the body continue descending in the most ventral aspect of each component of the brainstem—the crus cerebri of the midbrain, the basis pontis in the pons, and the pyramids in the medulla. In the pyramids, the corticospinal tracts decussate and continue descending to the spinal level responsible for their innervation. At that level, fibers exit the main corticospinal tract to then innervate lower motor neurons whose cell bodies reside in the ventral horn of the spinal cord. These neurons exit the spinal cord through ventral roots and end up innervating target muscles.

One key distinction in the localization of weakness is the distinction between damage to upper motor neurons and lower motor neurons. Lesions of upper motor neurons often affect groups of muscles, whereas lesions of lower motor neurons can affect single muscles. Lesions of upper motor neurons result in spasticity (i.e., velocity-dependent increase in tone), whereas lesions of lower motor neurons result in atrophy (decrease in muscle size) and fasciculations (spontaneous twitching of muscles). Deep tendon reflexes can also help distinguish between upper motor neurons and lower motor neurons lesions. With upper motor neuron lesions, reflexes are typically increased (along with the presence of the Babinski sign); with lower motor neuron lesions, reflexes are typically reduced.