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The anatomical location of the lesion is established by determining if the weakness is spastic or flaccid. Spastic weakness is characterized by increased muscle stretch reflexes, sustained ankle clonus, and excessive resistance and recoil of the leg when the leg is suddenly pulled by the foot and let go. Clonus is often present. Spastic weakness occurs with upper motor neuron lesions (Figure 234.1 A-E). Flaccid weakness is characterized by decreased or absent muscle stretch reflexes, no resistance of the leg when suddenly pulled by the foot, and no recoil when let go. Flaccid weakness occurs with upper or lower motor neuron lesions (Figure 234.1 F-H).

 

Figure 234.1. Schematic representation of the cortical component of the somatic motor system and sites of possible injuries causing leg monoparesis. The colored rectangles indicate the location of weakness produced by damage to the various components of the somatic motor system. V: ventricles; T: thalamus; UQ: upper quadrant; LQ: lower quadrant; FN: facial nerve; BP: brachial plexus; LSP: lumbosacral plexus. A: brain and midbrain; B: upper pons; C: lower pons and medulla; D: upper spinal cord above the brachial center; E: lower spinal cord below the brachial center but above the lumbosacral plexus; F: lumbosacral motor center; G: lumbosacral plexus; H: lower extremity peripheral nerves.

 

SPASTIC LEG MONOPARESIS

Spastic leg weakness may occur after several weeks with lesions that involve the central component of the lumbosacral somatic motor system in the brain, brainstem, or spinal cord (Figure 234.1 A-E). Brain lesions in the mesial aspect of the precentral gyrus, or in the fibers from the neurons in this area before they reach the internal capsule, may produce contralateral spastic leg monoparesis. Brain lesions that extend beyond the mesial aspect of the precentral gyrus, or the fibers from this region, are more likely to produce contralateral hemiparesis. Spastic leg monoplegia due to a lesion close to or in the cortex may be associated with seizures. Lesions in the lumbosacral motor system that occur between the internal capsule and the lower medulla rarely produce leg monoparesis, because a lesion in this area, unless extremely small and strategically located, will involve the arm fibers and produce hemiparesis. Unilateral spinal cord lesions between the lower medulla and first thoracic segment (Figure 234.1 D) usually do not produce leg monoplegia (they usually produce hemiparesis unless small and strategically located because the leg and the arm fibers travel very close together). A unilateral lesion below the second thoracic spinal segment and above the lumbosacral center (Figure 234.1 E) may produce spastic leg monoparesis but spastic diplegia occurs more frequently because most lesions in this area are tumors. Tumors usually produce mass effect and push the enlarged spinal cord against all sides of the bony spinal canal.

 

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lower extremity peripheral nerve lumbosacral plexus lumbosacral plexus brachial plexus lumbosacral motor center lower spinal cord upper spinal cord lower pons and medulla upper pons brain to midbrain facial nerve fibers to the lower facial quadrant fibers to the upper facial quadrant thalamus thalamus thalamus lateral ventricle lateral ventricle To identify a structure pause the pointer over the abbrevations, or the structure in question; to idenyify the sites of injury pause pointer over the letters; do not click. Not all structures are labeled. Figure must be centered.