Paraparesis refers to bilateral leg weakness. Paraparesis may occur with brain lesions, spinal cord lesions in the thoracic area, and lumbosacral center lesions (Figure 238.1 A-D). Brain and thoracic spine lesions may produce spastic or flaccid paraparesis. Lumbosacral center lesions produce flaccid weakness. Spastic weakness is characterized by increased muscle stretch reflexes, strong leg recoil to a sudden intense pull, and sustained ankle clonus. Flaccid weakness is characterized by decreased or absent muscle stretch reflexes, weak leg recoil to sudden intense pull of the leg, and no ankle clonus.
Brain lesions in the parasagittal region (Figure 238.1 A) or bilateral periventricular lesions (Figure 238.1 B) produce paraparesis. Paraparesis occurs with parasagittal lesions of the mesial regions of the postcentral gyrus. Bilateral periventricular lesions produce paraparesis because the fibers to the leg musculature travel closer to the lateral ventricles than the fibers to the arm and facial musculatures and, therefore, leg fibers are selectively affected with mild dilatation of the lateral ventricles.
Paraparesis may also occur with spinal cord lesions below T1 and above the lumbosacral center due to involvement of the descending corticospinal pathways (Figure 238.1 C). Paraparesis due to spinal injury may be associated with fecal and urinary incontinence and a sweat line may be present.

Figure 238.1.— Possible sites of anatomical injury producing paraparesis: A: parasagittal region; B: bilateral periventricular regions; C: spinal cord below T1; D: lumbosacral center; V: ventricles; T: thalamus; FN: facial nerve; UQ: upper quadrant; LQ: lower quadrant; BP: brachial plexus; LSP: lumbosacral plexus. The colored rectangles indicate the location of weakness produced by damage to the various components of the somatic motor system.