Normal pressure hydrocephalus (NPH) presents in adult patients with gait dysfunction, cognitive decline, and urinary incontinence. Gait dysfunction typically represents the first or most prominent of these symptoms, and commonly exhibits greatest improvement following cerebrospinal fluid (CSF) drainage [1–4]. Despite their importance and debilitating effect on NPH patients, gait abnormalities remain unexplained by a unified, accepted theory. In contrast, more appears to be known regarding the mechanism of urinary dysfunction in idiopathic NPH. In this context, bladder irregularity appears to arise from detrusor overactivity in relation to aberrant cerebral autonomic control and exaggerated micturition reflexes . Older theories regarding gait dysfunction in NPH targeted the pyramidal tracts controlling lower extremity movement. These hypotheses conjectured that third ventricular dilation compressed descending motor tracts within the internal capsule. Such compression could cause demyelination and/or axonal loss, resulting in amplitude reduction and latency prolongation . However, later research using motor evoked potentials (MEPs) showed no evidence of aberrant conduction along the central motor pathway . Furthermore, ventricular compression upon descending motor tracts in the internal capsule also should profoundly impact arm and hand movements. Nowak and Topka showed the hypokinetic movement disorder in NPH extends to upper limb motor control, specifically with grasp-lift synergy and force overshooting . Nonetheless, upper limb involvement remains secondary to the hypokinetic gait disorder in the primary symptoms of NPH. These multiple findings have raised questions regarding the role of pyramidal tracts in the pathophysiology of NPH gait dysfunction. Additionally, the typical lack of lower extremity weakness in NPH patients might argue against pyramidal tract dysfunction. No commonly accepted theory regarding the mechanism of gait impairment in NPH has been otherwise formulated.
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