Case 112, Video 1: This 75-year-old woman had a 3-year stepwise progression of gait, balance, and cognitive impairment, with falls and requirement of a walker after 2 years from symptom onset. She had arterial hypertension, hypercholesterolemia, diabetes, and was a smoker.

Case 112, Video 2: This 80-year-old man had a 2.5-year staggering progression of gait and balance impairment, sudden-onset freezing of gait hospitalizations, falls, and urinary incontinence. He had hypertension, hypercholesterolemia, Ménière disease; he accumulated a 60 pack/year history of smoking.

Both of these patients have a similar history of stepwise deterioration of gait over several years and shared several vascular risk factors. The initial working diagnosis was that of a lower-body parkinsonian syndrome, which was most suggestive of VaP. Both patients showed signal abnormalities in the periventricular and deep white matter, which further supported that assertion (Figs. 112.1 and 112.2).

However, in Patient 2 the degree of “small vessel disease” noted on magnetic resonance imaging (MRI) was of lesser magnitude than in Patient 1, and the extent of associated ventriculomegaly somewhat greater. These considerations were overshadowed by a heavy vasculopathic history and a stepwise deterioration suggesting strokelike events. Nevertheless and acquiescing to requests by his family physician, Patient 2 underwent a 3-day external lumbar drainage procedure, which in fact demonstrated a 40% gain in gait velocity and optimization of all of his gait parameters, as well as improvements in most of his cognitive endpoints, which had collectively crossed into the realm of moderate dementia prior to the procedure
(see third video). As a result, this patient underwent a ventriculoperitoneal shunt placement. Unfortunately, bowel perforation at the abdominal end of the shunt emerged as an immediate postoperative complication and the patient succumbed to septic peritonitis. Brain autopsy demonstrated typical findings previously reported in NPH, namely, dilatation of the lateral and third ventricles associated with fibrous thickening of the leptomeninges, gaps in the ependymal lining, and periventricular gliosis. Despite our clinical prediction, there was no direct evidence of the “small vessel” ischemic disease suggested by imaging (which would have included gliosis, perivascular pallor, hyaline thickening, and widening perivascular spaces).