Correlation of midbrain diameter and gait disturbance in patients with idiopathic normal pressure hydrocephalus

Abstract

The clinical elements of the NPH gait can be summarized as a hypokinetic gait which is characterized by diminished gait velocity, reduced stride length, reduced step height, and dynamic disequilibrium [17,28,31,34]. Patients with many other neurodegenerative diseases, such as Parkinson's disease, subcortical arteriosclerotic encephalopathy, progressive supranuclear palsy (PSP), and corticobasal degeneration, may develop hypokinetic gait during the disease progression [4,35,37] ■ Abstract Background and purpose Although gait disturbance is an important feature of idiopathic normal pressure hydrocephalus (NPH), only tentative theories have been offered to explain its pathophysiology. It has been suggested that the mesencephalic locomotor region is the anatomical substrate for the development of the hypokinetic NPH gait. To investigate this possibility, we evaluated the correlation between gait disturbance and midbrain diameter. Methods We enrolled 21 patients with NPH and 20 age-matched control subjects for the study. The maximal diameter of the midbrain and pons, and the width of the lateral and third ventricles were measured using midsagittal T1-weighted MRI and axial T2-weighted MRI, respectively. Gait disturbance, cognitive dysfunction, and incontinence were semiquantified. Results The maximal midbrain diameter was significantly smaller in the NPH group than in the controls (14.8 ± 0.9 vs. 17.1 ± 0.7 mm, p < 0.001). There were inverse correlations between the midbrain diameter and the widths of the two ventricles (r = -0.562, p = 0.008 for the third ventricle, and r = -0.510, p = 0.018 for the lateral ventricle). The severity of gait disturbance was negatively correlated with the midbrain diameter (r = -0.598, p = 0.004), but the degree of cognitive dysfunction and incontinence showed no significant correlation with midbrain diameter or ventricular width. Conclusions This study suggests that midbrain atrophy is significantly associated with gait disturbance in NPH.

Midbrain atrophy in subcortical ischemic vascular dementia

“…This degeneration appears to be responsible for gait freezing, gait ignition failure, and postural instability in patients with either PSP or advanced Parkinson's disease [18,26]. In patients with normal pressure hydrocephalus (NPH), gait disturbance was reported to be inversely related to midbrain diameter [19]. Since the present study was performed retrospectively, we could not assess any functional correlations between the AP diameter of the midbrain and changes in various cognitive domains or severity of gait disturbance.…”

Guidelines for Management of Idiopathic Normal Pressure Hydrocephalus Guidelines From the Guidelines Committee of Idiopathic Normal Pressure Hydrocephalus, the Japanese Society of Normal Pressure Hydrocephalus

“…3 as a reference for the differential diagnosis of both disorders. The diameter of the midbrain is reportedly decreased in iNPH, and negatively correlated with the severity of gait disturbance 60,81) (Recommendation grade C).…”

Global cerebral hypoperfusion in preclinical stage of idiopathic normal pressure hydrocephalus

“…The fact that rCBF was equally reduced in the AOS and NOS groups suggests that factors other than reduced rCBF are involved in the manifestation of symptoms in iNPH patients. Possible factors include (1) low availability of striatal D2 receptor, which is associated with hypokinetic gait and anhednic mentation in iNPH patients [40], (2) the compressive effect of the ventricles on several brain areas [41][42][43], (3) apoptosis of neuronal cells [44], and (4) dysfunction of the neurons [45].…”