TY - JOUR
T1 - Correlation of midbrain diameter and gait disturbance in patients with idiopathic normal pressure hydrocephalus
AU - Phil, Hyu Lee
AU - Suk, Woo Yong
AU - Young, Hwan Ahn
AU - Huh, K.
PY - 2005/8
Y1 - 2005/8
N2 - 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 ± 0.7mm, 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.
AB - 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 ± 0.7mm, 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.
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U2 - 10.1007/s00415-005-0791-2
DO - 10.1007/s00415-005-0791-2
M3 - Article
C2 - 15834647
AN - SCOPUS:23944485996
SN - 0340-5354
VL - 252
SP - 958
EP - 963
JO - Journal of Neurology
JF - Journal of Neurology
IS - 8
ER -