I read the article by Benson et al. [1] with interest. My own data,
based on CT imaging, support their conclusions. In a convenience sample of
343 patients, including patients with stroke, gait was examined with a
standardized scale [2] and leukoaraiosis rated in seven brain regions
using a modification of the van Swieten method [2, 3]. Neurologic
abnormalities were quantified using the NIH stroke scale and supplemental
scale. The brain region most correlated to gait disturbance was identified
by analysis of variance. Ordered logit models were then used for further
analysis (because of the ordinal nature of the gait scale).
The patients were predominantly male (96%) with a mean age of 68±10
years. Leukoaraiosis was found in 160 patients (47%). A history of stroke
was present in 179 patients (52%), and radiologic evidence of stroke was
present in 176 (51%). Leukoaraiosis correlated to the presence of
subcortical stroke (64% versus 37%, p=0.001), but not to cortical stroke
(47% vs 47%).
Analysis of variance found leukoaraiosis in the left frontal region
had the highest correlation coefficient to the gait scale (r=0.49,
p<0.0001; ordered logit coefficient 1.35, p<0.001). In the absence
of left frontal leukoaraiosis, no other region showed statistical
correlation to the gait scale (coefficients ranged from -0.13 to 0.19,
p=ns). A history of stroke (coefficient 1.06, p<0.001 and radiologic
evidence of stroke (particularly subcortical stroke: coefficient 0.73,
p<0.001) both correlated to gait disturbance. Leg weakness or ataxia
correlated to gait disturbance, but not to left frontal leukoaraiosis. In
models including all of the above, only leg weakness and ataxia
(coefficient 1.56, p<0.001) and left frontal leukoaraiosis (coefficient
1.32, p<0.001) were independent predictors of gait disturbance.
Thus, these data support the role of frontal white matter
leukoaraiosis, particularly on the left side, as a necessary lesion in
gait disturbance, but not more posterior leukoaraiosis. This may reflect
either different methodology or the larger number of patients examined.
Perhaps the specificity that Benson et al report with posterior
leukoaraiosis reflects greater disease severity. While leukoaraiosis does
appear to be a form of cerebrovascular disease [4], my data indicate the
effects are independent of those of overt stroke. I agree that
leukoaraiosis may be associated with a "significant portion of mobility
impairment" in older individuals and that further natural history studies
are necessary as this may portend a poor prognosis [5].
Acknowledgement: I acknowledge the help of Susan Sergent, PA-C in
data collection and Stuart Thomas, PhD in data analysis and my patients of
the Huntington VAMC, Huntington, WV.
References:
1) Benson RR, Guttmann CRG, Wei X et al. Older people with impaired
mobility have specific loci of periventricular abnormality on MRI.
Neurology 2002;58:48-55.
2) Briley DP, Wasay M, Sergent S, Thomas S. Cerebral white matter
changes (Leukoaraiosis), Stroke and Gait Disturbance. JAGS 1997;45;1434 -
1438.
3) van Swieten JC, Hijdra A, Koudstaal PJ, van Gijn J. Grading white
matter lesions on CT and MRI: a simple scale. J Neurol Neurosurg
Psychiatry 1990;53:1080-1083.
4) Pantoni L, Garcia JH. Pathogenesis of leukoaraiosis. Stroke
1997;28:652-659.
5) Briley DP, Haroon S, Sergent SM, Thomas S. Does leukoaraiosis
predict morbidity and mortality? Neurology 2000; 54:90-94.