Gait impairment, worse equilibrium scores and falls are associated with leukoaraiosis, as widely recognised [1-6]. In Binswanger’s disease with a severe leukoaraiosis gait disorders are clearly evident while patients with mild periventricular changes may present subclinical forms of gait disorders, as proposed by some authors (see data in [7]).
Gait disorders in the elderly are particularly relevant, since they can influence the loss of functional independence and death [8]. As anticipated, cerebral small vessel disease (both white matter lesions and lacunar infarcts) correlates with gait parameters: stride length and a lower gait velocity [8]. Most importantly, subcortical vascular lesions seem to increase the possibility of falls, even if clear evidences are still lacking [9-11].
Walking difficulties in Alzheimer’s disease are well described [12]: patients show slow and irregular steps, difficulties in turning and avoiding obstacles [13, 14]. These disturbances have been described also in patients free from extrapyramidal, ataxic, paretic signs, and clinically relevant musculoskeletal impairments [12, 14]. Moreover, Alzheimer’s disease patients have a worse balance [12, 14, 15] and a higher risk of falls compared with matched controls [16, 17]. The prevalence of gait abnormalities varies widely across the studies (from 8.7% [18] to over 90% [19]); this can be explained because of different inclusion criteria and/or assessment procedures.
These observations have been confirmed by studies demonstrating that patients with Alzheimer’s disease walk more slowly compared to healthy controls [12] and these gait problems have been interpreted as manifestations of the extrapyramidal deficits (well-known to affect 12–28% of Alzheimer patients), or as side effects of drug treatment (e.g. neuroleptic agents) [20]. Since a overt walking problems and trunk movement alterations can be seen also in absence of extrapyramidal signs, it has been proposed that some Alzheimer’s disease patients may present “frontal gait disorder”, a syndrome coterminous with gait apraxia [21, 15]. The lack of a standardised instrument to assess gait has been implicated as a possible cause for the low frequency of reports on the topic.
Since the walking assessment cannot discriminate between walking disorders caused by gait apraxia and other neurological causes of walking difficulty, there has been the necessity to exclude alternative causes of walking abnormalities in Alzheimer’s disease (overt extrapyramidal impairments or other concurrent neurological diseases); in order to assess gait capacity, a new test has been proposed and a large proportion of the sample (40%) scored below cut off, even if the percentage of severely impaired was smaller. Although the possibility of right–left confusion, working memory deficits, and problems with verbal comprehension was minimised by demonstrating the items, the complexity of some of them might have contributed to inflating the proportion of patients performing poorly. Even though, the presence of associated vascular pathology in a few patients also cannot account for the outcome. Neuroradiological signs of white matter changes were reported in three of the 24 patients (22.5%) in the Della Sala et al.’s study [12], who scored below cut off in the assessment of walking skills.
Therefore, in a well-defined population suffering from subcortical vascular dementia and Alzheimer’s disease (standing from a neurological, clinical, and radiological criteria), we tried to explore gait, balance and equilibrium alterations, and a behavioral complex symptom, such as apathy, even considering precipitant factors, such as concomitant pathologies and consequent therapies. We now present an extension of the work, with a speculation on what we observed for a two-year follow-up.
