Website Edition: April/May 2012

Understanding Gait in Aging: Finding the Way Forward: Part 2

Contributed by Dr. Richard Camicioli, MSc, MD and Dr. Caterina Rosano, MD

There is strong evidence that generalized brain atrophy, small vessel disease and lacunar infarcts are associated with slower gait and balance difficulties in older adults who live in the community and are free from overt neurological disorders or gait complaints. These associations have been shown in cross-sectional [1-6]  [7] [8] [9, 10] [11] [12] and in longitudinal [13, 14] [15] [16] [17] studies.

In the past decade, there has been a strong impetus to apply advanced neuroimaging technology to further understand these relationships and examine the spatial distribution of the neuro-anatomical correlates of slowing gait. Cross-sectional investigations of connectivity and gait speed underscore the importance of tracts localized in the anterior lobes, around the ventricles, [18] [19] [20] [21-23] and in the corpus callosum [24] [25-27].   In addition to  smaller sensorimotor regions and cerebellum,[28] [29] slowing gait is associated with smaller frontal lobes[30] and with atrophy of regions known to be related to information processing [28, 29, 31]. One study also identified significant correlations with the memory-related hippocampal region[32] . Consistent with these initial structural neuroimaging investigations, functional neuroimaging studies have also found significant associations between basal ganglia and prefrontal motor regions in relationship with gait [33-35].

Next steps

The emerging concept of brain adaptation in older adults [39] and the rapid progress of neuroimaging technology have the potential to change the approach to study physical functional impairment in older adults. The use of stronger magnetic fields, including 3Tesla and 7 Tesla, remarkably increases the precision and spatial localization of abnormalities’ quantification.  The application of imaging methods in carefully characterized populations of older adults living in the community can promote future studies to shift current research and clinical practice paradigms in several ways. First, these neuroimaging markers can be related to cognitive and motor behaviors to advance our understanding of the underlying mechanisms of mobility control (e.g. via overall processing speed and/or through distinct pathways). Secondly, they can advance our intervention approaches to ameliorate gait, including pharmacological and behavioral strategies such as exercise and diet. Lastly, neuroimaging measures can be used as biomarkers to identify the individuals that might benefit the most from intervention and to quantify response to therapy’s type and dose, and as newer targets of therapies.

What therapies deserve attention?

If the role of white matter abnormalities in determining physical functional loss is as prominent as studies suggest,   then intervention trials should focus on white matter biomarkers. Specific attention should be given to the fronto-parietal and subcortical areas, which are intrinsically vulnerable to damage, most likely due to poor collateral vascularization.[39, 40]   Recent findings that antihypertensive treatments stop or delay progression of small vessel disease,[41-44] and subsequent cognitive impairment,[45, 46] suggest the potential to prevent mobility impairment through hypertension control especially at younger and middle ages.  Additionally, there is the potential to use growth factors to stimulate production of new white matter cells even very late in age [47, 48].  White matter regeneration is already one of the main therapeutic targets in models of acute neuronal damage.[49, 50] Recent animal studies have shown that promoters of axonogenesis and of myelination have beneficial effects on behavioral measures and motor tasks.[47]
Recent evidence [51] also points to the potential for cross-over benefits of therapies targeting different domains. Therefore, studies should explore whether psychological intervention (e.g. to improve processing speed) alone or combined with motor intervention could delay the trajectories of slowing gait.


While intervention studies to improve gait in older adults appear premature because of the sparse evidence on the pathogenesis of mobility impairment, the rapid methodological advancements and the recent intervention trials are very promising.  Specifically, there remains the need for longitudinal studies of mobility control that integrate both peripheral and central components to fully understand the mechanisms underlying motor control.

As a step in this direction the NIA in cooperation with the Gerontological Society of America is sponsoring a series of workshops coupled to a thematic scientific program. The goal of this new initiative is to bring clinical and basic science and to develop a paradigm for the understanding of gait disorders of aging.


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Table: Pathological and age-related neurological changes that might contribute to gait impairment in older people.


Specific Anatomic Localization


Age-related correlate

Associated Findings





Waddling, slow/ Weakness, difficulty rising from a chair


Neuromuscular Junction

Myasthenia gravis

Neuromuscular junction dysfunction with aging

Slow, weak, fatiguable/
Oculomotor impairment, ptosis, fatiguable proximal weakness


Peripheral Nerve


Sensorimotor changes with aging

Slow, wide-based, steppage/
Hyporeflexia, weakness, sensory deficit


Motor neuron

Amyotrophic lateral sclerosis

Motor neuron loss

Slow, spastic/
Upper and lower motor neuron signs


White Matter

Stroke, White matter disease

Neurovascular coupling

Increased variability, shortened stride length, wide based/ Hyperreflexia, pyramidal sighs


Basal Ganglia

Parkinson’s disease (Lewy body disease)


Decreased stride length, narrow base/
Bradykinesia, rigidity, tremor


Basal Ganglia

Huntington Disease

“Senile” chorea

Variable base, flinging movements with chorea superimposed/
Cognitive impairment, chorea



Alcoholism, Multiple System Atrophy, Spinocerebellar ataxias, Essential tremor

Age-related cerebellar atrophy

Wide-based variable gait/Neuropathy (Alcohol), Parkinsonism and autonomic features (MSA)


Frontal-subcortical gait

Vascular, Progressive Supranuclear Palsy (PSP), Late Parkinson’s Disease, Normal Pressure Hydrocephalus

Most likely related to pathology

Impaired foot placement and stepping, Wide or variable base, dysquilibrium/
Cognitive impairment, frontal release signs, Vertical gaze palsy (PSP),  pyramidal findings


Gait Ignition Failure

Vascular, PSP, Late Parkinson’s Disease, Normal Pressure Hydrocephalus

Patient with extreme cautious gait

Inability to initiate walking, getting stuck on turns or after stopping. Festination/


Cautious Gait

Fear of Falling

Slowing with aging, to a lesser degree than seen with fear of falling

Very slow walking, needing to hold onto items to walk/
Anxiety, Normal physical exam