For many years, exercise was not a recommended rehabilitation strategy for persons with a diagnosis of idiopathic Parkinson’s disease (PD) [1]. Since it was believed that exercise had no measurable effect on PD, or might worsen the underlying pathology, it was to be avoided.

However, a rich vein of research now indicates that non-pharmological approaches- (exercise based physiotherapy), have a far greater effect on the cardinal features of PD than previously believed [2], [3], [4].


Exercise and brain health

There is an inverse relationship between activity level and risk of developing PD: moderate or vigorous levels (but not low levels) of physical activity are associated with lower risk of developing PD [5] [6].

Regular exercise delays the appearance of Parkinsonian features in persons already diagnosed with PD [7].

Paradoxically, studies suggest the following diagnosis, persons with PD reduce their physical activity levels [8] [9] and only 12-15% of these early diagnosed individuals are referred to physiotherapy. This is a significant and unfortunate problem, but amendable.

Research indicates that exercise triggers plasticity related changes in the central nervous system including synaptogenesis, enhanced glucose utilization, angiogenesis and neurogenesis [10].

Exercise promotes brain health by reducing inflammation, suppressing oxidative stress and stabilizing calcium homeostasis [10].

Chronic aerobic exercise is associated with synaptic plasticity, enhanced cognitive ability, learning and memory [11] Results from the above human studies are paralleled by studies with lesioned and intact laboratory animals, showing that motor training triggers lasting neuronal changes throughout the brain such as glial cell proliferation, changes in neuro transmitter levels, changes in the expression of endogenous neurotrophic factors such as BDNF and GDNF the growth of neuronal processes, and neural changes which are associated with enhanced behavioral recovery [12].

Activity-dependent plasticity occurs in the human brain after a stroke in response to exercise (forced use) and skill learning [13] [14].

Recent studies utilizing animal models of PD have begun to explore the molecular mechanisms of exercise induced changes in the pathophysiology of PD [15], [16]. Animals injected with targeted neurotoxins demonstrated a remarkable capacity for improved motor performance with forced exercise. This occurred through a variety of molecular repair mechanisms from within the damaged basal ganglia circuits. The animals demonstrated robust molecular mechanisms for plasticity in response to injury —which can be useful for studying the effect of exercise that may enhance recovery [17],[18].


Inactivity is prodegenerative

A period of inactivity or stress may reverse the protection and behavioural benefits of exercise [19].

In addition, decreased physical activity, which is often a precursor of the diagnosis of PD and worsened by the symptoms of bradykinesia, fatigue or weakness, may be prodegenerative, contributing to further motor deterioration and pathogenesis of PD [19].

Inactivity is not only a symptom of PD, but a catalyst in the degenerative process [20].

Despite all the evidence, many clinicians and communities remain unaware of the scientific literature underlying exercise-induced brain repair or reorganization (neuroplasticity) and accompanying behavioral recovery in animal models of PD [21], [22].

Often persons in the early stages of PD do not request a referral to physiotherapy, or they do not ask about how much or what type of exercise to do, as they do not perceive that their function has declined or that their symptoms interfere with normal daily activities. Traditionally, it is not till patients reach stage III (within 5 years of diagnosis) that referrals to rehabilitation are initiated. This referral model does not allow for a proactive treatment approach during the early postdiagnosis period prior to loss of postural stability. Animal studies suggest that this is a lost window of opportunity [20].


These studies suggest an enormous capacity of the PD —brain to reshape itself in response PD produced activity and provide a plausible rationale for exercise-induced plasticity-related mechanisms in humans with PD. The animal data suggest that multiple time-dependent mechanisms (i.e., neuroprotection, neurorestoration) are capable of contributing to behavioural recovery in PD.

Research suggests that continuous, deficit targeted, intensive training may confer neuroprotection and thereby, slow, stop or reverse the progression of the disease or promote neurorestoration through adaptation of compromised signaling pathways [20], [21]. It remains that the major challenge in the field of non-pharmacological, rehabilitative intervention for PD is the extent to which healthcare providers are able to translate the science of exercise and PD to the level of the community [20].

Visit for more information on supervised, exercised based physiotherapy.


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