Academic journal article New Zealand Journal of Occupational Therapy

Movement Deficits in Parkinson's Disease and Restorative Occupational Therapy

Academic journal article New Zealand Journal of Occupational Therapy

Movement Deficits in Parkinson's Disease and Restorative Occupational Therapy

Article excerpt


This paper focuses on movement deficits that interfere with smooth execution of movement following Parkinson's disease. Difficulty in initiating, slowness in executing, inhibition of a current movement and preparation for a new movement as well as, switching between sets of movements, and freezing are explained.

Effectiveness of occupational therapy has been difficult to establish with methodological flaws in research. However, measurements that quantify movement deficits and the neuroinvestigative evidence based activities and contexts in occupational therapy could restore movement capabilities. Such focussed movement restitution in occupational therapy would, in turn, increase participation in daily life and improve the quality of life.

Key words

Parkinson's disease, movement deficit, occupational therapy, measurement outcome

Parkinson's disease (PD) is a chronic progressive neurological condition with reported incidence of 1:5 in western nations and a condition commonly requiring occupational therapy. A review of occupational therapy literature indicated there is a vast amount of information available on many aspects of PD. This includes: cardinal symptoms, self-care ability, ability to interact with the environment, home health and general care, nutritional matters, medications, coping, functional therapies, family education, general fitness, person and occupational centred occupational therapy, and overall quality of life (College of Occupational Therapists, 1996; Deane, Ellis-Hill, Dekker, Davies, & Clarke, 2003; National Parkinson Foundation, 2002). The above approaches utilise compensatory or adaptive methods such as independence in activities of daily living despite the loss suffered by PD, to improve the quality of life of the persons with PD. New pharmaceutical agents, surgical approaches, and brain stimulation focus on movement deficit restitution. However there is practically no information on specific aspects of restorative occupational therapy addressing the type, the degree, or the quality of deficit in movement ability, its measurement and the neurological basis of intervention.

Therefore this paper focuses on: (i) movement deficits and resulting impairments (ii) the need for quantifiable assessments to show a specific change in the quality of movement performance, and (iii) the restorative approaches in occupational therapy as they relate to restoring the quality of the movement deficits. Awareness and application of quantifiable assessments and intervention strategies are vital for occupational therapists to positively impact neurological recovery. This restorative focus in turn will allow increased participation in daily occupations and improved quality of life in persons with PD.

Movement deficits in Parkinson's disease

To explain restitution of movement deficits in Parkinson's disease, this section focuses on the deficits, mechanisms of the deficits, the deeper brain nuclei associated with the execution of smooth movement, and measuring the quality and neurological evidence for activity based occupational therapy.

Akinesia refers to difficulty in initiating movement and paucity of self-generated voluntary movement (Bear, Connors, & Paradiso, 2001) whereas bradykinesia from strial dopamine deficiency results in slowness in executing movement. The slowness comes from increased reaction time, delayed correction of an inaccurate attempt, prolonged time to recommence correct movement, and easy fatigability. Akinesia and bradykinesia are closely related but can be independent, and present in the absence of rigidity (Paulson & Stern, 1997). With Akinesia, automatic execution of learned motor plans is altered, but with dyskinesia resulting from the administration of neuroleptics, the motor plan could be executed by alternative movement strategies. This indicates that in dyskinesia, the form of motor plan is preserved but individual motor programs, which make up the motor plan, are distorted (Bear, Connors & Paradiso, 2001; Marsden, 1994). …

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