- MemberOctober 18, 2021 at 10:09 am
It is unknown as to what causes the dopamine deficiency in the substantia nigra pars compacta cells in basal ganglia/midbrain of people with IPD. Diagnosis usually occurs between 55-65years of age (in which up to 60% of cells can already have perished), but symptoms can be present up to 20years prior.
There are stages of progression of the disease: Braak Stages 1-2 (autonomic disturbances), 3-4 (sleep and motor disturbances), 5-6 (emotional and cognitive impairment) which correlate with progressive brain disease and infiltration of Lewy bodies.
Clinical Diagnosis of IPD based on presence of primary motor impairments and non-motor symptoms, exclusion of other neurological conditions and response to medication.
Primary motor impairments include: hypo/bradykinesia, tremor, rigidity, weakness, akinesia
The types of IPD are: bradykinesia (target amplitude, scale, symmetry), tremor dominant (target forced use, motor output, high effort), agility impaired (target weight shift, agility, falls prevention, dynamic balance)
Non motor impairments, such as depression, apathy, anxiety, cognitive impairment, autonomic system dysfunction can greatly affect quality of life.
Secondary impairments like changes to mood, sedentary behaviours, and falls can also have a large impact.
Medications don’t have an effect on disease progression, only on symptoms, and are thought to support neurorestoration only. However, if clients can move better, there is more potential for a training effect. Therefore, it is important for medications and exercise to work in partnership for optimising outcomes.