Parkinson's disease
Also known as: parkinson disease, idiopathic parkinsonism
Parkinson's disease is a progressive neurodegenerative disorder caused by the loss of dopamine-producing neurons in the substantia nigra. It produces the cardinal motor signs of resting tremor, rigidity, bradykinesia, and postural instability, along with a wide range of non-motor symptoms.
The underlying pathology is degeneration of dopaminergic neurons in the substantia nigra pars compacta, part of the basal ganglia circuitry that regulates movement. Surviving neurons contain Lewy bodies, intracellular inclusions composed largely of aggregated alpha-synuclein. As dopaminergic input to the striatum falls, the basal ganglia output that normally permits smooth, automatic movement becomes inhibitory, and motor symptoms emerge — typically only after a substantial proportion of these neurons has already been lost.
The four cardinal motor features are often remembered as TRAP: resting tremor, classically a pill-rolling tremor of the hand that diminishes with voluntary movement; rigidity, felt as cogwheel or lead-pipe resistance to passive range of motion; akinesia or bradykinesia, meaning absent or slowed movement; and postural instability, which appears later and drives falls. Associated findings include a masked, expressionless face, small cramped handwriting known as micrographia, a stooped posture with a shuffling, festinating gait, reduced arm swing, quiet monotone speech, and episodes of freezing in doorways or turns. Signs usually begin asymmetrically.
Non-motor features often precede the movement disorder by years and include constipation, loss of smell, REM sleep behavior disorder, depression, and orthostatic hypotension; cognitive decline and dementia may develop in later stages. Pharmacologic management centers on restoring dopaminergic signaling: levodopa combined with carbidopa, which blocks peripheral conversion so more levodopa reaches the brain, remains the mainstay, supported by dopamine agonists, MAO-B inhibitors, COMT inhibitors, amantadine, and anticholinergics used mainly for tremor. Long-term levodopa use is associated with wearing-off and dyskinesias. Physical therapy addresses gait, balance, transfers, rigidity, and fall risk, often using external cueing strategies and high-amplitude movement training.
Parkinson's disease appears on several licensing exams from different angles. The PTCE tests it within drugs of the nervous system, emphasizing the levodopa-carbidopa combination and the other dopaminergic drug classes. The NPTE for physical therapists and the NPTE-PTA for assistants test it among central nervous system pathologies, where the emphasis falls on differentiating it from other neurological conditions, recognizing the cardinal signs and gait pattern, and selecting appropriate interventions for balance and mobility.
Key takeaways
- Parkinson's disease results from loss of dopaminergic neurons in the substantia nigra, with Lewy bodies containing alpha-synuclein.
- The cardinal motor signs are resting tremor, rigidity, bradykinesia, and postural instability, usually starting asymmetrically.
- Characteristic findings include masked facies, micrographia, reduced arm swing, and a shuffling, festinating gait.
- Non-motor symptoms such as anosmia, constipation, and REM sleep behavior disorder often precede motor signs.
- Levodopa combined with carbidopa is the mainstay drug therapy, with carbidopa preventing peripheral conversion of levodopa.
