Introduction to Parkinson’s Disease

Core Concepts

The basal ganglia and the nigrostriatal pathway

The basal ganglia govern movement: selecting which movements to make, suppressing unwanted ones, and regulating force and smoothness. The nigrostriatal pathway is the dopamine “supply line” from the substantia nigra to the striatum; in PD it fails. Without dopamine’s braking influence, the motor cortex receives excessive, poorly organized output — tremor, stiffness, and difficulty initiating movement. This circuit explains why PD looks the way it does.

The dopamine–acetylcholine balance

Within the striatum, dopamine and acetylcholine have opposing effects: dopamine suppresses excessive movement output; acetylcholine promotes it. In PD, dopamine loss leaves acetylcholine relatively unopposed. This balance is the most important concept for the pharmacology that follows: anti-Parkinsonian drugs either replace dopamine, mimic dopamine, slow dopamine breakdown, or reduce acetylcholine activity. Every class in the next topic aims to rebalance these two transmitters.

The cardinal motor signs (TRAP)

• Tremor — a rhythmic “pill-rolling” tremor of the hand at rest that often lessens with voluntary movement; it can also affect the jaw or lips.
• Rigidity — increased muscle tone felt as resistance to passive movement; it may be continuous (“lead-pipe”) or ratchety (“cogwheel”).
• Akinesia/bradykinesia — poverty and slowness of movement: reduced arm swing, masked facial expression, small handwriting, difficulty starting to walk.
• Postural instability — impaired balance and righting reflexes; usually later, and a major fall risk.

Non-motor symptoms

PD affects much more than movement. Early clues include hyposmia (reduced sense of smell), REM sleep behavior disorder, and constipation — sometimes years before motor signs. Depression and anxiety are common; later, people may develop orthostatic hypotension, urinary urgency, pain, fatigue, and cognitive changes. Non-motor symptoms often affect quality of life more than tremor, so nursing assessment never stops at motor signs.

Who gets Parkinson’s disease and why

Most cases are idiopathic — no single cause is identified. Age is the strongest risk factor; onset is typically after age 60, and men are affected somewhat more often. A small percentage of cases are inherited, involving genes such as those coding for alpha-synuclein (the protein that clumps into Lewy bodies, PD’s hallmark) or LRRK2. Environmental exposures (e.g., certain pesticides) are proposed contributors, with research ongoing. Importantly, parkinsonism — the same movement signs — can also be caused by drugs (notably some antipsychotics) or strokes; that is a different problem from Parkinson’s disease itself.

Diagnosis and staging

There is no single definitive test. Diagnosis is largely clinical: a history of gradually progressive motor signs plus a response to levodopa-based therapy supports it. A dopamine transporter (DaT) scan can help distinguish PD from other tremor disorders but is not routine. Clinicians use tools such as Hoehn and Yahr staging and the UPDRS to track severity; frameworks vary over time — verify the version in local use.

Nursing assessment and safety

Nursing priorities: fall-risk assessment (postural instability, freezing), swallowing and nutrition screening (aspiration risk), medication reconciliation, and emotional support. Observe for subtle signs — reduced arm swing, soft voice, expressionless face, small handwriting — and ask about sleep, mood, bowel function, and lightheadedness, not just tremor. Diagnosis, referral, and medication decisions follow regulated scope and institutional policy.

Common Confusions