Parkinson Disease
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Direct answer
Bradykinesia plus rest tremor, rigidity, or both — with a robust, sustained response to levodopa supporting the bedside impression — is the clinical core of Parkinson disease, a progressive α-synuclein neurodegeneration of the substantia nigra pars compacta. Treatment is symptomatic and staged: levodopa-carbidopa for the greatest motor benefit, dopamine agonists and MAO-B inhibitors in selected early or younger patients, amantadine for dyskinesias, and deep brain stimulation of the subthalamic nucleus or globus pallidus interna once fluctuations and dyskinesia become disabling.
What you must remember
- Bradykinesia is the obligatory core feature; the tremor is 4–6 Hz pill-rolling, maximal at rest, and the rigidity is lead-pipe with superimposed cogwheeling.
- Symptoms appear when roughly 60–80 per cent of nigrostriatal dopamine is lost; Lewy bodies (α-synuclein inclusions) are the pathological hallmark.
- Non-motor prodrome: constipation, rapid eye movement sleep behaviour disorder (acting out dreams), hyposmia and depression often precede motor signs by years.
- Levodopa remains the most effective drug; carbidopa blocks peripheral decarboxylation; motor complications — wearing-off and dyskinesia — develop in roughly half within about five years of therapy.
- Dopamine agonists (pramipexole, ropinirole) cause impulse control disorders (gambling, hypersexuality, shopping), somnolence with sudden sleep onset, hallucinations and ankle oedema — reasons younger, cognitively intact patients are preferred candidates.
- MAO-B inhibitors (rasagiline, selegiline) give mild benefit and are early-disease options; amantadine treats levodopa-induced dyskinesia.
- Deep brain stimulation suits levodopa-responsive patients disabled by fluctuations and dyskinesia with intact cognition; it does not help the non-motor progression.
- Red flags for atypical parkinsonism: early falls within the first year or postural instability, vertical supranuclear gaze palsy (progressive supranuclear palsy), cerebellar ataxia or autonomic failure early (multiple system atrophy), symmetric onset, absence of tremor, poor or waning levodopa response and early dementia.
- Essential tremor contrast: 8–12 Hz postural/action tremor, family history, improved by alcohol and propranolol, without bradykinesia or rigidity.
From first symptom to stimulator, in stages
A 58-year-old teacher notices smaller handwriting and a right-hand tremor while watching television; her right arm has stopped swinging on walks. The examination anchors on bradykinesia — decrementing finger taps, reduced blink — with a 4–6 Hz rest tremor and cogwheel rigidity, asymmetric, sensation and power normal, and no cerebellar or gaze abnormality; because she is under 60 and cognitively intact, therapy could begin with an MAO-B inhibitor or dopamine agonist, but her significant disability tips the shared decision toward low-dose levodopa-carbidopa, the most effective option, titrated weekly. Years later the disease renegotiates: each dose now wears off before the next is due, and peak-dose dyskinesia embarrasses her in class. The sequence of adjustments — shorten dosing intervals, consider adding amantadine for dyskinesia or a COMT inhibitor/MAO-B inhibitor to smooth levodopa, reassess for DBS candidacy — is walked one at a time, confirming first that the fluctuations are truly dopaminergic, since postural instability and autonomic failure do not respond to dose changes. If DBS is chosen: subthalamic nucleus stimulation in a cognitively intact, levodopa-responsive patient reduces off time and dyskinesia substantially; it is not offered when levodopa never helped — an exam-worthy point — nor when dementia or unstable psychiatric disease dominates. Had her first presentation been recurrent falls and a staring gaze at 66, the pathway would not be DBS work-up but a search for progressive supranuclear palsy.
Where students slip
Three confusions recur. First, prescribing dopamine agonists as the reflex first line in an elderly patient — impulse control disorders and hallucinations argue for levodopa there, while agonists are better justified in younger patients. Second, mistaking the tremor: an action tremor that alcohol improves is essential tremor, not Parkinson's, and marking "rest tremor improves with intention" as parkinsonian is backwards. Third, missing the atypical red flags hidden in the vignette — falls in year one, vertical gaze palsy, early symmetrical akinesia without tremor, or no response to an adequate levodopa trial each redirect the diagnosis away from Parkinson disease.
Frequently asked questions
Which combination of signs establishes Parkinson disease clinically?
Bradykinesia plus rest tremor or rigidity, asymmetric onset, and a clear sustained response to levodopa — with exclusion of atypical and secondary causes.
Which drug is first-line for levodopa-induced dyskinesia?
Amantadine; adjusting levodopa timing and dose, and considering deep brain stimulation when dyskinesia is refractory, are the companion moves.
What are the signature adverse effects of dopamine agonists?
Impulse control disorders (pathological gambling, hypersexuality, compulsive shopping), sudden-onset sleep, hallucinations, peripheral oedema and orthostatic hypotension.
When is deep brain stimulation indicated?
For levodopa-responsive Parkinson disease with disabling motor fluctuations or dyskinesia despite optimised medical therapy, in a patient without significant dementia or unstable psychosis.
How is essential tremor distinguished from parkinsonian tremor?
Essential tremor is a faster 8–12 Hz action and postural tremor, often familial, improved by alcohol and propranolol, without bradykinesia, rigidity or gait change.