Movement Phenomenology
The classification of abnormal movements by their character — the foundation for all movement disorder diagnosis.
The two categories
Hypokinetic
Diminished movement. Cardinal example: Parkinsonism (bradykinesia, rigidity, resting tremor).
Hyperkinetic
Excessive movement. Includes tremor, dystonia, chorea, tics, and myoclonus.
Hyperkinetic movement disorders
Tremor
Rhythmic
CharacterRegular, rhythmic oscillation — the only truly regular hyperkinetic movement
TimingRest (PD), action, postural
SuppressDifficult
Dystonia
Patterned
CharacterSustained, patterned muscle contractions — predictable postures
Key featureSensory trick (geste antagoniste) — unique to dystonia
ContextTask-specific (writer's cramp), postural, or at rest (severe)
Chorea
Random
CharacterRandom, flowing, dance-like — migrates unpredictably between body parts
Key featureMotor impersistence (cannot sustain tongue protrusion), milkmaid's grip
MaskingParakinesia — patient incorporates movement into purposeful gesture
Tics
Suppressible
CharacterRapid, non-rhythmic, stereotyped movements or vocalisations
Key featurePremonitory urge — uncomfortable sensation relieved by performing the tic
SuppressYes — voluntarily, at cost of building urge. Also suggestible.
Myoclonus
Lightning-like
CharacterSudden, brief, lightning-fast jerks — too fast to suppress
TypesPositive (muscle firing) or negative (asterixis — sudden muscle silence)
Key featureSpeed — briefer than any other hyperkinetic movement
Five bedside differentiators: (1) Suppressibility — only tics. (2) Sensory trick — only dystonia. (3) Rhythm — only tremor. (4) Speed — myoclonus is too fast. (5) Randomness — chorea flows unpredictably.
Quick comparison table
| Disorder | Rhythm | Suppressible | Trigger | Distinguishing clue |
|---|---|---|---|---|
| Tremor | Regular, rhythmic | Difficult | Action or rest | Regularity — metronome-like |
| Dystonia | Non-rhythmic (sustained) | Partially — sensory trick | Task-specific, postural | Geste antagoniste |
| Chorea | Arrhythmic, unpredictable | Briefly (parakinesia) | Spontaneous, migrating | Motor impersistence, milkmaid's grip |
| Tics | Non-rhythmic but stereotyped | Yes — briefly | Stress, suggestion | Premonitory urge |
| Myoclonus | Arrhythmic (sometimes rhythmic) | Cannot suppress | Action, stimuli, spontaneous | Lightning speed, can be negative (asterixis) |
Tremor Classification
Classification by when the tremor occurs and what causes it.
Tremor types by timing
Resting tremor
WhenPresent at rest, suppressed by voluntary movement, may re-emerge with sustained posture (latency)
CauseParkinsonism (idiopathic PD, atypical syndromes)
Frequency4–6 Hz
Action tremor
WhenDuring voluntary movement or posture holding
SubtypesPostural, kinetic, intention (cerebellar)
Frequency4–12 Hz depending on type
Common tremor causes
Enhanced physiologic tremor Benign
CharacterFine, postural, symmetric
TriggersAnxiety, adrenergic surge, caffeine, thyroid disease, being in clinic
Key pointNot persistent, not progressive — resolves when trigger removed
Essential tremor Most common
CharacterPostural + kinetic, immediate on posture hold, symmetric
DistributionHands/arms most common, also head (yes-yes or no-no) and voice
TestArchimedean spiral — jagged, irregular vs smooth normal
Parkinsonian tremor Resting
Character"Pill-rolling" — thumb rubs against index/middle finger in circular motion. Multiple joints, multiple planes.
TimingAt rest, 4–6 Hz. Re-emergent pattern on posture hold (latency before re-appearing)
AsymmetryAsymmetric onset — one side first
Cerebellar tremor Intention
CharacterAbsent at rest, worsens approaching target (terminal dysmetria)
ExamFinger-to-nose: worsens near target. Sit back — full arm stretch required.
AssociatedWide-based gait, dysdiadochokinesia, dysmetria
Re-emergence trap: after raising arms to posture hold, PD tremor disappears briefly then re-emerges after a latency of seconds. Essential tremor is immediate. Don't call re-emergent tremor "action tremor" and misdiagnose PD as ET.
Key drug causes of tremor
AntiarrhythmicsAntidepressants (SSRIs, TCAs)Glucocorticoids
Beta-agonistsCaffeineLevothyroxine
Mood stabilisers (lithium, valproate)Anti-epileptics
Antipsychotics (D2 blockers)Metoclopramide
Always take a medication history before labelling a tremor as pathological. Enhanced physiologic tremor from a drug is common and fully reversible.
DaTScan — what it tells you (and what it doesn't)
Normal DaTScan
Dopaminergic neurons are intact. Strongly supports essential tremor or drug-induced parkinsonism over degenerative disease. Rules out PD, PSP, CBD, MSA.
Abnormal DaTScan
Dopaminergic neuronal loss is present. Does NOT distinguish PD from PSP, CBD, or MSA — all show reduced uptake. Clinical assessment and response to levodopa still required.
Examination Approach
Systematic bedside assessment of the patient with a movement disorder.
1
Resting tremor assessment
Patient seated, arms relaxed in lap, semi-supinated thumbs toward ceiling
TechniqueObserve for 20–30 seconds. Distract with counting backwards to unmask subtle tremor — eliminates voluntary suppression.
2
Postural tremor
Arms outstretched, fingers spread wide
TechniqueObserve immediately, then wait 10+ seconds. Immediate = ET. After latency = re-emergent PD. Paper trick: place sheet on dorsum to amplify fine tremors.
3
Kinetic & intention tremor (finger-to-nose)
Sit back — ensure full arm extension to your still finger
KineticTremor present throughout movement — essential tremor pattern
IntentionTremor worsens specifically approaching the target — cerebellar sign
Ask the patient to stretch as far as possible — a short reach misses distal intention tremor.
4
Rigidity
Passive wrist movement — velocity-independent resistance
TechniqueAsk patient to completely relax and "give you the weight". Passively flex/extend wrist — any direction, any speed.
ActivationAsk patient to tap contralateral hand on thigh — unmasks subtle rigidity via basal ganglia contralateral overflow.
CogwheelRatchety interruption of smooth rigidity = rigidity + superimposed tremor. Hallmark of PD.
Spasticity is velocity-dependent (clasp-knife); rigidity is not. This is the key bedside distinction.
5
Bradykinesia
Speed, amplitude, and fatigability
Upper limbFinger tapping (index to thumb), hand opening/closing, wrist pronation/supination
Lower limbToe tapping (heel stays down), heel tapping
Look forDecrement in amplitude over 10–15 repetitions — the hallmark. Not just slowness.
Pure slowness without decrement is non-specific. Parkinsonism is characterised by fatiguing amplitude.
6
Ataxia — finger-to-nose & heel-to-shin
Cerebellar coordination testing
DysmetriaPast-pointing or under-shooting the target
DDKIrregular rhythm on alternating movements (dysdiadochokinesia)
DecompositionMovement broken into jerky segments
7
Gait and balance
Rising from chair, walking, turning
Step lengthShuffling short steps = Parkinsonism. Wide-based = cerebellar or fear of falling.
Arm swingReduced unilateral arm swing — often earliest Parkinsonian gait sign
TurnsEn bloc turning (multiple small steps, trunk and head together) = Parkinsonism
TandemHeel-to-toe walking sensitively exposes cerebellar midline ataxia
Foot motionFestination = accelerating, shuffling forward. Foot dragging. High steppage in foot drop.
8
Pull test (retropulsion)
Postural reflex testing — warn patient and supervise closely
TechniqueStand directly behind patient. Warn them. Firm brisk pull backward on shoulders. Be ready to catch.
Normal1–2 corrective steps backward
Impaired3+ steps or no correction at all — impaired postural reflexes, major fall risk
Never perform without being positioned to catch the patient — some will fall straight back with no corrective response.
Diagnostic Framework
A three-step approach to evaluating a patient with parkinsonism.
1
Establish parkinsonism
Required before asking what is causing it
Bradykinesia (mandatory)
Slowness with decrement in amplitude or speed on repetitive movements. Cannot diagnose parkinsonism without this.
Plus at least one of:
Rigidity — velocity-independent resistance.
Resting tremor — 4–6 Hz, suppressed by movement.
Resting tremor — 4–6 Hz, suppressed by movement.
↓
2
Support the diagnosis of Parkinson's disease
Positive features that increase confidence in idiopathic PD
Unilateral / asymmetric onset
PD almost always begins on one side. Symmetric onset from the start is a red flag against PD.
Rest tremor (pill-rolling)
Present in ~70% of PD. Its presence is strongly supportive; absence does not exclude PD.
Sustained levodopa response
Good, maintained response to levodopa is one of the strongest clinical supports. Lack of response should trigger reconsideration.
Nonmotor prodromal features
Hyposmia, REM sleep behaviour disorder, constipation, depression — especially if preceding motor onset by years.
Slowly progressive course
PD progresses over decades. Rapid deterioration suggests an atypical syndrome.
Levodopa-induced dyskinesia
Development of dyskinesias with levodopa is itself supportive — atypical syndromes rarely develop dyskinesias.
↓
3
Consider exclusions and red flags
Any red flag should prompt reconsideration of the diagnosis
Absent levodopa response
Most important single red flag. No response to adequate levodopa trial = almost certainly not PD.
Absent nonmotor features of PD
If hyposmia, constipation, REM sleep behaviour disorder, and mood symptoms are all completely absent, PD is less likely.
Early prominent gait impairment and falls
Falls within year 1 — especially backward — points toward PSP. PD preserves postural stability for years.
Early dementia
Dementia within 1 year of motor onset suggests DLB. PD dementia emerges late.
Bulbar dysfunction
Early severe dysarthria or dysphagia suggests PSP or MSA.
Early autonomic failure
Orthostatic hypotension, urinary incontinence, erectile dysfunction disproportionate to motor severity = MSA.
History of predisposing conditions
Dopamine-blocking drugs, prior strokes, TBI, heavy metal/pesticide exposure — all suggest secondary parkinsonism.
If a patient is not responding to levodopa as expected, or red flags accumulate, revisit the diagnosis. It is better to reconsider than to continue treating the wrong condition.
Disease Timeline
Parkinson's disease progresses through prodromal, early, mid, and late stages over decades.
Symptom progression over time
Prodromal
REM sleep behaviour disorder
Constipation
Depression
Anxiety
Hyposmia
~40s — years before motor Dx
Early
Tremor
Rigidity
Bradykinesia
Fatigue
Pain
Daytime sleepiness
~50s — diagnosis made
Mid-stage
Orthostatic hypotension
Urinary symptoms
Psychotic symptoms
Visual hallucinations
Years post-diagnosis
Late-stage
Postural instability
Falls
Dysphagia
Dementia
Advanced disease
By the time motor symptoms appear and the diagnosis is made, roughly 50–70% of dopaminergic neurons in the substantia nigra are already lost. REM sleep behaviour disorder is one of the strongest prodromal markers — high conversion rate to synucleinopathy over 10–15 years.
Key non-motor features of PD (prodromal)
Hyposmia
Loss of smell — often earliest feature, predates motor symptoms by years. Test with scratch-and-sniff cards.
REM sleep behaviour disorder
Acting out dreams — punching, kicking during sleep. Highly specific prodromal marker for synucleinopathies.
Constipation
Autonomic involvement of enteric nervous system. Can precede motor symptoms by many years.
Depression / anxiety
Dopaminergic and serotonergic involvement. Often predates motor onset. Not merely a reaction to diagnosis.
Fatigue
Common and often underappreciated. Distinct from sleepiness. Can be the most disabling symptom early.
Hypophonia
Soft voice — reduced vocal amplitude. Often noticed by family before the patient.
Treatment of Parkinson's Disease
Pharmacological approaches — when to start, what to use, and how to choose.
First principle: if symptoms are not bothersome and the patient does not want treatment, no medication needs to be prescribed. Initiation is driven by functional impact, not diagnosis alone.
Mechanism overview
| Class | Examples | Mechanism | Pros | Cons |
|---|---|---|---|---|
| Levodopa | Levodopa/carbidopa, levodopa/benserazide | Crosses BBB → converted to dopamine by AADC in nigrostriatal neurons | Most effective. Safe. Does not accelerate disease progression. | Motor fluctuations, dyskinesias, GI SE, multiple daily doses, impulse control |
| Dopamine agonists | Pramipexole, ropinirole, rotigotine, apomorphine | Directly stimulate D1/D2 receptors — bypass degenerating presynaptic neuron | Less dyskinesia. Longer lasting. Once or twice daily dosing. | More cognitive/psychiatric SE. Impulse control disorders. Less efficacious. Avoid in elderly. |
| MAO-B inhibitors | Selegiline, rasagiline, safinamide | Inhibit MAO-B → reduce dopamine breakdown in presynaptic terminal | Possible neuroprotection. Mild symptoms. Convenient OD dosing. | Poor efficacy. Cognitive SE. Serotonin syndrome risk with SSRIs/SNRIs/tramadol. |
| COMT inhibitors | Entacapone, opicapone, tolcapone | Block COMT → reduce peripheral levodopa breakdown → prolong half-life | Extend on time. Reduce wearing-off. Used as adjunct to levodopa. | Worsen dyskinesias if levodopa not reduced. Tolcapone — hepatotoxicity (monitor LFTs). |
| NMDA antagonist | Amantadine | Blocks NMDA glutamate receptors → reduces dyskinesias. Also mild dopaminergic effect. | Treats peak-dose dyskinesias. Useful adjunct. | Confusion, hallucinations, nightmares. Livedo reticularis. Ankle oedema. |
| Anticholinergics | Trihexyphenidyl, benztropine | Block muscarinic receptors → reduce cholinergic excess in striatum | Useful for tremor, dystonia, dysautonomia. | Cognitive SE (avoid in elderly). Urinary retention, dry mouth, constipation, dyskinesias. |
In a patient under 60, many neurologists start a dopamine agonist first to delay levodopa-related dyskinesias — accepting slightly higher psychiatric risk in exchange for preserving years of clean levodopa response. In older patients, levodopa is generally preferred given the cognitive risks of dopamine agonists.
What is dyskinesia?
Dyskinesia is not a specific movement type — it is an umbrella term for any abnormal involuntary movement caused by dopaminergic therapy. It encompasses:
Chorea Most common
Random, flowing movements. Appears during peak drug levels ("peak-dose dyskinesia").
Dystonia
Sustained postures. Common in off periods (early morning foot dystonia) and at peak dose.
Tics
Less common in drug-induced dyskinesia but can occur.
Tremor Rare
Occasionally a component but not the predominant form.
Early (peak-dose) dyskinesia
Levodopa levels at peak. Managed by smaller, more frequent doses, or adding adjuncts (amantadine, COMT inhibitor).
Levodopa levels at peak. Managed by smaller, more frequent doses, or adding adjuncts (amantadine, COMT inhibitor).
Tardive dyskinesia
Caused by long-term dopamine receptor blockade (antipsychotics, metoclopramide). Orofacial movements classic. Can be irreversible. Opposite mechanism to levodopa-induced dyskinesia.
Caused by long-term dopamine receptor blockade (antipsychotics, metoclopramide). Orofacial movements classic. Can be irreversible. Opposite mechanism to levodopa-induced dyskinesia.
Levodopa-induced dyskinesia = pulsatile overstimulation of sensitised receptors. Tardive dyskinesia = chronic blockade causing receptor upregulation. Opposite mechanisms.
Motor Fluctuations & DBS
Managing on/off fluctuations as disease progresses and the therapeutic window narrows.
On and off states
"On" state
Levodopa is active, brain dopamine levels adequate. Motor symptoms controlled — patient can move, speak, and function. May develop dyskinesias at peak levels.
"Off" state
Levodopa levels have fallen. Parkinsonism returns — bradykinesia, rigidity, tremor, freezing. Painful off-period dystonia (early morning foot cramps) is common.
Why the therapeutic window narrows
Early in PD, surviving dopaminergic neurons buffer levodopa — storing it, releasing it steadily, and smoothing out peaks and troughs of oral dosing. As disease progresses and neurons are lost, this buffering disappears. The brain becomes dependent on the timing of each oral dose. The window between "too little" (off) and "too much" (dyskinesia) narrows progressively over years.
Strategies to optimise motor fluctuations
1
Increase dosing frequency, reduce dose size
More frequent smaller doses smooth peaks and troughs. Reduces peak-dose dyskinesia while maintaining on time. Total daily dose may remain similar.
2
Add a COMT inhibitor
Entacapone, opicapone, or tolcapone. Extends levodopa half-life by blocking peripheral breakdown. Prolongs on time. Reduce levodopa dose when adding to avoid worsening dyskinesias.
3
Add a MAO-B inhibitor
Rasagiline or safinamide. Reduces central dopamine breakdown. Safinamide also has glutamate-modulating effects useful for motor fluctuations.
4
Add amantadine for dyskinesias
NMDA antagonist — reduces peak-dose dyskinesias without worsening parkinsonism. Particularly useful when dyskinesias are dominant rather than off time.
5
Continuous delivery systems
Levodopa-carbidopa intestinal gel (Duodopa) via jejunal pump, or subcutaneous infusion — provides steady-state levels, bypassing oral pharmacokinetics. Reserved for advanced disease with severe fluctuations.
6
Dietary protein timing
Large neutral amino acids compete with levodopa for intestinal absorption and BBB transport. Protein redistribution diet (low protein daytime, main intake evening) can smooth fluctuations.
Goal: maximise on time without troublesome dyskinesias. A patient with mild dyskinesias but good function has a better outcome than one with extended off periods and no dyskinesias.
Deep brain stimulation (DBS)
Surgical therapy for advanced PD where motor fluctuations and dyskinesias are no longer adequately controlled by medications. Does not cure PD or stop progression, but can dramatically improve quality of life and on time.
Targets
Subthalamic nucleus (STN) Most common
Most used target in PD. Reduces off time, dyskinesias, often allows levodopa dose reduction. Effective for tremor, rigidity, and bradykinesia.
Globus pallidus internus (GPi)
Preferred when dyskinesias are dominant, or in patients with cognitive concerns where levodopa reduction is undesirable.
VIM thalamus
Highly effective for tremor but does not address other PD features. More commonly used for essential tremor.
Responds to DBS
Tremor · Rigidity · Bradykinesia · Motor fluctuations · Levodopa-induced dyskinesias · On time extension
Does NOT respond to DBS
Axial symptoms (falls, freezing) · Speech/swallowing · Autonomic dysfunction · Dementia · Non-motor symptoms
DBS provides the equivalent of the patient's best on state on medication, but continuously. If a patient has a poor best-on state, DBS will not improve them beyond that ceiling. Good levodopa response is the best predictor of DBS benefit.
Causes of Parkinsonism
Parkinsonism is required to diagnose PD, but most people with parkinsonism do not have idiopathic PD.
Idiopathic PD
Most common. Alpha-synuclein / Lewy body pathology. Responds to levodopa.
Drug-induced
Antipsychotics, metoclopramide, prochlorperazine, valproate, calcium channel blockers. Reversible on withdrawal.
Vascular parkinsonism
Small vessel disease, strategic infarcts. Lower body predominant. Step-wise progression. Neuroimaging key.
Structural lesions
Normal pressure hydrocephalus, subdural haematoma, tumours (frontal or basal ganglia).
Metabolic
Wilson's disease (young patient — treatable), manganese toxicity, hypoparathyroidism.
Occupational / toxic
Heavy metals (manganese, mercury), pesticides (MPTP, rotenone). Occupational history essential.
TBI / CTE
Chronic traumatic encephalopathy. Consider in boxers and contact sport athletes.
Atypical parkinsonisms
PSP, CBD, MSA — degenerative, poor levodopa response, faster progression, ~7 year survival.
Always take a drug history before diagnosing PD — dopamine-blocking drugs are a common and fully reversible cause. In a young patient, always consider Wilson's disease (treatable with copper chelation).
Atypical Parkinsonisms — PSP, CBD, MSA
Degenerative syndromes that share parkinsonism but reflect degeneration of different brain regions.
~14 yrs
Typical survival after PD diagnosis
~7 yrs
Typical survival after atypical parkinsonism diagnosis
Red flags for atypical parkinsonism (not PD)
Early autonomic dysfunction disproportionate to motor severity · Poor or absent levodopa response · Early falls (especially backward) within year 1 · Rapid progression · Vertical gaze palsy · Cerebellar signs · Alien limb phenomenon
Tauopathy
Progressive supranuclear palsy (PSP)
PathologyTau — neurofibrillary tangles in brainstem, basal ganglia, cerebellum
RegionBrainstem predominant
Key features
Vertical gaze palsy
Early backward falls (year 1)
Oculomotor dysfunction
Bulbar signs
Axial > limb rigidity
"Surprised" facies
Hummingbird sign (MRI)
Midbrain atrophy on sagittal MRI gives the appearance of a hummingbird in flight — the atrophied midbrain forms the beak, relatively preserved pons the body. Reflects brainstem-predominant degeneration of PSP.
Vertical supranuclear gaze palsy — inability to look down voluntarily — is the defining sign. Falls within year 1, especially backward, are a strong early clue.
Tauopathy
Corticobasal degeneration (CBD)
PathologyTau — frontoparietal cortex and basal ganglia
RegionFrontal and parietal lobes predominant
Key features
Alien limb phenomenon
Cortical sensory loss
Visuospatial deficits
Behavioural / personality changes
Asymmetric apraxia
Myoclonus
Alien limb phenomenon — mechanism
Cortical dysfunction in the frontoparietal regions disrupts integration of motor intention and sensory feedback. The limb moves involuntarily and purposelessly — reaching, grasping, interfering with voluntary actions — as if belonging to someone else. The patient is aware and cannot suppress it. Direct manifestation of cortical (not subcortical) degeneration.
Alien limb in a patient with parkinsonism should immediately raise CBD as the leading diagnosis.
Alpha-synucleinopathy
Multiple system atrophy (MSA)
PathologyAlpha-synuclein in oligodendroglia (glial cytoplasmic inclusions) — same protein as PD but different cell type
RegionCentral autonomic pathways, cerebellum, striatum
Key features
Severe early autonomic failure
Orthostatic hypotension
Urinary incontinence / retention
Cerebellar ataxia (MSA-C)
Parkinsonism (MSA-P)
Inspiratory stridor
Hot cross bun sign (MRI)
Cruciform T2 hyperintensity in the pons reflecting pontine atrophy — MSA's equivalent of the hummingbird sign. Reflects the cerebellar/pontine degeneration seen in MSA-C subtype.
Inspiratory stridor from vocal cord paralysis carries a poor prognosis. Severe autonomic failure early and disproportionate to motor symptoms is the defining feature of MSA.
Side-by-side comparison
| Feature | PSP | CBD | MSA | Idiopathic PD |
|---|---|---|---|---|
| Pathology | Tau | Tau | Alpha-synuclein (oligodendroglia) | Alpha-synuclein (neurons) |
| Region | Brainstem | Frontal / parietal | Autonomic / cerebellar | Substantia nigra |
| Resting tremor | Uncommon | Uncommon | Uncommon | Characteristic |
| Early falls | Backward, year 1 | Late | Late | Late |
| Eye movement | Vertical gaze palsy | Variable | Variable | Normal early |
| Autonomic failure | Mild | Mild | Severe, early | Mild-mod, late |
| Cortical signs | Frontal only | Alien limb, apraxia, cortical sensory loss | Absent | Late dementia only |
| MRI sign | Hummingbird sign | Asymmetric frontoparietal atrophy | Hot cross bun sign | Normal early |
| Levodopa response | Poor | Poor | Poor / partial | Good |
| Survival after Dx | ~7 years | ~7 years | ~7 years | ~14 years |
| DaTScan | Abnormal | Abnormal | Abnormal | Abnormal |
DaTScan cannot distinguish PD from atypical parkinsonisms — all show dopaminergic loss. Poor levodopa response in a patient thought to have PD should always prompt reconsideration of an atypical syndrome.
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