Step 2 CK · Neurology

Movement Disorders

Name: Movement Disorders
Creator: Veli Bakalov, MD

Read the tremor and the movement to reach the diagnosis, then match the drug

Neurology·Cognitive & Movement Disorders·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Parkinson disease = TRAP (resting pill-rolling tremor, cogwheel rigidity, bradykinesia, postural instability) with asymmetric onset, masked facies, shuffling gait, and micrographia, from nigral dopaminergic loss with α-synuclein Lewy bodies.
Levodopa-carbidopa is the most effective Parkinson therapy (carbidopa blocks peripheral dopa decarboxylase, reducing nausea); long-term use brings motor fluctuations and dyskinesias.
Dopamine agonists (pramipexole, ropinirole) suit younger patients but cause impulse-control disorders (gambling, hypersexuality, shopping); MAO-B and COMT inhibitors are adjuncts; subthalamic DBS helps advanced disease.
Essential tremor = bilateral, symmetric action or postural tremor, often autosomal dominant, better with alcohol → propranolol or primidone; the Parkinson tremor is present at rest and fades with action.
Huntington = autosomal dominant CAG expansion in HTT (chromosome 4) with anticipation: chorea, psychiatric change, and dementia at ages 30–50 with caudate atrophy; tetrabenazine treats chorea.
Wilson = autosomal recessive ATP7B defect (chromosome 13): young patient with tremor, dystonia, or parkinsonism plus liver or psychiatric disease; Kayser-Fleischer rings, low ceruloplasmin, high urinary copper → penicillamine or trientine and zinc.
D2 blockers: acute dystonia (hours–days) → benztropine or diphenhydramine; drug-induced parkinsonism (symmetric) → stop the drug; tardive dyskinesia (orofacial, often irreversible) → switch to an atypical plus a VMAT2 inhibitor.
Restless legs syndrome (urge to move, worse at rest and in the evening): check iron studies and replace iron if ferritin is 75 ng/mL or lower or transferrin saturation is below 20%; also linked to pregnancy and renal failure; treat with gabapentin or pregabalin (dopamine agonists discouraged: augmentation).
Tourette = multiple motor tics plus ≥1 vocal tic for >1 year from childhood (comorbid OCD, ADHD) → habit reversal, α2 agonists, antipsychotics if severe; Sydenham chorea follows group A strep.

Tremor: Parkinson disease vs essential tremor

Parkinson disease (PD) is a clinical diagnosis built on TRAP: resting Tremor (pill-rolling, 4–6 Hz), Rigidity (cogwheel), Akinesia or bradykinesia, and Postural instability. Onset is asymmetric, with masked facies, a shuffling gait, and micrographia. Nonmotor features such as anosmia, constipation, REM sleep behavior disorder, and depression often precede the motor signs.

Essential tremor is a bilateral action or postural tremor of the hands (sometimes the head or voice) that worsens with sustained posture or movement, such as holding a cup, and improves with alcohol. It is often autosomal dominant. First-line treatment is propranolol or primidone.

Parkinson tremor vs essential tremor

Feature	Parkinson tremor	Essential tremor
When present	At rest; disappears with action	With action or posture; absent at rest
Pattern	Pill-rolling, asymmetric	Symmetric; may involve head and voice
Other clues	Rigidity, bradykinesia, postural instability	Familial; improves with alcohol
Treatment	Levodopa-carbidopa	Propranolol or primidone

A tremor that worsens as the hand approaches a target (intention tremor) points to the cerebellum instead.

Treating Parkinson disease

Substantia nigra degenerationLoss of dopaminergic neurons in the pars compacta, with α-synuclein Lewy bodies.
Dopamine deficiencyNigrostriatal pathway.
Impaired movement initiationBradykinesia, rigidity, tremor.
Levodopa replaces dopamineCarbidopa limits peripheral loss.

Parkinson pathophysiology and the logic of therapy

Levodopa-carbidopa is the most effective symptomatic therapy. Carbidopa blocks peripheral dopa decarboxylase, so more levodopa reaches the brain and nausea falls. Long-term use brings motor fluctuations and dyskinesias.
Dopamine agonists (pramipexole, ropinirole) are used in younger patients. They can trigger impulse-control disorders: pathologic gambling, hypersexuality, and compulsive shopping.
Adjuncts: MAO-B inhibitors (selegiline, rasagiline) and COMT inhibitors (entacapone) prolong the effect of dopamine and levodopa; amantadine reduces levodopa-induced dyskinesias.

Ask every patient on a dopamine agonist about new gambling or shopping behaviors.

Advanced disease. Deep brain stimulation of the subthalamic nucleus helps motor fluctuations. For PD psychosis, avoid typical antipsychotics, which worsen parkinsonism; quetiapine, clozapine, or pimavanserin are used instead.

Parkinson-plus clues. A poor levodopa response, early falls, or symmetric onset suggests another disorder: vertical gaze palsy (progressive supranuclear palsy), early autonomic failure (multiple system atrophy), or early hallucinations with fluctuating cognition (dementia with Lewy bodies).

Chorea, Huntington, and Wilson disease

Chorea is rapid, irregular, flowing involuntary movement. Causes include Huntington disease, Sydenham chorea (a major Jones criterion of acute rheumatic fever, appearing weeks after group A strep pharyngitis in a child), drugs, pregnancy (chorea gravidarum), and SLE.

Huntington disease vs Wilson disease

Feature	Huntington disease	Wilson disease
Inheritance	Autosomal dominant, with anticipation	Autosomal recessive
Defect	CAG trinucleotide repeat expansion in HTT, chromosome 4	ATP7B copper-transport defect, chromosome 13
Onset	Ages 30–50	Young, usually under 40
Clinical picture	Chorea, psychiatric and behavioral change, dementia	Tremor, dystonia, parkinsonism, dysarthria; liver disease; psychiatric symptoms
Key findings	Caudate atrophy (boxcar ventricles); reduced GABA and acetylcholine	Kayser-Fleischer rings, low ceruloplasmin, high urinary copper
Treatment	Tetrabenazine (VMAT2 inhibitor) for chorea	Chelation (penicillamine, trientine) and zinc

Anticipation. In Huntington disease, more CAG repeats in successive generations mean earlier, more severe disease. Predictive genetic testing of at-risk relatives is preceded by genetic counseling.

Consider Wilson disease in any patient under 40 with a new movement disorder plus liver or psychiatric disease; a slit-lamp exam looks for Kayser-Fleischer rings.

Drug-induced movement disorders

Movement reactions to dopamine (D2) blockers

Disorder	Timing	Features	Treatment
Acute dystonia	Hours to days after an antipsychotic	Sustained contractions: torticollis, oculogyric crisis, laryngospasm	Benztropine or diphenhydramine, promptly
Drug-induced parkinsonism	Subacute	Symmetric parkinsonism from typical antipsychotics or metoclopramide	Stop the drug; it resolves
Tardive dyskinesia	After prolonged D2-blocker use	Orofacial lip-smacking, tongue protrusion, chewing; often irreversible	Switch to an atypical agent; VMAT2 inhibitor (valbenazine, deutetrabenazine)

Key points. Drug-induced parkinsonism is the most common secondary parkinsonism, and its symmetry helps separate it from PD. Anticholinergics rapidly reverse acute dystonia but do not help, and may worsen, tardive dyskinesia; raising the antipsychotic dose only masks TD.

Restless legs syndrome and tics

Restless legs syndrome is an uncomfortable urge to move the legs that is worse in the evening and at rest and relieved by movement. It is associated with iron deficiency, pregnancy, and renal failure, so check ferritin and transferrin saturation first and replace iron when ferritin is 75 ng/mL or lower or transferrin saturation is below 20% (AASM 2024), cutoffs higher than those used for anemia. Alpha-2-delta ligands (gabapentin, pregabalin) are first-line symptomatic therapy; dopamine agonists (pramipexole) are now discouraged (AASM 2024) because long-term dopaminergic therapy causes augmentation, with symptoms starting earlier and becoming more intense.

Tourette syndrome is multiple motor tics plus at least one vocal tic for over a year, beginning in childhood, commonly with comorbid OCD and ADHD. Treat with habit-reversal behavioral therapy, α2 agonists (guanfacine, clonidine), or antipsychotics for severe tics.

Tics are briefly suppressible and preceded by a premonitory urge, unlike other hyperkinetic movements.