Abnormal Movements Catalog
Abnormal involuntary movements are some of the most visible findings in clinical neurology, and the diagnostic information they carry is often complete at first glance. A patient sitting in the waiting room may declare their diagnosis from across the room: the resting tremor of Parkinson disease, the jerky undulations of chorea, the sustained postures of dystonia, the lightning-fast jerks of myoclonus, the brief stereotyped movements of tics. Recognizing the type of movement is the first step; the differential of each type is the second; the localization within the extrapyramidal system is the third. By the time the history begins, an experienced examiner has often narrowed the differential more than the patient will know.
This page is a catalog of abnormal movements, organized by category, with a focus on the bedside features that distinguish each from its mimics. The point is to give the trainee a mental library of movement phenomenology so that, on seeing a new movement, they can name it. Once named, the differential becomes manageable.
The Approach to Any Abnormal Movement
A handful of questions, applied to any movement, place it in a phenomenological category:
- Is it rhythmic or irregular? Tremor is rhythmic; chorea and myoclonus are not.
- Is it sustained or brief? Dystonia sustains a posture; tics and myoclonus are brief.
- What is the patient doing when it occurs? Rest? Holding a posture? Performing an action? Reaching for a target? Different tremors emerge in different contexts.
- Is it voluntary, semi-voluntary, or involuntary? Tics are semi-voluntary (suppressible with effort, often accompanied by a premonitory urge). Chorea and dystonia are involuntary.
- Does it disappear in sleep? Almost all movement disorders disappear in sleep, with the notable exception of palatal myoclonus and some myoclonic epilepsies.
- Does it have a trigger? Some movements are reflexive, triggered by tactile or proprioceptive stimuli; others occur in response to specific actions.
- What does the patient feel? Some movements are accompanied by characteristic sensations (the premonitory urge of tics, the relief of dystonia by the “geste antagoniste”).
Tremor
Tremor is rhythmic oscillation of a body part around a fixed axis. The most clinically useful classification is by context — when the tremor appears:
Rest Tremor
Present when the limb is at rest and unsupported, typically reduced or absent during voluntary movement. The classical rest tremor is the 4-6 Hz pill-rolling tremor of Parkinson disease — a flexion-extension and pronation-supination of the thumb and fingers that looks as though the patient is rolling a small object between thumb and forefinger. The tremor is often unilateral or asymmetric at onset, asymmetric throughout the early course, and may spread to the contralateral side over years.
Rest tremor in a patient with bradykinesia and rigidity defines parkinsonism. Other parkinsonian syndromes can produce rest tremor (vascular parkinsonism, drug-induced parkinsonism), and some have more typical postural tremor (MSA, PSP, corticobasal syndrome have less rest tremor than idiopathic PD). Holmes (rubral) tremor — coarse, low-frequency tremor with rest, postural, and intention components — points to lesions of the midbrain involving the red nucleus.
Postural Tremor
Emerges when the patient holds a posture against gravity. Test by asking the patient to hold the arms outstretched, hands flat, fingers extended. The most common postural tremor is essential tremor — a bilateral, symmetric, 6-12 Hz tremor of the hands that often involves the head (titubation, “yes-yes” or “no-no” head tremor) and sometimes the voice. Essential tremor classically improves with alcohol (a useful historical clue but not a treatment recommendation) and may have a family history.
Essential tremor is the most common adult-onset movement disorder. The differential includes physiologic tremor enhanced by anxiety or fatigue, drug-induced tremor (lithium, valproate, beta-agonists, amiodarone, theophylline, SSRIs), thyrotoxicosis, alcohol withdrawal, and early Parkinson disease (when the tremor at this stage may be more postural than rest).
Intention (Action) Tremor
Worsens as the limb approaches a target. The classical bedside test is the finger-to-nose maneuver: the patient touches your fingertip and then their own nose alternately. The intention tremor is most prominent in the last few centimeters of the movement, with the finger increasingly off-target as it approaches the goal. Intention tremor localizes to the cerebellum or its outflow pathways (dentatorubrothalamic tract). MS, cerebellar stroke, cerebellar degeneration, Wilson disease, and drug toxicity (lithium, phenytoin) are the main causes.
Other Tremor Categories
- Orthostatic tremor: a high-frequency (13-18 Hz) tremor of the legs that appears only on standing. The patient describes leg unsteadiness or shaking when standing still, relieved by walking or sitting. Often missed because it is invisible to the eye; auscultation of the calves reveals the high-frequency rumble.
- Task-specific tremor: emerges only with a specific action — writing tremor (primary writing tremor), musical instrument tremors, occupational tremors.
- Dystonic tremor: irregular, sometimes jerky tremor in a body part affected by dystonia. Often appears or worsens in specific postures and disappears in the geste antagoniste posture.
- Functional tremor: variable frequency, distractibility (changes or stops when the patient attends to another task), entrainment (matches the frequency of voluntary movements in another limb when those are requested). Often present at rest, in posture, and on action — an “all-positions” tremor — and often abruptly variable.
Chorea, Athetosis, and Ballism
This family of hyperkinetic movements represents a continuum from small, distal, rapid (chorea) through slow, writhing (athetosis) to large, proximal, ballistic (ballism). All three reflect basal ganglia dysfunction, particularly involving the striatum, subthalamic nucleus, or their projections.
Chorea
Brief, irregular, non-rhythmic movements that flow from one body part to another. Each individual movement looks purposeful in isolation but the overall pattern is unpredictable and unintegrated. Patients often incorporate the choreiform movements into seemingly voluntary actions (the “parakinetic” posturing of Huntington disease — the patient appears to be moving with intention, but the movements are not under control).
Patients with mild chorea often appear fidgety or restless rather than overtly choreic. The clinical exam:
- Have the patient sit with hands in lap and observe — chorea often appears as irregular finger movements.
- Ask the patient to grip your two fingers tightly and hold (“milkmaid grip”) — choreic patients cannot sustain a steady grip; their hands repeatedly relax and re-grip, producing a milking sensation.
- Ask the patient to protrude the tongue and hold it out — patients with chorea cannot keep the tongue still (“trombone tongue,” the tongue darting in and out repeatedly).
The differential of chorea:
- Huntington disease: autosomal dominant; CAG repeat expansion in HTT gene; combines chorea with cognitive decline (executive dysfunction prominent) and psychiatric features (depression, irritability, sometimes psychosis). Onset usually in middle age. Juvenile Huntington presents more often with rigidity and parkinsonism than chorea.
- Sydenham chorea: postinfectious chorea, mostly in children, following streptococcal infection (rheumatic chorea). Resolves over weeks to months.
- Chorea gravidarum: pregnancy-related chorea, often with underlying rheumatic history or systemic lupus.
- Drug-induced chorea: levodopa (in Parkinson disease, peak-dose dyskinesias), oral contraceptives, cocaine, methamphetamine, anticholinergics.
- Wilson disease: any movement disorder in a young person, with hepatic dysfunction and Kayser-Fleischer rings.
- Vascular chorea: contralateral subthalamic, caudate, or putaminal infarct.
- Systemic lupus, antiphospholipid syndrome, polycythemia vera, hyperthyroidism: rarer causes of acquired chorea.
- Neuroacanthocytosis syndromes: rare genetic chorea with red cell membrane abnormalities and neuromuscular features.
Athetosis
Slow, writhing, sinuous movements, especially of the distal extremities. Pure athetosis is uncommon; the more common pattern is choreoathetosis — a combination with both fast (choreic) and slow (athetoid) components. Causes overlap with chorea; cerebral palsy is the classical cause of pure athetosis (athetoid cerebral palsy, often from perinatal injury to the basal ganglia).
Ballism
Large-amplitude flinging movements of a proximal limb, often violent enough to throw a glass off a table. Unilateral ballism (hemiballism) is the more common form and classically reflects a contralateral subthalamic nucleus lesion — most often a small lacunar stroke. Bilateral ballism is rare. Treatment is symptomatic (dopamine receptor antagonists). The condition often improves spontaneously over weeks to months.
Dystonia
Sustained or intermittent muscle contractions producing twisting, repetitive movements or abnormal postures. The cardinal features:
- Sustained posture: the affected body part is held in an abnormal position, often for prolonged periods.
- Patterned, repetitive movements: the same posture is assumed repeatedly.
- Triggering by action: many dystonias are worse during specific actions (writer’s cramp during writing, musician’s dystonia during playing).
- Overflow: the dystonic movement spreads beyond the intended muscle group to involve adjacent muscles.
- The geste antagoniste (sensory trick): a light touch or maneuver — touching the chin in cervical dystonia, putting a finger to the cheek — transiently and dramatically relieves the dystonia. This phenomenon is highly characteristic of dystonia and rare in other movement disorders.
Classification by Distribution
- Focal dystonia: a single body region affected. Examples: cervical dystonia (spasmodic torticollis), blepharospasm, oromandibular dystonia, writer’s cramp, musician’s dystonias, spasmodic dysphonia.
- Segmental dystonia: two or more contiguous regions (e.g., neck and arm).
- Multifocal dystonia: two or more non-contiguous regions.
- Hemidystonia: an entire half of the body, typically pointing to a contralateral basal ganglia lesion.
- Generalized dystonia: trunk and at least two other regions; typically pediatric onset (DYT1 dystonia and other genetic forms).
Classification by Cause
- Primary (idiopathic) dystonia: includes genetic dystonias (DYT1, DYT6, others), focal idiopathic dystonias of adulthood.
- Secondary dystonia: due to identifiable cause — stroke, perinatal injury, traumatic brain injury, neurodegenerative disease.
- Drug-induced dystonia: acute dystonic reaction (after dopamine receptor antagonists, classically in young men, rapidly responsive to anticholinergics); tardive dystonia (chronic use of dopamine receptor antagonists).
- Dystonia-plus syndromes: dopa-responsive dystonia (Segawa disease, GTP cyclohydrolase 1 deficiency, dramatic response to small-dose levodopa), myoclonus-dystonia, paroxysmal dystonias.
- Heredodegenerative dystonias: dystonia in the context of a degenerative disorder (Wilson, Huntington, neurodegeneration with brain iron accumulation, mitochondrial diseases).
Specific Bedside Patterns
- Cervical dystonia (spasmodic torticollis): head turned (torticollis), tilted (laterocollis), pulled forward (antecollis) or backward (retrocollis), often with shoulder elevation and tremor. The geste antagoniste (touching the chin or the side of the face) is highly characteristic. Treatment is botulinum toxin injection.
- Blepharospasm: forceful, involuntary eye closure. Often combined with oromandibular dystonia (Meige syndrome).
- Writer’s cramp: dystonic posturing of the hand during writing, with relative sparing of other activities. Task-specific dystonia.
- Spasmodic dysphonia: adductor type (strangled voice) or abductor type (whispered voice). Treatment is botulinum toxin to the vocal cord muscles.
- Dopa-responsive dystonia: childhood-onset dystonia, often with diurnal variation (better in the morning, worse by evening), with dramatic response to small doses of levodopa. The diagnosis is often missed for years; a trial of levodopa is appropriate in any childhood-onset dystonia.
Myoclonus
Brief, sudden, shock-like jerks of a muscle or muscle group. Each jerk is over in a fraction of a second. Myoclonus can be focal (a single muscle), segmental (several adjacent muscles), multifocal, or generalized.
Classification by Distribution and Origin
- Cortical myoclonus: from cerebral cortex; small distal jerks, often stimulus-sensitive (responding to touch, sound, light); associated EEG correlates. Causes include cortical reflex myoclonus, post-hypoxic myoclonus (Lance-Adams syndrome), various epileptic myoclonus syndromes, neurodegenerative disorders.
- Subcortical myoclonus: from brainstem, basal ganglia, or thalamus; often larger, more proximal jerks. Reticular reflex myoclonus, palatal myoclonus.
- Spinal myoclonus: from cord; rhythmic jerks in a segmental distribution, persistent in sleep.
- Peripheral myoclonus: from peripheral nerve; rare, typically reflects nerve hyperexcitability.
Specific Syndromes
- Physiologic myoclonus: hypnic jerks (the body jerk that occurs as one falls asleep), hiccups, anxiety-related jerks. Not pathological.
- Essential myoclonus: idiopathic, often familial, present from childhood.
- Post-hypoxic myoclonus (Lance-Adams): appearing during recovery from anoxic brain injury, often action-induced.
- Toxic-metabolic myoclonus: uremia, hepatic failure, hyponatremia, serotonin syndrome, drug toxicity (opioids, lithium).
- Asterixis (“negative myoclonus”): a brief LOSS of postural tone — the patient holds the hands extended and the wrists “drop” intermittently. Classic in hepatic encephalopathy and metabolic encephalopathies.
- Palatal myoclonus: rhythmic 1.5-3 Hz movements of the palate (and sometimes adjacent muscles), often persistent during sleep; reflects lesions of the Mollaret triangle (dentate, red nucleus, inferior olive).
- Opsoclonus-myoclonus-ataxia syndrome: chaotic, multidirectional eye movements (“dancing eyes”) with limb myoclonus and ataxia. Paraneoplastic (children: neuroblastoma; adults: lung, breast, ovarian cancers) or postinfectious.
- Epileptic myoclonus: part of juvenile myoclonic epilepsy, Lennox-Gastaut syndrome, progressive myoclonic epilepsies (Unverricht-Lundborg, Lafora body disease, MERRF, sialidosis).
Tics
Tics are brief, stereotyped, semi-voluntary movements (motor tics) or sounds (phonic tics). They are distinguished from other movement disorders by:
- Stereotypy: the same movement or sound repeats.
- Semi-voluntary character: tics can be suppressed for a while with effort, but suppression creates rising discomfort that is relieved by the tic.
- Premonitory urge: a sensation in the affected body part — itching, pressure, urge — that precedes the tic and is relieved by it.
- Distractibility: tics often diminish when the patient is engaged in absorbing tasks.
- Persistence in sleep is uncommon; tics usually disappear in sleep.
Motor tics range from simple (eye blinking, shoulder shrugging, head jerking, facial grimacing) to complex (jumping, touching objects, copropraxia). Phonic tics range from simple (sniffing, throat clearing, grunting) to complex (echolalia, coprolalia).
Tic disorders:
- Tourette syndrome: multiple motor tics and at least one phonic tic, onset before age 18, persisting for more than a year. Comorbid OCD and ADHD are common.
- Persistent (chronic) motor or phonic tic disorder: one or the other for more than a year.
- Provisional tic disorder: tics for less than a year (often transient childhood tics that resolve).
- Tardive tics: rare, after long-term neuroleptic use.
- PANDAS / PANS: pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections; abrupt onset of tics and OCD in children after infections.
Other Movement Disorders
Stereotypies
Repetitive, patterned, purposeless movements (rocking, hand flapping, head banging). Common in autism, intellectual disability, schizophrenia, and tardive movement disorders. Distinguished from tics by the absence of premonitory urge and the typical inability to suppress.
Restless Legs Syndrome (Willis-Ekbom Disease)
An uncomfortable urge to move the legs, worse at rest (especially at night), partially relieved by movement. Often associated with periodic limb movements of sleep — rhythmic flexion of the leg every 20-40 seconds during sleep. Associated with iron deficiency, uremia, pregnancy, and peripheral neuropathy. Treatment includes dopamine agonists, gabapentinoids, and iron supplementation if ferritin is low.
Akathisia
Inner restlessness with a compulsion to move, often manifested by walking, leg crossing, or shifting in the chair. Most commonly drug-induced (dopamine receptor antagonists, SSRIs); also a feature of Parkinson disease. Treatment of drug-induced akathisia is reduction of the offending agent, with beta-blockers, anticholinergics, or benzodiazepines as second-line.
Functional Movement Disorders
Movements that do not fit physiologic patterns, with positive features of functional disease:
- Distractibility (movements diminish or change when the patient attends to another task).
- Entrainment (a functional tremor matches the frequency of voluntary movements in another limb when those are requested).
- Variable frequency, amplitude, and direction.
- Inconsistency over time.
- Suggestibility.
- Sudden onset with peak severity from the start.
- Multiple movement types coexisting in implausible combinations.
- Resolution with placebo or distraction.
The diagnosis is made on positive features, not on exclusion. Functional movement disorders are common, often responsive to physical therapy and education, and deserve specific recognition rather than “I cannot find anything organic.”
🔍 Did You Know?
Palatal myoclonus is one of the few movement disorders that persists in sleep. The rhythmic movements of the soft palate, sometimes with ear clicks audible to the patient or examiner, reflect rhythmic activity in the Guillain-Mollaret triangle (dentate nucleus → contralateral red nucleus → contralateral inferior olive → back to dentate). Acquired palatal myoclonus often follows a lesion of the central tegmental tract; essential palatal myoclonus is idiopathic and lacks identifiable structural cause. The ear clicks are caused by the rhythmic contraction of the tensor veli palatini.
Pitfalls and Pearls
- Watch the patient before you touch them. Many movement disorders declare themselves in the first thirty seconds of observation.
- Tremor is rhythmic; chorea is not. A rhythmic involuntary movement is one of the tremors; an irregular, flowing involuntary movement is chorea, athetosis, or ballism.
- Rest tremor + bradykinesia + rigidity = parkinsonism. The diagnosis is essentially complete at the bedside.
- Asymmetric onset of parkinsonism favors idiopathic Parkinson disease. Symmetric onset, early postural instability, or rapid progression suggests an atypical syndrome.
- The geste antagoniste is highly characteristic of dystonia. Ask the patient if there is any maneuver that briefly improves the abnormal posture.
- Childhood-onset dystonia with diurnal variation may be dopa-responsive dystonia. A trial of levodopa is appropriate.
- Hemiballism is a small subthalamic lesion until proven otherwise, typically a lacunar infarct.
- A young person with any movement disorder, hepatic dysfunction, or psychiatric symptoms deserves evaluation for Wilson disease — including Kayser-Fleischer rings, ceruloplasmin, urine copper, and slit-lamp exam.
- Drug-induced movement disorders are common and reversible. Always review the medication list — dopamine receptor antagonists are the most common culprit.
- Functional movement disorders have positive features. Distractibility, entrainment, variability, and the dramatic effect of placebo are positive signs, not just absence of organic findings.
- Asterixis is “negative myoclonus.” Brief loss of postural tone in metabolic encephalopathy; not a tremor and not a true myoclonus.
References
- Campbell WW. DeJong’s The Neurologic Examination. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2013. Chapter 30.
- Albanese A, Bhatia K, Bressman SB, et al. Phenomenology and classification of dystonia: a consensus update. Mov Disord. 2013;28(7):863-873.
- Bhatia KP, Bain P, Bajaj N, et al. Consensus statement on the classification of tremors. From the task force on tremor of the International Parkinson and Movement Disorder Society. Mov Disord. 2018;33(1):75-87.
- Caviness JN, Brown P. Myoclonus: current concepts and recent advances. Lancet Neurol. 2004;3(10):598-607.
- Walker RH. Differential diagnosis of chorea. Curr Neurol Neurosci Rep. 2011;11(4):385-395.
- Espay AJ, Aybek S, Carson A, et al. Current concepts in diagnosis and treatment of functional neurological disorders. JAMA Neurol. 2018;75(9):1132-1141.
- Fahn S, Jankovic J, Hallett M. Principles and Practice of Movement Disorders. 2nd ed. Saunders; 2011.