The Movement Disorder Examination: A Region-by-Region Phenomenology Atlas

A rhythmic, oscillatory, roughly sinusoidal movement of a body part produced by alternating or synchronous contraction of antagonist muscles. Tremor is the only involuntary movement that is truly rhythmic and oscillatory — that single feature (axis 1 + 7: regular, repeating about a fixed point) separates it from every other hyperkinesia.

A sudden, brief, shock-like involuntary movement. Positive myoclonus is caused by an abrupt muscle contraction (<50–100 ms); negative myoclonus (asterixis) by an abrupt, brief loss of tone. Myoclonus is the fastest hyperkinesia — so fast it can look like a "twitch" or a jerk of a whole limb.

Brief lapses of posture from sudden loss of muscle tone, classically at the wrists with the arms outstretched and hands dorsiflexed — the "flapping tremor" of metabolic encephalopathy (hepatic, uremic, hypercapnic) and some drugs. Despite the old name it is not a tremor: it is arrhythmic, and the movement is a drop-and-recovery, not an oscillation.

A continuous stream of random, brief, non-rhythmic, unpredictable movements that flow from one body part to another. Unlike myoclonus (discrete jerks) chorea is fluid; unlike tremor it has no rhythm; unlike dystonia it has no consistent direction. Patients often camouflage chorea by folding it into semi-purposeful acts (parakinesia). Two classic bedside signs: milkmaid's grip (inability to maintain a steady grip — waxing/waning squeeze) and motor impersistence of the tongue (cannot keep it protruded — "harlequin" or "flycatcher" tongue), plus choreic (pronator) drift and "spooning" of the outstretched hands.

Slow, continuous, writhing, sinuous movements, most prominent distally (fingers, hands, toes). Modern usage treats athetosis as slow, mobile distal dystonia — the boundary is blurred, and choreoathetosis names the common admixture of fast choreic and slow athetoid movement (e.g., in cerebral palsy, Huntington disease, levodopa-induced dyskinesia).

Large-amplitude, violent, flinging movements of the proximal limb — essentially chorea "turned up" to involve proximal joints with great force. Usually unilateral (hemiballism), classically from a lesion of the contralateral subthalamic nucleus, and often evolving into distal chorea as it subsides.

Sustained or intermittent muscle contractions causing abnormal, often repetitive movements, postures, or both. Dystonic movements are patterned (the same muscles, pulling the same direction, every time), twisting in quality, and frequently tremulous. They are typically initiated or worsened by voluntary action (action-specific) and show overflow to adjacent muscles. Dystonia is defined more by its pattern and directionality (axes 7) than by its speed.

Brief, stereotyped, intermittent movements (motor) or sounds (phonic) that are semi-voluntary: preceded by a premonitory urge, temporarily suppressible (with mounting inner tension and a rebound flurry on release), and suggestible. Simple tics involve one muscle group (blink, shoulder shrug, sniff); complex tics are coordinated sequences (touching, echopraxia, coprolalia). The urge + suppressibility + rebound triad is close to specific for tics.

A repetitive, rhythmic, patterned, purposeless movement that is identical each time (hand-flapping, body-rocking, mouthing). Unlike tics, there is usually no premonitory urge, onset is earlier, and the movement is more fixed and often occurs during excitement or absorption. Seen in autism, intellectual disability, tardive syndromes, and some frontotemporal disorders.

A subjective inner restlessness and compulsion to move, expressed as semi-purposeful movements: shifting weight, rocking, marching in place, crossing/uncrossing legs, an inability to remain still. The subjective urge distinguishes it from chorea or stereotypy; classically drug-induced (dopamine antagonists). Rate with the Barnes Akathisia Rating Scale.

Bradykinesia = slowness of movement. Hypokinesia = smallness (reduced amplitude). Akinesia = poverty/absence of movement and delay in initiation. The MDS-diagnostic core of parkinsonism is bradykinesia plus the defining feature: decrement — a progressive reduction in amplitude and/or speed on repetitive movement (finger tapping, hand open–close, pronation–supination, toe tapping) — often with hesitations and arrests ("freezing" of the repetition). Look also for reduced automatic movements: hypomimia (face), reduced arm swing (gait), micrographia (writing), hypophonia (voice).

Freezing is a sudden, transient (usually <10 s) block of an ongoing movement — most often of gait ("feet glued to the floor") at initiation, on turning, in doorways, or approaching a target. Festination is an involuntary acceleration into progressively shorter, faster steps (or faster speech, tachyphemia) as the center of mass outruns the feet. Both are hallmarks of parkinsonism and are covered in the gait region (§21).

Slow, writhing, athetosis-like movements of the outstretched fingers that appear or worsen with eyes closed, caused by loss of proprioception (dorsal-column or large-fiber neuropathy), not basal-ganglia disease. Test: arms out, fingers spread, eyes open then closed — pseudoathetosis and finger drift emerge in the dark and correct with vision. This single maneuver keeps you from mislabeling a sensory sign as dystonia/athetosis.

Involuntary, bilateral, forceful eyelid closure from spasm of orbicularis oculi — a focal dystonia of the eyelids. Ranges from increased blinking to sustained functional blindness; worsened by bright light, reading, wind, and stress; often relieved by a sensory trick (talking, humming, touching the lateral canthus). When combined with lower-facial/oromandibular dystonia it is Meige syndrome (cranial segmental dystonia).

Difficulty initiating eyelid elevation despite no orbicularis spasm and intact levator — the patient struggles to open the eyes, often thrusting the brow/head back and touching the lids to help. Frequently coexists with blepharospasm and parkinsonian syndromes (esp. PSP).

Eyelid myokymia is a continuous fine rippling of the lower lid — extremely common, benign, fatigue/caffeine-related. Eyelid/ocular tics are brief, stereotyped, suppressible blinks or winks with a premonitory urge (Tourette spectrum). Distinguish both from the sustained closure of blepharospasm.

A staring appearance from lid retraction (PSP — the "astonished/worried" facies; also thyroid eye disease) and reduced blink rate (parkinsonism). These hypokinetic lid signs pair with hypomimia (§14).

Continuous chewing, rolling, and writhing of the tongue with lip smacking and puckering — the classic tardive dyskinesia pattern (a stereotypy/chorea from chronic dopamine-receptor blockade). Often the tongue rolls within the mouth and pushes against the cheek ("bon-bon sign"). Scored on the AIMS.

Involuntary, patterned, forceful tongue protrusion (a focal dystonia) — action-induced (talking/eating) tongue-protrusion dystonia is a red flag for neuroacanthocytosis and tardive dystonia; distinguish from the darting impersistence of chorea. May respond to a sensory trick (touching the lips, chewing gum).

Tremor — rhythmic oscillation on protrusion (essential tremor, parkinsonism, alcohol/enhanced physiologic). Lingual myorhythmia — slow (1–4 Hz) rhythmic movement persisting at rest (Whipple, brainstem). The "trombone tremor" of the tongue (rhythmic in–out) is described in general paresis and advanced PD.

Flickering fasciculations with atrophy and furrowing, seen best with the tongue at rest in the mouth (protrusion produces normal tremor that mimics fasciculation) — a sign of bulbar motor-neuron disease, not a movement disorder. Always assess the tongue at rest before calling fasciculations.

Focal dystonia of the jaw and lower face producing patterned jaw-opening, jaw-closing (with bruxism/trismus and tongue/cheek biting), or jaw-deviation/retraction spasms, often action-induced (speaking, chewing) with sensory tricks (touching the lips/chin, chewing gum, a toothpick). With blepharospasm = Meige syndrome.

Lip smacking, puckering, and chewing movements of tardive dyskinesia (see tongue, §12). Rabbit syndrome is a fast (~5 Hz), rhythmic, vertical perioral tremor sparing the tongue — a drug-induced parkinsonian (not tardive) phenomenon that responds to anticholinergics.

Rhythmic (1–3 Hz) elevation of the soft palate. Essential palatal tremor (tensor veli palatini) produces an ear click and typically stops in sleep; symptomatic palatal tremor (levator veli palatini) arises from a lesion of the Guillain–Mollaret triangle with hypertrophic olivary degeneration, persists in sleep, and often involves the eyes/face (myorhythmia).

Task-specific focal dystonia of the vocal folds. Adductor type: strained-strangled voice with abrupt voiced breaks; abductor type: breathy, whispered breaks on voiceless consonants. A voice tremor may coexist. Singing or a falsetto register may bypass it (a task-specific "trick").

Trismus — sustained jaw-closing spasm (acute dystonic reaction, tetanus, local pathology). Bruxism — involuntary grinding/clenching (often nocturnal; may be tardive or medication-related). Both are jaw-closing phenomena to distinguish from OMD's patterned, action-induced spasms.

Reduced facial expression, blink, and spontaneous movement — a hypokinetic sign of parkinsonism (bradykinesia of facial musculature). Pairs with reduced blink and lid signs (§11) and hypophonia.

Unilateral, involuntary, irregular twitching that usually begins in the orbicularis oculi and spreads down one hemiface; may become tonic; persists in sleep; often from vascular compression of CN VII at the root exit zone (a peripherally generated segmental myoclonus). The other Babinski sign (brow-up with eye closure) is characteristic. Unilaterality separates it from (bilateral) blepharospasm.

Continuous, fine, undulating "bag-of-worms" rippling across one side of the face — a brainstem (pontine) localizing sign (MS plaque, brainstem glioma), distinct from the discrete twitches of hemifacial spasm.

Grimacing from facial chorea (Huntington, tardive) is random and flowing; facial tics (blinks, nose-wrinkling, grimaces) are stereotyped, suppressible, urge-preceded; facial stereotypies are fixed and repetitive. Risus sardonicus is a sustained fixed grin from tetanus or strychnine.

A 4–6 Hz supination–pronation/flexion–extension oscillation of the fingers/hand at rest that damps with action; the thumb rubbing the fingers gives "pill-rolling." A postural tremor that reappears after a latency of several seconds (re-emergent tremor) is the same PD tremor re-expressing in posture.

On the tapping battery, progressive decrement in amplitude and/or speed, with hesitations and arrests, is the defining feature of parkinsonism (see §5). Contrast with cerebellar dysrhythmia (irregular timing/amplitude but no true decrement) and functional slowness (effortful, non-decrementing).

Writer's cramp is a task-specific focal hand dystonia: abnormal finger/wrist posturing with excessive grip and proximal overflow appearing only when writing (simple type) or also in the writing posture (dystonic/complex type); may show mirror dystonia. The striatal hand is a more fixed dystonic posture — MCP flexion, PIP extension, DIP flexion, ulnar deviation — seen in PD and atypical parkinsonism.

Milkmaid's grip (waxing/waning squeeze — motor impersistence), spooning (hyperextended MCPs with flexed wrists on outstretched arms), choreic (pronator) drift (arms drift and pronate/hyperextend when held out), and "piano-playing" fingers (independent, random finger movements). Together they flag chorea (Huntington, Sydenham, others).

Minipolymyoclonus — tiny, arrhythmic, twitch-like finger displacements of the outstretched hands (cortical myoclonus, or motor-neuron/neuropathic origin). Asterixis — brief postural lapses (negative myoclonus) at the wrists (metabolic; see §4.2). Distinguish both from tremor: neither is rhythmic.

An often irregular, jerky, direction-dependent tremor in a hand with dystonic posturing — worse away from the null point, sometimes relieved by a sensory trick. Its irregularity and null-point behavior separate it from the regular kinetic tremor of ET.

A high-amplitude, low-frequency proximal tremor most evident in the wing-beating posture — the classic tremor of Wilson disease (also cerebellar-outflow lesions). Its proximal, coarse quality separates it from the distal tremors of PD and ET.

A slow (<4.5 Hz), irregular tremor present at rest, on posture, and on action (worsening with action), from lesions affecting the cerebello-thalamic and nigro-striatal pathways (midbrain/"rubral"). Its presence in all three activation states is the giveaway.

Large, flinging proximal-limb movements (see §4.3) — usually hemibody, from a contralateral subthalamic lesion; watch the whole arm swing violently at the shoulder. As it subsides it becomes distal chorea.

Involuntary elevation, internal rotation, or extension of the arm — often action-induced and appearing during gait ("dystonic posturing of the arm on walking," an early sign of young-onset/DYT dystonia and of parkinsonism-with-dystonia). Overflow from a hand task (writer's cramp) into the proximal arm belongs here too.

Focal dystonia of the neck producing patterned, often tremulous, abnormal head/neck postures. Name every component by its direction: torticollis (rotation — chin turns to one side), laterocollis (tilt — ear toward shoulder), anterocollis (flexion — chin down), retrocollis (extension — chin up), and lateral/sagittal shift. Most patients have a combination. Look for a sensory trick, muscle hypertrophy, and dystonic head tremor; rate with TWSTRS.

Dystonic head tremor is irregular, direction-dependent, has a null point, and often accompanies an abnormal head posture and a sensory trick. Essential head tremor is more regular ("yes-yes" or "no-no"), occurs without a fixed posture, is worse upright and better supine, and usually comes with hand tremor. Titubation is a slow (~3 Hz) cerebellar head/trunk oscillation with other cerebellar signs.

Axial rigidity/retrocollis (neck extension) is characteristic of PSP. Dropped head (severe neck flexion from extensor weakness — "head ptosis") is seen in myasthenia, myopathy, ALS, and MSA; antecollis (dystonic neck flexion) is a red flag for MSA. Distinguish weakness-driven dropped head (correctable, floppy) from dystonic antecollis (patterned, resistant).

A rhythmic, low-frequency (~3 Hz) nodding oscillation of the head and trunk from disease of the cerebellar midline (vermis); worse when sitting/standing unsupported and accompanied by other cerebellar signs.

Bobble-head doll syndrome — a to-and-fro "yes-yes" head bobbing (~2–3 Hz) in children, associated with third-ventricular/suprasellar lesions (e.g., a cyst causing hydrocephalus). Spasmus nutans — the infantile triad of head nodding, asymmetric nystagmus, and anomalous head posture; usually benign and self-limited but requires exclusion of a chiasmal glioma.

Striatal toe — spontaneous, dystonic extension of the great toe (a pseudo-Babinski without the rest of the reflex), seen in PD and atypical parkinsonism. Foot/ankle dystonia — patterned inversion and plantarflexion with toe curling or great-toe extension; in PD it classically appears as painful early-morning or "off"-period off-dystonia, and in young-onset dystonia it may be the presenting, action-induced sign (worse on walking).

A very fast (13–18 Hz) tremor of the legs and trunk present only on standing still, causing a subjective unsteadiness relieved by walking, leaning, or sitting. Too fast to see well — palpate the thigh (a fine "hum," the "helicopter sign" on auscultation) or confirm with surface EMG.

RLS is a clinical diagnosis by history: an urge to move the legs, usually with uncomfortable sensations, that (1) begins/worsens at rest, (2) is relieved by movement, and (3) is worse in the evening/night. Periodic limb movements of sleep — stereotyped dorsiflexions of the great toe/ankle recurring every ~20–40 s — are often associated and seen on polysomnography.

Continuous, involuntary, writhing/wriggling movements of the toes (and feet) accompanied by deep leg pain — a peripheral/spinal-generated dyskinesia often following nerve or root injury. The pain-plus-movement combination is the clue.

Velocity-dependent ankle resistance, sustained ankle clonus, and an extensor plantar response mark an upper-motor-neuron process that shapes gait (spastic/scissoring, §21) — distinguish from the lead-pipe rigidity of parkinsonism.

Marked forward flexion of the thoraco-lumbar spine that appears on standing/walking and resolves when lying supine or against a backrest. Seen in PD, atypical parkinsonism, and axial myopathy; a mix of dystonic and myopathic mechanisms. The supine-correction test is diagnostic of the reducible form.

Sustained lateral trunk flexion (± slight rotation) resembling the leaning tower — an axial dystonia, often drug-related (dopaminergic or antidopaminergic) or part of PD; typically improves supine.

Opisthotonus — extreme extensor arching of the neck and trunk (severe generalized dystonia, acute dystonic reactions, tetanus, some genetic/metabolic dystonias). Generalized/axial dystonia may also produce tortipelvis and truncal twisting.

Truncal chorea — random, flowing trunk/pelvic movements (Huntington, tardive) producing a rocking, lurching seated posture. Belly-dancer's dyskinesia — slow, writhing, undulating movements of the abdominal wall/diaphragm. Respiratory dyskinesia — irregular, rapid, involuntary breathing movements (often tardive) causing grunting and dyspnea unexplained by cardiopulmonary disease.

Propriospinal myoclonus — repetitive, arrhythmic truncal flexion (or extension) jerks, often supine, spreading slowly up and down the cord from a spinal generator (organic or functional — test for distractibility/variability). Stiff-person spectrum — continuous co-contraction of axial (and proximal-limb) muscles producing a rigid, hyperlordotic trunk with superimposed painful, stimulus-triggered spasms.

Loss of postural reflexes — retropulsion or a fall on the pull test — is a late sign in PD but an early one in PSP and MSA. Grade by the number of corrective steps and whether the examiner must catch the patient. It is the single most important predictor of falls.