Associated movements are the unconscious accompaniments of voluntary action. Most of them are so automatic that the patient is unaware of them. The arm swings when we walk. The opposite hand opens when we squeeze something with the dominant hand. The face changes expression when we move our eyes. The trunk shifts when we reach. These automatic accompaniments are the hidden choreography of normal motor function, and when they fail or persist abnormally, they reveal disease in the underlying systems that produce them.

This page covers two related categories of associated movements: the normal accompaniments that are reduced or lost in disease (most notably the loss of arm swing in parkinsonism), and the abnormal associated movements that emerge in disease (synkinesias, the mirror movements of corticospinal tract disease, and the pathological associated reactions after stroke). The page complements the gait, motor unit, and postural reflexes pages by addressing motor phenomenology that often does not fit into other categories.

Normal Associated Movements and Their Loss

Arm Swing During Gait

Reciprocal arm swing during walking is one of the most fundamental associated movements. The left arm swings forward as the right leg swings forward, and vice versa. The rotational forces of the swinging arms balance the rotational forces of the swinging legs, smoothing the gait and reducing the work required to maintain posture.

Reduced arm swing is one of the most useful early signs of parkinsonism. The reduction is often asymmetric, with the side that first developed parkinsonism showing less swing than the other. A patient who has noticed that “my left arm doesn’t seem to swing when I walk” or whose spouse has noticed it, may be reporting the earliest motor sign of Parkinson disease — sometimes years before tremor, bradykinesia, or rigidity become evident on examination.

The bedside test is simple: watch the patient walk a normal distance — across the room, down the corridor — and observe the arm swing. Note its presence, symmetry, and amplitude. In the patient with possible parkinsonism, look specifically for asymmetric reduction; in patients with already-diagnosed parkinsonism, track the arm swing over time as a marker of progression.

Other Lost Associated Movements in Parkinsonism

  • Facial expression (reduced spontaneous emotional movement, “hypomimia”): the patient’s face is less expressive than it would be in a healthy individual of the same age. Reduced blink rate (normal 15-20/min, parkinsonian 5-7/min) is part of this pattern.
  • Spontaneous postural adjustments: a healthy person at rest makes constant small adjustments of posture; the parkinsonian patient sits or stands with more fixity.
  • Speech prosody: emotional inflection of voice is reduced.
  • Spontaneous gestures during conversation: the patient uses fewer hand gestures, particularly on the more affected side.

The cumulative effect is a patient who appears subdued, less reactive, and less spontaneously engaged than they actually are. Families often describe this as “he seems depressed,” and the patient may indeed have depression — but the apparent affective flatness is often largely due to reduced emotional facial movement rather than to genuine depression.

Abnormal Associated Movements

Mirror Movements

Mirror movements are involuntary movements of one limb that occur simultaneously with voluntary movements of the contralateral limb. Asked to make a fist with one hand, the patient with mirror movements simultaneously makes a fist with the other. The phenomenon is normal in young children, decreases with age, and is usually absent by adolescence.

Persistent mirror movements in adults are pathological. They are seen in:

  • Congenital syndromes: Klippel-Feil syndrome and X-linked Kallmann syndrome are the classical associations.
  • Acquired in the wake of stroke: motor recovery from contralateral cortical stroke sometimes produces mirror movements during attempted voluntary movement, reflecting reorganization of cortical motor representation.
  • Multiple sclerosis: occasional finding, particularly with cortical or callosal involvement.
  • Parkinson disease: a few patients show mirror movements, more often with rigidity than tremor.

The bedside test: ask the patient to perform a unilateral task (clenching the fist, tapping fingers, opening and closing the hand) and watch the contralateral hand for involuntary movement. Mirror movements are easier to elicit with novel motor tasks than with familiar ones.

Synkinetic Movements (Synkinesias)

Synkinesias are involuntary movements that occur during voluntary movement of a related body part, after aberrant regeneration of nerve fibers. The classical example is the synkinesis that develops after recovery from facial nerve palsy: voluntary eye closure produces involuntary elevation of the corner of the mouth, or voluntary smiling produces involuntary eye closure. The mechanism is misdirected regrowth of damaged facial nerve fibers — the axon intended for the orbicularis oculi grows back to a muscle of the lower face instead.

Other examples:

  • Marin-Amat syndrome: eye closure on opening the mouth; reverse facial synkinesis.
  • Crocodile tears (gusto-lacrimal reflex): lacrimation during eating, from misdirected regeneration of parasympathetic salivary fibers reaching the lacrimal gland.
  • Aberrant regeneration of the third nerve: lid retraction on attempted downward or medial gaze (Pseudo-Graefe sign), pupillary constriction on attempted adduction (pseudo-Argyll-Robertson). These follow recovery from CN III palsy.
  • Brachial plexus synkinesis: after Erb palsy recovery, the deltoid may contract simultaneously with the biceps because of misdirected reinnervation.
  • Trigeminal-abducens synkinesis (Duane syndrome): congenital aberrant innervation pattern producing characteristic eye movement abnormalities.

Spasticity-Related Associated Reactions

Patients with hemiplegic stroke and spasticity often develop involuntary movements of the affected limb during voluntary movement of the unaffected limb. Squeezing the unaffected hand may produce a synergistic flexion posture in the affected arm — shoulder adduction, elbow flexion, wrist flexion, finger flexion. The phenomenon reflects disinhibition of spinal motor programs by the corticospinal tract lesion.

Similar reactions are sometimes seen during yawning (a normal mass synergistic movement that can be exaggerated in hemiplegia) and during effortful movement of any kind. Recognition matters because these movements can interfere with rehabilitation and can be confused with voluntary movement.

Synkinesis in Motor Recovery

During recovery from hemiplegic stroke, patients often pass through stages of mass-pattern synergistic movement before regaining selective control of individual muscles. The classical Brunnstrom stages of recovery describe this progression: from no movement → mass flexion synergy → mass extension synergy → some selective control → near-normal isolated movement. The associated movements during this recovery are a normal part of the process, not a pathological finding.

The Babinski Sign and Other “Associated” Responses

Several reflex responses can be considered associated movements. The Babinski sign (extension of the great toe with fanning of the other toes) is an associated component of the triple-flexion response (the leg withdraws from noxious stimulus with flexion at hip, knee, and ankle). Most of the other extensor toe responses are variants of this — the response is the same, the maneuver to elicit it differs. Detailed coverage is on the Pyramidal Signs Catalog page.

Reduced Spontaneous Movements

Beyond the loss of arm swing in parkinsonism, reduced spontaneous movement is a clinical sign with several possible localizations:

  • Akinesia: absence of movement; severe form of bradykinesia. Seen in advanced parkinsonism, in advanced PSP, and in catatonia.
  • Hypokinesia: reduced amplitude of movement when movement does occur.
  • Bradykinesia: slowness of movement.
  • Akinetic mutism: severe akinesia with absence of speech; the patient is alert but does not initiate movement or speech. Bilateral medial frontal lesions or severe diffuse brain injury are the typical causes.
  • Abulia: reduction in spontaneous initiative; a milder form of akinetic mutism.
  • Apathy: loss of motivation and emotional engagement; often combined with reduced movement.

The differential between these is sometimes subtle but clinically important. A patient with parkinsonism can be apathetic, but they are clearly bradykinetic, with tremor and rigidity. A patient with akinetic mutism from a medial frontal lesion may have entirely normal motor function on examination once the patient is engaged in the task, but does not initiate anything spontaneously. Catatonic patients may have rigidity, posturing, and waxy flexibility on examination but no other parkinsonian features.

Specific Syndromes

Catatonia

Catatonia is a psychomotor syndrome with several characteristic features: immobility, mutism, posturing (the patient maintains positions imposed by the examiner), waxy flexibility (the limbs can be molded into positions and remain), echolalia and echopraxia (repeating the examiner’s words and actions), stupor, negativism (resistance to all attempts at movement), and stereotypies. Catatonia can occur in primary psychiatric illness (schizophrenia, severe depression) and in medical disorders (especially anti-NMDA receptor encephalitis, in which catatonia is a common presenting feature). The syndrome typically responds dramatically to benzodiazepines (lorazepam is the agent of choice).

Akinetic Mutism

The patient is awake, with open eyes that may track briefly, but does not move spontaneously, does not speak, and does not respond to most stimuli. Distinguished from coma by the preserved arousal and from locked-in syndrome by the absence of motor pathway disruption (the patient could move if they would). Caused by bilateral medial frontal or anterior cingulate lesions, severe diffuse brain injury, or rarely by midbrain reticular formation lesions.

Tic Disorders

Discussed in detail on the Abnormal Movements page. Tics are particular kinds of involuntary movements that are semi-voluntary — suppressible with effort, accompanied by premonitory urge. They are not associated movements in the formal sense but are sometimes elicited or worsened by voluntary movements in other body parts.

🔍 Did You Know?

The arm swing during normal gait is so automatic that it is preserved even when one arm is voluntarily occupied (carrying a briefcase, holding a phone). When voluntary action ceases, the arm resumes swinging within a few steps. In Parkinson disease, the asymmetric loss of arm swing is one of the few motor features that family members commonly notice and bring to medical attention before the patient does. The early loss of left-sided arm swing in a patient who eventually develops left-sided tremor and bradykinesia represents the natural history of the asymmetric Parkinson disease syndrome.

Pitfalls and Pearls

  • Watch the patient walk in. Asymmetric reduction in arm swing may be the earliest sign of parkinsonism — visible across the room before any other testing.
  • “Reduced facial expression” is hypomimia, not necessarily depression. A patient who appears depressed may have parkinsonism producing a masked face; the actual mood may be unaffected.
  • Synkinesias declare the history of nerve injury. A patient with crocodile tears has had a facial nerve injury, even if the apparent palsy resolved years ago.
  • Mirror movements are normal in children, abnormal in adults. Persistent mirror movements in an adult deserve attention.
  • Synergistic mass movements during early stroke recovery are part of the natural history. They are not regression and should not be interpreted as worsening.
  • Akinetic mutism is awake immobility, not coma. Test pupillary responses, response to noxious stimuli, and eye tracking before concluding the patient is unconscious.
  • Catatonia responds to benzodiazepines. A trial of lorazepam is both diagnostic and therapeutic; refractory catatonia often responds to ECT.
  • Aberrant regeneration of CN III (pseudo-Graefe sign, pseudo-Argyll-Robertson) tells you the patient has had a third nerve palsy in the past, even if the current exam appears otherwise normal.
  • Apathy and depression overlap but differ. The apathetic patient is not subjectively distressed about their lack of motivation; the depressed patient typically is.

References

  1. Campbell WW. DeJong’s The Neurologic Examination. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2013. Chapter 42.
  2. Cohen LG, Meer J, Tarkka I, et al. Congenital mirror movements. Abnormal organization of motor pathways in two patients. Brain. 1991;114(1):381-403.
  3. Kim YH, You SH, Kwon YH, et al. Mirror movements after stroke: pathologic patterns and clinical relevance. Stroke. 2007;38(6):1809-1814.
  4. Vincent A, Bien CG, Irani SR, Waters P. Autoantibodies associated with diseases of the CNS: new developments and future challenges. Lancet Neurol. 2011;10(8):759-772.
  5. Daniels J. Catatonia: clinical aspects and neurobiological correlates. J Neuropsychiatry Clin Neurosci. 2009;21(4):371-380.
  6. Cummings JL. Frontal-subcortical circuits and human behavior. Arch Neurol. 1993;50(8):873-880.