Should Paratonia Be Considered a Movement Disorder? Implications for Clinical Management

Abstract

Paratonia is an involuntary and variable resistance to passive movement that emerges with cognitive decline in dementias of different etiologies, with prevalence approaching 90% to 100% in end‐stage disease. It is common in Parkinson disease and the atypical parkinsonisms. The involuntary resistance is frequently interpreted as volitional refusal of care and may be managed with psychotropic medication. We propose that paratonia meets the criterion by which a movement disorder is defined, with a reproducible and distinct clinical phenomenology that is operationalized in a validated bedside instrument and is distinguishable from parkinsonian rigidity, spasticity, and dystonia. We present a preliminary staging schematic in which treatment with botulinum toxin A (BoNT‐A) is indicated when the posturing interferes with care and the contraction remains dynamic, before fixed contracture. Preliminary evidence from a randomized pilot trial and observational studies supports BoNT‐A for care‐interfering paratonia. Classification of paratonia as a movement disorder would enable a dedicated research, education and advocacy platform to advance clinical care.

Paratonia is a form of increased muscle tone, defined through international consensus as an involuntary and variable resistance to passive movement not under voluntary control. ¹ It emerges with cognitive decline across dementia etiologies, with prevalence approaching 90% to 100% in end‐stage disease. ² The neural basis of paratonia is thought to involve frontal and frontal‐subcortical dysfunction with loss of cortical inhibitory control over motor output. ² It is common in the conditions seen in movement disorders practice, including Parkinson's disease, in which dementia develops in more than three quarters of those surviving beyond a decade, ³ and the atypical parkinsonisms of progressive supranuclear palsy, corticobasal syndrome, and dementia with Lewy bodies. It manifests along a continuum, from facilitatory paratonia (mitgehen, “to go with”), in which the individual involuntarily assists the examiner's movement and which appears in healthy subjects and mild cognitive impairment, to oppositional paratonia (gegenhalten, “to hold against”), in which the individual involuntarily resists. The resistance grows stronger as dementia advances. ¹ , ² Despite this well‐established phenomenology, the diagnosis is often missed and the involuntary resistance interpreted as volitional refusal of care. ⁴ , ⁵

The consequences of untreated paratonia are considerable. Attempts to move a limb against the involuntary resistance provoke distress, and the increasingly sustained abnormal postures that develop as paratonia progresses result in prolonged pressure on skin over bony prominences, producing breakdown and pressure injury. A clenched hand causes fingernails to dig into the palm, and adducted thighs impede perineal care, causing poor hygiene and infection. ⁴ Because paratonia is generalized throughout the body, the involuntary resistance may impede feeding, positioning, bathing, and dressing, burdening caregivers. ⁶ , ⁷ With the dementia population projected to reach 139 million by 2050, this burden will grow for caregivers and the health system. ⁸ , ⁹

When the resistance is interpreted as behavioral, it may be managed with antipsychotic medication, which does not alleviate the underlying hypertonia while adding risk of sedation, cognitive impairment, parkinsonism, and mortality. ¹⁰ , ¹¹ No treatment is approved for paratonia‐induced postures, and passive movement therapy continues as standard care despite level 1 evidence from a multicenter randomized trial that it does not reduce muscle resistance. ¹² Further confusion arises when postures in advanced dementia are labeled as established contracture, a premature designation that prevents the assessment of a posture that may still retain a dynamic component amenable to treatment. ⁵ The common theme is a failure to recognize paratonia, a disorder of muscle tone, as the condition producing the disability.

We propose that paratonia meets the criterion by which a movement disorder is defined, with a reproducible and distinct clinical phenomenology, as outlined later. Although paratonia, dystonia, and spasticity arise from distinct central nervous system pathologies, they converge on a common peripheral endpoint, involuntary muscle contraction mediated by the lower motor neuron. Botulinum toxin A (BoNT‐A), whose established efficacy in dystonia and spasticity provides the rationale for its use in paratonia, acts through reversible chemodenervation at the neuromuscular junction, irrespective of the upstream lesion. ¹³ , ¹⁴ Direct evidence for BoNT‐A in paratonia is limited but consistent, comprising a proof‐of‐concept randomized trial and supportive observational data. ¹⁵ , ¹⁶ , ¹⁷ Given the burden of these postures and the absence of any alternative with demonstrated benefit, repurposing an agent used safely for decades in a parallel indication is reasonable. The preliminary evidence, although encouraging, requires confirmation in larger trials.

Paratonia as a Movement Disorder

A movement disorder is defined by a reproducible clinical phenomenology of involuntary or impaired movement, classified by observable motor features shared across conditions of differing cause, ¹³ , ¹⁸ which paratonia fulfills. Its phenomenology, specified through an international Delphi consensus, is operationalized in the validated Paratonia Assessment Instrument (PAI), a bedside instrument that differentiates paratonia from parkinsonian rigidity and spasticity by requiring involuntary, variable resistance increasing with the speed of passive movement and present in multiple directions. ¹ , ¹⁹ Surface electromyography provides an electrophysiological correlate with paratonia showing involuntary activity that increases with repeated movement, in contrast to the habituation seen in spasticity. ²⁰ , ²¹

The characteristics of paratonia that distinguish it from parkinsonian rigidity, spasticity, and dystonia are summarized in Table 1. The distinction from dystonia is clinically relevant. In the atypical parkinsonisms, limb posturing is often attributed to dystonia, though paratonia and dystonia differ in distribution and mechanism. Paratonia is generalized, though its stage and severity may vary across muscle groups, whereas the dystonia of atypical parkinsonism is commonly focal. Paratonia is an involuntary resistance to passive movement that increases with repetition, whereas dystonia is an active, patterned contraction often triggered by voluntary action. ² , ¹³ , ²³ A clenched fist, when severe or fixed as a contracture, can be difficult to distinguish from focal dystonia on attempted passive resistance in that limb alone. It is recognized as paratonia when other limbs are also involved, often more mildly, showing the characteristic resistance to passive movement, in the setting of advanced cognitive impairment in contrast to focal dystonia that is limited to 1 region. Distinguishing the 2, including where they coexist, is a core competency of the movement disorders clinician. ²⁴

TABLE 1.

Differentiation of paratonia from other conditions of increased muscle tone

Feature	Paratonia	Spasticity	Parkinsonian rigidity	Dystonia
Quality of resistance	Variable, increasing with force and speed of movement 1	Velocity dependent, with catch and release 22	Constant through range (lead pipe), with or without cogwheeling	Sustained or intermittent involuntary contraction. Does not increase with force or speed of passive movement 13
Effect of repeated passive movement	Increases	Decreases	No change	No change
Direction of resistance	Multidirectional	Directional, greatest on stretching the spastic muscle, classically upper‐limb flexors and lower‐limb extensors	Uniform in all directions	Directional, greatest on moving the limb away from the dystonic posture, opposite to the direction of involuntary contraction 13 , 24
Distribution	Generalized, affecting all limbs, with severity of posturing varying by region	Focal or regional, determined by the site of the upper motor neuron lesion	Bilateral, often asymmetric	Focal, segmental, multifocal, or generalized 13
Associated signs	Cognitive impairment	Hyperreflexia, clonus, extensor plantar response	Bradykinesia, tremor, postural instability	Twisting or patterned posturing, with dystonic tremor
Pathophysiology	Frontal and frontal‐subcortical dysfunction with loss of cortical inhibitory control 2	Upper motor neuron (corticospinal) lesion 22	Basal ganglia, with nigrostriatal dopaminergic loss	Basal ganglia and sensorimotor network dysfunction 13
Surface electromyography	Involuntary activity that increases with movement repetition, in the lengthening muscle in the oppositional form and the shortening muscle in the facilitatory form 20 , 21	Velocity‐dependent stretch reflex activity in the lengthening muscle 22	Tonic activity in agonist and antagonist with failure to relax, present at rest	Co‐contraction of agonist and antagonist, with tonic or phasic bursts 13
Response to botulinum toxin A	Preliminary evidence of reduced involuntary contraction and care‐related burden; no approved indication 15 , 16	Established, level A evidence 14	Not indicated; responds to dopaminergic replacement	Established, level A evidence 14

Despite meeting this criterion, paratonia lacks formal classification as a movement disorder and remains widely underrecognized. Dystonia offers a historical precedent, having been dismissed for much of the 20th century as hysteria until formal characterization established it as an organic movement disorder. ²⁵ Paratonia is at a comparable stage, its involuntary resistance frequently mislabeled and rarely correctly identified.

Implications for Clinical Management

Recognition and Diagnosis

Accurate diagnosis of paratonia depends on familiarity with its clinical features. Improving recognition requires dissemination through the scientific literature and conferences, alongside education of caregivers and point‐of‐care staff who manage the condition daily, the organizations representing patients with Parkinson's disease and those representing patients with dementia, and the specialists who confirm the diagnosis and plan treatment. Care interference, the criterion that determines treatment eligibility alongside a dynamic stage of muscle contraction prior to contracture, describes involuntary posturing that obstructs the tasks of daily care, including dressing, bathing, perineal and oral hygiene, positioning, and feeding, and that causes distress, pain, or skin injury when care is delivered against the resistance.

Because individuals with advanced paratonia are rarely referred to specialists, identification must also proceed at the population level. To this end we have developed a preliminary screening tool that flags probable care‐interfering paratonia from variables already in the Resident Assessment Instrument‐Minimal Dataset (RAI‐MDS 2.0), a resident assessment instrument used in nursing home and home care in more than 35 countries, with its validation a next step. ²⁶ , ²⁷ Ascertainment at this scale would identify those with care‐interfering paratonia who could benefit from treatment.

Staging and the Therapeutic Window

We propose a preliminary staging schematic (Fig. 1), with validation planned. Paratonia progresses with advancing dementia, evolving from involuntary assistance of passive movement, through involuntary resistance, to posturing that is at first intermittent and then sustained at rest, and finally to muscle contracture, in which the restriction of range of motion has become a fixed orthopedic deformity. This pattern mirrors the progression of cognitive impairment. It reflects the effect of increasingly sustained contraction, as a muscle maintained in a shortened position undergoes structural change, with sarcomere loss and collagen deposition consolidating a once‐dynamic posture into established contracture. ²⁸ , ²⁹

FIG. 1.

Proposed paratonia stages with advancing dementia. Passive range of motion, preserved early, declines with sustained posturing and is absent at fixed contracture. The therapeutic window (shaded) marks the phase where contraction stays dynamic and range is recoverable. Treatment is indicated within this window where the posturing interferes with care or causes distress and a treatment goal can be defined.

Chemodenervation can reduce the involuntary contraction while the posture remains dynamic, but not once a fixed contracture has formed. Treatment eligibility for BoNT‐A is determined both by the dynamic stage of the muscle and by a defined goal for the posture to be relieved. This second requirement parallels treatment decisions in other conditions where spasticity or dystonia may be present but not cause a specific impairment. Paratonia may also be present and well tolerated, in which case the posture is not treated, but due to the progressive nature of dementia, paratonia may progress to care‐interfering postures at a later date and should be monitored over time. Early treatment, when care‐interfering postures first emerge, may slow or prevent progression to contracture, and although cognitive impairment continues to advance, the involuntary postures of paratonia may be reduced or stabilized. Such an effect is supported by poststroke spasticity, where early BoNT‐A has been reported to reduce contracture development and may prevent disabling finger flexor stiffness. ³⁰ , ³¹

BoNT‐A Treatment

The direct evidence remains preliminary but consistent. A small, randomized placebo‐controlled pilot trial in individuals with advanced dementia reported improved range of motion and ease of care. ¹⁵ A recent retrospective review documented substantial reduction in caregiver burden and pain, ¹⁶ and clinician surveys reported benefit without serious adverse events. ¹⁷ , ³²

Determining BoNT‐A treatment protocols begins by defining how a posture obstructs care and setting the goal accordingly, whether loosening a clenched fist, abducting a thigh, or reducing jaw clenching. The problematic posture is not always evident at rest and may appear only during the task it impedes, such as dressing, hygiene, or oral care, so identifying treatable postures requires direct observation of care procedures and a careful history elicited from the caregiver regarding the circumstances under which impairments arise. Clarifying priority goals and observing postures under variable conditions extend a skill set injectors already apply to postures that fluctuate with position or action, as in cervical or task‐specific dystonia. Because paratonia‐induced postures are often multiple and bilateral, cumulative doses may exceed those in focal indications, and injection protocols may alternate between cycles. As with all targeted therapies, shared decision‐making between patient (if able), caregiver, and specialist‐injector is required to achieve treatment goals.

Movement disorders physicians and physiatrists are trained in tone assessment and chemodenervation within their scope of practice. However, the number of experienced injectors is limited relative to the number of individuals likely affected by care‐interfering paratonia, and meeting the need may require consideration of expanding the scope of practice of others, including nurse practitioners, physiotherapists, and palliative care physicians making home visits for homebound patients unable to travel to outpatient clinics. Precedent exists in the United Kingdom, where physiotherapists with independent prescribing qualifications administer BoNT‐A for spasticity, with outcomes comparable to rehabilitation physicians. ³³

Measuring Benefit

The Modified Ashworth Scale, developed to grade the severity of resistance to passive movement in spasticity, has not been validated in paratonia, where fluctuating resistance limits its reliability and a measure of resistance does not capture the functional burden treatment aims to relieve. That burden lends itself to observer‐reported outcomes, which regulatory guidance permits when patients cannot self‐report. ³⁴ We are developing a Paratonia Burden Scale, in which each affected posture is rated for its burden and for goal attainment after treatment. Delphi consensus has established its content, and clinimetric validation is planned. Once validated, it would structure goal‐directed treatment and provide an outcome measure for clinical trials, in addition to other tools such as goniometric joint measurements where feasible, clinical global impression of change, and pain ratings.

What Classification of Paratonia as a Movement Disorder Would Enable

Classifying paratonia as a movement disorder would establish it as a recognized diagnostic entity within an established medical specialty. A task force convened by the International Movement Disorders Society (MDS) could bring together the expertise to set research priorities. A dedicated International Classification of Diseases 11th Revision (ICD‐11) diagnostic code, an achievable near‐term objective, could be pursued through the MDS in conjunction with patient advocacy organizations and would allow paratonia to be captured in health data and its prevalence, natural history, and outcomes studied.

Establishing paratonia as a movement disorder of dementia would also anchor the prospective studies needed to chart its course. Following individuals from mild cognitive impairment onward, with paratonia assessed alongside imaging, biomarkers, and clinical measures, would delineate how and when it emerges and evolves, which at present is inferred only from cross‐sectional data. Such cohorts would also let the field test an exploratory but compelling possibility, that facilitatory paratonia, which precedes the oppositional form and accompanies early motor change, ²³ , ³⁵ , ³⁶ , ³⁷ is an early motor marker of cognitive decline. ²¹

Classification would similarly advance treatment. The evidence for BoNT‐A is preliminary but promising, and moving it from exploratory use toward established therapy requires a clinical development program, with staging criteria to select patients, a validated outcome measure, and natural history data. To that end, we are undertaking a retrospective analysis of how posturing evolved and was treated in a cohort of 107 patients managed at our center over 18 years. Regulatory approval would ultimately require an industry sponsor, ⁶ likelier to engage once a professional society, with patient and caregiver organizations and long‐term care bodies, shows this population can and should be identified and studied at scale.

Conclusion

Paratonia has a reproducible and distinct clinical phenomenology, distinguishable from the other disorders of increased tone, meeting the criterion by which a movement disorder is defined. Recognizing it as a movement disorder changes clinical care directly. When the resistance of paratonia is understood as an involuntary motor sign rather than deliberate refusal of care, the individual is met with compassion, and their postures are addressed as a potentially treatable source of discomfort, an approach consistent with neuropalliative care and its focus on comfort, dignity, and quality of life in advanced neurological illness. This recognition also begins to address a long‐standing inequity, as people with advanced dementia have seen little research or investment directed at their symptom burden, despite the scale of what they and their caregivers endure at this stage of disease. A promising treatment exists, but establishing standards of care for this population will require sustained effort across research, education, advocacy, and policy. Recognizing paratonia as a movement disorder would give this neglected area a direction and a community of clinicians and researchers to advance its study and care.

Author Roles

(1) Research project: A. Conception, B. Organization, C. Execution. (2) Literature review: A. Design, B. Execution, C. Review and critique. (3) Manuscript preparation: A. Writing of the first draft, B. Review and critique.

G.K.: 1A, 1B, 1C, 2A, 2B, 2C, 3A, 3B

C.G.: 2C, 3B

A.E.L.: 2C, 3B

Disclosures

Ethical Compliance Statement: This article is a viewpoint and did not involve original research, human participants, or animal subjects. Institutional review board or ethics committee approval was therefore not required and was not sought for this work. Informed patient consent was not necessary for this work. We confirm that we have read the journal's position on issues involved in ethical publication and affirm that this work is consistent with those guidelines.

Financial Disclosures and Conflicts of Interest: Author disclosures are available in the Supporting Information.

Supporting information

Data S1. COI_disclosure.

Data Availability Statement

Data sharing not applicable to this article as no datasets were generated or analysed during the current study.