Abstract
Background:
Acute-onset movement disorders, often termed movement disorder emergencies, present in emergency and inpatient neurology settings and may arise from diverse causes, including potentially reversible metabolic and medication-related conditions.
Objectives:
We aimed to describe the clinical phenomenology and etiological spectrum of movement disorder emergencies presenting to a tertiary care center.
Methods:
We conducted a prospective, single-center, hospital-based cross-sectional observational study over 12 months (February 2023 to January 2024) at a tertiary-care hospital in Kolkata, Eastern India. Patients aged 12 years or older with a movement disorder onset within 4 weeks were enrolled. Movement disorder presentations were categorized as hyperkinetic, hypokinetic, or mixed.
Results:
Eighty patients were included (mean age 48.0 years, standard deviation 18.0; 57.5% male). Hyperkinetic presentations predominated (80.0%), followed by mixed (13.7%) and hypokinetic (6.2%) presentations. The most frequent phenomenologies were hemichorea and myoclonus (18.7% each), followed by acute parkinsonism (17.5%), dystonia (16.2%), and tremor (15.0%). Mean symptom duration at presentation did not differ across movement disorder categories (p = 0.36). The movement disorder category was not associated with sex (p = 0.68), age group (p = 0.39), or timing of presentation (p = 0.632). The leading etiologies were metabolic (26.2%) and drug-induced (25.0%), followed by vascular (15.0%), functional (8.7%), and infectious (6.2%) causes. Functional etiologies presented exclusively with hyperkinetic phenomenology.
Conclusions:
In this tertiary-care cohort, movement disorder emergencies were predominantly hyperkinetic, and metabolic and drug-induced causes accounted for over half of the cases. These findings support an expeditious diagnostic approach that prioritizes rapid metabolic screening, careful medication review, and targeted neuroimaging when clinically indicated.
Keywords: Acute-onset movement disorders, Movement disorder emergencies, Hyperkinetic movement disorders, Hypokinetic movement disorders, Diabetic striatopathy, Drug-induced movement disorders, Functional movement disorders, Vascular movement disorders
Introduction
Movement disorders are traditionally viewed as chronic neurological conditions; however, a growing number of patients present with acute, severe movement disorder syndromes that constitute true neurological emergencies [1]. Acute-onset movement disorders, often termed movement disorder emergencies, are characterized by the sudden or subacute emergence of abnormal involuntary movements (e.g., chorea, dystonia, tremor, myoclonus, or parkinsonism) evolving over hours to several weeks and prompting urgent medical evaluation. These scenarios demand prompt recognition and management because delays can lead to significant morbidity [2]. Indeed, certain acute hyperkinetic syndromes (for example, neuroleptic malignant syndrome or status dystonicus) carry substantial mortality if not treated early [1,3]. Fortunately, many movement disorder emergencies are potentially reversible with timely intervention [2], making early diagnosis critical.
Hyperkinetic movement disorders are the predominant clinical profile encountered in the emergency department. For example, a recent prospective study from South India reported that 91.5% of movement disorder emergencies were hyperkinetic (most commonly chorea and dystonia), aligning with anecdotal experience that sudden hyperkinetic movements tend to precipitate urgent care more than akinetic-rigid syndromes [4]. In children, an Italian emergency-department series similarly found >95% hyperkinetic cases (tics, tremors, chorea, dystonia, myoclonus, and stereotypies) among acute movement disorders [5].
The etiological spectrum of acute movement disorders is remarkably broad. Common causes include drug-induced extrapyramidal reactions, metabolic derangements, stroke and other structural brain lesions, autoimmune or inflammatory encephalitis, and functional (psychogenic) movement disorders [6]. Pediatric acute movement disorders, however, show a distinct etiologic profile—often dominated by Sydenham’s chorea following group-A streptococcal infection, autoimmune encephalitides such as anti-NMDA receptor encephalitis, and genetic or metabolic syndromes—that differs meaningfully from that in adults [5,7–11]. Notwithstanding, there are clear racial and regional differences in the etiological spectrum of acute-onset movement disorders, driven in part by underlying epidemiological patterns. Importantly, the distribution of etiologies also varies across racial and geographic contexts, reflecting differences in underlying epidemiology and treatment exposures. For example, an Indian case series highlighted diabetic striatopathy as a leading cause of acute hemichorea, illustrating how local disease burden shapes acute movement-disorder phenotypes [12]. This pattern is biologically and epidemiologically plausible: diabetes is disproportionately prevalent in Asian populations, and South Asians are particularly susceptible to developing type 2 diabetes mellitus compared with ethnic Europeans [13]. By contrast, in many Western settings, broader exposure to antidopaminergic medications and differing autoimmune predispositions contribute to a different mix of acute presentations, including drug-induced dystonia or parkinsonism and immune-mediated choreiform syndromes [6,14–18]. Defining the clinico-etiological profile of acute-onset movement disorders within specific populations is therefore essential to optimize early diagnostic pathways, guide prevention strategies, and improve time-sensitive management.
Despite this diversity, patients with acute movement phenomena typically present through emergency or general neurology pathways, where early bedside clues may be subtle and easily overlooked, especially when systems are optimized for stroke and seizures rather than abnormal movements [1,2,6,19,20]. This reality underscores the need for neurologists and emergency physicians to maintain a high index of suspicion, to take a meticulous medication history, and to apply a systematic diagnostic approach tailored to acute movement phenomenology.
In this context, we conducted a hospital-based observational study to characterize the clinical phenomenology and etiological spectrum of acute-onset movement disorders presenting to a large tertiary-care center in Eastern India. We aimed to describe the distribution of hyperkinetic, hypokinetic, and mixed presentations; identify the leading etiologies in our setting; and explore whether basic demographic features were associated with movement disorder category or etiology.
Methods
Ethical approval for the study was obtained from the Institutional Ethics Committee of Medical College and Hospital, Kolkata. All procedures were in accordance with the Declaration of Helsinki. Informed consent was obtained from all participants (or their guardians) in their native language, and confidentiality was strictly maintained. The study did not incur any additional patient expenses, as the researchers covered all investigation-specific costs.
Medical College and Hospital, Kolkata, is a large government tertiary-care teaching hospital that receives both direct walk-in (“open-door”) presentations through the emergency department/outpatient clinics and interfacility referrals from across West Bengal and neighboring regions. There was no subspecialty pre-selection for movement disorders; patients entered routine emergency, inpatient, and outpatient pathways. The study spanned 12 months (February 2023 through January 2024) across outpatient, inpatient, emergency, and critical care units. We aimed to assess the clinical profile and etiology of patients presenting with acute-onset movement disorders.
Case Definition:
We defined a movement disorder emergency as an acute or subacute movement disorder (onset over hours to ≤4 weeks) leading to urgent medical evaluation and presentation to our hospital within that interval [21,22]. This definition encompassed (i) new-onset movement disorders and (ii) acute worsening of a previously diagnosed and stable movement disorder, provided the worsening began within ≤4 weeks and represented a clear change from baseline.
Inclusion and Exclusion Criteria:
We included patients aged ≥12 years who met the case definition and provided informed consent. We excluded: (i) chronic movement disorders without acute/subacute worsening in the preceding ≤4 weeks; (ii) refusal of consent; (iii) diagnostic ambiguity or unclear phenomenology after expert evaluation; (iv) epileptic events misclassified as movement disorders (confirmed by clinical assessment and, when indicated, electroencephalography and/or neuroimaging); and (v) functional neurological presentations lacking a clearly defined movement disorder phenotype (e.g., predominant weakness/flaccidity without involuntary movements). Acute functional hyperkinetic movement disorders (e.g., functional tremor, dystonia, chorea) were included when positive diagnostic features supported a functional movement disorder diagnosis.
Diagnostic Protocol:
All patients underwent a standardized assessment, including a detailed history (time course; drug/toxin exposure; metabolic triggers), a neurological examination emphasizing movement phenomenology, and first-line laboratory testing (capillary and serum glucose, complete blood count, electrolytes, renal and liver function). Neuroimaging (computed tomography and/or brain magnetic resonance imaging) was obtained when focal/lateralized movements were present, when vascular risk factors or focal neurological deficits suggested a structural lesion, or when the presentation was clinically atypical. An electroencephalogram was obtained when paroxysmal events, fluctuating symptoms, impaired awareness, or clinical concern for seizures/non-convulsive status epilepticus existed. Cerebrospinal fluid analysis was performed when fever, encephalopathy, seizures, meningism, or other features suggested infection or autoimmune encephalitis.
Autoimmune/paraneoplastic testing was performed when encephalopathy combined with movement disorder and supporting clinical or red-flag features indicated an immune-mediated disease, or when a malignancy-associated syndrome was suspected.
Audit of investigations and etiologic assignment. In practice, neuroimaging was performed in 65/80 (81.3%), electroencephalogram in 15/80 (18.8%), cerebrospinal fluid analysis in 9/80 (11.3%), and autoimmune/paraneoplastic panels in 6/80 (7.5%). Final etiologic diagnoses were assigned after a consensus among the neurology team (≥2 neurologists) on all available clinical and investigative data. If more than one plausible contributor was present, we classified a primary etiology (the factor most temporally and clinically linked to onset) and recorded additional contributors as secondary, where appropriate. Cases in which the phenomenology or etiology remained indeterminate after evaluation were excluded per protocol; therefore, no included cases were classified as undetermined.
Statistical Analysis:
This was a prospective consecutive-case series conducted over a fixed 12-month period; therefore, no a priori sample size calculation was performed. We enrolled all eligible patients presenting during the study period (complete enumeration), yielding a final sample of 80 cases. Data collected included socio-demographic variables, clinical features (movement disorder phenomenology and associated symptoms), and biochemical and radiological findings.
Statistical analysis was carried out using SPSS (IBM SPSS Statistics, Version 25) and Python. Descriptive statistics (mean [standard deviation] or median [interquartile range], as appropriate) summarized continuous variables, while frequencies (%) were used for categorical variables. Group comparisons employed chi-square or Fisher’s exact tests for categorical variables and independent-samples t tests or one-way analysis of variance for continuous variables, as appropriate. A two-sided p-value <0.05 was considered statistically significant. Missing data were minimal and handled with complete-case analysis; no imputation was performed.
Results
Participant characteristics and movement disorder type
Eighty patients with movement disorder emergencies were enrolled. The mean age was 48.0 ± 18.0 years (range 12–78), with a mild male predominance (46 males, 57.5%; 34 females, 42.5%). Mean age did not differ significantly between males (50.0 ± 18.5 years) and females (45.4 ± 17.3 years; independent-samples t-test, p = 0.28).
Hyperkinetic presentations predominated (64 of 80, 80.0%), whereas hypokinetic movement disorders were uncommon (5 of 80, 6.2%), and mixed presentations accounted for 11 of 80 (13.7%). There was no significant association between sex and movement disorder type (chi-square test, p = 0.68).
When stratified by age category, 71 of 80 patients (88.7%) were adults (≥18 years), and 9 of 80 (11.2%) were younger than 18 years. The distribution of movement disorder type did not differ significantly between pediatric and adult patients (chi-square test, χ2 = 1.88, p = 0.39; Table 1). Age distributions overlapped across movement disorder types (one-way analysis of variance, p = 0.46; Fig. 1).
Table 1.
Distribution of movement disorder type by age category and sex (N = 80).
| Characteristic | Hyperkinetic n (%) | Hypokinetic n (%) | Mixed n (%) | Row total, n | P value |
|---|---|---|---|---|---|
| Age <18 years | 8 (88.9) | 1 (11.1) | 0 (0.0) | 9 | 0.39 |
| Age ≥18 years | 56 (78.9) | 4 (5.6) | 11 (15.5) | 71 | |
| Male sex | 38 (82.6) | 3 (6.5) | 5 (10.9) | 46 | 0.68 |
| Female sex | 26 (76.5) | 2 (5.9) | 6 (17.6) | 34 |
Percentages are row percentages.
Fig. 1.
Boxplot diagram showing age distribution of study participants according to type of movement disorder.
Movement disorder phenomenology
The phenomenological profile is summarized in Table 2. The most frequent movement disorder phenomenologies were hemichorea and myoclonus (15/80 each; 18.7%), followed by acute parkinsonism (14/80; 17.5%), dystonia (13/80; 16.2%), and tremor (12/80; 15.0%). Dyskinesia and oculogyric crisis occurred in 6 patients each (7.5%). Less frequent phenomenologies (each ≤5.0%) included myokymia, ballism, choreodystonia, catatonia, ataxia, pseudoathetosis, myorrhythmia-like craniofacial rhythmic movements, tonic spasm, choreobalism, and opsoclonus.
Table 2.
Frequency of individual movement disorder phenomenologies (non-mutually exclusive; N = 80).
| Phenomenology | n | % |
|---|---|---|
| Hemichorea | 15 | 18.7 |
| Myoclonus | 15 | 18.7 |
| Acute parkinsonism | 14 | 17.5 |
| Dystonia | 13 | 16.3 |
| Tremor | 12 | 15.0 |
| Dyskinesia | 6 | 7.5 |
| Oculogyric crisis | 6 | 7.5 |
| Myokymia | 4 | 5.0 |
| Ballism | 3 | 3.7 |
| Choreodystonia | 3 | 3.7 |
| Catatonia | 2 | 2.5 |
| Ataxia | 2 | 2.5 |
| Pseudoathetosis | 1 | 1.2 |
| Myorrhythmia-like craniofacial rhythmic movements | 1 | 1.2 |
| Tonic spasm | 1 | 1.2 |
| Choreobalism | 1 | 1.2 |
| Opsoclonus | 1 | 1.2 |
Percentages are calculated using the total cohort as the denominator. Totals may exceed 100% because multiple phenomenologies could co-occur in a single patient.
At the patient level, several distinct single-phenomenology and multi-phenomenology patterns were observed (Table 3). Multi-phenomenology presentations most commonly comprised acute parkinsonism with dyskinesia and oculogyric crisis (n = 4) and choreodystonia (n = 3).
Table 3.
Patient-wise distribution of movement disorder phenomenology patterns (mutually exclusive; N = 80).
| Phenomenology pattern | n | % |
|---|---|---|
| Isolated hemichorea | 15 | 18.7 |
| Isolated myoclonus | 13 | 16.3 |
| Isolated tremor | 10 | 12.5 |
| Isolated dystonia | 9 | 11.2 |
| Myokymia | 4 | 5.0 |
| Acute parkinsonism + dyskinesia + oculogyric crisis | 4 | 5.0 |
| Isolated acute parkinsonism | 3 | 3.7 |
| Choreodystonia | 3 | 3.7 |
| Ballism | 3 | 3.7 |
| Acute parkinsonism + dystonia + tremor | 2 | 2.5 |
| Catatonia | 2 | 2.5 |
| Dyskinesia (isolated) | 1 | 1.2 |
| Acute parkinsonism + oculogyric crisis | 1 | 1.2 |
| Myorrhythmia-like craniofacial rhythmic movements | 1 | 1.2 |
| Ataxia (isolated) | 1 | 1.2 |
| Choreobalism | 1 | 1.2 |
| Acute parkinsonism + dystonia + oculogyric crisis | 1 | 1.2 |
| Tonic spasm | 1 | 1.2 |
| Acute parkinsonism + dyskinesia | 1 | 1.2 |
| Pseudoathetosis | 1 | 1.2 |
| Acute parkinsonism + dystonia | 1 | 1.2 |
| Acute parkinsonism + myoclonus | 1 | 1.2 |
| Opsoclonus + myoclonus + ataxia | 1 | 1.2 |
Acute parkinsonism was classified as a phenomenon and appeared both as a standalone hypokinetic presentation and as part of mixed syndromes (e.g., parkinsonism with dyskinesia or oculogyric crisis), which explains why the number of cases of parkinsonism exceeds the count of purely hypokinetic presentations (Tables 3 and 4).
Table 4.
Phenomomenology categorized by movement disorder type (N = 80).
| Patient-wise phenomenology | Hyperkinetic (n = 64) | Hypokinetic (n = 5) | Mixed (n = 11) |
|---|---|---|---|
| Hemichorea | 15 | 0 | 0 |
| Myoclonus | 13 | 0 | 0 |
| Tremor | 10 | 0 | 0 |
| Dystonia | 9 | 0 | 0 |
| Myokymia | 4 | 0 | 0 |
| Ballism | 3 | 0 | 0 |
| Choreodystonia | 3 | 0 | 0 |
| Ataxia | 1 | 0 | 0 |
| Choreobalism | 1 | 0 | 0 |
| Dyskinesia | 1 | 0 | 0 |
| Myorrhythmia-like craniofacial rhythmic movements | 1 | 0 | 0 |
| Opsoclonus + myoclonus + ataxia | 1 | 0 | 0 |
| Pseudoathetosis | 1 | 0 | 0 |
| Tonic spasm | 1 | 0 | 0 |
| Acute parkinsonism + oculogyric crisis | 0 | 0 | 1 |
| Acute parkinsonism + dyskinesia | 0 | 0 | 1 |
| Acute parkinsonism + dystonia + tremor | 0 | 0 | 2 |
| Acute parkinsonism + dystonia + oculogyric crisis | 0 | 0 | 1 |
| Acute parkinsonism + dystonia | 0 | 0 | 1 |
| Acute parkinsonism + dyskinesia + oculogyric crisis | 0 | 0 | 4 |
| Acute parkinsonism + myoclonus | 0 | 0 | 1 |
| Acute parkinsonism (isolated) | 0 | 3 | 0 |
| Catatonia | 0 | 2 | 0 |
Opisthotonus was not observed. One suspected case could not complete the diagnostic work-up and was excluded per protocol.
Phenomenology categorized by movement disorder type (hyperkinetic, hypokinetic, mixed) is shown in Table 4.
Duration of symptoms and timing of presentation
The mean duration of symptoms at presentation did not differ significantly among the three movement disorder types (hyperkinetic: 12.3 ± 9.3 days; hypokinetic: 8.0 ± 7.6 days; mixed: 8.9 ± 7.5 days; one-way analysis of variance, F = 1.04, p = 0.36; Fig. 2).
Fig. 2.
Boxplot showing the distribution of movement disorder duration (in days) across hyperkinetic, hypokinetic, and mixed types.
Overall, 3 of 80 patients (3.7%) presented within 24 h of symptom onset, 43 of 80 (53.7%) within 2–7 days, and 34 of 80 (42.5%) after >7 days. The timing of presentation was not significantly associated with movement disorder type (Fisher’s exact test, p = 0.632; Fig. 3).
Fig. 3.
Bar chart showing the distribution of types of movement disorders (hyperkinetic, hypokinetic, and mixed) according to the day of presentation: within 1 day, between 2–7 days, and after 7 days.
Etiology
The etiological spectrum is summarized in Table 5. Metabolic (21/80, 26.2%) and drug-induced (20/80, 25.0%) causes were most common, followed by vascular (12/80, 15.0%), functional (7/80, 8.7%), and infectious (5/80, 6.2%) etiologies. Less frequent etiologies (15/80, 18.7%) included neoplastic/paraneoplastic (3/80, 3.7%), autoimmune (2/80, 2.5%), traumatic (2/80, 2.5%), degenerative (2/80, 2.5%), post-hypoxic (2/80, 2.5%), malignant catatonia (2/80, 2.5%), toxin-induced (1/80, 1.2%), and genetic causes (1/80, 1.2%).
Table 5.
Distribution of etiological categories among patients with movement disorder emergencies (N = 80).
| Etiology | N | % (of 80) |
|---|---|---|
| Metabolic (diabetic striatopathy, hypocalcemic tetany, and osmotic demyelination syndrome) | 21 | 26.2 |
| Drug-induced (levosulpiride, haloperidol, amlodipine, cyclosporine, flunarizine, lurasidone, mirtazapine, olanzapine, phenytoin, prochlorperazine maleate, risperidone, and trihexyphenidyl) | 20 | 25.0 |
| Vascular (ischemic stroke and acute subdural hematoma) | 12 | 15.0 |
| Functional | 7 | 8.7 |
| Infectious (Creutzfeldt–Jakob disease, tuberculosis, and cryptococcus) | 5 | 6.2 |
| Other etiologies (total) | 15 | 18.7 |
| — Neoplastic/paraneoplastic (Holmes tremor due to brainstem glioma and post-radiotherapy brainstem glioma) | 3 | 3.7 |
| — Autoimmune | 2 | 2.5 |
| — Traumatic | 2 | 2.5 |
| — Degenerative | 2 | 2.5 |
| — Post-hypoxic (cardiac arrest, right parieto-occipital hypoxic brain damage) | 2 | 2.5 |
| — Malignant catatonia | 2 | 2.5 |
| — Toxin-induced | 1 | 1.2 |
| — Genetic (neuroacanthocytosis) | 1 | 1.2 |
Percentages are calculated using the total cohort as the denominator.
Metabolic etiologies were predominantly associated with hyperkinetic presentations, whereas drug-induced etiologies presented with both hyperkinetic and mixed phenomenology. Functional movement disorders were exclusively hyperkinetic.
Notable rare etiologies included osmotic demyelination syndrome presenting with parkinsonism and myoclonus, Holmes tremor associated with brainstem glioma (including a post-radiotherapy case), and post-hypoxic myoclonus (Lance–Adams syndrome) following cardiac arrest with parieto-occipital hypoxic brain injury.
Functional movement disorders accounted for 7 cases (8.8%), all presenting with hyperkinetic phenomenology. Because we required a predominant, clearly classifiable movement phenotype for inclusion, functional cases were categorized by their dominant presentation: functional myoclonus (n = 3), functional tremor (n = 3), and myorrhythmia-like craniofacial rhythmic movements (n = 1).
Among drug-induced cases (n = 20), tardive dyskinesia accounted for 10 cases (50.0%); the remainder included acute dystonia/oculogyric crisis and drug-induced parkinsonism.
Discussion
In this hospital-based series of 80 patients with movement disorder emergencies, hyperkinetic syndromes constituted the majority of presentations (80.0%), with mixed hyperkinetic–hypokinetic phenomenology in a further 13.7%. Hemichorea and myoclonus were the most frequent individual phenomenologies (each 18.7%), followed by acute parkinsonism (17.5%), dystonia (16.2%), and tremor (15.0%). Metabolic (26.2%) and drug-induced (25.0%) etiologies together accounted for just over half of all cases, with vascular (15.0%) and functional (8.7%) disorders comprising additional major contributors. Taken together, these findings emphasize that acute movement disorders in real-world emergency neurology are commonly hyperkinetic, frequently multifactorial in phenomenology, and often potentially reversible, provided that the underlying cause is identified early [23,24].
Compared with prior predominantly retrospective descriptions, our study provides a prospective, consecutive-case series from Eastern India with predefined operational triggers for key investigations and audited denominators for these investigations, improving reproducibility and practical applicability in acute neurology settings.
Acute movement disorders become “emergencies” when rapid evolution, systemic instability, or a treatable underlying cause is likely [23,24]. Emergency-oriented reviews recommend a structured early approach that prioritizes stabilization and recognition of toxic–metabolic syndromes (e.g., neuroleptic malignant syndrome) or catatonia-spectrum illness, while concurrently pursuing reversible causes such as medication toxicity, metabolic derangements, and acute structural lesions [23–25]. This conceptual framework is particularly relevant to our cohort because the most frequent etiological categories (metabolic and drug-induced) are largely diagnosable with targeted bedside history-taking and first-line investigations, and are commonly amenable to prompt intervention [23,24].
Metabolic etiologies: diabetic striatopathy and the broader metabolic differential
Metabolic disorders were the most common etiological category in our cohort, and diabetic striatopathy was the predominant metabolic diagnosis. Diabetic striatopathy is classically characterized by an acute or subacute onset of unilateral hyperkinetic movements (most often hemichorea/hemiballismus) in the context of hyperglycemia, accompanied by reversible striatal abnormalities on neuroimaging [12,26–28]. Current syntheses highlight diabetic striatopathy as an important “stroke mimic” in emergency practice, because acute focal hyperkinesias may prompt a primary cerebrovascular work-up unless hyperglycemia-related basal ganglia syndromes are actively considered [12,26–28]. Importantly, the diabetic striatopathy literature emphasizes that glycemic optimization is central to management, whereas symptomatic antidopaminergic therapy is individualized and may not be required in all cases [12,26–28].
The prominence of diabetic striatopathy is also epidemiologically plausible in regions facing a high and rising burden of diabetes. The IDF Diabetes Atlas (11th edition, 2025) documents continuing global increases in diabetes prevalence and projects further growth by 2050, underscoring why hyperglycemia-related neurological presentations are likely to remain common in acute neurology [29]. In such contexts, our findings support incorporating capillary glucose measurement and serum metabolic panels as “first-line investigations” for acute chorea/ballism or unexplained focal hyperkinesias, alongside early neuroimaging when focal or lateralized movements are present [12,26–28].
Although diabetic striatopathy was prominent, the metabolic differential in movement disorder emergencies extends beyond hyperglycemia. Osmotic demyelination syndrome, for example, can present with parkinsonism, dystonia, tremor, chorea, and myoclonus [30]. A 2021 synthesis summarized the spectrum of movement disorders associated with osmotic demyelination syndrome and emphasized frequent mixed phenomenology and delayed evolution after the precipitating electrolyte disturbance [31]. The presence of osmotic demyelination syndrome within our cohort reinforces the importance of reviewing recent sodium correction or major osmotic shifts when acute parkinsonism or mixed hyperkinetic–hypokinetic syndromes occur, particularly when magnetic resonance imaging shows pontine or extrapontine demyelination [31].
Drug-induced movement disorders: medication history as a diagnostic cornerstone
Drug-induced movement disorders accounted for one-quarter of cases in our series. This aligns with the fact that dopamine receptor blocking agents and related drugs are widely used across specialties, and adverse motor effects may be misattributed to primary neurological disease without a systematic exposure history [14–17]. The 2024 evidence-based update on anticholinergic use in drug-induced movement disorders provides a practical framework: identify and withdraw (or reduce) the offending agent when feasible; use anticholinergics selectively for syndromes where evidence supports benefit (e.g., acute dystonia and some cases of drug-induced parkinsonism); and avoid inappropriate use in disorders where anticholinergics are ineffective or may worsen outcomes [32]. In our series, as high as 50% of drug-induced cases were tardive dyskinesia, further highlighting the need for awareness among clinicians of judicious use of possible offending agents.
Acute dystonia—including oculogyric crisis—is a prototypical emergency-presenting drug-induced movement disorder. Oculogyric crisis is described as a paroxysmal dystonic phenomenon with sustained conjugate eye deviation and can be triggered by dopamine receptor blocking agents, metabolic abnormalities, and focal brain lesions [33]. In emergency department cohorts, rapid improvement following anticholinergic administration is frequently reported and can be diagnostically informative when acute dystonia is suspected [33,34]. In our cohort, the prominence of acute dystonic syndromes reinforces the need for high-quality medication reconciliation—particularly recent exposure to antipsychotics and antiemetics—as an essential component of acute movement disorder assessment [14–17].
Drug-induced parkinsonism is another clinically important entity because it can be misclassified as idiopathic Parkinson’s disease, particularly in older adults [14,16]. Benzamide derivatives prescribed for gastrointestinal symptoms—such as levosulpiride—have been repeatedly implicated in the development of parkinsonism and other movement disorders, such as dyskinesia and dystonia [35,36]. Case-based and observational literature also emphasizes that drug-induced parkinsonism may persist after drug withdrawal in a subset of patients, supporting early recognition and prompt cessation of the culprit drug whenever clinically feasible [16,37,38]. In our cohort, exposure to dopamine receptor–blocking agents—particularly haloperidol and levosulpiride—was common among drug-induced cases, reinforcing that meticulous medication reconciliation functions as a high-yield diagnostic tool in the evaluation of acute movement disorders [16,37,38].
Vascular and structural causes: maintaining a parallel differential
Vascular etiologies comprised 15.0% of cases, emphasizing that acute movement disorders can be a presenting feature of structural brain injury even without classic stroke syndromes. Post-stroke movement disorders are well described, and hemichorea–hemiballismus is an archetypal acute phenotype linked to lesions involving basal ganglia–-thalamocortical circuitry [39]. Clinically, the overlap between vascular hemichorea and diabetic striatopathy has two practical implications: acute hemichorea should trigger parallel assessment for both vascular and metabolic causes, and neuroimaging should be obtained with a low threshold when the presentation is focal, lateralized, or accompanied by new neurological deficits [39–41].
Acute parkinsonism within an “acute-onset movement disorder” cohort also warrants careful interpretation. Although idiopathic Parkinson’s disease is typically insidious, drug exposures, metabolic disturbances (including osmotic demyelination syndrome), and vascular lesions can precipitate acute parkinsonism or unmask latent parkinsonian features [30,39]. This reinforces the importance of avoiding pre-mature diagnostic closure on neurodegenerative etiologies in the emergency setting, particularly when onset is abrupt or subacute and potentially reversible precipitants are present.
Functional movement disorders: the importance of “rule-in” diagnosis
Functional movement disorders accounted for nearly 9% of cases in our series and were confined to hyperkinetic presentations. Contemporary reviews emphasize that functional neurological disorder can present with tremor, myoclonus, dystonia, and gait-disorder phenotypes, and should be diagnosed using positive clinical signs rather than by exclusion [42,43]. In support of this “rule-in” approach, a recent narrative review and decision-tool synthesis highlights the bedside utility of distractibility, variability, and incongruity as key features that strengthen diagnostic confidence across functional neurological disorder subtypes [43]. Within acute care settings, early identification of functional neurological disorder has the potential to reduce unnecessary investigations and facilitate timely referral to appropriate management pathways, provided that communication is clear and non-stigmatizing and that organic mimics are responsibly excluded when clinically indicated [42,43].
Immune-mediated and infectious etiologies: low frequency but high clinical stakes
Immune-mediated and infectious causes formed a smaller proportion of cases in our cohort, but these categories remain critical because they are often treatable and because delayed therapy can lead to preventable disability [44]. For suspected autoimmune encephalitis, a syndrome-based diagnostic approach is recommended: early diagnosis should rely on clinical assessment plus conventional investigations (magnetic resonance imaging, cerebrospinal fluid studies, electroencephalography) available at the time of initial presentation, rather than waiting for antibody results [44]. In practice, this means that acute movement disorders accompanied by encephalopathy, seizures, psychiatric symptoms, or autonomic instability should prompt consideration of autoimmune encephalitis in the appropriate clinical context, with early initiation of supportive care and timely immunotherapy where clinically appropriate, alongside parallel infectious work-up [44].
Hypokinetic emergencies: catatonia-spectrum illness and systemic toxicity syndromes
Although hypokinetic presentations were uncommon in our cohort, catatonia-spectrum disorders and systemic toxicity syndromes remain essential differentials in acute neurology. The British Association for Psychopharmacology consensus guideline provides structured recommendations for assessment and management of catatonia (including malignant catatonia), emphasizing first-line benzodiazepines, the role of electroconvulsive therapy, and careful consideration of neuroleptic malignant syndrome in overlapping presentations [45]. A recent comprehensive review summarises diagnostic and management principles for neuroleptic malignant syndrome and reinforces its potential for high morbidity without prompt recognition [25]. These frameworks provide a useful scaffold for early decisions in emergency care, especially where rigidity, mutism, autonomic instability, fever, or marked psychomotor disturbance are present [25,45].
Although opisthotonus is an uncommon emergency phenotype with a broad differential (including dystonia/toxic etiologies and functional presentations) [46], it was not observed in our cohort.
Rare and mixed presentations: reinforcing breadth in differential diagnosis
Our cohort included rare etiologies such as osmotic demyelination syndrome with mixed movement phenomenology and a structural lesion associated with Holmes tremor. Mixed hyperkinetic–hypokinetic syndromes are well described in osmotic demyelination syndrome, and systematic synthesis demonstrates that movement phenomenology can be broad and may coexist with other neurological deficits, supporting vigilance for mixed presentations when magnetic resonance imaging abnormalities are present [31]. Holmes tremor remains therapeutically challenging; a 2025 scoping review highlights heterogeneous treatment responses and suggests that levodopa and selected surgical strategies may benefit some patients depending on lesion localization and network involvement [47]. We encountered one patient with cranial (facial) rhythmic movements resembling myorrhythmia, but with clear positive features of a functional movement disorder (marked variability, distractibility/entrainment, and improvement after explanation and counseling). Because organic myorrhythmia is classically associated with brainstem or diencephalic network pathology, targeted evaluation did not identify a structural correlate, supporting a functional diagnosis.
These observations reinforce a core clinical message: acute movement disorder evaluation should remain anchored in a broad differential diagnosis guided by time course, exposure history, metabolic status, and neuroimaging, with escalation to an immune/infectious evaluation when red flags are present.
Strengths, limitations, and future directions
A key strength of this study is the systematic clinical phenotyping of acute-onset movement disorders presenting to a tertiary-care service, with categorization by both phenomenology and etiology. Several limitations should be considered. First, this is a single-center hospital cohort and may be shaped by local referral pathways and prescribing practices, which can influence the apparent frequency of metabolic and drug-induced presentations. Second, immune-mediated and paraneoplastic testing was performed based on clinical indication rather than uniformly across all participants; therefore, the relative contribution of immune-mediated etiologies could be underestimated compared with cohorts employing systematic antibody screening.44 Third, our center does not provide deep-brain stimulation (DBS) services; therefore, DBS-related emergencies were not encountered in this study. Future prospective multicenter studies with standardized diagnostic pathways and longitudinal outcome assessment could better clarify etiology-specific prognosis and inform local emergency pathways.
Conclusion
In this prospective tertiary-care cohort, movement disorder emergencies were predominantly hyperkinetic, and metabolic and drug-induced etiologies together accounted for more than half of presentations, underscoring the high yield of identifying reversible precipitants in acute care. Clinically, these data support an expeditious, structured diagnostic approach in the emergency and inpatient setting—one that begins with rapid metabolic screening (including bedside glucose and electrolyte assessment), a systematic medication and toxin exposure review (with particular attention to dopamine receptor–blocking agents, antiemetics, and other commonly implicated drugs), and targeted neuroimaging when focal or lateralized phenomenology, vascular risk factors, atypical features, or additional neurological deficits are present.
Beyond toxic–metabolic causes, the observed contributions of vascular, infectious, immune-mediated, and functional etiologies reinforce the need to maintain a broad, time-sensitive differential diagnosis. In particular, early recognition of functional movement disorders based on positive bedside signs may help reduce unnecessary investigations and enable timely referral to appropriate care pathways. Overall, our findings provide a pragmatic, evidence-informed framework for frontline clinicians and highlight the importance of standardized assessment pathways to shorten time to diagnosis and treatment. Future multicenter studies with harmonized diagnostic protocols and longitudinal follow-up are warranted to refine etiology-specific predictors and outcomes and to improve emergency care algorithms for acute-onset movement disorders.
Acknowledgments
Julián Benito-León is supported by the National Institutes of Health (NINDS R01 NS039422 and R01 NS094607) and by Spain’s Ministry of Science and Innovation through the Recovery, Transformation, and Resilience Plan (grants TED2021-130174B-C33, NETremor, PID2022-138585OB-C33, Resonate, and CPP2023-010465).
Funding statement
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Declaration of competing interest
The authors declare that they have no conflicts of interest relevant to this work. No financial support, grants, or funding were received for this study. Additionally, the authors affirm that there are no personal, professional, or financial relationships that could be perceived as influencing the content of this manuscript.
Footnotes
CRediT authorship contribution statement
Dinesh Kumar Manna: Writing – original draft, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Formal analysis, Data curation, Conceptualization. Ankur Banik: Writing – original draft, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Formal analysis, Conceptualization. Debsadhan Biswas: Writing – review & editing, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Data curation, Conceptualization. Sandip Pal: Writing – review & editing, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Formal analysis, Data curation, Conceptualization. Asutosh Pal: Writing – review & editing, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Formal analysis, Data curation, Conceptualization. Arkaprabha Sau: Writing – review & editing, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Data curation, Conceptualization. Mihira Chakravarthy: Writing – review & editing, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Formal analysis, Data curation, Conceptualization. Julián Benito-León: Writing – original draft, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Funding acquisition, Formal analysis, Conceptualization.
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