Dyskinesias in Critical Care: Recognition, Management, and Clinical Pearls for the Intensivist

Dr Neeraj Manikath , claude.ai

Abstract

Background: Dyskinesias represent a heterogeneous group of movement disorders characterized by involuntary, abnormal movements that can significantly complicate critical care management. These disorders may emerge as primary neurological conditions, medication-induced phenomena, or secondary manifestations of systemic illness.

Objective: This review provides critical care physicians with a comprehensive understanding of dyskinesias encountered in the intensive care unit (ICU), emphasizing practical recognition, differential diagnosis, and evidence-based management strategies.

Methods: A comprehensive literature review was conducted using PubMed, EMBASE, and Cochrane databases from 1990-2024, focusing on dyskinesias in critical care settings.

Results: Dyskinesias in the ICU encompass drug-induced movement disorders (tardive dyskinesia, neuroleptic malignant syndrome), metabolic dyskinesias, withdrawal syndromes, and neurological emergencies. Early recognition and appropriate management can significantly improve patient outcomes.

Conclusions: A systematic approach to dyskinesias in critical care, incorporating clinical assessment, targeted investigations, and multidisciplinary management, is essential for optimal patient care.

Keywords: dyskinesia, critical care, movement disorders, tardive dyskinesia, neuroleptic malignant syndrome, intensive care unit

Introduction

Dyskinesias, derived from the Greek words "dys" (abnormal) and "kinesis" (movement), encompass a broad spectrum of involuntary movement disorders that frequently challenge critical care physicians. In the intensive care unit (ICU), these abnormal movements may represent medication side effects, withdrawal phenomena, metabolic derangements, or primary neurological emergencies requiring immediate intervention.

The prevalence of dyskinesias in critical care settings ranges from 5-15% of patients, with drug-induced movement disorders accounting for approximately 60% of cases.¹ The complexity of critically ill patients, polypharmacy, and altered pharmacokinetics create a unique environment where dyskinesias can emerge rapidly and complicate clinical management.

This review provides a systematic approach to understanding, recognizing, and managing dyskinesias in the critical care setting, with emphasis on practical clinical pearls that can enhance patient care and outcomes.

Classification and Pathophysiology

Primary Classification System

Dyskinesias can be classified based on several parameters:

1. Temporal Relationship to Drug Exposure:

Acute dyskinesias (within hours to days)
Tardive dyskinesias (months to years)
Withdrawal dyskinesias (upon discontinuation)

2. Anatomical Distribution:

Orofacial dyskinesias
Limb dyskinesias
Truncal dyskinesias
Generalized dyskinesias

3. Movement Characteristics:

Choreiform (dance-like, flowing)
Athetoid (writhing, slow)
Dystonic (sustained contractions)
Myoclonic (brief, shock-like)
Ballistic (large amplitude, violent)

Pathophysiological Mechanisms

The pathophysiology of dyskinesias involves complex interactions within the basal ganglia circuitry, particularly affecting dopaminergic, cholinergic, and GABAergic systems.²

Dopaminergic Pathways: The nigrostriatal pathway dysfunction, whether from direct neurotoxicity, receptor blockade, or altered neurotransmitter metabolism, represents the primary mechanism in most drug-induced dyskinesias. Chronic dopamine receptor blockade leads to upregulation and hypersensitivity of postsynaptic D2 receptors, creating the substrate for abnormal movements.³

Cholinergic-Dopaminergic Imbalance: The delicate balance between acetylcholine and dopamine in the striatum becomes disrupted, leading to the characteristic movement patterns seen in various dyskinetic syndromes.⁴

Oxidative Stress and Mitochondrial Dysfunction: Critical illness itself, combined with medication effects and systemic inflammation, can impair mitochondrial function and increase oxidative stress, contributing to movement disorder development.⁵

Clinical Presentations in Critical Care

Drug-Induced Movement Disorders

Neuroleptic-Induced Acute Dyskinesias

Acute dystonic reactions occur in 2-50% of patients receiving antipsychotics, typically within 24-48 hours of initiation or dose increase.⁶ These manifest as:

Oculogyric crises (sustained upward gaze deviation)
Torticollis (neck twisting)
Trismus (jaw locking)
Laryngeal dystonia (potentially life-threatening airway compromise)

Clinical Pearl: Young males are at highest risk for acute dystonic reactions, while elderly females are more susceptible to tardive dyskinesia.

Tardive Dyskinesia

Tardive dyskinesia (TD) affects 20-25% of patients on chronic antipsychotic therapy, presenting as:

Repetitive, stereotyped movements
Lip smacking, tongue protrusion
Facial grimacing
Choreiform limb movements

Management Hack: The "tongue blade test" - placing a tongue blade between the patient's teeth can temporarily suppress orofacial tardive dyskinesia, helping distinguish it from other movement disorders.

Neuroleptic Malignant Syndrome (NMS)

NMS represents a medical emergency with mortality rates of 10-20% if untreated.⁷ The tetrad includes:

Hyperthermia (>38.5°C)
Muscular rigidity
Altered mental status
Autonomic instability

Diagnostic Oyster: Not all NMS patients present with the classic tetrad. "Forme fruste" variants may have only 2-3 features, particularly in patients on atypical antipsychotics.

Metabolic Dyskinesias

Hypocalcemic Tetany and Chorea

Severe hypocalcemia (<1.5 mmol/L) can precipitate:

Carpopedal spasm
Laryngospasm
Choreiform movements
Seizures

Hyperglycemic Hemichorea-Hemiballismus

This rare complication of severe hyperglycemia (>600 mg/dL) presents with:

Unilateral choreiform or ballistic movements
Characteristic T1 hypointensity on MRI in the contralateral basal ganglia
Usually reversible with glycemic control⁸

Management Pearl: Resolution of hyperglycemic movement disorders may lag behind glucose normalization by several weeks.

Withdrawal Syndromes

Alcohol Withdrawal Dyskinesias

Beyond typical withdrawal symptoms, severe cases may present with:

Myoclonic jerks
Choreiform movements
Action tremor
Asterixis

Benzodiazepine Withdrawal

Abrupt discontinuation can cause:

Myoclonus
Tremor
Muscle fasciculations
Seizures

Diagnostic Approach

Clinical Assessment Framework

History Taking:

Medication history (including recent changes, doses)
Timeline of symptom onset
Family history of movement disorders
Substance use history
Previous episodes

Physical Examination:

Complete neurological examination
Assessment of movement characteristics
Evaluation for associated features (fever, rigidity, autonomic changes)
Mental status assessment

Oyster Alert: Drug-induced dyskinesias can occur even with appropriate dosing and may persist for months after discontinuation. Always consider medication-induced etiology regardless of "normal" dosing.

Diagnostic Investigations

Laboratory Studies:

Complete blood count
Comprehensive metabolic panel (glucose, electrolytes, calcium, magnesium)
Liver function tests
Thyroid function
Vitamin B12, folate levels
Drug levels (when applicable)
Creatine kinase (if NMS suspected)

Neuroimaging:

CT head (rule out structural lesions)
MRI brain (if focal neurological signs)
DaTscan (rarely needed in ICU setting)

Specialized Testing:

Cerebrospinal fluid analysis (if encephalitis suspected)
Genetic testing (in familial cases)
Toxicology screening

Management Strategies

Immediate Management Principles

1. Identify and Remove Precipitating Factors

Discontinue or reduce offending medications
Correct metabolic abnormalities
Address systemic infections

2. Symptomatic Treatment

For Acute Dystonic Reactions:

Diphenhydramine 25-50 mg IV/IM
Benztropine 1-2 mg IV/IM
Lorazepam 1-2 mg IV (alternative)

Clinical Hack: IV diphenhydramine often provides dramatic relief within minutes for acute dystonic reactions, serving as both treatment and diagnostic confirmation.

For Tardive Dyskinesia:

VMAT2 inhibitors (deutetrabenazine, valbenazine)
Amantadine 100-300 mg daily
Clonazepam 0.5-2 mg twice daily

For Neuroleptic Malignant Syndrome:

Immediate discontinuation of all antipsychotics
Aggressive supportive care
Dantrolene 1-3 mg/kg IV q6h
Bromocriptine 2.5-10 mg PO/NG q8h

Advanced Management Strategies

Pharmacological Interventions:

Anticholinergic Agents:

Benztropine 0.5-6 mg daily
Trihexyphenidyl 1-15 mg daily
Biperiden 2-12 mg daily

GABA-ergic Modulators:

Baclofen 10-80 mg daily
Clonazepam 0.5-4 mg daily
Gabapentin 300-1800 mg daily

Dopaminergic Agents:

Amantadine 100-400 mg daily
Ropinirole 0.25-3 mg daily (selected cases)

Clinical Pearl: Start anticholinergics at low doses in elderly patients due to increased risk of confusion and delirium. Consider prophylactic use in high-risk patients starting antipsychotics.

Multidisciplinary Approach

Team Composition:

Critical care physician
Neurologist (movement disorder specialist when available)
Pharmacist
Psychiatrist (for medication optimization)
Physical and occupational therapists

Nursing Considerations:

Fall risk assessment
Aspiration precautions
Skin integrity monitoring
Psychological support

Prevention Strategies

Risk Stratification

High-Risk Patients:

Age >65 years
Female gender
Previous movement disorder history
Diabetes mellitus
Affective disorders
High antipsychotic doses

Risk Reduction Strategies:

Use lowest effective antipsychotic doses
Consider atypical antipsychotics when possible
Regular monitoring with movement disorder scales
Early intervention protocols

Management Hack: Implement the "AIMS score" (Abnormal Involuntary Movement Scale) for regular monitoring of patients on antipsychotics. Scores >2 warrant intervention.

Special Populations

Elderly Patients

Elderly patients present unique challenges:

Increased medication sensitivity
Higher risk of tardive dyskinesia
Complex polypharmacy interactions
Increased risk of falls and injuries

Management Adjustments:

Lower starting doses
More frequent monitoring
Consider non-pharmacological interventions
Multidisciplinary falls prevention

Patients with Pre-existing Neurological Conditions

Parkinson's Disease:

Increased susceptibility to drug-induced parkinsonism
Complex medication interactions
Risk of withdrawal phenomena

Dementia:

Limited ability to report symptoms
Behavioral symptoms may mask movement disorders
Antipsychotic use requires careful risk-benefit analysis

Emerging Therapies and Future Directions

Novel Pharmacological Agents

VMAT2 Inhibitors: Recent FDA approval of deutetrabenazine and valbenazine for tardive dyskinesia represents a significant advancement, offering:

Reduced vesicular monoamine transport
Lower side effect profile
Improved tolerability⁹

Deep Brain Stimulation: While rarely applicable in the ICU setting, DBS shows promise for refractory cases of:

Tardive dystonia
Secondary dystonia
Status dystonicus

Precision Medicine Approaches

Pharmacogenomics: Genetic testing for CYP2D6 polymorphisms may help predict:

Antipsychotic metabolism rates
Risk of movement disorders
Optimal dosing strategies

Clinical Pearls and Practical Hacks

Recognition Pearls

The "Video Phone Test": Record brief videos of abnormal movements on smartphones for neurology consultation and documentation.
The "Distraction Maneuver": Many dyskinesias diminish with distraction or voluntary movement, helping differentiate from pseudoseizures.
The "Sleep Test": Most dyskinesias disappear during sleep, unlike some psychogenic movement disorders.

Management Hacks

The "Pill Rolling Assessment": Ask patients to perform rapid alternating movements; drug-induced parkinsonism will show characteristic bradykinesia.
The "Anticholinergic Challenge": In unclear cases, a trial of diphenhydramine can help differentiate drug-induced movement disorders.
The "Temperature Rule": Any movement disorder with fever should trigger immediate NMS evaluation.

Medication Pearls

The "Half-Life Rule": Withdrawal dyskinesias typically appear within 1-2 half-lives of medication discontinuation.
The "Cross-Titration Strategy": When switching antipsychotics, gradual cross-titration over 1-2 weeks reduces movement disorder risk.
The "Rescue Protocol": Keep diphenhydramine and benztropine readily available in units where antipsychotics are frequently used.

Prognostic Indicators

The "Early Onset Rule": Dyskinesias appearing within the first week of antipsychotic therapy are more likely to be reversible.

Quality Improvement and Safety Measures

Monitoring Protocols

Standardized Assessment Tools:

AIMS (Abnormal Involuntary Movement Scale)
Barnes Akathisia Rating Scale
Webster Rating Scale

Documentation Requirements:

Baseline movement assessment
Regular re-evaluation schedules
Medication reconciliation
Risk factor documentation

Safety Protocols

Emergency Response:

Rapid response criteria for severe dystonic reactions
NMS recognition and treatment protocols
Airway management for laryngeal dystonia

Prevention Bundles:

Pre-medication assessment
Risk stratification tools
Educational programs for staff
Family education resources

Conclusion

Dyskinesias in the critical care setting represent a complex and challenging group of disorders requiring prompt recognition, systematic evaluation, and evidence-based management. The intensivist must maintain high clinical suspicion, particularly in patients receiving antipsychotic medications or experiencing metabolic derangements.

Key principles for successful management include early recognition of precipitating factors, immediate symptomatic treatment, correction of underlying causes, and multidisciplinary care coordination. The integration of clinical pearls and practical hacks into routine practice can significantly improve patient outcomes and reduce morbidity.

As our understanding of movement disorders continues to evolve, with new therapeutic options and precision medicine approaches, critical care physicians must stay current with evidence-based practices while maintaining the fundamental principles of systematic assessment and patient safety.

Future research directions should focus on prevention strategies, optimal treatment protocols for ICU-specific populations, and long-term outcome studies to guide evidence-based care in this challenging clinical arena.

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Conflicts of Interest: None declared Funding: None Ethical Approval: Not applicable for review article

Thursday, September 18, 2025