is the residual category for clinically significant motor disturbances attributable to a medication that do not fit the criteria for the named entities: , , medication-induced , medication-induced acute akathisia, , , tardive , or . It sits in the chapter Medication-Induced Movement Disorders and Other Adverse Effects of Medication, which exists in DSM-5-TR precisely because these phenomena routinely complicate psychiatric care and require coded recognition for treatment planning and billing. Clinically the category captures heterogeneous presentations — drug-induced myoclonus, restless-legs-like phenomena attributed to medication, mixed or atypical hyperkinetic syndromes, and movement disturbances from non-antipsychotic agents such as , , stimulants, and antiepileptics — that nevertheless cause distress or impair function. The bottom line for the resident at the bedside: when a patient on psychotropic medication develops a movement problem that does not look like classical parkinsonism, dystonia, akathisia, tardive dyskinesia, or NMS, this is the diagnosis that captures it, and the workup centers on temporal association, exclusion of mimics, and a structured deprescribing or substitution trial.
Precise prevalence is unknown because the category is residual and registry coding is inconsistent; the contributing phenomena have better epidemiologic data than the umbrella diagnosis itself.[1-2]
Contributing-phenomenon rates
- Lithium tremor occurs in approximately 25% of patients on therapeutic doses (reported range 4-65% depending on case definition), with higher rates at supratherapeutic levels.[3]
- SSRI- and -associated bruxism, jaw clenching, and myoclonus are reported in case series and pharmacovigilance data, with frank myoclonus in fewer than 1% of users but subclinical jerks far more common.[4-5]
- Stimulant-associated tics, stereotypies, and choreiform movements are reported in pediatric and adult ADHD populations, generally dose-related and reversible.[6]
- Valproate-induced postural and action tremor occurs in approximately 25% of long-term users.[7]
Demographic and risk factors
- Older adults have higher absolute risk for any drug-induced movement disorder owing to polypharmacy, reduced renal and hepatic clearance, and age-related dopaminergic decline.[8]
- Female sex carries higher risk for some serotonergic movement phenomena and for tardive presentations generally.[9]
- Comorbid neurodegenerative disease (early Parkinson disease, Lewy body disease) lowers the threshold for medication-induced motor symptoms and complicates attribution.[10]
The unifying thread is iatrogenic perturbation of motor circuits — most often the and related basal ganglia loops — but the precise mechanism varies by drug class.[1,11]
Dopaminergic mechanisms
- Postsynaptic D2 blockade by antipsychotics, antiemetics (metoclopramide, prochlorperazine), and some calcium channel blockers (flunarizine, cinnarizine) drives parkinsonism, dystonia, akathisia, and ; the residual category captures mixed or atypical hyperkinetic presentations that do not fit those named entities.[11-12]
- Dopamine-depleting agents (tetrabenazine, valbenazine, deutetrabenazine, reserpine) reduce presynaptic vesicular dopamine and can produce parkinsonism, depression, and akathisia-like restlessness even while treating chorea.[13]
Serotonergic mechanisms
- SSRI and SNRI agents can produce bruxism, jaw clenching, myoclonus, and akathisia-like restlessness, hypothesized to reflect 5-HT2 modulation of mesocortical dopamine output.[4-5]
- at the severe end produces myoclonus, tremor, hyperreflexia, and clonus with autonomic features, and is coded separately as a toxidrome rather than under this residual category.[14]
Other mechanisms
- Lithium produces a fine postural tremor through poorly understood effects on cerebellar and thalamic circuits; coarse tremor signals toxicity.[3,15]
- Valproate tremor is dose-related and often resembles in frequency and distribution.[7]
- Stimulants drive striatal dopamine release and can unmask tics, stereotypies, or chorea, particularly in genetically predisposed individuals.[6]
- Antiepileptics (lamotrigine, carbamazepine, phenytoin, gabapentin) can cause asterixis, myoclonus, or tremor, often dose- or level-related.[16]
Genetic and individual susceptibility
DSM-5-TR places this entry in the chapter Medication-Induced Movement Disorders and Other Adverse Effects of Medication, alongside the named entities; it is intended for clinically significant medication-induced motor phenomena that the named diagnoses do not capture.[1]
Core requirements
- A motor disturbance is present and is clinically significant — it causes distress, impairs function, or requires intervention.[1]
- The motor disturbance is judged to be due to a medication, based on temporal relationship to initiation, dose change, or discontinuation, and on the known pharmacology of the agent.[1]
- The presentation does not meet criteria for one of the named medication-induced movement disorders in the same chapter.[1]
- The clinician documents the implicated agent and the phenomenology.[1]
Phenomenology that commonly maps to this category:
- Drug-induced myoclonus (e.g. from SSRIs, opioids, lithium toxicity, gabapentin).[4,15-16]
- Drug-induced chorea or choreoathetosis (e.g. from levodopa in Parkinson disease, stimulants, oral contraceptives, lamotrigine).[16,18]
- Drug-induced restless-legs-like phenomena (e.g. from antihistamines, antidepressants, dopamine antagonists) that do not fulfill primary RLS criteria.[19]
- Drug-induced stereotypies, tics, or punding (e.g. from stimulants, dopamine agonists in Parkinson disease).[6,20]
- Mixed hyperkinetic syndromes that combine features without fitting a single named entity.[1]
ICD-11 differences
- organizes medication-induced movement disorders under chapter 06 with finer-grained entity codes and a residual ''other specified'' category analogous in function to the DSM-5-TR entry.[21]
- The clinical content is largely equivalent; coding granularity differs by registry.[21]
DSM-5-TR moved several of these entries from an appendix in DSM-IV-TR into the main text to acknowledge that medication-induced movement disorders are coded diagnoses, not merely side-effect notes.[1]
The presentation depends on the offending agent and the phenomenology; the common thread is temporal linkage to a medication and a motor disturbance that does not match the named entities.[1-2]
Common presentations
- Drug-induced myoclonus: brief, shock-like jerks, often multifocal, sometimes only at sleep onset; ask specifically about sleep-onset jerks in patients on SSRIs, gabapentinoids, or opioids.[4,16]
- Drug-induced chorea: irregular, flowing, non-rhythmic movements affecting limbs or face; consider stimulants, levodopa, lamotrigine, and oral contraceptives.[18]
- Drug-induced restless-legs-like symptoms: urge to move with rest, evening predominance, partial relief with movement, but onset clearly tied to medication initiation rather than primary RLS course.[19]
- Drug-induced stereotypies and punding: repetitive, purposeless motor sequences, classically described with dopamine agonists in Parkinson disease and with high-dose stimulants.[20]
- Mixed tremor-myoclonus syndromes on lithium, valproate, or antidepressant combinations.[3-4,7]
Course features
- Onset is typically within days to weeks of initiation or dose escalation, though late-onset presentations occur.[2]
- Most presentations are reversible with dose reduction or discontinuation, but symptoms can persist for weeks to months and rarely longer.[2,13]
- Severity ranges from a private nuisance to functional impairment requiring hospitalization or interruption of essential therapy.[1]
Red flags that argue against the residual category:
- Fever, rigidity, autonomic instability, and altered mental status point toward NMS, not this category.[22]
- Hyperreflexia, clonus, and autonomic features after a serotonergic combination point toward serotonin syndrome.[14]
- Sustained twisting postures within hours of a high-potency antipsychotic point toward medication-induced acute dystonia, which has its own code.[23]
A patient on antipsychotics or antiemetics who develops fever, rigidity, and altered mental status has NMS until proven otherwise; do not code this as Other Medication-Induced Movement Disorder while the diagnosis is in question.[22]
The differential is broad because the category captures whatever the named entities do not; the workup is built around excluding mimics and confirming the temporal link to the implicated agent.[1-2]
Named medication-induced entities (must be excluded first):
- Neuroleptic-induced parkinsonism: bradykinesia, rigidity, rest tremor, often symmetric; onset within weeks of antipsychotic initiation.[11]
- Medication-induced acute dystonia: sustained muscle contractions, often oculogyric, torticollic, or laryngeal, typically within 4 days of antipsychotic initiation.[23]
- Medication-induced acute akathisia: subjective restlessness with objective movement, within weeks of starting or escalating a .[24]
- Tardive dyskinesia: choreiform orobuccolingual movements after months to years of dopamine antagonist exposure.[25]
- Tardive dystonia and tardive akathisia: tardive analogues of the acute entities, each with its own DSM-5-TR code.[1]
- NMS and medication-induced postural tremor: distinct entries with their own criteria.[1,22]
Primary movement disorders
- Essential tremor: postural and action tremor, often familial, no clear temporal link to a new medication.[26]
- Idiopathic Parkinson disease: asymmetric onset, rest tremor, anosmia, REM sleep behavior disorder; medications can unmask but not solely cause the .[27]
- , , neuroacanthocytosis, and other genetic choreas: family history, age of onset, additional neurologic and systemic features.[28]
- Primary tic disorders and primary myoclonus syndromes: onset typically in childhood or adolescence, with a course independent of any specific medication.[29]
Medical mimics
- Hyperthyroidism (tremor, chorea), hypoparathyroidism (tetany, chorea), Wilson disease (tremor, dystonia, parkinsonism), and autoimmune encephalitis (varied hyperkinetic features) all mimic drug-induced presentations.[30]
- Stroke, especially involving basal ganglia or thalamus, can produce hemichorea or hemiballismus; the temporal profile usually differentiates.[31]
- Hepatic and uremic encephalopathy produce asterixis and myoclonus that can mimic drug-induced phenomena, particularly in patients on multiple psychotropics.[32]
Substance-induced presentations
Diagnosis is clinical and rests on a careful medication history, a structured neurologic examination, and selective laboratory testing rather than on advanced imaging.[1-2]
History elements that must not be skipped:
- Complete medication list including over-the-counter agents, supplements, antiemetics, antihistamines, and recent dose changes.[2]
- Temporal relationship between symptom onset and each medication's initiation, escalation, or recent discontinuation.[2]
- Prior episodes of movement disorder with this or related agents, including childhood tics or family history of essential tremor or Parkinson disease.[10,26]
- Substance use, including stimulants, cannabis, and alcohol, which can confound attribution.[6,32]
Examination approach
- Inspect at rest, with arms outstretched, with finger-to-nose movement, while writing or pouring water, and during gait.[2]
- Characterize each movement by phenomenology (tremor, myoclonus, chorea, tic, , dystonia), distribution, frequency, and triggers.[2]
- Look specifically for parkinsonian signs, sustained postures, hyperreflexia, and clonus before defaulting to the residual category.[14,22]
Validated rating scales
- AIMS for tardive dyskinesia screening, useful at baseline and serially in any patient on antipsychotics.[33]
- BARS for akathisia detection and quantification.[34]
- SAS for drug-induced parkinsonism.[35]
- The Unified Myoclonus Rating Scale and the Unified Huntington Disease Rating Scale motor section can quantify myoclonus and chorea when those are the dominant features.[36-37]
Laboratory and imaging
- Targeted labs based on phenomenology: TSH, electrolytes including calcium and magnesium, renal and hepatic panels, glucose, and drug levels for lithium, valproate, and antiepileptics.[2,15]
- Ceruloplasmin and 24-hour urinary copper in any patient under 50 with new chorea, dystonia, or parkinsonism to exclude Wilson disease.[28]
- Brain MRI when focal signs, , or absence of a plausible drug culprit raise concern for structural disease.[2]
- Dopamine transporter SPECT (DaTscan) can help when the question is medication-induced parkinsonism versus idiopathic Parkinson disease, but it is not first-line.[27]
What not to order routinely
- Whole-genome sequencing, generic neurodegeneration panels, and CSF studies are not first-line in a typical medication-induced presentation; reserve them for atypical, progressive, or focal findings.[2]
When attribution is uncertain, a structured deprescribing trial — reducing or holding the most likely offender for a defined interval and reassessing with a rating scale — is more informative than reflexive imaging.[2]
DRUGS
Dopamine antagonists, Reuptake inhibitors (SSRIs/), Useful mood stabilizers (lithium, valproate), Gabapentinoids and antiepileptics, Stimulants — the five classes that produce most non-named medication-induced movement phenomena.
Treatment is organized around three principles: confirm the culprit, reduce or remove exposure when feasible, and add symptomatic agents only when deprescribing is impossible or insufficient.[2,38]
Pharmacotherapy
- Dose reduction or discontinuation of the offending agent is first-line; evidence suggests this is the most reliable intervention across phenomenologies.[2,38]
- Substitution with a lower-risk agent within the same therapeutic class is commonly recommended when continued treatment is required; for example, from a high-potency to a lower-potency or partial-agonist antipsychotic for movement-related intolerance.[12,38]
- For lithium tremor that is functionally significant, evidence supports propranolol 10-40 mg PO TID as a symptomatic option, with dose reduction of lithium where therapeutically feasible.[3,15]
- For valproate tremor, evidence supports dose reduction; limited evidence suggests propranolol or primidone as adjuncts.[7]
- For SSRI-associated bruxism or myoclonus, limited evidence suggests dose reduction or switch to a less serotonergic agent; case reports describe benefit from buspirone 5-10 mg PO TID for bruxism.[4-5]
- For drug-induced chorea, removing the implicated agent is first-line; symptomatic tetrabenazine 12.5-25 mg PO BID or valbenazine 40-80 mg PO QD may be used when chorea persists or cannot be deprescribed.[13]
- For drug-induced restless-legs-like symptoms, switching the suspected agent is first-line; iron repletion is recommended if ferritin is low, consistent with primary RLS guidance.[19]
Psychotherapy
- Psychoeducation about the iatrogenic nature of the symptom, expected reversibility, and the rationale for any medication change improves adherence and reduces distress.[38]
- Cognitive-behavioral strategies for symptom-related distress are commonly recommended when movements persist during deprescribing.[38]
Neuromodulation
- Neuromodulation is not indicated for the typical presentations covered by this residual category.[38]
- has a role in selected refractory primary movement disorders (essential tremor, Parkinson disease, dystonia) but not in drug-induced phenomena that resolve with deprescribing.[39]
Adjunctive
- Iron repletion for low ferritin in drug-induced restless-legs-like presentations.[19]
- Treatment of contributing metabolic derangements (hyponatremia, hypocalcemia, hepatic or renal dysfunction).[2]
- Sleep optimization and reduction of caffeine and alcohol, which exacerbate tremor and myoclonus.[26]
Lithium has a narrow therapeutic window of 0.6-1.2 mEq/L for maintenance; coarse new tremor with confusion, ataxia, or GI symptoms suggests toxicity and warrants an urgent level rather than reassurance.[15]
| Intervention | Evidence base/Comparator | Benefits | Harms | Certainty | Notes |
|---|---|---|---|---|---|
| Dose reduction or discontinuation of offender | Observational and pharmacovigilance data; clinical consensus | Resolution or marked reduction in symptoms in most cases | Loss of therapeutic benefit; risk of relapse of primary illness | moderate | First-line across phenomenologies |
| Switch to lower-risk agent in same class | Comparative observational data, guideline consensus | Maintains primary indication while reducing motor risk | Switch failure; new adverse effects | moderate | Common strategy with antipsychotic-related presentations |
| Propranolol for lithium or valproate tremor | RCT and observational data | Reduces tremor amplitude | Bradycardia, hypotension, fatigue | moderate | Symptomatic only; does not treat cause |
| for drug-induced chorea | RCT data in tardive dyskinesia and Huntington disease, extrapolated | Symptom reduction when deprescribing fails | Parkinsonism, depression, somnolence | low | Off-label use outside named indications |
| Iron repletion for drug-induced RLS-like symptoms | Extrapolated from primary RLS RCTs | Symptom reduction when ferritin is low | GI effects of oral iron | low | Mirrors primary RLS guidance |
The harms picture is dominated by the trade-off between the motor symptom and the indication for which the offending medication was prescribed; the evidence base is fragmented across phenomenologies and drug classes.[1-2]
- Common adverse effects of deprescribing include relapse of the primary psychiatric illness, withdrawal phenomena, and patient mistrust if the rationale is not communicated clearly.[38]
- Serious harms include destabilization of bipolar or psychotic illness during abrupt antipsychotic or mood-stabilizer discontinuation.[38]
- Symptomatic agents carry their own risks: propranolol can cause bradycardia and bronchospasm, VMAT2 inhibitors can produce parkinsonism and depression, and used for myoclonus carry dependence and falls risk.[13,15]
- Monitoring burden is real: serial rating scales, levels for lithium and valproate, and re-evaluation visits add to the patient's appointment load.[2,33]
- Limitations of the evidence base include heterogeneous case definitions, small sample sizes for non-antipsychotic phenomena, short follow-up in most studies, and underrepresentation of older adults and patients with polypharmacy in trial populations.[1-2]
Attribution and management differ meaningfully in age extremes, perinatal patients, and those with neurodegenerative disease; thresholds for action shift accordingly.[2,8]
Pediatric
- Stimulant-associated tics and stereotypies are common questions in care; most are reversible and do not require stimulant discontinuation when the symptom is mild and the therapeutic benefit is clear.[6]
- SSRI-associated activation, including jitteriness and myoclonus, is more common in children and adolescents than in adults.[40]
Geriatric
- Older adults have higher rates of any drug-induced movement disorder and lower thresholds for falls, fracture, and delirium when symptomatic agents are added.[8]
- burden should be minimized rather than expanded when treating geriatric drug-induced movement symptoms.[8]
Perinatal
- Medication-induced tremor and akathisia may emerge or worsen during pregnancy because of pharmacokinetic shifts; lithium, in particular, requires more frequent level monitoring.[15]
- Decisions about deprescribing must weigh fetal exposure against maternal psychiatric stability and are best made in shared decision-making with obstetric and psychiatric input.[38]
Comorbid medical illness
- Renal or hepatic impairment alters clearance of lithium, valproate, and many antipsychotics, increasing the risk of dose-related motor symptoms.[15]
- Neurodegenerative comorbidity (early Parkinson disease, Lewy body disease) markedly lowers the threshold for medication-induced parkinsonism and atypical movement phenomena.[10,27]
Cultural considerations
- Patient-reported terms for involuntary movements vary by language and culture; structured rating scales reduce reliance on idiomatic descriptions.[33-34]
Most presentations covered by this residual category are reversible with timely deprescribing; persistence and progression are the exceptions and warrant reconsideration of the diagnosis.[2,38]
- Tremor from lithium and valproate typically improves within days to weeks of dose reduction.[3,7]
- SSRI-associated bruxism and myoclonus generally remit within weeks of discontinuation or switch.[4-5]
- Drug-induced chorea from levodopa or stimulants usually resolves with dose adjustment, though levodopa-induced dyskinesia in advanced Parkinson disease is a separate, often persistent problem.[18]
- Stimulant-associated tics in children commonly remit on discontinuation or dose reduction; persistence raises suspicion of an underlying primary tic disorder.[6]
- Persistent symptoms despite deprescribing should prompt reconsideration of the diagnosis, in particular tardive syndromes or an unmasked primary movement disorder.[25,27]
- Functional outcome is generally good when the offending agent can be safely changed; outcome is worse when the patient requires continued exposure (e.g. for treatment-resistant with associated tremor).[12,38]
Most presentations are outpatient problems, but a small subset requires urgent recognition and escalation; the residual category should never be used as a holding diagnosis for a true emergency.[14,22]
- Hospitalization is warranted when movements impair airway protection (severe oromandibular or laryngeal involvement), when there is suspicion of NMS or serotonin syndrome, or when the underlying psychiatric illness is destabilized by the symptom or by required deprescribing.[14,22,38]
- Suicide risk can rise during acute distress from akathisia or akathisia-like restlessness; specifically ask about suicidal ideation in any patient presenting with new restlessness on a serotonergic or antidopaminergic agent.[24]
- Agitation management in this population avoids reflexive use of additional high-potency antipsychotics, which may worsen the motor problem.[12]
- Safety-relevant comorbid presentations include falls in older adults with tremor and ataxia, aspiration in patients with significant oromandibular movements, and motor vehicle risk in patients with prominent myoclonus or sedation from symptomatic agents.[8]
Fever, rigidity, autonomic instability, and altered mental status on an antipsychotic is NMS, not Other Medication-Induced Movement Disorder.[22]
The category is useful precisely because it captures heterogeneity, but that heterogeneity drives most of the unresolved questions about boundaries, coding, and evidence quality.[1-2]
- Boundary with tardive syndromes: late-onset hyperkinetic movements after prolonged dopamine antagonist exposure should be coded as tardive dyskinesia or tardive dystonia rather than under the residual category, but real-world presentations are often mixed.[25]
- Boundary with primary movement disorders: medication exposure can unmask latent essential tremor, RLS, or Parkinson disease, and whether to code the syndrome as medication-induced, primary, or both is a recurring uncertainty.[10,26-27]
- Restless-legs-like presentations on antidepressants and antipsychotics are inconsistently classified across literature, with some authors arguing for a distinct subtype and others for inclusion under this residual category.[19]
- Punding and stereotypies from dopamine agonists in Parkinson disease overlap with impulse-control disorders, raising questions about the right diagnostic chapter.[20]
- Evidence for symptomatic agents (propranolol, VMAT2 inhibitors, buspirone) is largely extrapolated from named entities; head-to-head trials within the residual category are absent.[3,7,13]
- ICD-11 and DSM-5-TR are largely concordant in scope but differ in coding granularity, which complicates registry-based epidemiology.[1,21]
- Other Medication-Induced Movement Disorder is the DSM-5-TR residual category for clinically significant medication-induced motor disturbances that do not meet criteria for the named entities.[1]
- The named entities to exclude first are neuroleptic-induced parkinsonism, NMS, medication-induced acute dystonia, medication-induced acute akathisia, tardive dyskinesia, tardive dystonia, tardive akathisia, and medication-induced postural tremor.[1]
- Lithium tremor is fine and postural; coarse tremor with confusion or ataxia signals toxicity and warrants an urgent level.[3,15]
- Valproate produces a postural and action tremor in roughly 25% of long-term users, often resembling essential tremor.[7]
- SSRIs and SNRIs can produce bruxism, jaw clenching, and myoclonus; the dominant hypothesized mechanism is 5-HT2 modulation of dopaminergic output.[4-5]
- Stimulants can unmask tics, stereotypies, and chorea, particularly in genetically predisposed children.[6]
- Antiemetics (metoclopramide, prochlorperazine) and calcium channel blockers (flunarizine, cinnarizine) are commonly overlooked dopamine antagonists.[12]
- , Barnes, and Simpson-Angus are the standard scales for tardive dyskinesia, akathisia, and parkinsonism respectively; their absence at baseline is a quality-of-care marker.[33-35]
- Wilson disease must be excluded in any patient under 50 with new chorea, dystonia, or parkinsonism, regardless of medication history.[28]
- First-line treatment across phenomenologies is dose reduction or discontinuation of the offending agent; symptomatic agents are second-line.[2,38]
- Propranolol is the most evidence-supported symptomatic treatment for lithium tremor.[3,15]
- VMAT2 inhibitors (tetrabenazine, valbenazine, deutetrabenazine) treat chorea but can produce parkinsonism, depression, and akathisia.[13]
- Fever, rigidity, autonomic instability, and altered mental status on an antipsychotic is NMS, not the residual category.[22]
- Hyperreflexia and clonus with serotonergic combination therapy is serotonin syndrome, not the residual category.[14]
- ICD-11 organizes medication-induced movement disorders under chapter 06 with finer-grained codes and an analogous residual category.[21]
No external funding. No conflicts of interest declared. Peer-review status: pending.
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A clinical reference on tardive dyskinesia: DSM-5-TR placement, risk factors, AIMS-based assessment, and VMAT2 inhibitor first-line treatment.
PsychopharmacologyMedication-Induced Movement Disorders and Other Adverse Effects of MedicationTardive DyskinesiaMedication-Induced Acute Akathisia
A practical guide to recognizing, differentiating, and treating acute drug-induced akathisia, with emphasis on antipsychotic-related presentations.
PsychopharmacologyMedication-Induced Acute AkathisiaMedication-Induced Acute Dystonia: Recognition, Mechanism, and Bedside Management
Acute dystonia is a dramatic, painful, and treatable extrapyramidal reaction to dopamine-blocking agents — recognize it fast, reverse it faster.
Extrapyramidal SymptomsPsychopharmacologyMedication-Induced Acute DystoniaNeuroleptic-Induced Parkinsonism: Diagnosis, Mechanism, and Management
A clinical reference on drug-induced parkinsonism from antipsychotics — risk factors, differential diagnosis from Parkinson disease, and evidence-based management.
Extrapyramidal SymptomsPsychopharmacologyNeuroleptic-Induced ParkinsonismMedication-Induced Movement Disorders and Other Adverse Effects of Medication
A clinical reference to antipsychotic and psychotropic movement disorders — dystonia, akathisia, parkinsonism, tardive dyskinesia, NMS, and serotonin syndrome.
PsychopharmacologySerotonin SyndromeNeuroleptic Malignant SyndromeBinge-Eating Disorder: Diagnosis, Evaluation, and Evidence-Based Treatment
A clinical reference on binge-eating disorder covering DSM-5-TR criteria, differential diagnosis, evidence-based pharmacotherapy and psychotherapy, and exam-ready pearls.
PsychopharmacologyPicaBinge-Eating DisorderDepersonalization/Derealization Disorder: Clinical Recognition, Differential Diagnosis, and Management
A clinical reference on depersonalization/derealization disorder, covering DSM-5-TR criteria, assessment, differential diagnosis, and evidence-based management.
Dissociative DisordersAnxiety DisordersPsychopharmacology