Tardive akathisia is a delayed-onset, often persistent movement disorder marked by a subjective sense of inner restlessness and an observable urge to move, emerging months to years after exposure to dopamine receptor blocking agents. It sits within the broader family of tardive syndromes alongside Tardive Dyskinesia and tardive dystonia, but its dominant feature is distress rather than dyskinetic movement, which makes it easy to miss and easy to misread as worsening psychiatric illness. DSM-5-TR codes medication-induced akathisia within the medication-induced movement disorders chapter; the tardive subtype is distinguished by latency of onset and tendency toward chronicity. The clinical stakes are high: untreated Akathisia is linked to medication nonadherence, functional impairment, and elevated suicide risk. The bottom line: in a patient with months of antipsychotic exposure who reports restlessness, agitation, or "feeling worse," consider tardive akathisia before escalating the antipsychotic dose.

Tardive akathisia is less well characterized than tardive dyskinesia, but it accounts for a meaningful share of chronic movement burden in patients on long-term dopamine-blocking therapy. Prevalence estimates vary by case definition, exposure duration, and the antipsychotic generation studied.

Frequency and exposure

• Chronic akathisia prevalence in patients on long-term first-generation antipsychotics has been reported in the range of 15-35% across clinical cohorts.^[1-2]
• Second-generation antipsychotics carry a lower but non-negligible risk; aripiprazole and lurasidone have the highest akathisia signal within the second-generation class in the broad comparative literature, with cariprazine showing a similar signal in its registration trials.^[3-4,22]
• True tardive akathisia (delayed onset, persistent after dose change) is rarer than acute akathisia but is plausibly underdiagnosed because clinicians attribute the restlessness to anxiety or psychotic agitation.^[1,5]

Demographic and risk factors

• Older age, female sex, and longer cumulative antipsychotic exposure increase risk for tardive syndromes generally, paralleling the better-studied risk profile for tardive dyskinesia.^[6]
• Mood disorder diagnosis (versus primary psychotic disorder) is associated with higher tardive syndrome risk at equivalent antipsychotic exposure.^[6-7]
• Concomitant exposure to antiemetic dopamine blockers (metoclopramide, prochlorperazine) is an underrecognized contributor and shows up frequently in older outpatients.^[8]
• A history of acute extrapyramidal symptoms during early treatment predicts later tardive syndromes.^[6]

The mechanism of tardive akathisia overlaps with, but is not identical to, the mechanism proposed for tardive dyskinesia. Chronic Dopamine Receptor Blockade drives compensatory changes in basal ganglia circuits that outlast the original blockade.

Receptor and circuit hypotheses

• The dominant model is postsynaptic D2 receptor upregulation and supersensitivity in the striatum, producing paradoxical hyperkinetic phenomena when blockade is reduced or unmasked.^[9]
• A complementary model implicates dysfunction in the mesocortical and nigrostriatal pathways, with imbalance between direct and indirect basal ganglia output pathways generating the subjective restlessness and motor urge.^[1,9]
• Akathisia specifically has been linked to mesocortical dopaminergic hypofunction, which may explain why Aripiprazole—a D2 partial agonist—produces high rates of akathisia despite a low overall extrapyramidal profile.^[3,9]

Neurochemical contributors

• Serotonergic modulation of dopamine release contributes; 5-HT2A antagonism is part of why some second-generation agents reduce akathisia risk relative to high-potency first-generation drugs.^[9]
• Noradrenergic hyperactivity is implicated in the subjective restlessness; this is the rationale for Beta-blocker trials (propranolol) in akathisia.^[10]
• GABAergic deficits in striatal interneurons have been proposed as a substrate for the persistence of tardive phenomena after the offending agent is removed.^[1,9]

Genetic and patient-level vulnerability

• Polymorphisms in dopamine receptor genes (DRD2, DRD3) and in genes affecting oxidative stress pathways (MnSOD) have been associated with tardive syndrome risk in candidate-gene studies, though replication is inconsistent.^[6]
• Iron deficiency has been linked to akathisia severity and is worth screening when restlessness is prominent.^[10]

DSM-5-TR groups medication-induced akathisia under medication-induced movement disorders. Tardive akathisia is distinguished from the acute form by latency and persistence; the diagnostic move is recognizing both the phenomenology and the temporal relationship to dopamine-blocking exposure.

Core diagnostic features

• Subjective complaints of inner restlessness, most often referable to the legs, with an irresistible urge to move.^[11]
• Observable movements: rocking from foot to foot, pacing, inability to sit or stand still, and stereotyped leg crossing or shifting.^[1,11]
• Temporal relationship to a dopamine receptor blocking agent—either ongoing exposure or recent dose change.^[11]
• Symptoms are not better explained by anxiety, psychotic agitation, restless legs syndrome, or another medical condition.^[11]

Tardive subtype features

• Onset after at least three months of cumulative exposure to a dopamine receptor blocking agent (one month in patients over 60).^[1,12]
• Symptoms persist for at least one month after the offending agent is discontinued or reduced, distinguishing the syndrome from withdrawal akathisia.^[1,12]
• Symptoms may paradoxically worsen with dose reduction or discontinuation of the offending agent—a defining feature that helps separate tardive from acute akathisia.^[1,12]

ICD-11 placement

• ICD-11 codes drug-induced akathisia under chapter 08 (diseases of the nervous system) rather than the mental disorders chapter, reflecting its neurological character.^[13]
• ICD-11 does not separately code a tardive akathisia subtype; the persistent presentation is captured descriptively.^[13]

The hallmark is the combination of subjective restlessness and stereotyped, semi-voluntary movements that the patient cannot suppress for long. Severity ranges from mild fidgeting to constant pacing that prevents sleep and erodes quality of life.

Symptom phenomenology

• Subjective component: a sense of inner restlessness, tension, or "needing to move," most often localized to the legs but sometimes generalized.^[1,11]
• Objective component: rocking, marching in place, shifting weight, crossing and uncrossing legs, pacing, or repeatedly standing and sitting.^[1,11]
• Diurnal pattern: symptoms are typically constant throughout waking hours and improve with sleep, which distinguishes akathisia from Restless Legs Syndrome.^[10]
• Suppressibility: brief voluntary suppression is possible but generates mounting distress and rebound movement.^[1]

Tardive-specific features

• Insidious onset months into therapy, often after a dose increase or addition of a second dopamine blocker.^[1,12]
• Paradoxical worsening on dose reduction—a near-pathognomonic feature that should immediately raise suspicion for the tardive variant.^[1,12]
• Coexistence with other tardive phenomena: orofacial dyskinesia, limb-truncal dyskinesia, or tardive dystonia is common and supports the diagnosis.^[1]
• Persistence after the offending agent is withdrawn, sometimes for months to years; spontaneous remission rates are modest.^[1,14]

Functional consequences

• Sleep disruption, particularly difficulty initiating sleep, is among the most common patient complaints.^[10]
• Functional impairment in work, social roles, and self-care is frequent and correlates with akathisia severity.^[2]
• Akathisia is independently associated with suicidal ideation and completed suicide in patients on antipsychotics.^[15]
• Medication nonadherence is common and frequently precipitates psychiatric relapse, which can be misattributed to the underlying illness rather than to the adverse effect.^[2,15]

Tardive akathisia is frequently misdiagnosed as psychiatric worsening or as an unrelated medical condition, and clarifying the differential is the single most important diagnostic step.

Psychiatric mimics

• Psychotic agitation: typically context-dependent, tied to internal stimuli, and accompanied by other psychotic features; akathisia is mechanical, monotonous, and the patient often labels it as physical rather than mental distress.^[1,11]
• Anxiety disorders: psychic anxiety predominates over motor urge, and the restlessness is not localized to the legs; in akathisia, the patient often says "I just can't keep my legs still."^[1,11]
• Agitated depression: motor agitation co-occurs with depressive cognition; in pure akathisia, mood may be secondary to the physical restlessness.^[1]
• Mania: distinguishable by elevated mood, sleep loss without fatigue, and goal-directed activity, none of which characterize akathisia.^[1]

Other movement and neurologic causes

• Restless Legs Syndrome: circadian (evening/nighttime) symptoms, relief with movement, association with sleep onset; akathisia lacks the strong circadian rhythm and is present during waking hours.^[10]
• Tardive dyskinesia: choreiform orofacial or limb movements without the subjective restlessness; the two often coexist.^[1]
• Parkinsonian tremor or drug-induced parkinsonism: bradykinesia and rigidity dominate; akathisia is by definition hyperkinetic.^[1]
• Stereotypies in autism spectrum disorder or stimulant use: history and context typically clarify.^[1]

Medical mimics worth excluding

• Hyperthyroidism: TSH should be checked in any new restlessness presentation.^[10]
• Iron deficiency: ferritin is appropriate when akathisia features or restless legs overlap.^[10]
• Serotonin syndrome or NMS in the appropriate temporal window; both involve restlessness but with autonomic and neurologic signs absent in pure akathisia.^[16]
• Substance intoxication (stimulants, cocaine) or withdrawal (opioids, benzodiazepines, alcohol) can mimic akathisia.^[1]

Akathisia variants to distinguish

• Acute akathisia: onset within days to weeks of starting or increasing a dopamine blocker; resolves with dose reduction.^[1,11]
• Withdrawal (rebound) akathisia: emerges within six weeks of dose reduction or discontinuation and resolves within six weeks.^[1,12]
• Tardive akathisia: delayed onset, persistence beyond one month off the offending agent, and often paradoxical worsening with dose reduction.^[1,12]
• Pseudoakathisia: objective restless movements without the subjective component, often in patients with longstanding chronic exposure and frequently a marker of chronicity rather than a separate entity.^[1]

Assessment hinges on a careful exposure history, structured symptom inventory, and use of a validated rating scale. Examination should include a focused movement disorder exam.

History to obtain

• Complete dopamine receptor blocking agent history: every antipsychotic, every antiemetic (especially metoclopramide, prochlorperazine), and any over-the-counter combination products containing promethazine.^[1,8]
• Cumulative exposure duration, dose changes, and the temporal relationship between dose changes and symptom emergence.^[1,12]
• Specific question for "needing to move" or "legs that won't stay still"—patients often do not volunteer this complaint unless asked directly.^[1,11]
• History of acute extrapyramidal symptoms, mood disorder diagnosis, and substance use (especially stimulants).^[6]

Examination

• Observe the patient at rest and during conversation for foot tapping, weight shifting, leg crossing, and inability to sit still.^[1,11]
• Look for coexisting tardive dyskinesia (orofacial, limb, truncal) and tardive dystonia (focal sustained postures).^[1]
• Assess for parkinsonism (tremor, cogwheel rigidity, bradykinesia)—frequently coexists and informs treatment selection.^[1]

Validated rating scales

• Barnes Akathisia Rating Scale (BARS) is the standard instrument; it captures objective restlessness, subjective awareness, subjective distress, and a global clinical assessment.^[19]
• A BARS global score of two or higher (mild akathisia present) is the conventional threshold for clinically meaningful symptoms.^[19]
• Abnormal Involuntary Movement Scale (AIMS) should be administered at the same visit to screen for coexisting tardive dyskinesia.^[20]

Investigations

• TSH to exclude hyperthyroidism.^[10]
• Ferritin and iron studies; low ferritin (below 50 ng/mL) is associated with akathisia severity and is correctable.^[10]
• Basic metabolic panel and pregnancy test as appropriate for treatment planning (relevant before initiating a VMAT2 inhibitor).^[17-18]

What not to order

• Routine neuroimaging is not indicated unless atypical features (focal signs, sudden onset, cognitive decline) suggest an alternative diagnosis.^[1]
• Genetic testing for dopamine receptor polymorphisms has no current role in clinical care.^[6]

Treatment requires a deliberate balance between managing the underlying psychiatric illness and reducing the iatrogenic movement disorder. The single most important step is to recognize that escalating the offending antipsychotic typically worsens tardive akathisia.

General principles

• Confirm the diagnosis with a structured exam and BARS rating; document the offending agent and cumulative exposure.^[1,19]
• Avoid further dose increases of the suspected agent; consider switching to a lower-risk antipsychotic when the psychiatric indication allows.^[1,17]
• Correct contributing factors: replete iron, treat hyperthyroidism, taper concomitant stimulants when feasible.^[10]
• Engage the patient in shared decision-making; tardive symptoms can be chronic and require sustained management.^[1]

Pharmacotherapy

• VMAT2 inhibitors have the strongest evidence base in tardive syndromes generally and are first-line for moderate-to-severe persistent tardive akathisia. Strong evidence supports valbenazine 40-80 mg PO QD and deutetrabenazine 12-48 mg PO BID for tardive dyskinesia; evidence in tardive akathisia specifically is more limited but increasingly supportive given the shared pathophysiology.^[17-18,21]
• propranolol 10-40 mg PO TID is first-line for acute akathisia and is commonly tried in tardive akathisia, with limited evidence suggesting modest benefit.^[10,22]
• mirtazapine 7.5-15 mg PO QHS has moderate evidence for acute akathisia (via 5-HT2A antagonism) and is commonly used adjunctively in tardive presentations; lower-quality evidence in the tardive subtype.^[22-23]
• clonazepam 0.5-2 mg PO QD can reduce subjective distress; benzodiazepines carry dependence and falls risk and are best used short-term.^[22]
• Anticholinergic agents (benztropine 0.5-2 mg PO BID) are useful for parkinsonism and dystonia but generally not effective for akathisia and may worsen tardive dyskinesia; avoid as monotherapy.^[1,22]
• Switching to clozapine has the most robust evidence among antipsychotic switches for tardive syndromes; it may improve akathisia and dyskinesia and is reasonable when the psychiatric indication and monitoring infrastructure allow.^[24]

Psychotherapy

• Targeted psychoeducation reduces misattribution of restlessness to psychiatric illness and supports adherence to a revised regimen.^[1]
• Supportive therapy for distress, sleep hygiene interventions, and management of comorbid depression are reasonable adjuncts; psychotherapy alone does not treat the movement disorder.^[1]

Neuromodulation

• Deep brain stimulation of the globus pallidus internus has limited case-series evidence for severe, refractory tardive syndromes including tardive akathisia; expert opinion, not first-line.^[25]
• Repetitive transcranial magnetic stimulation has been studied in tardive dyskinesia with mixed results; evidence in tardive akathisia is very limited.^[25]

Adjunctive

• Vitamin B6 (pyridoxine) at high doses has limited evidence in tardive dyskinesia and akathisia; some experts recommend it as a low-risk adjunct.^[1,22]
• Ginkgo biloba extract has shown benefit in small tardive dyskinesia trials and is mentioned in treatment algorithms as a possible adjunct; direct evidence in tardive akathisia is limited.^[21-22]
• Vitamin E does not improve established tardive dyskinesia symptoms in pooled analysis but may protect against deterioration; evidence in tardive akathisia is absent and the role is at best a low-risk adjunct.^[26]
• Discontinue or switch antiemetic dopamine blockers (metoclopramide, prochlorperazine) whenever possible; substitute ondansetron or non-dopaminergic alternatives.^[8]

The harms picture in tardive akathisia is twofold: harms from the syndrome itself and harms from the treatments used to manage it. Both deserve explicit discussion with the patient.

Harms of the syndrome

• Persistent distress, sleep disruption, and functional impairment that often outlast the offending agent by months to years ^[1,14]
• Independent association with suicidal ideation and completed suicide, particularly during episodes of severe restlessness ^[15]
• Medication nonadherence and psychiatric relapse, which can be misattributed to the underlying illness ^[2,15]

Harms of treatment

• VMAT2 inhibitors: parkinsonism, somnolence, QT prolongation, and treatment-emergent depression with suicidality have been reported with valbenazine and deutetrabenazine ^[17-18]
• Propranolol: bradycardia, hypotension, bronchospasm in patients with reactive airway disease, and fatigue ^[10,22]
• Benzodiazepines: tolerance, dependence, cognitive blunting, and falls in older adults ^[22]
• Anticholinergics: cognitive impairment, urinary retention, and potential worsening of tardive dyskinesia ^[1,22]
• Clozapine switch: agranulocytosis, myocarditis, seizures, ileus, and metabolic syndrome; requires REMS monitoring ^[24]

Limitations of the evidence

• Most tardive akathisia trials are small, of short duration, and use heterogeneous case definitions that conflate acute and tardive presentations ^[1,22]
• Pivotal VMAT2 inhibitor trials enrolled patients with tardive dyskinesia; extrapolation to tardive akathisia rests on shared pathophysiology rather than dedicated trial data ^[17-18]
• Long-term outcome data beyond one to two years are sparse, limiting confidence in durable benefit ^[14]
• Publication bias toward positive findings is plausible across the small-trial literature ^[22]
• Patients with comorbid substance use, severe medical illness, and active psychosis are typically excluded from trials, limiting generalizability ^[22]

Risk and management differ meaningfully across the lifespan and clinical contexts. The principles are unchanged but the thresholds shift.

Pediatric

• Tardive syndromes occur in children and adolescents exposed to antipsychotics, though prevalence data are limited and lower than in adults ^[27]
• Withdrawal dyskinesias are particularly common in children after antipsychotic discontinuation and can be mistaken for tardive akathisia ^[27]
• VMAT2 inhibitors are not FDA-approved in pediatric populations; treatment is largely supportive with cautious dose reduction or switch ^[17-18]

Geriatric

• Older adults develop tardive syndromes more rapidly and at lower cumulative doses; the diagnostic threshold for tardive akathisia is one month of exposure rather than three ^[1,12]
• Concomitant dopamine-blocking antiemetics (metoclopramide, prochlorperazine) are a major contributor in older outpatients and are often overlooked ^[8]
• Falls risk, anticholinergic burden, and QT prolongation considerations narrow the treatment options; propranolol must be used cautiously given hypotension and bradycardia risk ^[10,22]

Perinatal

• VMAT2 inhibitors have limited pregnancy safety data; both valbenazine and deutetrabenazine were approved under the FDA Pregnancy and Lactation Labeling Rule and carry no letter category, with labeling noting embryofetal toxicity in animal studies and absent adequate human data ^[17-18]
• Avoid valbenazine and deutetrabenazine in pregnancy unless benefits clearly outweigh risks.^[17-18]
• Continuation of the offending antipsychotic may be required for maternal stability; treatment of tardive akathisia in this setting favors non-pharmacologic measures and propranolol when tolerated ^[10]

Comorbid medical illness

• Cardiac disease, particularly long QT or recent myocardial infarction, restricts VMAT2 inhibitor and antipsychotic options ^[17-18]
• Hepatic impairment requires dose adjustment for valbenazine and deutetrabenazine ^[17-18]
• Reactive airway disease contraindicates non-selective beta-blockade; metoprolol is a less-studied alternative ^[10]

Comorbid substance use

• Stimulant use (methamphetamine, cocaine, prescription stimulants) can both unmask and worsen akathisia; abstinence is part of the treatment plan ^[1]
• Concurrent benzodiazepine or alcohol use complicates pharmacologic adjuncts and raises overdose risk ^[22]

Cultural considerations

• Somatic presentations of distress vary across cultures; patients may describe akathisia in idioms of distress that obscure the movement disorder origin ^[1]
• Stigma around movement disorders can reduce reporting; a structured screen using BARS at every antipsychotic visit reduces missed cases ^[19]

Tardive akathisia is often chronic, but not universally so. Earlier recognition and intervention are associated with better outcomes.

Natural history

• Spontaneous remission occurs in a minority of patients after withdrawal of the offending agent, with estimates of 10-30% at one year in observational cohorts ^[1,14]
• Persistence beyond one year is common, and a meaningful subset of patients have lifelong symptoms ^[1,14]
• Coexisting tardive dyskinesia predicts a more chronic course ^[1]

Response to treatment

• VMAT2 inhibitors produce clinically meaningful reductions in tardive movement burden in a majority of treated patients, with sustained benefit at one to two years in extension studies of tardive dyskinesia trials ^[17-18]
• Switching to clozapine is associated with improvement in tardive symptoms in observational cohorts, though heterogeneity is high ^[24]
• Akathisia-specific symptomatic agents (propranolol, mirtazapine) produce modest benefit and rarely eliminate symptoms in the tardive variant ^[22-23]

Functional and mortality outcomes

• Functional outcome correlates with akathisia severity and with successful psychiatric stabilization on a tolerated regimen ^[2]
• Suicide risk is elevated during periods of severe restlessness and warrants explicit screening at each visit ^[15]
• All-cause mortality data specific to tardive akathisia are limited; mortality in tardive syndromes overall is driven primarily by the underlying psychiatric illness and its comorbidities ^[14]

Severe tardive akathisia is a psychiatric emergency in its own right, primarily because of its link to suicidality and to medication nonadherence with downstream relapse.

Hospitalization criteria

• Active suicidal ideation with intent or plan, particularly when attributed by the patient to the restlessness itself ^[15]
• Severe sleep deprivation and inability to perform basic self-care ^[2]
• Behavioral disorganization preventing safe outpatient management ^[1]

Suicide risk assessment

• Screen every patient with tardive akathisia for suicidal ideation using a structured tool at each visit ^[15]
• Document the contribution of restlessness to suicidal ideation; this distinction informs whether the priority intervention is symptomatic relief or treatment of comorbid depression ^[15]
• Means restriction, safety planning, and rapid follow-up are standard components ^[15]

Acute management

• Avoid increasing the offending antipsychotic; this is the most common iatrogenic error in the emergency setting ^[1,15]
• For severe distress, a short course of a benzodiazepine (clonazepam or lorazepam) can provide rapid relief while definitive management is initiated ^[22]
• Propranolol can be initiated at 10 mg PO TID with titration as tolerated ^[10,22]
• For patients on a high-risk agent, plan a deliberate switch to a lower-risk antipsychotic with the receiving outpatient team ^[1,17]

Safety-relevant comorbidities

• Comorbid depression with active suicidal ideation requires escalation to inpatient care if not safely manageable as outpatient ^[15]
• Active substance use, especially stimulants, can precipitate severe akathisia and warrants concurrent substance use treatment ^[1]

Several clinically relevant questions remain unsettled, and clinicians should be explicit with patients about the limits of current evidence.

Diagnostic boundaries

• The dividing line between chronic acute akathisia, withdrawal akathisia, and tardive akathisia is operationalized by duration thresholds that vary across diagnostic frameworks; this affects prevalence estimates and trial inclusion ^[1,12]
• Pseudoakathisia (objective movement without subjective component) remains contested as a separate entity versus a phenotype of chronic exposure ^[1]

Treatment evidence

• VMAT2 inhibitor approval is restricted to tardive dyskinesia; off-label use in tardive akathisia is supported by mechanism and case-level evidence but lacks dedicated randomized trial data ^[17-18]
• Whether switching antipsychotic class meaningfully alters the course of established tardive akathisia, or only prevents progression, remains uncertain outside the clozapine literature ^[1,24]
• The role of partial dopamine agonists (aripiprazole, brexpiprazole, cariprazine) in patients with established tardive akathisia is contested; case reports of both improvement and worsening exist ^[3-4]

Regulatory and access considerations

• VMAT2 inhibitor cost and insurance coverage are practical barriers; not all eligible patients can access them ^[17-18]
• Antiemetic dopamine blockers (metoclopramide) remain widely prescribed without consistent documentation of cumulative exposure, complicating risk stratification ^[8]

Long-term safety

• Long-term safety of VMAT2 inhibitors beyond two to three years is being characterized in post-marketing studies; particular attention to depression and parkinsonism is warranted ^[17-18]
• Whether tardive akathisia carries the same long-term mortality signal as severe tardive dyskinesia is not established ^[14]

• Tardive akathisia is defined by delayed onset (at least three months of cumulative dopamine receptor blocking agent exposure, one month if older than 60) and persistence beyond one month after the offending agent is withdrawn or reduced.^[1,12]
• Paradoxical worsening of akathisia on dose reduction of the offending antipsychotic is a near-pathognomonic feature of the tardive variant.^[1,12]
• Akathisia is independently associated with suicidal ideation and completed suicide; ask about suicide at every visit when akathisia is present.^[15]
• The Barnes Akathisia Rating Scale (BARS) is the standard instrument and captures objective restlessness, subjective awareness, subjective distress, and global clinical assessment.^[19]
• A BARS global score of 2 or higher indicates clinically meaningful akathisia.^[19]
• Aripiprazole has the highest akathisia signal among second-generation antipsychotics; clozapine and quetiapine have the lowest.^[3-4,24]
• Dopamine-blocking antiemetics, especially metoclopramide and prochlorperazine, are underrecognized causes of tardive syndromes including akathisia.^[8]
• VMAT2 inhibitors (valbenazine, deutetrabenazine) are FDA-approved for tardive dyskinesia and are first-line for moderate-to-severe persistent tardive akathisia based on shared pathophysiology.^[17-18]
• Propranolol 10-40 mg PO TID is first-line for acute akathisia and is commonly extrapolated to tardive akathisia, with limited dedicated evidence.^[10,22]
• Anticholinergics are generally ineffective for akathisia and may worsen coexisting tardive dyskinesia.^[1,22]
• Switching to clozapine has the most robust antipsychotic-switch evidence for tardive syndromes.^[24]
• Iron deficiency (ferritin below 50 ng/mL) is associated with akathisia severity and is correctable.^[10]
• Restless legs syndrome has a circadian (evening/nighttime) pattern; akathisia is constant during waking hours and improves with sleep.^[10]
• ICD-11 places drug-induced akathisia in chapter 08 (nervous system) rather than the mental disorders chapter.^[13]
• Coexisting tardive dyskinesia is common and predicts a more chronic course; examine for it with AIMS at every visit.^[1,20]

No external funding. No conflicts of interest declared. Peer-review status: pending.