Dystonia

Dystonia is a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both.^[1] Dystonic movements are typically patterned and twisting, sometimes tremulous, and it is the sustained twisted posture itself — not simply "abnormal movement" in general — that is the key to recognizing dystonia at the bedside.^[2] Movements are classically absent at rest, triggered or worsened by voluntary action, often somewhat better earlier in the day, and frequently eased by a sensory trick (geste antagoniste) — a light touch to the affected body part that transiently interrupts the abnormal muscle activity.^[2]

Current international consensus classifies dystonia along two axes.^[1] Axis I — clinical characteristics covers age at onset, body distribution, temporal pattern, and associated features. By distribution: focal dystonia affects a single body region — cervical dystonia (the neck), blepharospasm (the eyelids), oromandibular dystonia (the jaw), spasmodic dysphonia (the vocal cords), or a task-specific limb dystonia such as writer's cramp; segmental dystonia affects two or more contiguous regions; multifocal affects two or more non-contiguous regions; generalized dystonia affects the trunk plus at least two other regions; and hemidystonia affects one side of the body only, a pattern that should specifically prompt brain imaging for a structural secondary cause.^[2][1] Axis II — etiology spans nervous system pathology and inheritance (inherited, acquired, or idiopathic), with acquired causes including drug exposure, perinatal injury, infection, structural lesions, toxins, vascular disease, and trauma.^[1][2]

Onset pattern tracks with etiology in a genuinely useful way at the bedside: dystonia beginning in adulthood is usually primary and tends to stay focal, while dystonia beginning in childhood is usually secondary and is more likely to be — or become — generalized.^[2]

Chronic focal dystonia — the presentations pharmacists see most often

Acute dystonic reaction — the high-yield, pharmacist-relevant emergency

The acute dystonic reaction is an idiosyncratic, drug-induced movement disorder triggered by any dopamine D2 receptor-blocking drug, arising from the resulting dopaminergic-cholinergic imbalance in the basal ganglia. It is most strongly associated with first-generation (typical) antipsychotics — reported in roughly 10.5% of exposed patients, versus about 2.2% with second-generation (atypical) agents — and is also well documented with the antiemetics metoclopramide (approximately 8.3% in adults) and prochlorperazine (approximately 4%).^[3] Onset is fast: symptoms typically emerge within 96 hours of starting the drug or increasing its dose, and risk is highest in young patients, male patients, those with a prior dystonic reaction, and those with reduced CYP2D6 metabolizer status.^[3]

The presentation is dramatic and genuinely frightening for the patient: oculogyric crisis (a sustained, involuntary upward-and-lateral deviation of the eyes), torticollis, trismus (jaw clenching/lockjaw), blepharospasm, and — the presentation that matters most — laryngospasm/pharyngeal dystonia, which can progress to airway compromise. Patients are typically anxious and in real distress but remain fully alert; this combination of severe involuntary posturing with a clear sensorium in a patient recently started or increased on a dopamine-blocking drug is the pattern to recognize.^[3]

Tardive dystonia — a distinct, late, often-persistent complication

Tardive dystonia is a form of tardive syndrome: a persistent and potentially disabling movement disorder that emerges only after prolonged exposure to antipsychotics or other dopamine-receptor-blocking drugs.^[4] Unlike the acute dystonic reaction, which appears within days of starting or increasing the offending drug and resolves rapidly with an anticholinergic, tardive dystonia develops after months to years of cumulative exposure, can persist — sometimes permanently — even after the causative drug is stopped, and, critically, is not reliably treated with the anticholinergic drugs used for the acute reaction (see Choose Initial Treatment).^[4] Correctly identifying which of these two timelines a patient is on is the single most important diagnostic branch point in this chapter.

• Adult-onset dystonia is usually primary/idiopathic and tends to remain focal; childhood-onset dystonia is usually secondary and is more likely to generalize — age at onset is one of the most useful prognostic clues available at the bedside.^[2]
• A family history or a known genetic cause (inherited dystonia) — Axis II of the current classification framework explicitly separates inherited, acquired, and idiopathic dystonia, and early-onset generalized dystonia in particular should prompt genetic evaluation.^[1]
• Any dopamine D2 receptor-blocking drug — the largest modifiable risk factor in this entire chapter. First-generation antipsychotics carry the highest acute dystonic reaction risk (approximately 10.5%), followed by metoclopramide (approximately 8.3%) and prochlorperazine (approximately 4%); second-generation antipsychotics carry a lower but genuinely non-zero risk (approximately 2.2%).^[3]
• Male sex, younger age, a prior acute dystonic reaction, and reduced CYP2D6 metabolizer status all independently raise acute dystonic reaction risk.^[3]
• Cumulative, prolonged exposure to a dopamine-receptor-blocking drug — the specific risk driver for tardive dystonia, distinct from the acute reaction's dose-change trigger.^[4]
• A structural brain lesion, perinatal injury, prior stroke, infection, or toxin exposure — recognized causes of secondary dystonia, and specifically the reason hemidystonia (one side of the body only) warrants brain imaging.^[2][1]
• An underlying degenerative or genetic neurologic disease in which dystonia is one feature among several — evaluate for additional neurologic features rather than treating the dystonia in isolation.^[1]

Dystonia is a clinical diagnosis

There is no laboratory test or single imaging study that confirms dystonia; the diagnosis rests on recognizing the phenomenology described in Recognize the Condition — sustained or intermittent contractions producing a patterned, often twisting posture, triggered or worsened by action, and often eased by a sensory trick.^[2][1]

The first and most urgent diagnostic branch: timeline and drug exposure

Before classifying a patient's dystonia by body distribution, establish two facts: (1) has any dopamine-receptor-blocking drug been started or increased in the past hours to days, and (2) has the patient had prolonged (months-to-years) cumulative exposure to such a drug? These two questions separate the acute dystonic reaction and tardive dystonia from primary/idiopathic chronic dystonia, and each of the three requires different management (see Clinical Decision Algorithm).

Differential diagnosis of the acute presentation

Acute dystonic reactions are genuinely easy to misdiagnose, particularly when a medication history is not volunteered or not specifically asked about. Reports describe patients initially diagnosed with a seizure, meningitis, tetanus, or an unclear brain process before the correct diagnosis was reached.^[3] A directed medication history — any new antipsychotic, antiemetic, or other dopamine-blocking drug — is the single most useful diagnostic step, and response to an anticholinergic trial is itself both diagnostic and therapeutic (see Choose Initial Treatment).

Psychogenic (functional) dystonia — a genuine and difficult mimic

Dystonia, and the distress that accompanies an acute dystonic reaction in particular, is often misread as hysterical or psychiatric in origin — while true psychogenic dystonia is itself uncommon and genuinely hard to diagnose.^[5] A Canadian case series of 18 patients found the clinical characteristics of psychogenic dystonia to be inconsistent or incongruous with established forms of organic dystonia: onset was abrupt with rapid progression, often to fixed dystonic postures; leg involvement was common despite adult-life onset, atypical for organic dystonia; paroxysmal worsening occurred in the majority; and pain was a prominent feature in most patients.^[5] Do not use a "looks psychiatric" impression alone to withhold or delay treatment from a patient having a genuine acute dystonic reaction.

Investigations

Investigations are targeted, not routine, and exist mainly to identify a secondary cause or exclude a mimic rather than to "confirm" dystonia itself.

• Brain MRI — indicated for hemidystonia, any focal neurologic deficit, an atypical or rapidly progressive course, or childhood-onset generalized dystonia without a clear cause, to look for a structural secondary lesion.^[2]
• Genetic testing — considered for early-onset generalized dystonia, particularly with a family history, consistent with the inherited/acquired/idiopathic distinction built into the current classification framework.^[1]
• Medication and exposure history — the single most important "investigation" in this entire chapter: a careful, specific review of every dopamine-receptor-blocking drug (antipsychotics, metoclopramide, prochlorperazine) and its timing relative to symptom onset.^[3]
• Creatine kinase and renal function are reasonable to check in any patient with severe, diffuse, or prolonged dystonic contraction, given the general risk of muscle injury from sustained involuntary contraction.
• Routine bloodwork, EEG, and lumbar puncture are not needed to diagnose a typical acute dystonic reaction or typical focal dystonia, and reflexively pursuing them can delay the anticholinergic trial that both treats the acute reaction and helps confirm the diagnosis.

• Recognize and treat the acute dystonic reaction rapidly — anticholinergics work within minutes, and speed genuinely changes both how much the patient suffers and how much unnecessary escalation (unneeded testing, misdiagnosis-driven delay) occurs.
• Protect the airway proactively whenever laryngeal or pharyngeal involvement is possible, rather than waiting for overt respiratory distress.
• Correctly distinguish the acute dystonic reaction from tardive dystonia before choosing a drug — the two conditions require different, and in one respect opposite, pharmacotherapy.
• Provide effective, sustained symptom control for chronic focal dystonia (cervical dystonia, blepharospasm, writer's cramp) with botulinum toxin as first-line therapy, redosed on an appropriate interval.
• Reserve oral agents (anticholinergics, baclofen, benzodiazepines) for generalized/segmental dystonia or for focal disease inadequately controlled by botulinum toxin, titrating to the lowest effective dose given their genuine adverse-effect burden.
• For tardive dystonia: use a VMAT2 inhibitor, not an anticholinergic, and involve the prescriber in reassessing the causative antipsychotic.
• Prevent recurrence — of the acute reaction with an oral anticholinergic taper, and of tardive dystonia by using the lowest effective antipsychotic dose and monitoring for early signs.
• Support the genuine quality-of-life goals (return to work, driving, reading, social functioning) that chronic focal dystonia disrupts, alongside movement control itself.

Acute dystonic reaction — treat now, then prevent recurrence

First step, every time assess the airway before anything else — stridor, marked dysphonia, dyspnea, or difficulty handling secretions means laryngeal/pharyngeal dystonia, and emergency airway support must be arranged in parallel with (not instead of) giving the anticholinergic.^[3] No airway compromise give benztropine 1-2 mg IV or IM, or diphenhydramine 50 mg IV or IM (pediatric: 1 mg/kg up to 50 mg); both are equally effective first-line choices, and symptoms usually improve or resolve dramatically within 10-30 minutes.^[3] May repeat the dose once at 15-30 minutes if the response is inadequate.^[3] After acute resolution start an oral anticholinergic taper — benztropine 1-2 mg PO twice daily for 2-3 days, or diphenhydramine 25 mg PO four times daily for 24-72 hours — since dystonia commonly recurs once the parenteral dose wears off, particularly if the causative drug is continued.^[3] Always discuss discontinuing or switching the causative agent with the prescriber where clinically feasible; if it must be continued (for example, an antipsychotic that is otherwise working well psychiatrically), a scheduled prophylactic oral anticholinergic is a reasonable next discussion rather than repeated emergency visits.

Chronic focal and segmental dystonia — botulinum toxin first-line

Cervical dystonia, blepharospasm, writer's cramp, and most other focal dystonias botulinum toxin injection into the affected muscles is first-line therapy, ahead of oral agents, for essentially all patients able to access it.^[7] Injections are individualized — dose is not fixed but titrated to each patient's specific pattern of muscle involvement and response — and re-treatment should not be given sooner than 12 weeks from the prior injection, both to match the interval used in the placebo-controlled cervical dystonia trials and to limit the risk of neutralizing-antibody formation with more frequent dosing.^[7] For cervical dystonia specifically, published dosing for abobotulinumtoxinA is an initial 500 U divided intramuscularly among the affected muscles, with re-treatment doses of 250-1,000 U at intervals of no less than 12 weeks; onabotulinumtoxinA doses across controlled cervical dystonia trials have ranged from as low as 17 U to as high as 240 U, again individualized rather than fixed.^[7][8] Products are not unit-interchangeable onabotulinumtoxinA, abobotulinumtoxinA, incobotulinumtoxinA, prabotulinumtoxinA, and letibotulinumtoxinA each have their own dosing scale — confirm exactly which product a patient has been receiving before assuming a dose translates from one to another.

Inadequate response to botulinum toxin reassess muscle selection and injection technique (EMG or ultrasound guidance can help target deep or hard-to-localize muscles) before assuming treatment failure, then consider adding an oral agent (trihexyphenidyl or baclofen) or referral for the generalized/refractory-disease pathway below.

Generalized or refractory dystonia — oral agents, then specialist referral

Oral pharmacotherapy a trial of an anticholinergic (trihexyphenidyl, titrated slowly from a low starting dose — children and young adults typically tolerate substantially higher doses than older adults), baclofen, or a benzodiazepine (as an adjunct, not monotherapy) is reasonable for generalized or segmental dystonia, or for focal dystonia inadequately controlled by botulinum toxin.^[2] These oral agents carry a genuine anticholinergic and sedative burden, particularly in older adults, and should be titrated to the lowest effective dose. Refractory to oral therapy refer to a movement disorders specialist for deep brain stimulation candidacy assessment — outcomes vary widely by underlying cause, with the best results generally seen in primary/inherited dystonia without structural brain change and more modest results in dystonia secondary to a fixed structural brain injury.^[9]

Tardive dystonia — a different drug, and a genuinely important warning

Do not use anticholinergics they are appropriate for drug-induced parkinsonism and for the acute dystonic reaction, but are not recommended for tardive syndromes and may even worsen them.^[4] First-line in Canada tetrabenazine, a VMAT2 inhibitor Health Canada has approved for hyperkinetic movement disorders including tardive dyskinesia; movement disorder specialists extend the same drug to tardive dystonia given the shared underlying mechanism and drug class.^[6] Start low (12.5 mg PO twice or three times daily) and titrate slowly — by no more than 12.5 mg/day at weekly intervals — to the lowest effective, tolerated dose; most patients land at a maximal tolerated dose of about 25 mg three times daily, though the product monograph describes rare cases needing up to 200 mg/day.^[6] Not available in Canada valbenazine and deutetrabenazine are VMAT2 inhibitors approved specifically for tardive dyskinesia, with generally favourable comparative safety data, but neither is Health Canada-approved or stocked in Canadian pharmacies — a pharmacist may still encounter them on a cross-border or transferred prescription and should recognize the drug class rather than assume an error.^[10] Alongside drug therapy involve the prescriber in reassessing the causative antipsychotic — a dose reduction or a switch to a lower-risk agent, where psychiatrically safe to do so — since ongoing exposure to the causative drug class works against recovery.

• Sensory tricks (geste antagoniste) — many patients with cervical dystonia or other focal dystonias can find their own light touch or posture (for example, a touch to the chin or cheek) that transiently reduces the abnormal posture; encourage patients to find and use their own trick as a genuine, no-cost adjunct to drug therapy, not a curiosity.^[2]
• Physical and occupational therapy — stretching, postural retraining, and task modification (for example, adaptive writing tools for writer's cramp) support drug therapy, particularly between botulinum toxin cycles.
• Deep brain stimulation for generalized or severely disabling dystonia refractory to oral therapy — a genuine, recognized option, with outcomes that vary meaningfully by cause: generally better in primary/inherited dystonia without structural brain change, more modest in dystonia secondary to a fixed structural injury. Cervical dystonia and tardive dystonia are also recognized candidate indications for carefully selected patients.^[9] This decision is made by a movement disorders specialist and neurosurgical team, not initiated in general practice.^[9]
• Intrathecal baclofen — a pump-delivered option specifically for severe generalized dystonia, particularly of secondary/structural cause, when oral baclofen is inadequate or not tolerated at the doses needed.
• Avoid abrupt discontinuation of any chronic anticholinergic, baclofen, or benzodiazepine regimen — taper deliberately to avoid withdrawal effects (including, for baclofen, a withdrawal syndrome that can include seizures).
• For the acute dystonic reaction specifically: reassure the patient throughout — they are fully alert and often frightened by involuntary movements they cannot control, and clearly communicating that this is a known, treatable drug effect (not a seizure or a psychiatric event) is itself part of the treatment.
• Keep a clear, written record of exactly which drug caused an acute dystonic reaction, in the patient's allergy/intolerance record, to prevent inadvertent re-exposure — a genuinely preventable repeat event.

Children

Children tolerate high-dose oral anticholinergic therapy (trihexyphenidyl) for generalized dystonia substantially better than adults, making it a genuinely useful option in this population where adults would be limited by cognitive and anticholinergic side effects.^[2] Childhood-onset dystonia is more often secondary and prone to generalize, so investigate for an underlying cause more readily than in an adult with new focal dystonia.^[2] For acute dystonic reactions, dose diphenhydramine at 1 mg/kg IV/IM up to a 50 mg maximum.^[3] Tetrabenazine dosing under 18 years has not been established through adequately controlled trials; limited clinical experience suggests starting at roughly half the adult dose and titrating slowly and carefully according to tolerance and individual response.^[6]

Older adults

Anticholinergic drugs (benztropine, diphenhydramine, trihexyphenidyl) carry a disproportionate burden in older adults — confusion, falls, constipation, urinary retention, and a well-recognized contribution to anticholinergic cognitive load — so use the lowest effective dose and taper promptly once the acute indication has resolved. Tetrabenazine's pharmacokinetics have not been systematically evaluated in patients over 65; clinical experience favours a reduced initial and maintenance dose, since parkinsonian-like adverse effects are relatively common in this group and can be dose-limiting.^[6]

Pregnancy and breastfeeding

Tetrabenazine is not recommended during pregnancy or in patients of childbearing potential not using contraception, based on animal reproductive toxicity findings and the absence of adequate human safety data; it should also be avoided during breastfeeding, since it is excreted in milk.^[6] Botulinum toxin use in pregnancy is generally reserved for situations where the benefit clearly outweighs any theoretical risk, decided case by case with the prescriber. Discuss anticholinergic use in pregnancy or breastfeeding case by case with the prescriber given limited dedicated safety data for this specific indication.

Hepatic impairment

Tetrabenazine is contraindicated in hepatic impairment of any degree — plasma concentrations of its active metabolites rise markedly (peak concentrations 7- to 190-fold higher than in patients with normal liver function in the studied population), and there is no established way to adjust the dose safely for this increased exposure.^[6]

Renal impairment

No dedicated tetrabenazine dose adjustment is described for renal impairment in the Canadian product monograph; use standard clinical judgment and monitor for accumulation of anticholinergic and sedative adverse effects, which can be more pronounced with reduced clearance of other concomitant drugs.^[6]

CYP2D6 poor metabolizers and drug interactions

Tetrabenazine's active metabolites are principally cleared by CYP2D6; poor metabolizers, or patients on a strong CYP2D6 inhibitor (for example, fluoxetine, paroxetine, quinidine, bupropion, or terbinafine), have substantially increased exposure — roughly 3- to 10-fold increases across its two active metabolites with a strong inhibitor on board — and need a lower starting and maintenance dose.^[6] Tetrabenazine is contraindicated with MAOIs (allow at least 14 days between stopping one and starting the other) and with reserpine (allow at least 20 days after stopping reserpine), and should be avoided with other QT-prolonging drugs, including many antipsychotics.^[6] Reduced CYP2D6 metabolizer status is also an independent risk factor for the acute dystonic reaction itself.^[3]

For the acute dystonic reaction: follow up specifically to confirm the oral anticholinergic taper is being taken and completed, since recurrence once a single parenteral dose wears off is common, particularly if the causative drug is continued.^[3] Document the causative drug clearly in the patient's allergy/intolerance record so it is flagged before any future re-exposure.

For chronic focal dystonia on botulinum toxin: track response and duration of benefit at each visit, since both the interval between injections (no sooner than 12 weeks) and the dose may need individual adjustment over time.^[7] A pattern of shortening benefit or declining response despite dose increases should prompt reassessment for secondary non-response — including neutralizing antibodies — rather than simply escalating the dose further.

For tardive dystonia on tetrabenazine: monitor specifically for new or worsening depression and suicidal ideation at every visit — informing the patient and their caregivers of this risk up front, and instructing them to report concerning changes promptly, is a labelled expectation of therapy, not an optional add-on.^[6] Also monitor for sedation (the most common dose-limiting effect), parkinsonism, akathisia, and orthostatic symptoms, and periodically reassess the need for continued therapy alongside the underlying psychiatric condition and its own medications.^[6]

For any patient on a chronic anticholinergic or baclofen regimen: periodically reassess whether the dose remains the lowest effective one, particularly as patients age into a higher-risk group for anticholinergic burden.

1. Acute dystonic reaction not improving within 30 minutes of a first anticholinergic dose: give a second dose (benztropine or diphenhydramine) rather than switching agents or simply waiting longer, and reassess the airway again at each step.^[3]
2. Recurrent dystonic posturing after apparent resolution of an acute reaction: this usually means the oral taper was not started, was inadequate, or the causative drug was continued unchanged — confirm all three before assuming a new problem.
3. A presentation that looks like an acute dystonic reaction but does not respond at all to an anticholinergic trial: reconsider the diagnosis — a seizure, a primary psychiatric event, or true psychogenic dystonia are all real alternatives that have been reported to mimic this presentation.^[3][5]
4. Botulinum toxin with declining or absent benefit despite an adequate, individualized dose and correct muscle selection: consider secondary non-response (including neutralizing antibodies), and discuss a change of product (for example, to a formulation without complexing proteins) or of injection technique (EMG/ultrasound guidance) with the treating specialist, rather than simply repeating the same regimen.
5. Generalized dystonia inadequately controlled despite an adequate trial of oral agents: refer for deep brain stimulation candidacy assessment rather than continuing to escalate oral doses into a burdensome adverse-effect range.^[9]
6. Tardive dystonia not improving on an adequate tetrabenazine trial: confirm the antipsychotic dose has genuinely been minimized or switched where psychiatrically feasible, reconfirm the diagnosis is tardive dystonia rather than an evolving acute reaction or another movement disorder, and escalate to a movement disorders specialist — do not add an anticholinergic to try to "boost" the response, since this is the specific error most likely to worsen the syndrome.^[4]

• Treating tardive dystonia with an anticholinergic because "it worked for the last dystonia this patient had" — this is the single most important error in this chapter; anticholinergics are appropriate for the acute reaction and not for tardive syndromes, which they may worsen.^[4]
• Missing laryngeal/pharyngeal involvement in an acute dystonic reaction because the patient's limb or neck posturing is the most visually obvious finding — always specifically ask about and assess for stridor, dysphonia, and dyspnea.^[3]
• Assuming an acute dystonic reaction is a seizure, a primary psychiatric event, or "attention-seeking" because the presentation looks dramatic and the patient remains fully alert — alertness with severe involuntary posturing is precisely the pattern that should raise, not lower, suspicion for a dystonic reaction.^[3]
• Stopping at a single parenteral anticholinergic dose and sending the patient home without an oral taper — recurrence once the parenteral dose wears off is common, especially if the causative drug is continued.^[3]
• Reflexively escalating a botulinum toxin dose, or re-injecting sooner than 12 weeks, when response seems inadequate, rather than first reassessing muscle selection/technique or considering secondary non-response.^[7]
• Assuming botulinum toxin products are interchangeable unit-for-unit between brands — they are not.
• Starting tetrabenazine without asking about a personal history of depression or suicidality, or without setting the expectation of monitoring for this specific, labelled risk.^[6]
• Using tetrabenazine in a patient with any degree of hepatic impairment — this is a contraindication, not a relative caution.^[6]
• Dismissing a genuinely bizarre-looking movement presentation as purely psychogenic without a careful history and examination — true psychogenic dystonia exists but is uncommon and difficult to diagnose, and organic dystonia (including the acute drug-induced reaction) is far more often the real explanation.^[5]
• Forgetting that childhood-onset dystonia is usually secondary and prone to generalize — treating a child's new dystonia exactly like an adult's new focal dystonia risks missing an underlying cause.^[2]

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

Acute Dystonic Reaction — Emergency Anticholinergics and Oral Taper

Give the parenteral dose without delay once an airway assessment is complete; follow with an oral taper to prevent recurrence once the causative drug's effect has worn off.

Botulinum Toxin Products — First-Line for Chronic Focal Dystonia

Individualized dosing based on muscle involvement and response; re-treatment no sooner than 12 weeks from the prior injection. Products are not unit-interchangeable — confirm exactly which product a patient has received before assuming a dose translates from one to another.

Oral Pharmacotherapy — Generalized or Segmental Dystonia, or Botulinum Toxin-Inadequate Focal Disease

Second-line to botulinum toxin for focal/segmental dystonia; first-line oral options for generalized disease. Titrate to the lowest effective dose given the genuine anticholinergic/sedative burden of this class.

Tardive Dystonia — VMAT2 Inhibitors (NOT Anticholinergics)

Anticholinergics are not recommended here and may worsen tardive syndromes — this class, not the acute-reaction anticholinergics, is first-line. Tetrabenazine is the only Health Canada-approved, Canadian-available option in this class.

Avoid in Tardive Dystonia — the Acute-Reaction Anticholinergics

Listed here specifically because these are the exact drugs used first-line for the acute dystonic reaction (see above) — the single most important contrast to hold onto in this chapter. Do not substitute one of these for a VMAT2 inhibitor in tardive dystonia.