Formulary
Haloperidol: Uses, Dosing, Side Effects and Indian Brand Names
Haloperidol is a high-potency typical antipsychotic that blocks D2 receptors. It is first-line for acute psychosis and delirium but causes significant extrapyramidal side effects and carries the risk of neuroleptic malignant syndrome.
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Clinically reviewed by Awaiting clinical review
Haloperidol: Uses, Dosing, Side Effects and Indian Brand Names
Haloperidol is a high-potency typical antipsychotic that blocks D2 receptors. It is first-line for acute psychosis and delirium but causes significant extrapyramidal side effects and carries the risk of neuroleptic malignant syndrome.
NEET PG High-Yield: Haloperidol is the drug of choice for Tourette syndrome and delirium. Neuroleptic malignant syndrome (NMS) triad: hyperthermia + rigidity + elevated CPK -- treated with dantrolene and bromocriptine. High-potency antipsychotics like haloperidol cause MORE EPS but LESS sedation and anticholinergic effects than low-potency agents like chlorpromazine (the potency-side effect inverse rule).
Clinical overview
Haloperidol is a high-potency typical antipsychotic and one of the most widely used first-generation antipsychotics in India, particularly in acute psychiatric emergencies. It is the drug of choice for acute psychosis, delirium (including ICU delirium), and Tourette syndrome. Its high D2 receptor affinity makes it highly effective against positive symptoms of schizophrenia (hallucinations, delusions, thought disorder) but it is poorly effective against negative symptoms (flat affect, social withdrawal, anhedonia). The major drawback of haloperidol is its propensity to cause extrapyramidal side effects (EPS) -- acute dystonia, akathisia, parkinsonism, and tardive dyskinesia with chronic use. Acute dystonia (oculogyric crisis, torticollis, opisthotonus) typically occurs within hours to days of initiation and is treated with IV/IM anticholinergics (promethazine or trihexyphenidyl). Neuroleptic malignant syndrome (NMS) is a rare but life-threatening idiosyncratic reaction characterised by hyperthermia, lead-pipe rigidity, autonomic instability, and elevated CPK. Treatment of NMS includes stopping the drug, cooling, dantrolene, and bromocriptine. In Indian psychiatry, haloperidol remains widely used due to its low cost, effectiveness in acute agitation, and availability in injectable form. It is available in depot formulation (haloperidol decanoate) for maintenance therapy in non-compliant patients.
Pharmacological class
Haloperidol belongs to the Typical (first-generation) antipsychotic (butyrophenone derivative) class. Haloperidol is a potent antagonist at dopamine D2 receptors in the mesolimbic and mesocortical pathways, which mediates its antipsychotic effect. It blocks D2 receptors in the nigrostriatal pathway (causing extrapyramidal side effects), tuberoinfundibular pathway (causing hyperprolactinaemia), and the chemoreceptor trigger zone (antiemetic effect). It has weak anticholinergic and alpha-adrenergic blocking activity compared to chlorpromazine.
Indian brand names and formulations
Available as: Serenace (RPG Life Sciences), Trancodol (Torrent Pharmaceuticals), Haloperidol (Various generic manufacturers), Senorm (Intas Pharmaceuticals).
Tablets (0.25 mg, 1.5 mg, 5 mg, 10 mg), Oral drops (2 mg/mL), Injection (5 mg/mL for IM/IV), Depot injection -- haloperidol decanoate (50 mg/mL for IM, given monthly)
Regulatory status
Haloperidol is classified under Schedule H in India under the Drugs and Cosmetics Act, 1940. Schedule H prescription-only drug. Parenteral haloperidol is commonly used in psychiatric emergencies and ICU settings across India. Included in the NLEM 2022.
Indications
- Acute psychosis and schizophrenia (positive symptoms)
- Acute agitation and violent behaviour (IM rapid tranquillisation)
- Delirium (drug of choice, including ICU delirium)
- Tourette syndrome (drug of choice for severe tics)
- Huntington's chorea
- Intractable hiccups
- Nausea and vomiting (second-line antiemetic, especially post-operative)
- Mania (acute management)
Dosing
Acute psychosis: 5-10 mg IM/IV, may repeat every 30-60 minutes (max 20 mg/day in acute setting). Oral: 1.5-5 mg BD-TDS, titrate to 15-20 mg/day. Delirium: 0.5-2 mg IV every 4-6 hours. Tourette syndrome: 0.25-0.5 mg/day initially, titrate slowly. Depot (decanoate): 50-200 mg IM every 4 weeks for maintenance. Elderly: start at lowest dose (0.5-1 mg).
Contraindications
- Parkinson's disease (worsens by D2 blockade)
- Severe CNS depression or comatose states
- Known QT prolongation or history of torsades de pointes
- Lewy body dementia (extreme sensitivity to antipsychotics)
- Phaeochromocytoma (risk of hypertensive crisis)
Adverse effects
- Extrapyramidal side effects -- acute dystonia, akathisia, parkinsonism, tardive dyskinesia
- Neuroleptic malignant syndrome (hyperthermia, rigidity, autonomic instability, elevated CPK)
- Hyperprolactinaemia (galactorrhoea, amenorrhoea, gynaecomastia, sexual dysfunction)
- QT prolongation and risk of torsades de pointes (especially with IV use)
- Sedation (less than chlorpromazine)
- Weight gain (less than atypical antipsychotics)
- Anticholinergic effects (minimal compared to low-potency typical antipsychotics)
Drug interactions
- Drugs prolonging QT interval (amiodarone, quinidine, macrolides) -- additive risk of torsades de pointes
- Anticholinergic drugs -- may mask early signs of tardive dyskinesia
- Levodopa/dopamine agonists -- mutual antagonism (avoid combination)
- Lithium -- increased risk of neurotoxicity and NMS-like syndrome
- CYP3A4 and CYP2D6 inhibitors -- increased haloperidol levels
- CNS depressants (alcohol, opioids) -- additive sedation
Pregnancy and lactation
Category C. Limited human data; used when necessary for severe psychosis in pregnancy. Small increased risk of limb defects reported in early studies but not confirmed in larger datasets. Neonatal EPS and withdrawal symptoms may occur if used in the third trimester. Preferred over atypical antipsychotics in some guidelines due to longer safety experience.
Exam-style clinical scenario
A 30-year-old man on haloperidol for schizophrenia develops sudden-onset neck twisting to one side, tongue protrusion, and upward deviation of both eyes within 48 hours of starting the drug. What is the diagnosis and treatment? Answer: This is acute dystonia (oculogyric crisis + torticollis), an extrapyramidal side effect of haloperidol occurring early in treatment. Immediate treatment is IV/IM promethazine (25-50 mg) or benztropine (1-2 mg IV). The anticholinergic restores the dopamine-acetylcholine balance in the basal ganglia. Risk factors include young males, high-potency antipsychotics, and first exposure.
Cost in India
INR 10-25 per strip of 10 tablets (5 mg); Injection: INR 10-30 per ampoule (5 mg/mL)
Clinical governance
Author: MedNext Editorial Team. Clinical reviewer: Awaiting clinical review. Jurisdiction: India (Drugs and Cosmetics Act, 1940). Sources: CIMS India, Indian Pharmacopoeia. Publication state: Awaiting clinical review. Correction: Report errors at support@mednext.academy.
Frequently Asked Questions
What is the difference between acute dystonia, akathisia, and tardive dyskinesia?
Acute dystonia occurs within hours to days (sustained muscle contractions -- torticollis, oculogyric crisis); treated with anticholinergics. Akathisia occurs within days to weeks (subjective restlessness, inability to sit still); treated with propranolol or benzodiazepines. Tardive dyskinesia occurs after months to years of chronic use (involuntary choreoathetoid movements of face, tongue, lips); often irreversible, treated by switching to clozapine.
Why is haloperidol preferred for delirium over benzodiazepines?
Haloperidol reduces agitation and psychotic symptoms without significantly depressing respiration or worsening confusion (unlike benzodiazepines which can paradoxically worsen delirium, especially in the elderly). The exception is delirium tremens (alcohol withdrawal delirium), where benzodiazepines are the treatment of choice because the underlying pathology is GABA withdrawal.
How does neuroleptic malignant syndrome differ from serotonin syndrome?
NMS features lead-pipe rigidity, very high fever (>40 degrees C), autonomic instability, and markedly elevated CPK; onset is gradual (days). Serotonin syndrome features clonus, hyperreflexia, tremor, myoclonus, agitation, and diarrhoea; onset is rapid (hours). NMS is caused by D2 blockade; serotonin syndrome by serotonin excess. NMS is treated with dantrolene/bromocriptine; serotonin syndrome with cyproheptadine.
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