Acute Psychosis in Adults

Quick Reference

Critical Alerts

Critical Alert: SAFETY FIRST: Acute psychosis is a psychiatric emergency requiring immediate assessment of risk to self and others. Staff safety must be maintained at all times with appropriate security presence and environmental precautions.

• Always rule out organic causes first: Up to 10% of patients presenting with apparent psychiatric symptoms have an underlying medical etiology that requires urgent treatment. [1]
• Delirium mimics psychosis: Fluctuating consciousness and attention = NOT primary psychosis. This is the most important distinguishing feature. [2]
• Medical clearance is essential: Check glucose, electrolytes, toxicology screen, and vital signs in ALL patients before psychiatric disposition. [3]
• Never assume "known psychiatric patient": New organic causes may occur in patients with established psychiatric diagnoses. [4]
• Excited delirium syndrome: Can lead to sudden cardiac death - requires immediate intervention with cooling, sedation, and monitoring. [5]
• Duration of Untreated Psychosis (DUP): Shorter DUP correlates with better long-term outcomes; first-episode psychosis is a time-critical diagnosis. [6]

Key Diagnostics

Emergency Treatments

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Definition and Overview

Definition

Acute psychosis is a neuropsychiatric syndrome characterised by a significant disconnection from reality, manifesting through one or more of the following core features:

1. Hallucinations: Perceptions occurring without external stimulus that have the quality of true perception. [7]

• Auditory hallucinations: Most common in primary psychotic disorders (60-80% of schizophrenia patients). Typically third-person running commentary or command hallucinations.
• Visual hallucinations: More suggestive of organic aetiology (delirium, substance intoxication, neurological disease). [2]
• Tactile hallucinations: Characteristic of stimulant psychosis (formication - "bugs crawling under skin").
• Olfactory/gustatory hallucinations: Rare; consider temporal lobe epilepsy or brain tumour.

2. Delusions: Fixed, false beliefs that are not amenable to change in light of conflicting evidence, held with absolute conviction, and are not consistent with the individual's cultural or religious background. [7]

• Paranoid/Persecutory: Belief that one is being followed, monitored, poisoned, or conspired against.
• Grandiose: Inflated sense of power, wealth, knowledge, or identity.
• Referential: Belief that external events, objects, or people have particular significance specifically for the individual.
• Somatic: False belief about body function or structure.
• Thought insertion/withdrawal/broadcasting: Schneiderian first-rank symptoms.

3. Disorganised Thinking (Formal Thought Disorder): [7]

• Tangentiality: Responses drift off topic and never return.
• Loose associations: Shifting between unrelated topics without logical connection.
• Derailment: Gradual deviation from topic.
• Word salad: Incomprehensible speech with preserved grammar.
• Neologisms: Made-up words.
• Clang associations: Word choice governed by sound rather than meaning.

4. Grossly Disorganised or Catatonic Behaviour: [7]

• Disorganised behaviour: Unpredictable agitation, inappropriate affect, bizarre postures.
• Catatonic behaviour: Stupor, mutism, waxy flexibility, posturing, stereotypy, echolalia, echopraxia.

Clinical Significance

Acute psychosis represents a psychiatric emergency requiring rapid assessment, medical stabilisation, and appropriate intervention. The primary goals of emergency management are:

1. Ensure safety of patient, staff, and others
2. Exclude life-threatening medical causes through systematic evaluation
3. Provide symptomatic relief through verbal de-escalation and pharmacological intervention when necessary
4. Establish appropriate disposition for ongoing care

The lifetime prevalence of psychotic experiences in the general population is approximately 5-8%, while the prevalence of psychotic disorders requiring treatment is approximately 3%. [8] Schizophrenia, the most common chronic psychotic disorder, affects approximately 1% of the population worldwide. [9]

Exam Detail: First-Rank Symptoms of Schizophrenia (Schneider): Originally considered pathognomonic but now understood to occur in other conditions including bipolar disorder and organic psychosis:

• Auditory hallucinations: Third-person commentary, thought echo, voices discussing patient
• Thought insertion, withdrawal, or broadcasting
• Passivity experiences: Made actions, feelings, or impulses
• Delusional perception: Normal perception given delusional meaning
• Somatic passivity: External control of bodily functions

Sensitivity: ~60% for schizophrenia Specificity: ~50% (also seen in 10-20% of bipolar disorder)

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Epidemiology

Incidence and Prevalence

Demographics

Age of Onset:

• Males: Peak onset 15-25 years (earlier than females)
• Females: Peak onset 25-35 years (with second peak post-menopause)
• First episode after age 40 strongly suggests organic aetiology [1]

Sex Differences:

• Male:female ratio for schizophrenia approximately 1.4:1 [9]
• Males have earlier onset, more negative symptoms, poorer premorbid functioning
• Females have better treatment response, more affective symptoms

Risk Factors: [10]

• Family history of psychosis (OR 7-10 for first-degree relatives)
• Cannabis use, especially high-potency products in adolescence (OR 3-5)
• Childhood trauma and adversity
• Urban environment and migration
• Obstetric complications
• Developmental delay
• Social isolation

Duration of Untreated Psychosis (DUP)

The interval between onset of psychotic symptoms and initiation of adequate antipsychotic treatment is a critical prognostic factor. [6]

Clinical Pearl: The DUP Paradox: Despite decades of evidence supporting early intervention, the mean DUP remains 12-24 months in most healthcare systems. Barriers include poor illness insight (anosognosia), stigma, prodromal symptoms being misattributed, and access to specialist services.

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Aetiology and Classification

Classification by Aetiology

Primary Psychiatric Disorders

Substance-Induced Psychosis [11]

Exam Detail: Methamphetamine-Induced Psychosis:

• Prevalence: 10-60% of methamphetamine users will experience psychosis [11]
• Typically resolves within 1-2 weeks of abstinence
• ~25% develop persistent psychotic symptoms
• Features indistinguishable from paranoid schizophrenia
• Key history: timeline correlation with substance use
• Treatment: Benzodiazepines preferred first-line; antipsychotics if psychosis persists

Medical/Organic Causes (MUST EXCLUDE) [2,3]

Clinical Pearl: Anti-NMDA Receptor Encephalitis - Don't Miss This Diagnosis:

• Primarily affects young women (80%)
• Often misdiagnosed as psychiatric illness initially
• Classic progression: Prodrome (viral-like illness) → Psychiatric symptoms → Seizures → Movement disorders → Autonomic instability → Decreased consciousness
• Associated with ovarian teratoma (50% of female cases)
• CSF: Lymphocytic pleocytosis, anti-NMDA receptor antibodies
• MRI: Often normal or non-specific (50%)
• CRITICAL: Early immunotherapy dramatically improves outcomes [12]

Medication-Induced Psychosis

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Pathophysiology

Neurobiological Basis of Psychosis

The Dopamine Hypothesis [13]

The dopamine hypothesis remains the cornerstone of psychosis neurobiology, supported by:

1. Antipsychotic efficacy correlates with D2 receptor blockade
2. Dopamine-releasing drugs (amphetamines) produce psychosis
3. Increased dopamine synthesis capacity in striatum demonstrated on PET imaging

Mesolimbic Pathway (Hyperactivity):

• Projects from ventral tegmental area (VTA) to nucleus accumbens and limbic structures
• Hyperactivity → Positive symptoms (hallucinations, delusions)
• Target of antipsychotic medications (D2 receptor blockade)

Mesocortical Pathway (Hypoactivity):

• Projects from VTA to prefrontal cortex
• Hypoactivity → Negative symptoms (flat affect, avolition, anhedonia) and cognitive deficits
• D2 blockade may worsen these symptoms (typical antipsychotics)

Nigrostriatal Pathway:

• Substantia nigra to striatum (motor control)
• D2 blockade → Extrapyramidal side effects (EPS)

Tuberoinfundibular Pathway:

• Hypothalamus to pituitary
• D2 blockade → Hyperprolactinaemia

Exam Detail: The Revised Dopamine Hypothesis (Aberrant Salience): Modern understanding proposes that psychosis results from dysregulated dopamine release leading to aberrant attribution of salience (importance) to otherwise irrelevant stimuli, thoughts, and events. This explains how delusions form - normal stimuli become imbued with inappropriate significance. [13]

Presynaptic Dopamine Dysfunction: PET studies using [18F]DOPA demonstrate increased striatal dopamine synthesis capacity in:

• Schizophrenia (effect size: d = 0.79)
• Prodromal individuals who later transition to psychosis
• First-episode, drug-naïve patients (excluding medication effects)

Glutamate Hypothesis [14]

The glutamate hypothesis proposes NMDA receptor hypofunction as a key mechanism:

Evidence:

• NMDA receptor antagonists (ketamine, PCP) produce psychotic symptoms indistinguishable from schizophrenia, including negative and cognitive symptoms
• Genetic variants in glutamate pathway genes associated with schizophrenia risk
• Anti-NMDA receptor encephalitis causes psychosis

Proposed Mechanism:

• NMDA receptor hypofunction on GABAergic interneurons → Disinhibition of glutamate release → Excitotoxicity in cortical regions → Dopamine dysregulation downstream

Serotonin System [14]

• 5-HT2A receptor activation contributes to hallucinations
• Atypical antipsychotics have high 5-HT2A/D2 binding ratio
• Serotonergic hallucinogens (LSD, psilocybin) are potent 5-HT2A agonists
• May modulate dopamine release in prefrontal cortex

Substance-Induced Mechanisms

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Clinical Presentation

Core Symptom Domains

Positive Symptoms

Negative Symptoms (Deficit Syndrome)

Exam Detail: Primary vs Secondary Negative Symptoms:

• Primary: Intrinsic to illness, stable over time, poor treatment response
• Secondary: Result of depression, EPS (akinesia), medication sedation, positive symptoms (social withdrawal from paranoia), institutionalisation
• IMPORTANT: Always exclude secondary causes before attributing to primary deficit

Cognitive Symptoms

Cognitive deficits are core features of schizophrenia, present before onset and persistent:

• Working memory impairment
• Attention and concentration deficits
• Executive dysfunction (planning, abstraction)
• Processing speed reduction
• Verbal learning and memory deficits

Presentation by Acuity

Acute Agitated Presentation

Acute Non-Agitated Presentation

Physical Examination

Vital Signs (Abnormalities Suggest Medical Cause)

Neurological Examination

Mental State Examination

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Red Flags and Warning Signs

Organic Psychosis Indicators [1,2,3]

Psychiatric Emergency Red Flags

Clinical Pearl: The "4 A's" of Organic Psychosis:

• Acute onset (hours to days)
• Age > 40 at first episode
• Abnormal vital signs
• Abnormal level of consciousness

Any "A" = Medical workup mandatory before psychiatric disposition

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Differential Diagnosis

Medical Mimics of Psychosis

Psychiatric Differential

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Diagnostic Approach

Immediate Safety Assessment

Before ANY clinical assessment:

1. Environmental safety: Clear room of potential weapons, ensure clear exit path
2. Security presence: Call security if ANY concern about agitation/violence
3. Staff positioning: Maintain safe distance (arm's length minimum), never corner patient
4. Communication devices: Ensure duress alarm or phone accessible

Systematic Evaluation

Step 1: Primary Survey

Step 2: Focused History (from patient, collateral, records)

History of Present Episode:

• Symptom onset and progression (acute vs insidious)
• Type and content of psychotic symptoms
• Precipitating factors (stressors, substance use, medication changes)
• Associated symptoms (mood, anxiety, sleep disturbance)
• Functional impact

Psychiatric History:

• Previous psychiatric diagnoses and episodes
• Previous hospitalisations and treatments
• Medication history (current, past, adherence)
• Response to previous treatments

Substance Use History:

• Alcohol, cannabis, stimulants, opioids, hallucinogens
• Synthetic cannabinoids, novel psychoactive substances
• Last use, quantity, route
• Withdrawal symptoms

Medical History:

• Neurological conditions
• Endocrine disorders
• Autoimmune conditions
• Recent infections
• HIV status

Medication History:

• New medications started
• Recent changes
• Over-the-counter and herbal supplements

Collateral History (ESSENTIAL):

• Baseline functioning
• Timeline of symptom development
• Recent behaviour changes
• Medication adherence
• Substance use

Medical Clearance Algorithm [3,4]

ALL Patients (Minimum Workup)

First-Episode Psychosis OR High Suspicion for Organic Cause

Consider in Specific Situations

Clinical Decision Tool: Organic vs Primary Psychiatric

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Acute Management

Principles of Emergency Care [15]

1. Safety first: Staff and patient safety is paramount
2. De-escalation before medication: Verbal techniques should be attempted first when safe
3. Rule out organic causes: Medical workup before psychiatric disposition
4. Pharmacological intervention when needed: For safety of patient, staff, and others
5. Least restrictive intervention: Use minimum force/restraint necessary
6. Continuous monitoring: Especially with restraints or sedation

Verbal De-escalation Techniques [15]

Environmental Modifications:

• Move to quiet, low-stimulation area
• Remove potential weapons
• Reduce number of staff/observers
• Ensure adequate space

Communication Strategies:

De-escalation Script:

"My name is [X], I'm a doctor here to help you. I can see you're very distressed right now. You're safe here. I'd like to understand what's happening for you. Is there anything I can get you that might help - some water, a blanket? I'd like to offer you some medication that can help you feel calmer. Would you be willing to take something by mouth?"

Pharmacological Management

Oral Medications (Cooperative Patient - PREFERRED)

Intramuscular Medications (Uncooperative Patient) [15,16]

Critical Alert: CRITICAL WARNING: Olanzapine IM + Benzodiazepine IM Concomitant administration of IM olanzapine and IM benzodiazepine is associated with significant cardiorespiratory depression and deaths. If benzodiazepines are required after IM olanzapine, wait ≥1 hour and monitor closely. [15]

Special Situations

Monitoring Requirements

Post-Medication Monitoring

Patients in Restraints

Physical Restraints

Principles: [15]

• Last resort only after de-escalation and medication attempts have failed
• Documentation required: Indication, alternatives tried, ongoing necessity
• Time-limited: Regular reassessment (every 15-30 minutes)
• Continuous monitoring: Vital signs, respiratory status, circulation
• AVOID PRONE POSITIONING: Associated with positional asphyxia and death

Technique:

• Minimum 5 trained staff for safe restraint (one per limb + team leader)
• Supine or lateral positioning (NEVER prone)
• Ensure airway access and chest expansion
• Use approved restraint devices
• Document clearly

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First-Episode Psychosis (FEP)

Clinical Significance

First-episode psychosis is a critical window of opportunity for intervention that significantly impacts long-term outcomes. [6,18]

FEP-Specific Workup

In addition to standard workup, first-episode psychosis requires: [18]

Antipsychotic Selection in FEP [18,19]

First-Line Options:

Key Principles: [19]

• Start at 50% or less of adult dose
• Titrate slowly over weeks
• Allow adequate trial (4-6 weeks at therapeutic dose)
• Monitor response with standardised scales (PANSS, CGI)
• Assess for side effects at each visit
• Consider long-acting injectable early if adherence concerns

Early Intervention Services

Components of comprehensive FEP care: [6]

• Rapid access and assessment (less than 2 weeks from referral)
• Low-dose antipsychotic treatment
• Cognitive behavioural therapy for psychosis (CBTp)
• Family intervention and psychoeducation
• Supported employment/education
• Substance use intervention
• Physical health monitoring
• Case management

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Disposition and Follow-Up

Admission Criteria

Psychiatric Admission Indications

Medical Admission Indications

Discharge Criteria

All of the following must be met:

• Medical causes excluded or adequately treated
• No imminent danger to self or others
• Able to care for basic needs OR appropriate support in place
• Capacity to make decisions about care OR appropriate legal framework
• Outpatient follow-up arranged and accepted
• Medication plan in place with supply provided
• Family/support persons informed (with consent) and have crisis contacts
• Safety plan completed if any suicide risk

Involuntary Detention

Criteria vary by jurisdiction but generally require:

1. Mental disorder is present
2. Risk of harm to self or others OR inability to care for self
3. Treatment is available and will benefit the patient
4. Least restrictive option has been considered

Documentation requirements:

• Specific mental disorder or symptoms
• Specific risk behaviours or statements
• Why voluntary treatment is not appropriate
• Signatures and time limits per local legislation

Follow-Up Recommendations

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Special Populations

Elderly Patients [2]

Pregnant and Postpartum Patients

Adolescents [18]

Intellectual Disability

Comorbid Substance Use Disorder

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Complications and Emergencies

Neuroleptic Malignant Syndrome (NMS)

Diagnostic Criteria: [20]

• Recent antipsychotic exposure (within past 1-4 weeks)
• Hyperthermia (> 38°C)
• Muscle rigidity ("lead pipe")
• Autonomic instability (tachycardia, labile BP, diaphoresis)
• Altered mental status

Management:

1. STOP all antipsychotics immediately
2. Supportive care: IV fluids, cooling, ICU if severe
3. Dantrolene 1-2.5 mg/kg IV for severe rigidity
4. Bromocriptine 2.5mg PO TDS for dopamine agonism
5. Benzodiazepines for rigidity/agitation
6. Monitor CK, renal function, electrolytes
7. Consider ECT for refractory cases

Excited Delirium Syndrome [5]

Features:

• Extreme agitation and aggression
• Hyperthermia
• Diaphoresis
• Superhuman strength
• Pain tolerance
• Paranoia or bizarre behaviour
• Often associated with stimulant use or psychiatric illness

Management:

• This is a medical emergency with high mortality risk
• Call for help immediately
• Rapid sedation: Ketamine 4-5 mg/kg IM is most rapid
• Active cooling
• Avoid prolonged physical struggle/restraint
• Continuous cardiorespiratory monitoring
• IV access, fluids
• Transfer to resuscitation area/ICU

Catatonia

Clinical Features:

• Stupor, mutism, posturing
• Waxy flexibility (catalepsy)
• Negativism, stereotypy
• Echolalia, echopraxia

Bush-Francis Catatonia Rating Scale items:

• Immobility, staring, mutism, posturing, grimacing, stereotypy, mannerisms, verbigeration, rigidity, negativism, waxy flexibility, withdrawal

Management:

1. Benzodiazepine challenge: Lorazepam 1-2mg IV/IM
   • Positive response (improvement within 5-10 min) suggests catatonia
   • Continue lorazepam 1-2mg TDS-QID; doses up to 16mg/day may be needed
2. If benzodiazepines fail: ECT is highly effective
3. Monitor for lethal catatonia (fever, autonomic instability)

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Exam-Focused Content

Common Viva Questions

Q1: "A 22-year-old man is brought to ED by police, agitated and claiming people are trying to kill him. How would you approach this?"

Model Answer:

"This is a psychiatric emergency requiring a systematic approach to ensure safety while excluding organic causes.

Immediate priorities: First, I would ensure the safety of staff and the patient. I would request security presence, ensure the room is clear of potential weapons, and maintain a safe distance while positioning myself near the exit.

De-escalation: I would attempt verbal de-escalation using a calm, non-threatening approach, introducing myself, acknowledging his distress, and offering basic comforts. If willing to engage, I would offer oral medication such as lorazepam 2mg or olanzapine 5mg.

If de-escalation fails: I would proceed to IM medication - my choice would be haloperidol 5mg with lorazepam 2mg IM, or droperidol 5-10mg IM if available, given its rapid onset.

Medical assessment: Once safe, I would check vital signs and fingerstick glucose immediately. In a young man with first presentation, I would be particularly concerned about substance-induced psychosis, so a thorough toxicology screen is essential. My medical workup would include CBC, metabolic panel, LFTs, TFTs, and urinalysis. Given first episode, I would arrange CT head and consider MRI.

Key history: I would seek collateral from family or the accompanying officers regarding onset, substance use, baseline functioning, and any prodromal symptoms.

Disposition: This patient likely requires psychiatric admission for stabilisation, further workup, and initiation of treatment under the Mental Health Act if he lacks capacity to consent."

Q2: "What are the indications for neuroimaging in acute psychosis?"

Model Answer:

"Neuroimaging should be considered in any first-episode psychosis and is strongly indicated when clinical features suggest organic aetiology.

Absolute indications for CT head:

• First episode of psychosis at any age
• New focal neurological signs
• Altered level of consciousness
• Recent head injury
• Age over 40 at first presentation

Strong indications:

• Atypical features suggesting organic cause
• Treatment-resistant psychosis
• Cognitive impairment disproportionate to psychosis
• History of CNS pathology

MRI is preferred when:

• Investigating for demyelinating disease
• Temporal lobe pathology suspected
• Subtle structural abnormalities
• Autoimmune encephalitis suspected

A Cochrane review found that while routine CT in uncomplicated presentations of known psychiatric illness has low yield, first-episode psychosis warrants comprehensive investigation including neuroimaging."

Q3: "Describe the assessment and management of first-episode psychosis."

Model Answer:

"First-episode psychosis is a critical intervention window where early, optimal treatment significantly impacts long-term outcomes.

Assessment: This requires comprehensive evaluation to:

1. Confirm the diagnosis - distinguish from organic causes, substance-induced psychosis, and other psychiatric conditions
2. Establish baseline function and symptom severity
3. Identify risk factors and comorbidities

The workup should include bloods, toxicology, MRI brain, and baseline cognitive assessment. I would also screen for substance use, trauma history, and premorbid functioning.

Importance of Duration of Untreated Psychosis: Literature consistently shows that longer DUP predicts poorer outcomes. The target is treatment initiation within 3 months, ideally sooner.

Treatment:

• Start antipsychotic at low dose - for example, risperidone 1mg or aripiprazole 5mg
• Titrate slowly based on response and tolerability
• Allow adequate trial (4-6 weeks at therapeutic dose)
• Combine with psychological intervention - CBT for psychosis
• Family psychoeducation and involvement

Setting: Ideally, referral to an Early Intervention in Psychosis service, which provides intensive, specialised care and has been shown to improve outcomes compared to standard care."

High-Yield Facts for Examinations

Common Examination Mistakes

❌ Mistakes that fail candidates:

• Failing to rule out organic causes before psychiatric diagnosis
• Missing NMS or serotonin syndrome
• Using IM olanzapine with benzodiazepines
• Not checking glucose before sedation
• Forgetting to assess capacity
• Missing command hallucinations and suicide risk
• Not knowing the Mental Health Act criteria
• Ignoring substance use history

✅ What examiners want to hear:

• Systematic safety-first approach
• Clear understanding of organic vs primary distinction
• Knowledge of appropriate medication choices with doses
• Awareness of DUP and early intervention importance
• Understanding of legal framework for involuntary treatment
• Appropriate disposition planning and follow-up

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Quality Metrics

Performance Indicators

Documentation Requirements

• Safety assessment (risk to self and others)
• Medical clearance workup results
• Mental state examination
• Capacity assessment
• De-escalation attempts documented
• Medication administration with times, doses, route, response
• Restraint use: indication, duration, monitoring
• Collateral sources contacted
• Disposition decision with rationale
• Follow-up arrangements
• Information provided to patient/family
• Mental Health Act documentation if applicable

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References

1. Nordstrom K, Zun LS, Wilson MP, et al. Medical evaluation and triage of the agitated patient: consensus statement of the American Association for Emergency Psychiatry Project BETA Medical Evaluation Workgroup. West J Emerg Med. 2012;13(1):3-10. doi:10.5811/westjem.2011.9.6863

2. Inouye SK, Westendorp RG, Saczynski JS. Delirium in elderly people. Lancet. 2014;383(9920):911-922. doi:10.1016/S0140-6736(13)60688-1

3. Wilson MP, Nordstrom K, Anderson EL, et al. American Association for Emergency Psychiatry Task Force on Medical Clearance of Adult Psychiatric Patients. Part II: Controversies over Medical Assessment, and Consensus Recommendations. West J Emerg Med. 2017;18(4):640-646. doi:10.5811/westjem.2017.3.32259

4. Henneman PL, Mendoza R, Lewis RJ. Prospective evaluation of emergency department medical clearance. Ann Emerg Med. 1994;24(4):672-677. doi:10.1016/S0196-0644(94)70279-2

5. Takeuchi A, Ahern TL, Henderson SO. Excited delirium. West J Emerg Med. 2011;12(1):77-83. PMCID: PMC3088378

6. Marshall M, Lewis S, Lockwood A, et al. Association between duration of untreated psychosis and outcome in cohorts of first-episode patients: a systematic review. Arch Gen Psychiatry. 2005;62(9):975-983. doi:10.1001/archpsyc.62.9.975

7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Text Revision. Washington, DC: American Psychiatric Publishing; 2022.

8. Perälä J, Suvisaari J, Saarni SI, et al. Lifetime prevalence of psychotic and bipolar I disorders in a general population. Arch Gen Psychiatry. 2007;64(1):19-28. doi:10.1001/archpsyc.64.1.19

9. McGrath J, Saha S, Chant D, Welham J. Schizophrenia: a concise overview of incidence, prevalence, and mortality. Epidemiol Rev. 2008;30(1):67-76. doi:10.1093/epirev/mxn001

10. Kirkbride JB, Fearon P, Morgan C, et al. Heterogeneity in incidence rates of schizophrenia and other psychotic syndromes: findings from the 3-center AeSOP study. Arch Gen Psychiatry. 2006;63(3):250-258. doi:10.1001/archpsyc.63.3.250

11. Bramness JG, Gundersen ØH, Guterstam J, et al. Amphetamine-induced psychosis - a separate diagnostic entity or primary psychosis triggered in the vulnerable? BMC Psychiatry. 2012;12:221. doi:10.1186/1471-244X-12-221

12. Dalmau J, Gleichman AJ, Hughes EG, et al. Anti-NMDA-receptor encephalitis: case series and analysis of the effects of antibodies. Lancet Neurol. 2008;7(12):1091-1098. doi:10.1016/S1474-4422(08)70224-2

13. Howes OD, Kapur S. The dopamine hypothesis of schizophrenia: version III - the final common pathway. Schizophr Bull. 2009;35(3):549-562. doi:10.1093/schbul/sbp006

14. Coyle JT. Glutamate and schizophrenia: beyond the dopamine hypothesis. Cell Mol Neurobiol. 2006;26(4-6):365-384. doi:10.1007/s10571-006-9062-8

15. Wilson MP, Pepper D, Currier GW, Holloman GH Jr, Feifel D. The psychopharmacology of agitation: consensus statement of the American Association for Emergency Psychiatry Project BETA Psychopharmacology Workgroup. West J Emerg Med. 2012;13(1):26-34. doi:10.5811/westjem.2011.9.6866

16. Battaglia J. Pharmacological management of acute agitation. Drugs. 2005;65(9):1207-1222. doi:10.2165/00003495-200565090-00003

17. Riddell J, Tran A, Bengiamin R, Hendey GW, Armenian P. Ketamine as a first-line treatment for severely agitated emergency department patients. Am J Emerg Med. 2017;35(7):1000-1004. doi:10.1016/j.ajem.2017.02.026

18. National Institute for Health and Care Excellence. Psychosis and schizophrenia in adults: prevention and management. NICE guideline [CG178]. 2014. Updated 2019.

19. Correll CU, Galling B, Pawar A, et al. Comparison of early intervention services vs treatment as usual for early-phase psychosis: a systematic review, meta-analysis, and meta-regression. JAMA Psychiatry. 2018;75(6):555-565. doi:10.1001/jamapsychiatry.2018.0623

20. Ware MR, Feller DB, Hall KL. Neuroleptic malignant syndrome: diagnosis and management. Prim Care Companion CNS Disord. 2018;20(1):17r02185. doi:10.4088/PCC.17r02185

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Basic Cards

1. What is the lifetime prevalence of psychotic disorders? → 3%
2. What is the peak age of onset for schizophrenia in males vs females? → Males 15-25; Females 25-35
3. What type of hallucination is most suggestive of organic cause? → Visual hallucinations
4. What is the key distinguishing feature between psychosis and delirium? → Level of consciousness (clear vs fluctuating)
5. What is the target Duration of Untreated Psychosis? → less than 3 months

Cloze Cards

1. The "B52" IM regimen consists of haloperidol 5mg + lorazepam 2mg + diphenhydramine 50mg
2. Anti-NMDA receptor encephalitis primarily affects young women and is associated with ovarian teratoma in 50% of female cases
3. NMS is characterised by hyperthermia, rigidity, altered mental status, and autonomic instability
4. First-episode psychosis over age 40 should be considered organic until proven otherwise

Scenario Cards

1. A 25-year-old woman with no psychiatric history presents with psychosis, seizures, and bizarre movements. What diagnosis must you consider? → Anti-NMDA receptor encephalitis
2. A patient on antipsychotics develops fever 39°C, rigidity, and CK 15,000 U/L. Diagnosis and immediate management? → NMS; stop antipsychotic, supportive care, dantrolene, ICU
3. An agitated patient requires IM sedation. You give olanzapine 10mg IM. The nurse wants to give lorazepam 2mg IM. Your response? → Do NOT give - risk of cardiorespiratory depression. Wait ≥1 hour if benzodiazepine needed.