01 · Psychosis: symptoms, diagnosis and recovery

1.1 Hallucinations, illusions and unusual beliefs

A hallucination is a perception without a corresponding external stimulus. An illusion misinterprets something present: a coat becomes a person. Hallucinations may be auditory, visual, olfactory, gustatory or tactile. A voice heard “inside the head” can still be a hallucination; location alone does not settle it.

A delusion is a firmly held belief, unexplained by the person's cultural context, which persists despite compelling contrary evidence. It need not be impossible: a real event can acquire a delusional explanation.

An overvalued idea is an emotionally charged, dominating belief understandable from the person's circumstances and values. An obsession is an intrusive thought, image or urge, usually unwanted and resisted or neutralised. Conviction alone does not distinguish them: OCD and BDD can have poor or absent insight.

Primary delusions arise without an understandable preceding psychological explanation. Secondary delusions follow another experience, such as a voice or profound depressive guilt.

Delusional perception: normal perception acquires an immediate, unexplained personal significance. Seeing a red car suddenly means “I am going to be executed”. The perception itself is normal, so this is not a visual hallucination.

1.2 First-rank symptoms and thought disorder

Schneider's first-rank symptoms are useful vocabulary, but not specific to schizophrenia. ICD-11 no longer gives them special diagnostic weight.

Thought blocking is interrupted thought. It becomes thought withdrawal only when the person attributes the interruption to external removal.

Formal thought disorder concerns organisation, expressed through speech: derailment, tangentiality, loose associations, neologisms and, at its most severe, incomprehensibility. Delusions concern thought content.

A command voice does not automatically produce obedience. Its perceived authority, power to punish, previous compliance and the person's intention matter. Likewise, someone may jump to escape a persecutor without wanting to die. The mechanism behind the act matters more than the diagnostic label.

1.3 Schizophrenia and its nearest differentials

ICD-11: at least two characteristic symptom groups, most of the time, for at least one month. At least one must be persistent delusions, persistent hallucinations, disorganised thinking, or influence/passivity/control experiences. Other groups are negative symptoms, grossly disorganised behaviour and psychomotor disturbance. Exclude substance and medical causes. Prodromal withdrawal does not count as the active month.

ICD-11 uses symptom and course qualifiers. Paranoid and hebephrenic schizophrenia are historical subtypes, not current ICD-11 categories.

For ICD-11 schizoaffective disorder, establish the full psychotic and mood syndromes and their timing; the content of a belief alone does not settle the diagnosis.

1.4 Negative symptoms: what is actually missing?

The five main domains are avolition, alogia, blunted affect, anhedonia and asociality: reduced drive, speech, emotional expression, pleasure and social engagement. Anticipation of pleasure may be more impaired than enjoyment once an activity begins.

Exclude secondary causes before calling symptoms primary.

More dopamine blockade may worsen medication-related slowing. Negative symptoms often outlast voices, so recovery also means daily activity, relationships and independence.

1.5 First-episode psychosis and physical differentials

A first episode is a presentation, not a permanent diagnosis. Early intervention combines psychiatric, psychological, family, educational and occupational support. Young people need developmental assessment and age-appropriate prescribing.

Medical clues include abrupt onset, fluctuating consciousness, seizures, focal signs, cognitive change, autonomic instability or unusual age of onset. Think of intoxication/withdrawal, epilepsy, endocrine/metabolic disease, intracranial disease and encephalitis. Rapid psychiatric change with seizures, abnormal movements and autonomic disturbance particularly raises autoimmune encephalitis.

Olfactory hallucinations prompt consideration of seizures or focal pathology but diagnose neither. Routine brain imaging is not recommended for every uncomplicated first episode; examination and atypical features guide it.

Before antipsychotics, record weight/waist, pulse/BP, glucose or HbA1c, lipids, prolactin and movement findings. ECG is indicated by the drug, cardiac history/risk or inpatient admission. Baselines distinguish pre-existing problems from later adverse effects.

1.6 Medication choice, apparent failure and clozapine

Choose an antipsychotic using previous response, patient priorities and the individual drug's movement, metabolic, prolactin, sedative and QT effects. The older/newer distinction is too crude.

A long-acting injection changes delivery. It may suit preference or help avoid unrecognised missed doses; it does not imply treatment resistance or remove the drug's adverse effects.

Before calling treatment resistant, establish what was taken, the dose, duration and response. Reconsider diagnosis, adherence, substances, interactions, tolerability and stress. Persistent distress may reflect depression, trauma, negative symptoms or adverse effects rather than persistent psychosis.

Clozapine follows two sequential adequate antipsychotic trials, including at least one non-clozapine second-generation drug. NICE describes an optimum-dose trial of 4–6 weeks; some specialist resistance definitions use longer. Two prescriptions alone are insufficient. Before augmenting clozapine, review dose, level, adherence and alternative explanations.

Clozapine facts to retain:

• Neutropenia, myocarditis, severe constipation/intestinal hypomotility, seizures, sedation and metabolic effects are key hazards. Constipation can become fatal obstruction.

• FBC checks haematological safety; a plasma concentration checks exposure/toxicity. They answer different questions.

• Persistent tachycardia with fever, chest pain or breathlessness needs assessment, not automatic attribution to titration.

• A break over 48 hours needs urgent advice and re-titration, not the former full dose.

• Stopping smoking raises concentrations. Combustion products induce metabolism; nicotine replacement does not maintain that induction. Serious infection can also raise levels.

1.7 Why psychological and social treatments matter

CBT for psychosis addresses meanings, distress, coping and functioning. It is not an argument about whether the belief is true. Family intervention adds understanding, communication, problem solving and relapse planning.

Expressed emotion means criticism, hostility and emotional over-involvement associated with relapse. It does not mean relatives caused schizophrenia.

Know the NICE treatment dose: at least 16 individual CBT sessions; at least 10 family sessions over three months to one year. Arts therapies may support expression and engagement, especially with negative symptoms. Supported employment pursues ordinary paid work; occupational therapy develops daily skills and independence.

1.8 Relapse, prognosis and family risk

Treatment interruption, substances, disrupted sleep and stress can precipitate relapse. Earlier clues include changed sleep, withdrawal, reduced self-care, unusual preoccupation and suspiciousness. The person's previous pattern is especially useful.

Remission and social recovery are different. Courses range from one episode to recurrent or persistent illness; a fixed “rule of thirds” is misleading. Stopping medication within the first 1–2 years carries substantial relapse risk. Later duration depends on course and preference; withdrawal should be gradual with continued monitoring.

Schizophrenia is polygenic and multifactorial. One Danish study estimated schizophrenia by age 52 in roughly 7% of offspring with one affected parent and 27% with two, versus below 1% when neither parent had been admitted with schizophrenia. These are study-specific population estimates, not an individual prediction.

There is no routine predictive test for a well child. Targeted genomic investigation is different: early-onset illness, intellectual disability, congenital anomalies or a suggestive family history may justify looking for a pathogenic copy-number variant. Heritability is not a child's probability of inheriting the illness.

1.9 Later-life and substance-related psychosis

In later life, review cognition, attention, hearing, vision, medicines and neurological findings. A limited hallucination matching a delusional theme, such as crawling with infestation beliefs, can occur in delusional disorder. Persistent prominent hallucinations, thought disorder, passivity or negative symptoms favour a broader syndrome. Late-onset schizophrenia and very-late-onset schizophrenia-like psychosis are clinical descriptions, not separate ICD-11 categories.

Older adults are more susceptible to postural hypotension, falls, sedation, anticholinergic effects and movement disorders. Prescribe cautiously and review benefit. Dementia adds cerebrovascular and mortality concerns with antipsychotics, balanced against distress and danger from untreated symptoms.

Cannabis can precipitate psychosis and worsen relapse, particularly with frequent, high-potency use. Psychosis preceding use, recurring independently or persisting beyond expected drug effects raises concern for a primary disorder. A positive urine screen shows exposure, not causation or current intoxication. Treat both problems together.

Neither diagnosis nor poor insight alone proves incapacity or justifies detention.