First-Episode Psychosis in a 19-Year-Old with a Normal-Looking MRI Request

Distinguishing the two. The distinction is clinical and longitudinal, not a single test.

Features favouring a primary psychotic disorder (e.g. schizophrenia spectrum):

• Duration: psychotic symptoms persist beyond the expected window of the substance. Synthetic cannabinoids have a relatively short intoxication/withdrawal window (hours to a few days), so 5 months of continuous delusions is far longer than can be attributed to ongoing use alone.
• Persistence during verified abstinence: if symptoms continue after 4+ weeks of monitored abstinence, substance-induced psychosis becomes much less likely.
• Phenomenology: passivity phenomena (thought insertion) and bizarre persecutory delusions are more characteristic of a primary disorder; substance-induced psychosis more often features prominent visual hallucinations, confusion and agitation.
• Functional decline predating heavy use, negative symptoms, and a prolonged prodrome (social withdrawal, academic decline) suggest a primary disorder.
• Family history of psychosis increases risk, though its absence does not exclude.

Limitations of the urine drug screen:

• Standard immunoassays do not reliably detect synthetic cannabinoids ('spice'), so a negative screen does not exclude use.
• Cannabinoids are detectable only for days in heavy users; a negative result may simply reflect timing.
• The screen does not tell you whether use is causal, coincidental, or a self-medication attempt.

Investigations:

• Baseline physical: full blood count, renal and liver function, electrolytes, calcium, glucose/HbA1c, thyroid function, B12/folate, syphilis serology, HIV test, pregnancy test, and CK if agitated.
• Urine drug screen (with the caveat above) plus a careful collateral history of exactly which substances, how much, how often, and last use.
• MRI brain is not routinely indicated in first-episode psychosis with a normal neurological examination, but is indicated if there are neurological signs, atypical features, late onset, or rapid deterioration. In this patient, a normal exam makes routine MRI low-yield; it may still be requested to reassure the family if resources allow, but the reasoning must be explicit.
• EEG only if seizures, confusion, or atypical features suggest epilepsy.

Exam point: the answer is not 'negative screen means not drugs'. It is 'the duration and phenomenology already argue against a purely substance-induced picture, and the screen cannot rule out synthetic cannabinoids'.

Untreated psychosis. Longer duration of untreated psychosis is associated with poorer functional outcome, so prompt treatment is justified. The aim is rapid symptom control and engagement, not immediate commitment to lifelong medication.

What the evidence supports:

• Acute treatment with an antipsychotic at the lowest effective dose is standard; response usually appears within 2–4 weeks and should be reviewed at 4–6 weeks.
• Maintenance after a first episode reduces relapse substantially. Relapse risk is high in the first 1–2 years after stopping, so guidelines generally advise continuing antipsychotic treatment for at least 1–2 years after remission, with gradual, monitored withdrawal if the patient wishes to stop.
• Long-term, possibly indefinite, treatment is more likely if there are multiple relapses, persistent symptoms, strong family history, or substantial functional impairment. It is not inevitable after a single episode.

What guides the decision:

• Number and severity of relapses, residual symptoms, insight, premorbid and current functioning, substance use, social support, and the patient's own values and preferences.
• Shared decision-making with the patient (and family, with consent) and a documented relapse-prevention plan, including early warning signs.
• Metabolic and movement monitoring on any antipsychotic: weight, waist, BP, HbA1c, lipids, prolactin if relevant, and extrapyramidal symptoms.

Communicating with the mother: avoid both 'she will be on drugs forever' and 'she will be fine off everything in a few months'. The honest answer is that treatment now is important, that the first 1–2 years are a high-risk period, and that the long-term plan will be reviewed as her illness evolves. Also address the substance use as a modifiable relapse risk, and offer family psychoeducation and a first-episode service where available.

Step 1 - Clarify the cause. Amenorrhoea plus weight gain suggests hyperprolactinaemia, common with risperidone, amisulpride and paliperidone. Check serum prolactin (and pregnancy test, thyroid function). Weight gain of 4 kg in 6 weeks is clinically significant and predicts future metabolic problems.

Step 2 - Address the side effects without abandoning effective treatment.

• Switch to an agent with a lower prolactin and metabolic liability (e.g. aripiprazole) rather than stopping antipsychotic altogether. Cross-taper with monitoring.
• Lifestyle and metabolic monitoring: diet and activity advice, weight, waist, BP, HbA1c and lipids; consider referral to a dietitian.
• If hyperprolactinaemia persists, consider dose reduction or an alternative, and evaluate for osteoporosis risk with long-term elevation.

Step 3 - Manage the request to stop. Explore her reasons (side effects, stigma, feeling well, insight). Explain the relapse risk in the first 1–2 years and the plan for gradual reduction if she still wishes to stop after discussion. Document the conversation and agree a relapse plan with early warning signs and rapid access.

Step 4 - Broader care. Ensure psychological intervention (CBT for psychosis), family work, vocational/education support, and substance-use intervention are in place - medication is only one component.

Exam point: the correct response to distressing side effects is not 'stop the drug' or 'accept the side effects'; it is to identify the mechanism, switch to a better-tolerated agent, monitor, and involve the patient in a documented shared decision.