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Clinical Atlas Prestige · Evidence-first

Psych MEQs / SAQsGeneral adult psychiatry — psychosis

Psych MEQs / SAQs · General adult psychiatry — psychosis

Negative and cognitive symptoms of schizophrenia — primary vs secondary and treatment honesty (MEQ)

FRANZCP-style MEQ on primary vs secondary negatives, SANS/PANSS/MATRICS, limited pharmacotherapy evidence, cariprazine/clozapine nuance, cognitive remediation.

20 marks20 min
On this page & tools

Target exams

FRANZCPMRCPsychABPNMD-DNB

Target exams

FRANZCPMRCPsychABPNMD-DNB
Prompt
A 29-year-old man with schizophrenia is referred for 'untreatable negative symptoms'. He spends most days in bed, speaks little, has poor hygiene, and has not worked for three years. Current medicines: risperidone 6 mg orally daily, benztropine 2 mg orally twice daily, and quetiapine 300 mg at night 'for sleep'. He has bilateral cogwheel rigidity and a shuffling gait. Family say he still hears muffled voices occasionally and has seemed low in mood with passive death wishes. He cannot follow multi-step instructions at a supported-employment trial. (i) Separate primary from secondary negative contributors present. (ii) Outline your bedside assessment including scales/domains and risk. (iii) Propose a stepwise management plan including medication optimisation and psychosocial/cognitive interventions with evidence anchors. (iv) State careful nuances for cariprazine and clozapine in this context. (v) List exam pitfalls. (20 marks)

Model answer

Reveal model answer

(i) Primary vs secondary contributors. This is not yet established pure primary deficit syndrome. Secondary drivers present: EPS/parkinsonism (rigidity, shuffle) on high-dose risperidone with anticholinergic cover; sedating polypharmacy (quetiapine 300 mg night plus risperidone); possible depression (low mood, passive death wishes); residual positive symptoms (voices) that can drive withdrawal; understimulation and long unemployment. Primary negatives may coexist after secondary causes are treated, but labelling "untreatable" now is premature.[2][7]

(ii) Assessment. History: onset of negatives vs medication changes; premorbid function; typical day; pleasure/motivation; substances; medical. MSE for affect range, alogia, self-care, insight. Risk: suicide (explicit), self-neglect, vulnerability, capacity. Scales: SANS domains conceptually / PANSS negative items; note two-factor structure (expression vs avolition–apathy). Cognition: MATRICS-style domains (processing speed, attention, working memory, learning, reasoning, social cognition); consider formal testing/cognitive remediation referral. Collateral essential.[1][2][8]

(iii) Stepwise plan. (1) Treat secondary causes: reduce EPS (dose reduction or switch; review benztropine necessity — anticholinergics can worsen cognition); stop unnecessary sedation; treat depression if confirmed; optimise residual positives. (2) Measurement-based follow-up of negatives and function. (3) Cognitive remediation with link to supported employment/IPS and structured activity (Wykes meta-analytic support). (4) Family psychoeducation, skills training, housing support per RANZCP psychosocial framing. (5) Realistic goals; Fusar-Poli reminds overall drug effects on negatives are often small.[3][6][7][8]

(iv) Cariprazine and clozapine nuance. Cariprazine: Németh RCT showed benefit versus risperidone in a predominant negative symptoms population — cite phenotype carefully; not a panacea for all deficit syndromes; confirm local indication/label and titrate per product information after secondary causes addressed.[4] Clozapine: Kane superiority is for TRS after adequate failed trials with adherence — not automatic for isolated primary negatives without TRRIP-style resistance; do not claim clozapine as a proven primary-negative cure; if TRS criteria are later met, offer with full monitoring pathway.[5][7]

(v) Pitfalls. Calling secondary EPS "primary"; ignoring suicide under flat affect; stacking antipsychotics for avolition; overclaiming cariprazine beyond trial design; starting clozapine without TRS logic; omitting cognitive remediation and employment; inventing Mental Health Act section numbers.[2][3][4][5]

Common errors

  • Accepting "untreatable negatives" without secondary-cause checklist.
  • Leaving high-dose risperidone plus sedating polypharmacy unchanged.
  • Omitting suicide-risk assessment because affect is flat.
  • Marketing cariprazine or clozapine without trial/indication nuance.
  • Drug-only plan with no cognitive remediation or supported employment. [3][6][7]

Examiner notes

Reward primary/secondary separation, named domains (NIMH five; MATRICS cognition), Fusar-Poli humility, Németh and Kane careful citations, and a rehabilitation-heavy plan. Penalise stigma language and polypharmacy folklore. [1][3][4][5]

References

  1. [1]Kirkpatrick B, Fenton WS, Carpenter WT Jr, et al. The NIMH-MATRICS consensus statement on negative symptoms Schizophr Bull, 2006.PMID 16481659
  2. [2]Marder SR, Galderisi S The current conceptualization of negative symptoms in schizophrenia World Psychiatry, 2017.PMID 28127915
  3. [3]Fusar-Poli P, Papanastasiou E, Stahl D, et al. Treatments of Negative Symptoms in Schizophrenia: Meta-Analysis of 168 Randomized Placebo-Controlled Trials Schizophr Bull, 2015.PMID 25528757
  4. [4]Németh G, Laszlovszky I, Czobor P, et al. Cariprazine versus risperidone monotherapy for treatment of predominant negative symptoms in patients with schizophrenia Lancet, 2017.PMID 28185672
  5. [5]Kane J, Honigfeld G, Singer J, et al. Clozapine for the treatment-resistant schizophrenic. A double-blind comparison with chlorpromazine Arch Gen Psychiatry, 1988.PMID 3046553
  6. [6]Wykes T, Huddy V, Cellard C, et al. A meta-analysis of cognitive remediation for schizophrenia: methodology and effect sizes Am J Psychiatry, 2011.PMID 21406461
  7. [7]Galletly C, Castle D, Dark F, et al. Royal Australian and New Zealand College of Psychiatrists clinical practice guidelines for the management of schizophrenia and related disorders Aust N Z J Psychiatry, 2016.PMID 27106681
  8. [8]Green MF What are the functional consequences of neurocognitive deficits in schizophrenia? Am J Psychiatry, 1996.PMID 8610818