CH-13-Schizophrenia Spectrum & Other Psychotic Disorders – Comprehensive Study Notes

Perspectives on Schizophrenia

• Broad syndrome marked by disruption of perception, cognition, emotion, speech, and movement; affects virtually every domain of functioning.
• Stigmatized & misunderstood; societal costs exceed \$60\text{ billion} annually in the USA.
• Lifetime prevalence ≈ 0.2\text{--}1.5\% (≈ 1/100 people).
  • Men: earlier onset, poorer prognosis; risk peaks in late adolescence and declines with age.
  • Women: lower risk until age 36, then risk surpasses men; somewhat better course overall.
• Chronic course; full recovery in ≈ 1/7 patients; relapse common.
• High comorbidity with depression, anxiety, substance use, suicide (risk 10\text{--}15\%).

Early Figures in Diagnosing Schizophrenia

• John Haslam (1809) – first systematic clinical description ("form of insanity"; gradual onset, blunted sensibility, social withdrawal).
• Philippe Pinel (1801/1809) – French physician describing similar cases.
• Benedict Morel (1852) – coined "démence précoce" (early loss of mind).
• Emil Kraepelin (1898/1899)
  • Unified catatonia, hebephrenia, paranoia under dementia praecox.
  • Emphasised early onset + poor outcome; distinguished from manic–depressive illness.
• Eugen Bleuler (1908)
  • Introduced term schizophrenia (Greek skhizein + phren, split mind).
  • Core = "associative splitting" of thought; clarified that it is not multiple personality.

DSM-5: Schizophrenia Spectrum & Other Psychotic Disorders

• Disorders sharing extreme reality distortion (hallucinations, delusions) + disorganisation.
  • Schizophrenia
  • Schizophreniform Disorder
  • Schizoaffective Disorder
  • Delusional Disorder
  • Brief Psychotic Disorder
  • Substance/Medication-Induced & Medical-Condition Psychoses
  • Catatonia (specifier or separate diagnosis)
  • Attenuated Psychosis Syndrome (appendix; condition for further study)
  • Schizotypal Personality Disorder (Chapter 12) also within spectrum.

Diagnostic Criteria (core points)

• Schizophrenia
  • \geq 2 symptoms for \geq 1 month; at least one = delusions, hallucinations, disorganised speech.
  • Continuous disturbance \geq 6 months incl. prodromal/residual phases.
  • Marked functional decline.
  • Mood disorders, substances, medical conditions ruled out.
• Dimensional rating (0–4) for severity of each symptom cluster.

Symptom Clusters

Positive Symptoms (50–70 % experience)

• Delusions
  • Persecution, grandeur, erotomania, jealousy, somatic, Capgras (double), Cotard (dead), control, reference.
  • Motivational vs. deficit models; possible metacognitive origin.
• Hallucinations
  • Any modality; auditory most common (≈ 70\%).
  • SPECT: activation of Broca’s area ⇒ misattributed inner speech; deficits in emotional prosody & meta-worry.

Negative Symptoms (~25\% of patients)

• Avolition (apathy) – lack of initiation/persistence (e.g., hygiene).
• Alogia – poverty of speech/content; delayed responses.
• Anhedonia – lack of pleasure.
• Asociality – reduced social interest.
• Affective Flattening – reduced outward emotion; internal experience may remain.

Disorganised Symptoms

• Disorganised Speech – tangentiality, loose associations, derailment, neologisms.
• Disorganised/Bizarre Behaviour & Inappropriate Affect.
• Catatonia – stupor, waxy flexibility, negativism, echolalia/echopraxia, agitation; DSM-5 lists 12 features, need \geq3.

Historic Subtypes (dropped in DSM-5)

• Paranoid, Disorganised (Hebephrenic), Catatonic.
• Eliminated due to low stability & limited clinical utility; replaced by dimensional specifiers.

Other Psychotic Disorders

• Schizophreniform Disorder – criterion A met; duration 1\text{–}6 months; good-prognosis specifier. Prevalence ≈ 0.2\%.
• Schizoaffective Disorder – mood episode + criterion A; psychosis \ge 2 weeks without mood; bipolar vs. depressive type.
• Delusional Disorder – persistent non-bizarre or one bizarre delusion \ge 1 month; relatively intact functioning; subtypes as above; prevalence 24–60/100k; late onset (35–55 yrs).
• Brief Psychotic Disorder – \geq 1 positive/disorganised symptom lasting 1\text{–}<30 days; full return; with/without marked stressor; postpartum subtype.
• Substance/Medication-Induced Psychotic Disorder – psychosis temporally related to intoxication/withdrawal.
• Psychotic Disorder Due to Another Medical Condition – tumour, epilepsy, Huntington’s, Alzheimer’s, etc.
• Attenuated Psychosis Syndrome – subthreshold positive symptoms, intact insight; high risk; proposed for prevention research.

Course & Development

• Premorbid subtle motor, cognitive, social markers in childhood.
• Prodromal Stage (1–2 yrs): ideas of reference, magical thinking, illusions, social withdrawal, poor hygiene.
• Onset: late adolescence/early adulthood; men earlier.
• Delay from prodrome to full psychosis ≈ 2\text{–}10 yrs; longer untreated ⇒ poorer outcome.
• Chronic: cycles of relapse & remission; 22\% single-episode, 78\% multiple.
• Suicide risk high; mortality ↑ due to accidents/poor health.

Cultural & Social Considerations

• Universal phenomenon; symptom expression varies.
• Higher diagnosed rates in African-Americans & Afro-Caribbeans (bias, stress, discrimination).
• Urbanicity, migration, minority status ↑ risk.
• Course/outcome poorer in low-resource settings due to limited services; stigma & supernatural causal models impact help-seeking.

Etiology

Genetic Factors

• Family risk proportional to shared genes (MZ twin \approx 48\%; 1° relative \approx 6\%).
• Twin concordance: MZ > DZ; Genain quadruplets show gene–environment interplay.
• Adoption studies: risk remains if biological parent affected; good adoptive environments buffer.
• Offspring-of-twins design ⇒ “carrier” concept.
• Polygenic: loci on chromosomes 1,2,3,5,6,8 (NRG1),10,11,13,20,22 (COMT); GWAS => 108 risk loci.
• Endophenotypes: smooth-pursuit eye tracking deficits, working memory, emotion identification.

Neurobiological Factors

• Dopamine Hypothesis (revised)
  • Excess stimulation of striatal D2 receptors.
  • Deficient prefrontal D1 activity (hypofrontality).
  • Evidence: antipsychotics block D2; L-dopa & amphetamines exacerbate psychosis; imaging shows presynaptic dopamine ↑.
• Glutamate Hypothesis
  • NMDA receptor hypofunction (PCP, ketamine produce psychosis).
• Brain Structure
  • Enlarged lateral & third ventricles; more common in males, chronic cases, prenatal flu exposure.
  • Reduced gray matter; abnormal white-matter connectivity; dorsolateral prefrontal cortex inefficiency.
  • Hypo/hyperfrontality; disrupted thalamic–cortical circuits.
• Prenatal & Perinatal Insults
  • 2nd-trimester influenza, maternal stress, obstetric complications (anoxia), bleeding; cannabis exposure (gene \times environment with CNR1).

Psychological & Social Factors

• Stress – precipitates onset & relapse; e.g., urban living, discrimination, trauma, natural disasters.
• Expressed Emotion (EE) – criticism, hostility, emotional over-involvement in family predicts \approx3.7× relapse; cultural variation (high EE: UK ≈ 65\%, Mexico ≈ 30\%, India ≈ 25\%).
• Schizophrenogenic mother & double bind discredited.

Biological Interventions

• First-Generation (Typical) Antipsychotics: chlorpromazine, haloperidol, fluphenazine, etc.
  • Effective 60\text{–}70\%; strong D2 antagonism.
  • Side-effects: extrapyramidal symptoms (EPS) – Parkinsonism, akinesia, tardive dyskinesia (20–50%%; irreversible).
• Second-Generation (Atypical) Antipsychotics: clozapine, risperidone, olanzapine, quetiapine, ziprasidone, aripiprazole.
  • Mixed D2/5-HT actions; helpful for treatment-resistant; risk metabolic syndrome.
  • CATIE & CUtLASS: modest advantage; side-effects differ, not absent.
• Compliance Issues: \approx 74\% discontinue within 18 months; causes = EPS, sedation, cost, poor insight, stigma.
• Depot / LAI injections to improve adherence (variable success).
• rTMS to left temporoparietal area ↓ auditory hallucinations (small, short-term).
• Modafinil adjunct: possible cognitive & affective benefits (preliminary).
• ECT rarely used; psychosurgery & insulin coma obsolete.

Psychosocial Interventions

• Inpatient Token Economies – operant conditioning; increased self-care, social behaviour; expedite discharge.
• Social Skills Training – role-play, modelling, feedback → improved community functioning; needs maintenance.
• Independent Living Skills Programs – symptom management, medication adherence, substance avoidance.
• CBT for Psychosis – challenge delusional beliefs, coping with voices; moderate effect on positive symptoms.
• Cognitive Remediation – computerised drills + strategy coaching; improves attention, memory, executive function & employment outcomes.
• Family Psychoeducation / Behavioural Family Therapy – education, communication & problem-solving skills; reduces EE & relapse if ongoing.
• Supported Employment (IPS) – job coaching during competitive employment; increases work tenure.
• Assertive Community Treatment (ACT) – multidisciplinary 24/7 outreach; ↓ hospitalisation, ↑ housing stability.
• Consumer-run / Clubhouse Models (e.g., Fountain House) – peer support, empowerment; mixed evidence.

Treatment Across Cultures

• Variation in causal beliefs & help-seeking.
  • Xhosa (South Africa): traditional healers, emetics, animal sacrifice.
  • Bali: supernatural attribution, minimal neuroleptic use.
  • China: higher endorsement of karmic/ancestor causes; preference for herbal/alt treatments.
• Culturally adapted interventions (e.g., including extended family, bilingual groups) improve engagement & outcome.

Prevention & Early Intervention

• High-Risk Offspring Studies (Danish cohort) – maternal schizophrenia + unstable rearing environments ⇒ highest conversion.
• Prodromal Intervention – low-dose antipsychotics, CBT, omega-3, family education; aim to delay/avert psychosis.
• Public Health Approach – reduce obstetric complications, maternal infections, urban stress, discrimination; promote prenatal care.

Key Takeaways

• Schizophrenia entails heterogeneous symptoms clustering as positive, negative, disorganised.
• Etiology is multifactorial: polygenic liability + neurodevelopmental insults + neurochemical dysregulation + psychosocial stress.
• Optimal management is integrative: continuous antipsychotic medication + psychosocial rehabilitation + family/community support.
• Early detection and culturally sensitive prevention strategies hold promise for reducing incidence, severity, and societal burden.