Childhood Psychosis


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Childhood Psychosis

  1. 1. Childhood Psychosis Bivin Jay. B
  2. 2. Introduction • Pediatric schizophrenia, childhood onset schizophrenia, childhood psychoses (DSM III) • Dysregulation in thinking, motor, emotional processess in child and adoloscents under the age of 18 years • Rare among children of ages from 7-8 yrs • 50% of the young schizophrenics will experience severe neuropsychiatric disturbances in the future • Diagnostic criteria are same to adult population • Childhood psychoses was added to DSM III in 1980s.
  3. 3. Prevalence & Epidemiology • Studies using strict Dx criteria are limited (because of the diagnostic diversity) • Autism is more prevalent than childhood schizophrenia • 2/100,000 (based on the DSM III) • Male to female ratio= 1.5:1 to 2.5:1 • Diagnosis is made frequently in adults than children • The peak age of onset is 15 yrs
  4. 4. Clinical features • Almost similar to the adult schizophrenia • Earlier signs are developmental lags/ language and motor delays • Positive & negative symptoms • Auditory hallucinations are the most common Sx in 75% • Visual and somatic hallucinations are not rare but less frequent when compared to AH. • Delusions (50-80%) – persecutory, feeling of being tormented, somatic concerns, grandiose perception or religious ideation
  5. 5. Etiology • A neurodevelopmental disorder with no demonstrable single etiology • Genetic factors: – Schizophrenia & schizophrenia spectrum ds. are found in high rate among families of pts with F20 – Concordance rate: monozygotic twins (50%) & dizygotic twins (17%) – F20 is genetically mediated but not genetically determined and results from an interaction of gene & evmnt.
  6. 6. • Neurobiological deficits: – No clear premorbid personality profile explanations available – Enlargement of the ventricular structure & overall reduction in cortical grey matter and brain volumes (Brain imaging studies) • Psychology: – 10-20% of children with F20 have borderline IQ – Cognitive deficits include lowered IQ, low information processing, sustained attention, memory and executive functions especially working memory
  7. 7. • Family factors: – – – – Abberant communication patterns Double bound communications Levels of EE Communication deviance predispose to develop schizophrenia in adoloscents • Environment – Low SES is associated with higher rate of schizophrenia – Adverse life events such as death of a parent, rejection of the child – Relationship of schizophrenia onset with SES is still contradictory – Incidence of clinical syndrome similar in a variey of cultural settings
  8. 8. Assessment • • • Evaluate all areas of functioning Dignostic procedures are often prolonged and require multiple informants History and development – History of current difficulties – Age of onset – Course and nature of symptoms – Premorbid functioning – School & cognitive skills – Psychosocial adaptive skills – Precipitants – History of trauma – Family H/o – Family adaptive funtioning – Substance use H/o – Developmental H/o – Communication and speech functioning
  9. 9. • Mental status examination: – Level of consciousness and orientation – Hallucinations or delusions – Thought ds & negative symptoms – Affective symptoms – Assessment of dangerous and impulsive acts – Suicidality & homicidality
  10. 10. • Psycho logic evaluation – Projective testing for evaluation of thought disturbances, hallucinations etc – IQ and formal educational testing for assessment of achievement – Assessment of adaptive skills – Assessment of communication/speech and language • Medical & neurological history and evaluation • Physical examination for associated medical conditions • Toxicology screen for evaluation of substance abuse • Neurological consultation including EEG
  11. 11. • Autistic spectrum dis. – Aspergers dis., Autistic Dis., childhood disintegrative dis., PDDs • Psychoses associated with mood dis – BPAD., MDD • Other psychotic dis – Psychosis NOS, Schizoaffective Dis. • OCD • PTSD – Dissociative Dis. • PDs • Communication Dis • SUDs • Medical conditions – Delirium, epilepsy, CNS trauma or neoplasms • Infectious dis. – HIV, HSV, Neurosyphilis, Encephalitis.
  12. 12. Treatment • Require a multi-model approach • Goals: – ↓ the characteristic ψtic symptoms – Returning the child to more appropriate lines of management – Re-integrating the child into his/her community
  13. 13. Psychopharmacolgoy • Clozapine is effective than HPL • Clozapine has S/E of drowsiness, weight gain, non specific changes in EEG, and hypersalivation (Wt gain is approximately 7kg/6wks) • RSPN – weight gain, sedation, and EPS • OLZ- ↑ appetite, sedation • Quitiapine- well tollerated in longer term use/ sustained symptom improvement
  14. 14. • Care full practice parameters to be included in Antipsychotic dosage • Patient education abt the S/Es and informed consent • Baseline monitoring using AIMS for motor S/Es • Ongoing monitoring needs for SE of atypical APs • A combination of psychoeducational family Rx + medication Rx + social skill training has decreased relapse rate • Support the child and the family with proper explanations
  15. 15. • Supportive and CBT interventions are used to promote adaptive functioning • Individual/group interventions focus on improving conflict resolution, social skills, problem solving, and ADL • Advocacy and educational groups are beneficial- ↓ the stigma, and isolation experienced by the families. • School based interventions: spl education to address the possible learning and developmental disabilities • Community based interventions: case management, in-home therapeutic care, therapeutic recreational activities and vocational rehabilitation
  16. 16. Prognosis • Low IQ and poor premorbid functioning- ↓ outcome • Good prognosis: presence of affective symptoms, A/c and old age onset, better premorbid functioning and adjustment • Poor prognosis: poor premorbid character, non acute onset and early age of onset.
  17. 17. Thank You