This document discusses childhood psychosis. It begins by defining childhood psychosis and noting its rarity in children aged 7-8 years. While diagnostic criteria are the same as for adults, prevalence is estimated at 2 per 100,000 children based on DSM-III. Clinical features often resemble adult schizophrenia, including positive symptoms like hallucinations and delusions. Etiology is thought to involve genetic and neurobiological factors as well as family environment and low socioeconomic status. Treatment requires a multimodal approach including pharmacotherapy with atypical antipsychotics, psychoeducation, social skills training, and support for the child and family. Prognosis depends on factors like IQ, premorbid functioning, and age of onset.

1. Childhood Psychosis
Bivin Jay. B

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. 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. 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. 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. • 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. • 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. 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. • 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. • 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. • 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. 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. 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. • 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. • 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. 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. Thank You