Child  Psychiatry  
Paper  B   Syllabic  content  10  
 
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 1. Adult mental illness and children
¬ The  consequences  on  the  child  of  parental  mental  illness  affect  their  infancy,  toddlerhood,  preschool  
age,  school  age  and  adolescence.    The  best-­‐‑studied  example  of  the  influenced  of  parental  illness  on  
child’s  mental  health  is  that  of  maternal  depression.  
¬ It  is  important  to  note  that  the  effects  of  parental  mental  illness  on  children  are  mediated  by  complex  
factors.    
¬ Rutter  has  outlined  a  number  of  possible  mediators  of  the  effect  of  parental  psychiatric  disorder  on  a  
child.    First,  the  direct  pernicious  impact  of  exposure  to  the  parental  disorder.  Second,  an  indirect  
impact  due  to  altered  interpersonal  behaviour  and  parenting  capacity.  Third,  mediator  variables,  such  
as  the  social  adversity,  genetic  or  constitutional  factors  could  play  a  part  (Murray  &  Cooper,  1997).  
¬ Consequences  of  maternal  depression  on  a  growing  child  is  summarised  below:  
  Prenatal effects!
• Poor nutrition, higher preterm birth, low birth weight, pre-
  eclampsia!

  Effect on the infant!

• Anger and protective style of coping, passivity, withdrawal,
  reduced attention and lower IQ!

  Effect on toddler!
• Passive noncompliance, reduced expression of autonomy,
  internalizing and externalizing problems, and reduced social
interaction (e.g. no cooperative play)!

Effect on school-age children!

• Reduced adaptive functioning, affective, anxiety and
conduct disorders, ADHD-like presentation in some.!

Adolescents!
• Affective disorders (depression), anxiety disorders, phobias,
panic disorders, conduct disorders, substance abuse and
alcohol dependence!

Adapted  from  Canadian  Paediatric  Society,  Maternal  depression  and  child  development.  (2004).  Paediatrics  &  Child  Health,  9(8),  
575–583;    Murray,  L  &  Cooper,  PJ.  

©  SPMM  Course   2  
 2. Negative life events during development
¬ Childhood  adversities  are  significantly  associated  with  adult  mental  disorders  as  shown  in  numerous  
epidemiological  studies.  
¬ The  association  between  retrospectively  reported  childhood  adversities  and  the  first  onset  of  a  wide  
variety  of  mental  disorders  across  the  life  course  was  studied  in  epidemiological  surveys  in  21  
countries  in  the  World  Health  Organization  (WHO)  World  Mental  Health  (WMH)  Survey  Initiative  
(Kessler  et  al.,  2010).  Some  notable  findings  from  this  large  study  are  as  follows:  
o Parental  death  is  the  most  common  childhood  adversity  (11.0–14.8%).    
o Other  adversities  included  physical  abuse  (5.3–10.8%),  family  violence  (4.2–7.8%)  and  parental  
mental  illness  (5.3–6.7%).    
o Multiple  childhood  adversities  (mean  =  2  or  more  in  nearly  2/3rd)  were  common  among  
respondents  with  any  childhood  adversities.    
o Adversities  associated  with  maladaptive  family  functioning  elevate  the  risk  of  adult  psychiatric  
disorders  (all  major  DSM-­‐‑IV  disorders)  with  an  odds  ratio  of  1.3–2.4;  the  risk  was  lower  and  often  
insignificant  for  other  types  of  childhood  adversities.  These  results  were  strikingly  consistent  
globally.    

Child Abuse
¬ Physical  abuse  involves  the  intentional  injury  of  a  child  by  someone.  Physical  abuse  can  be  defined  as  
any  act  that  results  in  a  nonaccidental  physical  injury,  such  as  beating,  punching,  kicking,  biting,  
burning,  and  poisoning.
¬ Sexual  abuse  of  children  refers  to  sexual  behaviour  between  a  child  and  an  adult  or  between  two  
children  when  one  of  them  is  significantly  older  or  uses  coercion.  The  perpetrator  and  the  victim  may  
be  of  the  same  or  opposite  sex.  The  sexual  abuse  may  be  non  contact  or  contact  abuse  and  may  include  
exhibitionism;  nongenital  or  genital  fondling;  fellatio;  cunnilingus;  or  vaginal  or  anal  penetration.  
¬ Depression,  PTSD,  conduct  disorders,  somatisation  and  suicidal  behaviour  is  seen  in  those  with  a  h/o  
sexual  abuse.    Girls  are  more  often  the  victims  [4:1],  90%  abusers  are  male.  Avg  age  9-­‐‑11  years  
depending  on  the  study.
¬ Psychological  abuse  or  emotional  abuse  occurs  when  an  adult  repeatedly  conveys  to  a  child  that  he  or  
she  is  worthless,  defective,  flawed,  unloved,  or  unwanted,  flawed  or  endangered.  
¬ Neglect,  the  most  prevalent  form  of  child  maltreatment,  is  the  failure  to  provide  adequate  care  and  
protection  for  children.  Malicious  or  ignorant  withholding  of  physical,  emotional,  and  educational  
necessities  can  harm  children.  Neglect  includes  failure  to  feed  children  adequately  and  to  protect  them  
from  danger.  
¬ Of  the  cases  reported,  approximately  60%  are  for  neglect,  20%  for  physical  abuse,  10%  for  sexual  
abuse,  and  10%  for  other  forms  of  maltreatment  (e.g.,  psychological  abuse,  abandonment  etc)
¬ Child  maltreatment  is  a  non-­‐‑specific  risk  factor  for  multiple  forms  of  psychopathology.  They  also  have  
increased  rates  of  posttraumatic  stress  disorder,  depression,  self-­‐‑destructive  behaviour  and  borderline  
traits,  sexually  inappropriate  behaviours,  drug  and  alcohol  problems,  eating  disorders,  oppositional  
defiant  disorder  and  conduct  disorder.

©  SPMM  Course   3  
 Signs  of  possible  physical  abuse  
• Unexplained  injuries,bruises  or  burns,  especially  if  recurrent  
• Improbable  excuses  given  for  injuries  
• Refusal  to  discuss  injuries  
• Untreated  injuries  or  delay  in  reporting  them  
• Excessive  physical  punishment  
Signs  of  possible  physical  neglect  
• Constant  hunger  
• Poor  personal  hygiene  
• Constant  tiredness  
• Poor  state  of  clothing  
• Frequent  lateness  or  non-­‐‑attendance  at  school  
• Untreated  medical  problems  
 
Signs  of  possible  non-­‐‑organic  failure  to  thrive  
• Significant  lack  of  growth  
• Weight  loss  and  hair  loss  
• Poor  skin  or  muscle  tone  and  circulatory  disorders  
Signs  of  possible  emotional  abuse  
• Low  self-­‐‑esteem,  continual  self-­‐‑deprecation  
• Sudden  speech  disorder  
• Rocking,  head-­‐‑banging,  or  other  neurotic  behaviour  
• Self-­‐‑mutilation  
Signs  of  possible  sexual  abuse  
Behavioural  
• Lack  of  trust  in  adults  or  over-­‐‑familiarity  with  adults  
• Fear  of  a  particular  individual  
• Social  isolation,  withdrawal,  and  introversion  
• Sleep  disturbances  (nightmares,  irrational  fears,  bed  wetting,  fear  of  sleeping  alone,  needing  a  nightlight)  
• Running  away  from  home  
• Girls  taking  over  the  mothering  role  
• Unusual  interest  in  genitals  of  adults,  children,  or  animals  
• Expressing  affection  in  inappropriate  ways  
• Developmental  regression  
• Over-­‐‑sexualised  behaviour  
Physical/medical  
• Bruises,  scratches,  or  other  marks  to  the  thighs  or  genital  area  
• Itch,  soreness,  discharge,  unexplained  bleeding  from  the  rectum,  vagina,  or  penis  
• Pain  on  passing  urine  or  recurrent  urinary  tract  infection  
• Recurrent  vaginal  infection  
• Venereal  disease  
• Stained  underwear  
• Discomfort/difficulty  walking  or  sitting  
• Pregnancy,  particularly  when  reluctance  to  name  father  
• Higher  morning  cortisol  levels,  than  non  abused  children  
                                                                 Adapted  from;  Oxford  Handbook  of  Psychiatry,  1st  Edition  

©  SPMM  Course   4  
¬ Factitious  disorder/Munchausen’s  syndrome  by  proxy:  when  a  person  feigns  or  induces  illness  in  a  
child  or  others  in  order  to  obtain  medical  attention.  A  form  of  child  abuse.  Can  be  hard  to  detect  as  the  
perpetrator  may  cover  up  or  deny  behaviour.  Need  to  be  aware  when  a  young  person  repeatedly  
presents  for  medical  attention.

Aetiological factors for abuse

Physical  Abuse

¬ Although  child  abuse  occurs  at  all  socio-­‐‑economic  levels,  it  is  highly  associated  with  poverty  and  
psychosocial  stress,  especially  financial  stress.  
¬ Physical  abuse  most  commonly  begins  around  adolescence.  Child  maltreatment  is  strongly  correlated  
with  less  parental  education,  underemployment,  poor  housing,  welfare  reliance,  and  single  parenting.  
¬ Child  abuse  tends  to  occur  in  multiproblem  families,  that  is,  families  characterized  by  domestic  
violence,  social  isolation,  parental  mental  illness,  and  parental  substance  abuse,  especially  alcoholism.  
¬ Risk  factors  in  the  parent(s):  young  age,  low  IQ,  criminal  record,  poor  parenting  skills,  experience  of  
absue/neglect  as  a  child  and  psychiatrc  problems.
¬ Risk  factors  in  the  child  include  prematurity,  congenital  malformation,  intellectual  disability,  chronic  
illness,  difficult  temperament  (eg.  crying  a  lot).  
¬ The  risk  of  child  abuse  increases  in  families  with  many  children.

Sexual  Abuse

¬ Socioeconomic  status  is  unrelated  to  the  incidence  of  child  sexual  abuse,  but  lower  socioeconomic  
classes  are  more  likely  to  come  to  attention.
¬ There  is  an  inverse  relationship  between  self  blame  and  powerlessness  in  sexually  abused  children.  
¬ Most  common  relationship  is  stepfather  and  stepdaughter
¬ Social,  cultural,  physiological,  and  psychological  factors  all  contribute  to  the  breakdown  of  the  incest  
taboo.  Incestuous  behaviour  has  been  associated  with  alcohol  abuse,  overcrowding,  increased  physical  
proximity,  and  rural  isolation  that  prevent  adequate  extra  familial  contacts.  

©  SPMM  Course   5  
 3. Attention Deficit Hyperactivity Disorder

Clinical features of ADHD

¬ The  cardinal  features  of  ADHD  are  excessive  and  impairing  levels  of  hyperactivity,  inattention,  and  
impulsivity,  and  they  are  pervasive  over  time.  
¬ These  features  must  be  evident  in  more  than  one  setting,  cause  serious  impairment  and  be  excessive  in  
relation  to  the  person’s  mental  age  and  development,    and  must  not  be  due  to  other  causes  such  as  
anxiety,  schizophrenia  or  autism.  
¬ Hyperactivity-­‐‑impulsivity  symptoms  include:  fidgeting,   DSM-­‐‑5  AND  ADHD    
being  ‘always  on  the  go’,  talking  excessively;  unable  to  
For  ADHD  the  onset  criterion  has  been  
play  quietly;  continually  interrupting.  
changed  from  “symptoms  that  caused  
¬ Inattention  symptoms  include:  being  easily  distracted,  
impairment  were  present  before  age  7  
being  unable  to  sustain  attention,  difficulties  completing  
years”  to  “several  inattentive  or  
tasks,  difficulties  organizing,  avoiding  tasks  requiring  
hyperactive-­‐‑impulsive  symptoms  were  
mental  effort;  appearing  not  to  listen,  being  forgetful,  
present  prior  to  age  12”  
and  losing  things.
¬ Hyperactivity  is  more  impairing  and  more  noticeable  in   Subtypes  have  been  replaced  with  
pre-­‐‑school  children.  In  school  inattention  is  more   presentation  specifiers  that  map  directly  
noticeable,  and  inattention  and  impulsivity  is  noticeable   to  the  prior  subtypes  
in  both  adolescent  and  adult  populations,  especially  in  
social  situations. A  comorbid  diagnosis  with  autism  
¬ Connor’s  questionnaire  is  widely  used  to  obtain   spectrum  disorder  is  now  allowed  
information  from  schoolteachers  on  ADHD  symptoms.  
The  symptom  threshold  has  been  
There  are  also  parent  and  adolescent  versions
changed  for  adults  with  a  cutoff  for  
¬ Diagnostic  criteria: The  hyperkinetic  disorder  is  the  
ADHD  of  five  symptoms,  instead  of  six  
ADHD  equivalent  in  ICD-­‐‑10.  For  ADHD/HKD,  the  
required  for  younger  persons,  both  for  
diagnostic  criteria  are  considered  to  be  more  ‘relaxed’  in  
inattention  and  for  hyperactivity  and  
DSM  but  stricter  in  ICD-­‐‑10.    According  to  DSM-­‐‑IV  
impulsivity.  
criteria,  to  meet  the  diagnosis  of  ADHD,  some  symptoms  
must  be  present  before  the  age  of  7  years,  although  
ADHD  is  not  diagnosed  in  many  children  until  they  are  older  than  7  years  when  their  behaviours  
cause  problems  in  school  and  other  places.    
¬ To  confirm  a  diagnosis  of  ADHD,  impairment  from  inattention  and/or  hyperactivity-­‐‑impulsivity  must  
be  observable  in  at  least  2  settings  and  interfere  with  developmentally  appropriate  functioning  
socially,  academically,  or  in  extracurricular  activities  and  should  persist  for  at  least  six  months.  
¬ ADHD  is  not  diagnosed  when  symptoms  occur  in  a  child,  adolescent,  or  adult  with  a  pervasive  
developmental  disorder,  schizophrenia,  or  another  psychotic  disorder.  

©  SPMM  Course   6  
Prevalence:  
¬ Using  DSM-­‐‑IV  criteria,  proposed  general  prevalence  in  school  age  children  is  about  5%.  Using  ICD-­‐‑10  
criteria  ,  prevalence  is  approximately  1-­‐‑2%(Shorter  Oxford  Textbook  of  Psychiatry,  6th  Edition).
¬ The  prevalence  in  UK  children,  using  DSM  IV  criteria  is  3-­‐‑4%  (The  British  Child  and  Adolescent  
Mental  Health  Survey  1999:  the  prevalence  of  DSM-­‐‑IV  disorders)
¬ ADHD  is  3  times  more  prevalent  in  boys  than  in  girls,  and  more  common  in  areas  of  social  deprivation  
and  amongst  children  living  in  institutions  

Aetiology:
¬ Genetics:  Siblings  have  2-­‐‑3  times  increased  risk;  heritability  of  approximately  80%.  Greater  
concordance  in  monozygotic  compared  with  dizygotic  twins  [concordance  79%  in  monozygotic  and  
32%  in  dizygotic  twins].  Genes  5,  6,  and  11  implicated.  This  condition  is  associated  with  dopamine  
transporter  gene  [DAT1]  and  dopamine  D4  receptor  gene.  SNAP-­‐‑25  gene  may  also  have  a  role.
¬ Neuroimaging:  Areas  of  brain  affected  include:prefrontal  cortex,  striatum  and  cerebellum.  Studies  
using  positron  emission  tomography  (PET)  have  found  lower  cerebral  blood  flow  and  metabolic  rates  
in  the  frontal  lobe  areas  of  children  with  ADHD  than  in  controls.  PET  scans  have  also  shown  that  
adolescent  females  with  the  disorder  have  globally  lower  glucose  metabolism  than  both  normal  
control  females  and  males  with  the  disorder.
¬ Neurotransmitters:  DA  and  NA  dysregulation  in  the  prefrontal  cortex  is  implicated.  The  most  widely  
studied  drugs  in  the  treatment  of  ADHD,  the  stimulants,  affect  both  dopamine  and  norepinephrine,  
leading  to  neurotransmitter  hypotheses  that  include  possible  dysfunction  in  both  the  adrenergic  and  
the  dopaminergic  systems.  Serotonin  may  have  a  role  in  modulating  dopamine  transmission  and  the  
expression  of  ADHD.
¬ Potentially  important  environmental  factors  include  a)prenatal  and  perinatal  obstetric  complications  
b)  low  birth  weight  &  prematurity  c)  prenatal  exposure  to  alcohol,  nictine  and  benzodiazepines  d)  
poor  attachment  and  severe  early  deprivation  e)  institutional  rearing
¬ Idiosyncratic  reactions  to  food,  Other  food  additives,  lead  exposure  to  toxic  levels  are  not  supported  
by  research  evidence.
¬ Previous  research  shows  that  ADHD  occurs  in  head  injury  in  25%  cases.  Retrospective  cohort  study  
published  in  BMJ  found  that  head  injury  before  the  age  of  2  years  does  not  seem  to  be  causal  in  the  
development  of  ADHD.  Medically  attended  injury  before 2  years  of  age  may  be  a  ‘marker’  for  
 

subsequent  diagnosis  of  attention deficit  hyperactivity  disorder.

 

¬ The  quality  of  relationships  within  the  family  and  at  school  can  be  considered  as  protective  or  
maintaining  factors.
¬ Comorbidity:      50-­‐‑80%  of  children  with  ADHD  have  a  comorbid  disorder.  50%  children  may  meet  
criteria  of  2  comorbid  conditions.  Common  comorbid  problems  in  childhood  include  oppositional  
defiant  disorder  (40%),  anxiety  disorder  (34%);  conduct  disorder  (14%),  tics  (11%)  and  mood  disorder  
(6%)  (Young  et  al,  2011,  BMC  Psychiatry)

©  SPMM  Course   7  
Outcome:
¬ Approximately  15%  of  cases  continue  to  meet  diagnostic  criteria  for  ADHD  at  the  age  of  25  years.  
(Young  et  al,  2011,  BMC  Psychiatry).  A  further  50%  of  individuals  will  suffer  some  impairment  from  
residual  symptoms.  
¬ Children  with  hyperkinetic  disorders  are  5  times  greater  risk  for  antisocial  behaviour,  substance  abuse  
and  other  psychiatric  disorders.  15-­‐‑20%  develop  substance  misuse  problems
¬ Many  children  initially  diagnosed  with  ADHD,  combined  type,  exhibit  fewer  impulsive-­‐‑hyperactive  
symptoms  as  they  get  older  and,  by  the  time  they  are  adults,  will  meet  criteria  for  ADHD,  inattentive  
type.    
¬ Poor  prognosis  depends  on  early  stressful  life  experiences  such  as  due  poverty,  overcrowding,  
expressed  emotions  and  parental  psychopathology.  Prognosis  is  worse  when  the  symptoms  are  severe,  
predominantly  hyperactive-­‐‑impulsive  in  nature,  and  associated  with  conduct,  language  or  learning  
disorder.

Management
¬ Treatment  [long  term,  multimodal]:  Before  resorting  to  pharmacological  treatments,  efforts  should  be  
made  to  provide  psychological  and  social  interventions.  If  medication  is  being  considered,  the  young  
person/family    need  to  consent,  and  must  be  aware  of  the  possible  side  effects  of  treatment.  
¬ General  management  principles  are:
o Educational/remedial  interventions  
o Parent  training  programme  for  child  management  skills–  based  on  social  learning  theory  and  
behavioural  interventions
o Individual/family/group  therapies
o CBT  methods,  especially  behavioural,  are  often  effective
o Social  skills  training
¬ MTA  Study:  The  Multimodal  treatment  study  of  children  with  ADHD  was  the  largest,  most  rigorous  
randomised  controlled  trail  to  date,  involving  579  children.  Despite  methodological  issues  raised  by  
few  authors,  it  is  a  trial  that  confirmed  the  effectiveness  of  medication  management  in  children  and  
adolescents.  The  trial  also  found  that  intensive  behavioural  therapy  involving  the  child;  family  and  
teachers  added  little  to  well  supervised  medication  management.  However,  psychological  
interventions  are  important  for  families  who  do  not  wish  to  use  medication.  Also,  there  is  lack  of  
evidence  of  efficacy  over  prolonged  periods  of  treatment  with  medication.  
¬ Stimulants  –  release  noradrenaline,  dopamine  and  also  serotonin,  increasing  extracellular  dopamine  
and  thus  ‘inhibit’  impulses,  helping  persistence  in  motor  and  cognitive  functions.  They  are  rapidly  
absorbed  following  oral  administration.  
¬ Methylphenidate  has  most  rapid  onset  1-­‐‑3hr,  and  shortest  half-­‐‑life  2-­‐‑3  hours  so  the  effects  wear  off  in  
4-­‐‑6  hours.  Methylphenidate  dose  range  –  5-­‐‑60mg/day.    Growth  retardation  may  occur  during  acute  
treatment,  but  no  significant  retardation  seen  in  long  term.  Note:  Prescription  of  stimulants  does  not  
increase  the  rate  of  substance  abuse  by  the  patients.
¬ Pimoline  is  no  longer  licensed  in  UK  as  it  causes  abnormal  liver  function  tests,  and  in  some  cases  liver  
failure  following  long  term  use.
©  SPMM  Course   8  
¬ Atomoxetine  is  a  noradrenaline  reuptake  inhibitor  –  good  evidence  for  use  in  hyperkinetic  disorders.  
It  increases  noradrenaline  in  the  synaptic  cleft.  It  doesn’t  affect  dopamine  levels,  and  hence  doesn’t  
cause  more  tics.  In  December  2012,  MHRA  issued  a  note  highlighting  that  Atomoxetine  can  cause  
clinically  relevant  increases  in  blood  pressure  or  heart  rate,  or  both,  in  a  small  proportion  of  patients  
and  suggested  monitoring  heart  rate  and  BP.  
¬ Monitoring:    Height,  weight,  blood  pressure,  heart  rate  monitoring  is  recommended  for  
methylphenidate  (initially  3  monthly,  then  6  monthly).  Atomoxetine  rarely  causes  liver  damage;  so  
routine  monitoring  of  LFT  is  not  warranted.  The  MHRA  also  advises  that  patients  on  Atomoxetine  
should  be  monitored  for  signs  of  depression,  suicidal  thoughts  or  suicidal  behaviour.  Monitoring  of  
height  and  weight  is  also  recommended,  initially  three  monthly  and  then  six  monthly.  

Stimulants  (methylphenidate)  
1st  Line   Specifically  treat  ADHD  core  symptoms   Adverse  effects:  
Medication   [hyperactivity>inattention]   Appetite,  weight  loss  
Largest  and  most  rapid  effect  on  ADHD  of  any  drug   Sleep  disturbance  (if  taken  late  in  day)  
class,  indirect  sympathomimetic  by  increasing  DA  and   Cramps  (first  few  weeks)  
AND  release.     Headaches  
Calms  comorbid  aggression  and  oppositional-­‐‑defiant   Mild  BP  and  pulse  increase  
behaviour   Evening  crash  
Except  for  pemoline,  medically  safer  than  most   constricted  affect  and  spontaneity,  emotional  
psychoactive  drugs   blunting,  social  withdrawal,  
Results  of  given  dose  seen  immediately;  relatively  easy   Depression  
titration   Tics  
Now  available  in  XL  preparation   Hallucinations  (skin  crawling,  visions)  
Mild  growth  slowing  first  2  years    
Dose  for  behaviour  may  not  be  optimal  for  attention    
 
(normal  dose:  Initially  5-­‐‑10  mg  daily  titrated  up  to  a  
maximum  of  60  mg/day  in  divided  doses  using  
weekly  increments  of  5-­‐‑10  mg.)  
 
 
Atomoxetine  
  Noradrenaline  reuptake  inhibitor   Adverse  effects:  
Specifically  treats  ADHD  core  symptoms     Appetite,  weight  loss  
Nearly  as  effective  as  stimulants;  may  help  stimulant   Gastrointestinal  Sx  (nausea,  vomiting,  diarrhea,  
failures   constipation)  
Continuous  duration  of  effect   Fatigue,  dizziness  
Little  or  no  insomniac  side  effect   Probable,  mild  growth  slowing  
Can  be  given  any  time  of  day  –once  daily   Allergic  reactions  
No  tic  side  effect  (good  choice  with  comorbid  tics  )   Possibly  longer  time  than  stimulants  to  flush  out  if  
May  help  comorbid  depression   adverse  effect  
  Slower  attainment  of  full  effect  than  stimulants  
 
Antidepressants  
Tricyclics   Treat  both  ADHD  and  comorbid  depression  and  anxiety   Adverse  effects:  
Helps  some  stimulant  non-­‐‑responders   Sedation  
Third  most  effective  drug  class  for  ADHD  (except  for   BP  changes  (down  or  up)  
SSRIs,  which  are  not  very  effective)   Dizziness  (especially  on  standing)  
Some  patients/families  who  are  prejudiced  against   Dry  mouth  
stimulants  will  accept  antidepressants   Cardiac  conduction  block:  TCAs  require  ECG  
May  equal  stimulant  effectiveness  for  adults   monitoring  in  children  
©  SPMM  Course   9  
  
 
 
 
 
Alpha  2  agonists  
    Treat  both  hyperactivity-­‐‑impulsiveness  and  comorbid  tic   Adverse  effects:  
disorder  or  comorbid  aggression   Response  delayed  
Helps  some  nonresponders  to  stimulants  and   Sedation  
antidepressants   Hypotensive  dizziness  (especially  postural)  
Good  for  those  overaroused,  possibly  with  comorbid   Dry  mouth  
anxiety   Rare  hallucinations  
Hypertensive  rebound  if  dose  missed  
Not  as  helpful  for  attention  as  stimulants  
Antipsychotics  
    May  work  when  stimulant  or  atomoxetine  does  not,   Adverse  effects:  
especially  if  stimulant  makes  worse   Sedation  
Good  for  comorbid  anxiety,  aggression,  tic  disorder,  or  Extrapyramidal  side  effects  
bipolar  disorder   Endocrine  effects  
Tardive  dyskinesia  
Paradoxical  agitation  (akathisia)  
Weight  gain  
Not  specific.  generally  less  effective  than  stimulants  
or  atomoxetine  
Riskiest  drug,  last  resort  
Adapted  from  Lewis’s  Child  &  Adolescent  Psychiatry:  A  comprehensive  textbook  4th  edn  

©  SPMM  Course   10  
 4. Disorders of childhood conduct
Disorders  of  childhood  conduct  comprise  of  (a)  Conduct  Disorder  and  (b)  Oppositional  Defiant  Disorder.  
Conduct  disorder  (CD)  is  characterized  by  a  severe  and  persistent  pattern  of  antisocial,  aggressive  or  
defiant  behaviours  that  defy  age-­‐‑appropriate  societal  norms.  Oppositional  Defiant  Disorder  (ODD)  also  
involves  a  persitent  pattern  of  defiant  behaviour.  However,  the  behaviour  in  the  latter  does  not  defy  age-­‐‑
appropriate  societal  norms  to  the  same  extent  as  in  CD.    According  to  ICD10,  oppositional  defiant  
disorder  is  a  subtype  of  conduct  disorder.  DSM-­‐‑5  excludes  oppositional  disorder  if  a  conduct  disorder  is  
present.  

Conduct Disorder
Diagnostic criteria:
¬ Children  with  conduct  disorder  are  likely  to  demonstrate  behaviours  in  the  following  four  categories
o Physical  aggression  or  threats  of  harm  to  people,  cruelty  to  people  and  animals
o Destruction  of  their  own  property  or  that  of  others
o Theft  or  acts  of  deceit
o Frequent  and  serious  violation  of  age-­‐‑appropraite  rules  (Like  truating  or  running  away)
¬ ICD-­‐‑10  requires  at  least  one  behaviour  to  be  present  for  at  least  six  months.  According  to  DSM-­‐‑5  
criteria,  atleast  3  out  of  a  list  of  15  behaviours  should  begin  before  the  age  of  13,  for  a  period  of  12  
months.  DSM-­‐‑5  has  added  a  limited  prosocial  emotions  specifier  to  the  diagnosis  of  conduct  disorder  
for  children  who  do  not  meet  the  full  criteria  but  present  with  limited  prosocial  emotions,  such  as  
limited  empathy  and  guilt.  Other  specifiers  retained  from  DSM-­‐‑IV  a  childhood  onset  type  –  symptoms  
present  before  age  10  and  an  adolescent  onset  type  –  symptoms  develop  after  age  10.  
¬ CD  is  the  cause  of  great  suffering  in  both  the  individual  and  in  society;  it  is  one  of  the  major  risk  
factors  for  adult  antisocial  behaviour,  posing  a  major  burden  on  public  resources.  Conduct  disorder  
occurs  with  greater  frequency  in  the  children  of  parents  with  antisocial  personality  disorder  and  
alcohol  dependence  than  in  the  general  population.  In  the  Isle  of  White  study,  CD  was  found  to  be  the  
most  common  psychiatric  disorder  amongst  10-­‐‑11  year  olds.  
¬ A  prevalence  of  5-­‐‑7%  is  noted  in  the  UK  (Oxford  Handbook  of  Psychiatry,  3rd  Edn.).  The  disorder  is  
more  common  among  boys  than  girls,  and  the  male:  female  ratio  is  4:1.  

Aetiology:
¬ Ontario  Child  Health  Survey[1987]  :    Three  most  significant  risk  factors:  
o Family  dysfunction
o Parental  mental  illness
o Low  income
¬ Rutter  [1978]  :  
o Low  socioeconomic  status,  [Low  family  income]
o Criminality  of  father,  
o Overcrowding,  
o Maternal  neurosis,  
o Institutional  care
©  SPMM  Course   11  
 o Chronic  marital  discord
¬ Biological  risk  factors:  
o Genetic:  CD  clusters  in  families.  Heritable  trait  of  being  more  susceptible  to  externalizing  disorders  
in  general  (CD,  ODD  and  and  ADHD)  (Shorter  Oxford  Textbook  of  Psychiatry,  6th  Edition).
o Temperament:  ‘callous-­‐‑unemotional’
o Brain  injury  
o Neurochemical:  Low  CSF  serotonin,  deficient  serotonergic  activity  is  seen  in  those  with  early  onset  
and  more  aggressive  behaviour.    Autonomic  under-­‐‑arousal  e.g.,  consistent  lower  mean  resting  
heart  rates,  lower  electro  dermal  activity  etc.  HR  indices  can  predict  later  onset  of  aggression.    
Low  salivary  cortisol  levels  are  also  reported.
o Low  IQ.  Performance  IQ  may  be  higher  than  Verbal  IQ
o Neuroimaging:  Prefrontal  brain  regions  may  have  reduced  volumes  in  affected  children.
¬ Psychosocial  risk  factors:
o Maternal  smoking  during  pregnancy
o Parental  criminality  and  substance  abuse
o Harsh  and  inconsistent  parenting
o Lack  of  a  warm  parental  relationship  and  cold/rejecting  family  relationships
o Domestic  violence  in  the  family  and  child  abuse
o Large  family  size
o Low  socio-­‐‑economic  status  /  Low  family  income  and  social  disadvantage
o Early  loss  and  deprivation
o School  failure  and  poor  school  achievement
o Social  isolation;  
o Exposure  to  urban  life  does  not  increase  the  rate  of  conduct  disorders,  though  some  studies  have  
found  higher  prevalence  rates  in  urban  locations  

Outcome

¬ Childhood  conduct  disorders  further  predict  risk  for  numerous  problems  in  adulthood  that  includes  
(Moffitt  et  al-­‐‑2002)
o Criminality  and  antisocial  personality  disorder.  Less  than  50%  of  conduct  disorder  children  have  
persistent  and  severe  antisocial  problems  as  adults  (Zoccolillo  et  al  1992).
o Serious  difficulties  in  education,  work  and  finances
o Homelessness  and  abuse
o Drug  and  alcohol  dependence
o Poor  physical  health  including  injuries,  sexually  transmitted  infections,  compromised  immune  
function
o Variety  of  mental  disorders  and  suicidal  behaviour

©  SPMM  Course   12  
 Protective  factors

• Female  gender
• High  IQ
• Resilient  temperament
• Good  parenting
• Warm  relationship  with  a  key  adult
• Commitment  to  social  values
• Increased  economic  equality.

Poor  prognostic  factors

• Early  onset  (before  10  yrs)

• Increased  aggression  at  early  age
• Aggression  carried  out  in  isolation  and  not  in  groups
• Low  IQ
• Low  socio-­‐‑economic  status
• Poor  school  achievement
• Atentional  problems  and  hyperactivity  as  a  child
• Poor  parenting  and  family  criminality.

Treatment:
¬ As  the  causes  and  risk  factors  are  multifactorial,  treatment  is  multimodal.  Explore  specific  support  for  
academic  and  social  skills.  Psychological  therapies  form  the  mainstay  of  treatment  for  conduct  
problems.  Parent  Management  Training  based  on  the  principles  of  social  learning  theory  has  been  very  
successful  in  altering  the  course  of  conduct  disorders.  NICE  recommends  that  group  based  parent  
training/education  programmes  should  be  the  mainstay  of  treatment  for  children  of  12  years  and  
under  with  oppositional  defiant  disorder  and  conduct  disorder.
¬ Cognitive  behavioural  therapy:  CBT  for  conduct  problems  in  children  and  adolescents  typically  includes  
social  skills  training  and  anger  management.  The  most  common  targets  are  aggressive  behaviour,  
social  interactions,  self-­‐‑evaluation  and  emotional  dysregulation.
¬ Functional  family  therapy:  One  of  the  best-­‐‑known  interventions  for  serious  antisocial  behaviour  is  
functional  family  therapy.  It  is  designed  to  be  practicable  and  relatively  inexpensive.    The  target  age  
range  is  11-­‐‑18  years.  Between  eight  and  twelve  1-­‐‑hour  sessions  are  given  in  the  family  home  to  
overcome  attendance  problems.  For  more  intractable  cases,  12-­‐‑16  sessions  are  offered  and  it  usually  
lasts  for  three  months.  There  are  four  phases  of  treatment  which  includes  Engagement,  Motivation,  
Behavioural  Change  and  Generalisation.  The  aim  is  first  to  keep  the  family  in  treatment  and  only  then  
to  move  on  to  finding  what  precisely  they  want.  The  therapist  must  understand  the  parents’  goals  
before  specific  techniques  are  taught.  Functional  family  therapy  addresses  family  processes,  which  
need  to  be  present,  such  as  improving  communication  between  parent  and  young  person,  reducing  
interparental  inconsistency,  tightening  up  on  supervision  and  monitoring,  and  negotiating  rules  and  
the  sanctions  to  be  applied  for  breaking  them.  Functional  family  therapy  has  been  shown  to  reduce  
reoffending  rates  by  around  50  per  cent.
¬  Multisystemic  therapy:    It  is  one  of  the  best-­‐‑developed  treatments  of  conduct  disorder,  which  rests  on  
nine  treatment  principles.  The  clinicians  take  on  only  four  to  six  cases  at  a  time  and  the  team  is  
available  24  hours  a  day.  Treatment  is  usually  given  for  three  months  and  then  stopped.  In  

©  SPMM  Course   13  
 Multisystemic  therapy the  young  person'ʹs  and  family'ʹs  needs  are  assessed  in  their  own  context  at  
,  

home  and  in  their  relationships  with  other  systems  such  as  school  and  peers.  Following  the  
assessment,  proven  methods  of  intervention  is  used  to  address  difficulties  and  promote  strengths.  In  
this  therapy,  assessing  and  promoting  the  strengths  in  the  young  person  and  the  system  is  very  
important.  The  therapist  is  responsible  for  ensuring  appointments  are  kept  and  for  making  change  
happen—families  cannot  be  blamed  for  failing  to  attend  or  ‘not  being  ready'ʹ  to  change.  Regular  
written  feedback  on  progress  towards  goals  from  multiple  sources  is  gathered  by  the  therapist  and  
acted  upon  and  the  parents  and  teenagers  fill  in  weekly  questionnaires  on  whether  they  have  been  
receiving  therapy  as  planned.  There  is  close  attention  to  ‘quality  control’  by  offering  weekly  
supervisions  and  the  supervisor  checks  adherence  weekly.  Several  randomised  controlled  trial  attest  to  
effectiveness,  with  reoffending  rates  typically  cut  by  half  and  time  spent  in  psychiatric  inpatient  care  
further  reduced.  
¬ Other  treatment  options:  
o Treat  any  comorbidity  
o Address  any  child  protection  concerns  
o Anger  Management  Programmes  

Oppositional Defiant Disorder

¬ ODD  is  characterised  by  an  enduring  pattern  of  negative,  hostile,  disobedient  and  defiant  behaviour,  
without  serious  violations  of  societal  norms  or  the  rights  of  others.  Symptoms  must  be  persistent  and  
evident  for  at  least  6  months.  In  oppositional  defiant  disorder,  a  child'ʹs  temper  outbursts,  active  refusal  
to  comply  with  rules,  tendency  to  blame  others,  spiteful  and  annoying  behaviours  exceed  expectations  
for  these  behaviours  for  children  of  the  same  age.  
¬ Manifestations  of  the  disorder  are  almost  invariably  present  in  the  home,  but  they  may  not  be  present  
at  school  or  with  other  adults  or  peers.  In  some  cases,  features  of  the  disorder  from  the  beginning  of  
the  disturbance  are  displayed  outside  the  home;  in  other  cases,  the  behaviour  starts  in  the  home,  but  is  
later  displayed  outside.  Typically,  symptoms  of  the  disorder  are  most  evident  in  interactions  with  
adults  or  peers  whom  the  child  knows  well.    
¬ Although  ODD  can  begin  as  early  as  3  years  of  age,  it  typically  is  noted  by  8  years  of  age  and  usually  
not  later  than  adolescence.  Age  of  onset  of  ODD  is  generally  earlier  than  that  for  CD.  Prevalence  2-­‐‑5%  
(Oxford  Handbook  of  Psychiatry,  3rd  Edn).  The  disorder  seems  more  prevalent  in  boys  than  in  girls  
before  puberty,  and  the  sex  ratio  appears  to  be  equal  after  puberty.  25%  cases  show  no  symptoms  in  
later  life  (Oxford  Handbook  of  Psychiatry,  3rd  Edn)  but  many  progress  to  conduct  disorder    
¬ Aetiology  includes  temperamental  factors  like  sick  or  traumatised  child  and  power  struggle  between  
parents  &  child.  
¬ Longitudinal  studies  suggest  that  ADHD  in  early  life  is  a  predictor  of  oppositional  defiant  disorder  
and  conduct  disorder  later  in  life.  
¬ Chronic  oppositional  defiant  disorder  almost  always  interferes  with  interpersonal  relationships  and  
school  performance.  Secondary  to  these  difficulties  can  be  low  self-­‐‑esteem,  poor  frustration  tolerance,  
depressed  mood,  and  temper  outbursts.  Adolescents  may  abuse  alcohol  and  illegal  substances.  The  
disturbance  may  evolve  into  a  conduct  disorder  or  a  mood  disorder  
©  SPMM  Course   14  
¬ Poor  prognosis  is  associated  with  early  onset  of  symptoms,  longer  duration  of  symptoms,  co-­‐‑morbid  
anxiety,  impulse  control  &  substance  misuse  disorders  and  development  of  conduct  disorder.  
¬ Management:    The  principles  are  the  same  for  both  ODD  and  CD.  The  primary  treatment  of  ODD  is  
family  intervention  using  both  direct  training  of  the  parents  in  child  management  skills  and  careful  
assessment  of  family  interactions.  With  the  child,  use  methods  such  as  collaborative  problem  solving  
skills.  Behaviour  therapists  emphasize  teaching  parents  how  to  alter  their  behaviour  to  discourage  the  
child'ʹs  oppositional  behaviour  and  encourage  appropriate  behaviour.  Behaviour  therapy  focuses  on  
selectively  reinforcing  and  praising  appropriate  behaviour  and  ignoring  or  not  reinforcing  undesired  
behaviour.  

5. Early onset mood and psychotic disorders

Depressive disorder
¬ The  same  diagnostic  criteria  for  a  major  depressive  episode  apply  in  both adult  and  youth  
populations,  but  the  way  that  young  people  can  present  can  vary  (see  ‘clinical  features’  section  below).  
Core  symptoms  of  low  or  irritable  mood,  fatigue  or  anhedonia,  along  with  at  least  five  other  
symptoms,  such  as  social  withdrawal,  worthlessness,  guilt,  suicidal  thoughts  or  behaviour,  sleep  
increase  or  decrease,  decreased  motivation  and/or  concentration,  and  increased  or  decreased  appetite.    
¬ The  prevalence  of  depression  amongst  young  people  is  increasing.  Pre-­‐‑puberty:  about  1%,  no  sex  
difference;    Post-­‐‑puberty:  about  3%,  commoner  in  females.  
¬ 50%  of  young  people  with  depression  remain  clinically  depressed  after  12  months.  Most  young  people  
with  major  depression  will  recover  from  the  episode  within  2  years.  Adolescent  depression  however  
shows  significant  continuity  [eg    30%  will  have  a  recurrence  within  5  years]  into  adulthood.
¬ The  single  most  important  distinction  between  depression  as  an  illness  and  the  normal  ups  and  downs  
of  childhood  and  adolescence  is  that  depression  is  associated  with  functional  impairment,  mediated  
through  the  intensity,  duration,  and  lack  of  responsiveness  of  depressed  mood  and  associated  
symptoms.    
¬ The  full,  pure  clinical  syndrome  of  depression  is  very  uncommon  before  puberty.  In  early  adolescence,  
cognitive  changes  such  as  formal  operational  thought  allow  hopelessness  to  be  experienced  and  a  
clinical  picture  akin  to  adult  depression  can  be  seen.  Depression  should  only  be  diagnosed  when  there  
is  impairment  of  social  role  functioning,  or  with  symptoms  leading  to  significant  suffering,  or  
psychopathy  eg  suicidality.
¬ It  is  important  to  rule  out  organic  pathology  and  ask  about  possible  substance  misuse/abuse  .  

Clinical  features:

¬ Young  children:  Poor  feeding,  failure  to  thrive,  tantrums,  irritability,  separation  anxiety,  hyperactivity,  
regressed  behaviour  such  as  enuresis,  soiling  etc.
¬ Older  children:    Somatisation  like  pain  in  head,  abdomen,  chest  and/or  Hypochondriacal  ideas,  school  
refusal,  Poor  academic  achievement  at  school,  decline  in  school  work,  sleep  disturbance,  antisocial  
behaviour

©  SPMM  Course   15  
¬ Adolescents:  Low  mood  may  not  be  fixed  and  is  more  influenced  by  environment.    Anhedonia  and  
social  withdrawal  are  powerful  indicators  of  the  presence  of  depression.  Other  features  may  include  
Low  self-­‐‑esteem,  biological  symptoms,  suicidal  acts,  behavioural  problems,  and  substance  abuse.
¬ Serious  depressive  episodes  are  rare  before  puberty,  increasing  in  mid  and  late  adolescence  to  adult  
levels.  Clinical  features  are  essentially  the  same  as  in  adulthood  but  impairment  may  not  be  as  salient,  
as  in  adults.  
¬ Dysthymic  disorder  is  a  chronic  condition  with  fewer  symptoms  than  major  depression,  but  lasts  a  
minimum  of  one  year.
¬ Risk  factors:  95%  of  major  depression  in  young  people  is  seen  in  children  with  longstanding  
psychosocial  dificulties.  Other  risk  factors  include
o Family  history  of  depression
o Early  loss  of  a  parent
o Parental  separation,  divorce  and  marital  conflict
o Stressful  life  events
o History  of  abuse  (physical,  emotional  and  sexual)
¬ Maintaining  factors
o Persistence  of  subthreshold  symptoms
o Scarring:  First  episode  of  depression  sensitizes  people  to  further  episodes
o Personality,  temperament,  cognitive  abiities
o Persisting  adversity
o Comorbidity
¬ Comorbidity:  Comorbidity  is  the  rule  (50-­‐‑80%)  rather  than  the  exception  in  depressed  children  and  
adolescents.  Anxiety  [50  –  80%]  is  frequently  a  precursor  of  mood  disorder  and  may  also  occur  
simultaneously  with  depression.  Conduct  disorder  –  25%  ,  OCD  –  15%,  eating  disorder  –  5%
¬ ADHD  and  depression  are  also  often  co  morbid  and  the  two  disorders  may  be  co  transmitted  in  
families.  Alcohol,  drug,  and  tobacco  abuse  and  conduct  disorder  are  associated  with  depression

Treatment

¬ Establish  therapeutic  alliance  and  provide  education  to  the  child  and  family.  A  multidisciplinary  
approach  should  be  adopted.
¬ Mild  depression:  2  weeks  of  watchful  waiting.  After  4  weeks  –  supportive  therapy,  self  help  or  group  
CBT.  With  self  help  consider,  advice  on  exercise,  sleep  hygiene  and  anxiety  management  to  the  young  
person.  Moderate  to  severe  depression  –  CAMHS  review,  +/-­‐‑  3  months  of    individual  CBT,  IPT,  or  
shorter  term  family  therapy.  Consider  an  alternate  psychotherapy  if  first  mode  doesn’t  help.  CBT  can  
reduce  the  duration  of  illness  as  compared  to  the  other  psychological  treatments.  NICE  guidance  for  
moderate  to  severe  depression  recommends  psychotherapy  before  considering  pharmacotherapy.  
¬ Combination  treatment  should  be  considered  in  all  cases  (i.e.  psychotherapy  +  medication).  
¬ Several  studies  have  demonstrated  efficacy  with  selective  serotonin  reuptake  inhibitors  (SSRI)  
antidepressants,  especially  using  fluoxetine.  NICE  guideline  recommends  fluoxetine  as  first  line  and  
sertraline  or  citalopram  as  second  line.  Fluoxetine  is  the  best-­‐‑studied  antidepressant  with  the  strongest  

©  SPMM  Course   16  
 efficacy  data,  and  consequently  is  the  only  antidepressant  to  receive  FDA  and  MHRA  approval  and  
has  been  allowed  by  CSM  for  use  for  the  treatment  of  depression  in  children  and  adolescents.  Monitor  
for  emergence  of  agitation,  irritability,  unusual  changes  in  behaviour  and  emergence  of  suicidality  at  
initiation  and  when  dosages  are  changed.  Paroxetine  –  evidence  shows  that  Paroxetine  has  little  
impact  to  treatment,  symptom  levels,  functional  status  or  clinical  improvement.  Paroxetive  is  also  
more  likely  to  bring  serious  adverse  effects  [and  discontinuation]  and  increased  suicidal  behaviour.
¬ TCAs  are  not  supported  by  trials  and  have  been  associated  with  cardiac  toxicity.  
¬ Psychotherapy  is  considered  as  a  reasonable  initial  treatment  in  mild  to  moderate  depression  and  this  
may  be  individual,  group,  or  family  therapy.  CBT  is  one  of  the  most  researched  techniques,  but  IPT,  
behaviour  therapy,  psychodynamic  therapy,  and  supportive  therapy  are  used.  
¬ Treatment  of  Adolescents  with  Depression  Study  (TADS)  :  TADS  is  the  only  published  study  to  compare  
CBT,  fluoxetine,  their  combination,  and  placebo.  In  this  large  [n=439],  well-­‐‑powered  investigation,  CBT  
(43%  significantly  improved)  was  not  superior  to  placebo  (35%),  whereas  both  combination  (71%)  
including  fluoxetine,  and  fluoxetine  alone  (61%),  were  markedly  superior  to  both  CBT  and  to  placebo.  
The  combination  treatment  (CBT  +  fluoxetine)  showed  a  faster  recovery  than  any  of  the  other  
treatments,  although  fluoxetine  alone  had  a  favourable  outcomes  with  respect  to  the  Clinical  Global  
Impression  Improvement  (CGI-­‐‑I)  and  baseline-­‐‑adjusted  endpoints  and  in  more  severely  depressed  
patients.  Combined  treatment  was  superior  to  fluoxetine  alone  with  regard  to  remission  (37  vs.  20%).
¬ A  possible  explanation  for  the  relatively  weak  performance  of  CBT  in  this  study  could  be  the  nature  of  
TADS  treatment  package,  which  attempted  to  deliver  a  large  number  of  approaches  such  as  problem  
solving,  behaviour  activation,  cognitive  restructuring,  emotion  regulation,  relaxation  training  etc  in  a  
brief  period.    
¬ ECT  not  recommended  for  5-­‐‑11  year  olds.    In  older  persons,  only  in  severe  depression,  life  threatening  
symptoms,  or  severe  intractable  symptoms  not  responding  to  other  treatment.

Suicide  and  Deliberate  Self  Harm:

¬ Suicide  is  the  third  leading  cause  of  death  for  adolescents,  following  accidents  and  homicides  (Hawton  
1986).  12%  of  adolescent  deaths  are  due  to  suicide.    Male  suicides  outnumber  females  at  all  ages  and  in  
all  cultures.  
¬ Suicidal  ideation  is  very  common    in  adolescents  –  14%  boys,  25%  girls.  Suicide  attempts  and  
deliberate  self  harm  (DSH)  are  more  common  in  females,  completed  suicides  are  more  common  in  
males.
¬ Few  adolescents  who  make  suicide  attempts  actually  have  psychiatric  disorder  and  serious  suicidal  
intent  is  low.  In  contrast,  almost  all  children  and  teenagers  who  commit  suicide  suffer  from  a  
psychiatric  disorder  at  the  time  of  death  –  mood  disorder,  alcohol/substance  abuse,  anxiety  disorders,  
or  conduct  disorders.  
¬ Self-­‐‑poisoning  is  the  commonest  form  of  parasuicide-­‐‑the  usual  agents,  being  analgesics  and  
psychotropic  agents.  Others  include  attempted  hanging,  jumping  from  heights,  car  exhaust  fumes  and  
shooting  being  most  frequent.  Hanging  is  the  most  common  method  used  by  boys  who  completed  

©  SPMM  Course   17  
 suicide.  Overdose  or  jumping  from  heights  is  the  most  common  method  used  by  girls  who  completed  
suicide.
¬ 10%  of  adolescents  who  attempt  suicide  repeat  within  a  year.   40%  suicides  will  have  made  a  previous  
suicide  attempt.

Comparison  of  suicide  and  non-­‐‑fatal  deliberate  self-­‐‑harm  

  Completed  suicide   Non  fatal  DSH  

Incidence     Declining  until  recently   Rising  
Sex   Males     Female  
Age     Older  (rare  in  children)   Younger  (rare  in  children)  
Social  class   Upper  and  lower   Lower  
Childhood   Death  of  a  parent   Broken  home  
Precipitants   Guilt,  hopelessness   Situational  crisis  
Family   2-­‐‑4  times  likely  to  have  a  1st  degree  relative  who  committed    
History   suicide  
Setting   Often  premeditated  and  alone   Impulsive  and  often  others  
present  
 

Bipolar disorder
¬ The  symptoms  of  mania  commonly  reported  in  children  include:    increased  energy,distractibility,  
pressured  speech,  irritability,  grandiosity,  racing  thoughts,  decreased  need  for  sleep,  euphoria/elation,  
flight  of  ideas  and  poor  judgement.  
¬ Children  experiencing  a  manic  episode  typically  present  with  atypical  or  mixed  features  characterized  
by  irritability,  labile  mood  and  behavioural  problems.  Mood  lability  is  a  common  and  impairing  
presentation  in  youth,  which  may  not  always  be  a  sign  of  mood  disorder.
¬ Elated/euphoric  mood  and  irritability  are  the  two  symptoms  with  the  most  variability  in  rates  across  
studies.  However,  though  there  was  also  significant  heterogeneity  in  the  rates  of  decreased  need  for  
sleep,  racing  thoughts,  poor  judgment,  pressured  speech,  and  distractibility.  
¬ Epidemiology:    Prevalence  in  adolescents  is  approximately  1%  and  as  high  as  6%  when  including  soft  
subsyndromal  symptoms.  M>F  in  childhood  cases;  M=F  in  adolescents.  Retrospective  studies  in  adults  
with  Bipolar  Affective  Disorder  have  consistently  reported  that  up  to  60%  had  the  onset  of  their  mood  
symptoms  before  the  age  of  20  years.
¬ Co-­‐‑morbidity:  Approximately  70%  have  ADHD,  40%  ODD,  30%  anxiety  disorder,  40%  have  substance  
misuse  problems,  8%  Tourette’s  syndrome  and  3%  bulimia  nervosa.  
¬ Outcome:    Early  onset  BPD  has  a  poor  outcome  with  50%  showing  long-­‐‑term  decline  in  function.  The  
course  is  often  chronic  and  less  responsive  to  treatment,  with  atypical  and  rapid-­‐‑cycling  features  
especially  difficult  to  treat.  
¬ Some  studies  suggest  that  approximately  20%  of  adolescents  who  have  an  episode  of  major  depression  
experience  a  subsequent  manic  episode  by  adulthood. In  depressed  children  and  adolescents,  the  
following  features  predict  subsequent  development  of  mania
o Rapid  onset  depressive  episode  with  psychomotor  features  

©  SPMM  Course   18  
 o Depressive  episode  with  psychotic  features
o Family  history  of  mood  disorder,  especially  mania
o History  of  hypomania  or  mania  following  treatment  with  antidepressant  medications
¬ Suicide  risk  is  high  with  rates  of  completed  suicide  approximately  10%.
¬ Treatment:  NICE  guidelines  on  bipolar  disorder  in  children  &  adolescents  recommend  using  adult  
medication  guidelines  but  in  lower  doses.  Atypical  antipsychotics  (Olanzapine,  Risperidone)  are  
preferred  first  line  for  acute  mania  followed  by  valproate/lithium.For  maintenance  the  same  choice  of  
medication  that  controlled  manic  symptoms  is  preferred.
¬ Polycystic  ovaries  and  associated  infertility  are  particular  concerns  when  valproate  is  used  for  
adolescent  girls  and  NICE  recommends  avoiding  its  use  in  girls  and  young  women.
¬ As  children  have  a  higher  renal  filtration  rate,  and  higher  proportion  of  body  water,  higher  doses  of  
lithium  (mg/kg  of  body  weight)  may  be  needed  [to  achieve  a  level  of  0.4-­‐‑1.0  mEq/L].  In  younger  
children,  neurological  side  effects  such  as  tremors  ,  drowsiness,  ataxia  and  confusion  may  be  seen  moe  
often  than  in  adults.

Childhood onset schizophrenia:

¬ Childhood-­‐‑onset  schizophrenia  (COS)  is  a  rare  and  severe  form  of  schizophrenia  characterized  by  an  
onset  of  psychotic  symptoms  by  age  12  years,  believed  to  represent  a  subgroup  of  affected  individuals  
with  an  increased  heritable  etiology.  
¬ The  term  early-­‐‑onset  schizophrenia  is  used  for  onset  before  age  18.  Very  early-­‐‑onset  schizophrenia  
(VEOS)  refers  to  onset  before  13  yrs

Epidemiology:  

¬ Schizophrenia  in  prepubertal  children  is  exceedingly  rare;  In  adolescents,  the  prevalence  of  
schizophrenia  is  estimated  to  be  50  times  that  in  younger  children,  with  probable  rates  of  1  to  2  per  
1,000.  Boys  seem  to  have  a  slight  preponderance  among  children  diagnosed  with  schizophrenia  and  
are  often  identified  at  a  younger  age  than  girls.
¬ In  very  early  onset  schizophrenia,  onset  before  age  13,  the  sex  ratio  is  approximately  2:1  with  males  
predominating.  
¬ All  of  the  symptoms  included  in  adult-­‐‑onset  schizophrenia  may  be  manifest  in  children  with  the  
disorder.    Childhood  onset  schizophrenia  is  characterised  by  more  negative  symptoms,  disorganised  
behaviour,  greater  disorganisation  both  of  thought  and  sense  of  self  and  fewer  systematized  or  
persecutory  delusions.  It  also  runs  a  more  chronic  course  with  less  chance  of  a  full  recovery.  The  onset  
is  frequently  insidious;  after  first  exhibiting  inappropriate  affects  of  unusual  behaviour,  a  child  may  
take  months  or  years  to  meet  all  of  the  diagnostic  criteria  for  schizophrenia.  
¬ Premorbid  course:  EOS  cases  have  increased  delays  in    language,  reading,  bladder  control,  and  social  
functioning  than  adult-­‐‑onset  cases.  Reports  have  documented  marked  neuropsychological  deficits  in  
attention,  working  memory,  and  premorbid  IQ  among  children  who  develop  schizophrenia  and  its  
spectrum  disorders.  These  premorbid  manifestations  also  indicate  a  genetic/developmental  
component  to  schizophrenia
©  SPMM  Course   19  
Clinical  features

¬ Children  who  eventually  meet  the  criteria  often  are  socially  rejected  and  clingy  and  have  limited  social  
skills.  They  may  have  histories  of  delayed  motor  and  verbal  milestones  and  do  poorly  in  school,  
despite  normal  intelligence.    They  often  have  an  insidious  onset.  Desuions  and  hallucinations  are  
prominent  especially  in  those  whopresent  to  services.    Visual  hallucinations  are  experienced  by  a  
significant  number  of  children  with  schizophrenia  and  are  often  frightening.  Delusions  are  present  in  
more  than  one  half  of  children  with  schizophrenia;  the  delusions  take  various  forms,  including  
persecutory,  grandiose,  and  religious.  Delusions  increase  in  frequency  with  increased  age  Blunted  or  
inappropriate  affects  appear  almost  universally  in  children  with  schizophrenia.  Children  with  
schizophrenia  may  giggle  inappropriately  or  cry  without  being  able  to  explain  why.  
Formal  thought  disorders,  including  loosening  of  associations  and  thought  blocking,  are  common  
features  among  children  with  schizophrenia.  Illogical  thinking  and  poverty  of  thought  are  also  often  
present.  These  clincal  symptoms  are  associated  with  poor  premorbid  function  with  developmental  
delays.
¬ It  is  important  to  rule  out  organic  conditions  (such  as  TLE,  Thyroid  disease,  brain  tumour,  Wilson’s  
disease).  

Aetiology:

¬ Genetic  factors:  Schizophrenia  is  known  to  be  up  to  eight  times  more  prevalent  among  first-­‐‑degree  
relatives  of  those  with  schizophrenia  than  in  the  general  population.  Heritability  estimates  are  as  high  
as  82%.  5-­‐‑10%  risk  amongst  first  degree  relatives  of  people  with  schizophrenia  compared  with  0.2-­‐‑0.6%  
amongst  first  degree  reltives  of  controls.  Adoption  studies  of  patients  with  adult-­‐‑onset  schizophrenia  
have  shown  that  schizophrenia  occurs  in  the  biological  relatives,  not  the  adoptive  relatives.  Genetic  
evidence  is  supported  by  higher  concordance  rates  for  schizophrenia  in  monozygotic  twins  than  in  
dizygotic  twins;  cytogenetic  abnormalities  are  more  common  in  early  onset  cases  than  in  Adult  onset  
cases.
¬ Brain  imaging:  enlarged  lateral  ventricles  compared  with  AOS;  Recent  studies  have  documented  grey  
matter  loss  in  the  brains  of  children  with  COS  that  started  in  the  parietal  region  and  proceeded  
frontally  to  dorsolateral  prefrontal  and  temporal  cortices,  including  superior  temporal  gyri.
¬ Obstetric  complications  similarly  implicated  as  in  AOS.  (maternal  infections  like  rubella,  obstertric  
complications  eg  hypoxia)
¬ High  expressed  emotion,  characterized  by  overly  critical  responses  in  families,  has  been  shown  to  be  
correlated  with  increased  relapse  rates  among  patients  with  schizophrenia
¬ Early  attentional  deficits, deficits  in  social  functioning, deficits  in  organisiational  ability and a  lower  
intellectual  ability  at  age  16  and  17  predict  later  development  of  schizophrenia  in  at-­‐‑risk  individuals.  
(The  Oxford  Handbook  of  Child  and  Adolescent  Psychiatry-­‐‑219)
¬ Course  and  outcome:  Childhood-­‐‑onset  schizophrenia  appears  to  be  a  more  malignant  type  of  
schizophrenia,  which  presents  a  greater  challenge  to  treat  with  pharmacology  and  psychosocial  
interventions.  It  seems  to  respond  less  to  medication  than  schizophrenia  with  adult  onset  or  adolescent  
onset,  and  the  prognosis  may  be  poorer.  
©  SPMM  Course   20  
¬ Important  predictors  of  the  course  and  outcome  of  early-­‐‑onset  schizophrenia  include  the  child'ʹs  level  
of  functioning  before  the  onset  of  schizophrenia,  the  age  of  onset,  IQ,  duration  of  first  episode,  
duration  of  untreated  psychsis,  presence  of  negative  symptoms,  response  to  pharmacological  
interventions,  how  much  functioning  the  child  regained  after  the  first  episode,  and  the  amount  of  
support  available  from  the  family.
¬ Risk  of  premature  death  is  higher  than  in  adult  form  of  the  disorder.  8.5%  in  a  study  of  106  cases.  The  
risk  of  suicide  or  accidental  death  as  a  result  of  psychotic  symptoms  appears  to  be  about  5%.  (Adult  
suicide  rate  for  schizophrenia  is  10%)

Treatment:

¬ Algorithms  for  treating  psychosis  in  young  people  are  the  same  as  those  for  adult  patients.  Metabolic  
side  effects  are  more  common  in  this  age  group  and  more  intensive  monitoring  is  required.
¬ Atypical  antipsychotics  favoured  over  typical  ones.  Although  first  generation  drugs  such  as  
haloperidol  are  effective,  young  people  are  more  prone  to  EPSEs  than  adults.  Drug  induced  akathasia  
is  less  common  in  children,  but  acute  dystonia  is  more  common.
¬ Randomised  controlled  trails  of  antipsychotics  in  early  onset  psychosis  suggest  that  olanzapine  and  
risperidone  are  effective,  with  advantages  over  Haloperidol.  Atypicals  are  commonly  used  as  first-­‐‑line  
agents  in  EOS.
¬ Clozapine  seems  to  be  effective  in  treatment  resistant  psychosis  in  adolescents  although  this  
population  may  be  more  prone  to  neutropenia  and  seizures  than  adults.
¬ Avoid  depot  and  sedating  antipsychotics
¬ Psychosocial  treatments  should  include  family  work  and  focus  on  psychoeducation,  social  skills,  and  
problem-­‐‑solving  strategies  and  CBT  methods.    

©  SPMM  Course   21  
 6. Anxiety Disorders
¬ Fear  and  anxiety  represent  normal  reactions  to  danger.  One  critical  differentiation  between  normal  
fears  or  anxiety  and  an  anxiety  disorder  derives  from  the  so-­‐‑called  impairment  criterion:  to  receive  an  
anxiety  disorder  diagnosis,  there  must  be  evidence  of  significant  impairment  or  interference  in  the  
child'ʹs  everyday  functioning.  Anxiety  disorders  adversely  impact  self-­‐‑esteem,  social  relationships,  and  
academic  performance.  
¬ Behavioural  avoidance  is  a  primary  area  of  impairment  that  might  lead  children  to  avoid  many  typical  
experiences  enjoyed  by  peers.  Anxiety  or  fear  is  also  considered  abnormal  when  the  level  of  distress  
evoked  by  danger  is  considered  extreme,  relative  to  a  child'ʹs  peers  

Prevalence
¬ Prevalence  rates  seem  to  vary.  Overall  rates  range  from  5-­‐‑15%,  with  8%  requiring  clinical  treatment  
(Oxford  Textbook  of  Psychiatry  3rd  edn.)  Male:  female  ratio  is  equal  in  childhood;  Prevalence  increase  
in  girls  after  adolescence  when  the  female:  male  ratio  is  around  2:1.  Prevalence  rates  (Oxford  
Handbook  of  Psychiatry,  3rd  edn):  
o Separation  anxiety  disorder-­‐‑3.5%  in  children  and  0.8%  in  adolescents  
o Generalized  anxiety  disorder-­‐‑  approximately  4%  of  adolescents.  
o Simple  Phobia-­‐‑  10%  in  some  studies;  twice  as  common  in  females.  
o Social  phobia-­‐‑1%  in  children  and  between  5-­‐‑15%  in  adolescents  
o Panic  disorder-­‐‑3-­‐‑6%,  peak  onset  15-­‐‑19  years.    
¬ Age  of  onset  and  presentation  of  symptoms  vary  for  each  disorder.    Anxiety  symptoms  vary  with  age.  
Tearfulness  and  clinging  in  preschool  children.  Somatic  complaints  and  hypochondriacal  fretting  are  
common  in  middle  childhood  (5-­‐‑12  years)  as  are  irritability  and  aggressive  behaviour.  Separation  
anxiety  disorder  and  specific  phobia  usually  have  onset  in  early  childhood.  Generalized  anxiety  
disorder  occurs  across  all  age  groups,  while  obsessive-­‐‑compulsive  disorder,  social  phobia,  and  panic  
disorder  tend  to  occur  in  later  childhood  and  adolescence.  
¬ Co-­‐‑morbidity:  Children  with  SAD  are  more  likely  to  have  co  morbid  specific  phobia  than  children  
with  GAD  or  social  phobia.  In  contrast,  children  with  GAD  and  social  phobia  are  more  likely  to  have  
comorbid  mood  disorders  as  compared  to  children  with  SAD.  Up  to  90%  of  young  people  with  GAD  
have  a  comorbid  diagnosis-­‐‑  anxiety  disorders,  CD  and  substance  abuse  are  most  common.  Depression  
is  8.2  times  as  likely  in  children  with  anxiety  disorders  than  in  children  without  anxiety  disorders.  
Specifically,  there  is  a  significant  link  between  GAD  and  depression  that  persists  into  adulthood.  

Clinical presentations
Separation anxiety disorder
¬ Separation  anxiety  disorder  (SAD)  is  defined  as  developmentally  inappropriate  and  excessive  anxiety  
concerning  separation  from  home  or  from  those  to  whom  the  individual  is  attached.  This  anxiety  will  
interfere  with  normal  age-­‐‑appropriate  functioning.    The  essential  clinical  feature  of  separation  anxiety  
is  excessive  worry  about  losing  or  being  permanently  separated  from  a  major  attachment  figure.    
¬ Symptoms:  anxiety  about  actual  or  anticipated  separation  from  or  danger  to  attachment  figure;  sleep  
disturbances  and  nightmares  -­‐‑  Persistent  reluctance  or  refusal  to  go  to  sleep  without  being  near  or  next  
©  SPMM  Course   22  
 to  a  major  attachment  figure,  repeated  nightmares  about  separation;  Somatisation  -­‐‑  Repeated  
occurrence  of  physical  symptoms  that  includes  nausea,  vomiting,  headache,  stomach  aches  etc.  
especially  on  occasions  that  involves  separation  from  a  major  attachment  figure;  School  refusal  
(especially  in  adolescents)  -­‐‑  Persistent  reluctance  or  refusal  to  go  to  school  because  of  fear  of  
separation.  School  refusal  and  excessive  somatic  complaints  in  the  context  of  actual  or  anticipated  
separations  are  the  most  common  reasons  for  parents  and  children  to  seek  treatment  for  SAD    
¬ The  disturbance  must  last  at  least  4  weeks  and  cause  clinically  significant  impairment  in  social,  
academic,  and  occupational  domains.  The  onset  must  occur  before  18  years  of  age,  and  it  is  generally  
not  expected  to  occur  below  6  years  of  age.  If  the  onset  occurs  before  the  child  is  6  years  old,  it  is  
labeled  as  early  onset  separation  anxiety  disorder.    

Attachment disorders:
¬ Attachment:  the  emotional  bond  between  child  and  caregiver.  Develops  though  appropriate  parental  
responses  to  child’s  behaviour.  It  allows  the  child  to  understand  their  ‘inner  world’  and  it  is  the  
foundation  for  safe  separation  and  development  of  autonomy  (Oxford  Handbook  of  Psychiatry,  3rd  
edn).  
¬ Children  exhibit  considerable  variation  in  their  attachment  relationships  to  their  mothers.  Different  
patterns  of  attachment  have  been  described:  
o Secure  (about  60%)  –  child  uses  carer  as  secure  base  but  able  to  explore  freely  and  go  back  to  
caregiver  for  comfort  if  necessary,  carer  sensitive  to  child’s  cues)  
o Insecure,  avoidant/anxious  type  (about  15%)  –  appears  interested  in  caregiver,  minimal  distress  at  
separation,  sometimes  ignores/avoids  caregiver  
o Insecure,  ambivalent/resistant  type  (about  10%)  –  high  levels  of  distress  upon  separation,  resist  
comforting  and  can  take  a  while  to  settle.  Thought  to  be  due  to  inconsistent  care  giving.    
o Disorganized/disorientated  (about  15%)  –  child  displays  contradictory  behaviour  patterns.  
Thought  to  arise  from  either  the  child  experiencing  the  caregiver  as  frightening  or  the  caregiver  
being  frightened  themselves.    
¬ Mary  Ainsworth  created  a  way  of  studying  the  quality  of  the  attachment  of  a  child  to  their  
mother/caregiver-­‐‑  she  developed  the  Strange  Situation  procedure  (1978).  
¬ Romanian  Adoptees  Study  –  Data  on  severe  attachment  disorders  have  been  obtained  from  follow  up  of  
children  taken  from  severely  deprived  institutions  in  Romania  and  adopted  by  families  in  Canada  or  
UK.    20%  had  severe  disturbances  at  the  age  of  6.  Duration  of  exposure  to  deprivation  was  strongly  
associated  with  severe  disinhibited  behaviour.    

A.  Reactive  attachment  disorder:    

¬ This  disorder,  occurring  in  infants  and  young  children  is  characterized  by  persistent  abnormalities  in  
the  child’s  pattern  of  social  relationships,  which  are  associated  with  emotional  disturbance  and  
reactive  to  changes  in  environmental  circumstances.      
¬ It  is  diagnosed  before  the  age  of  5  years,  and  may  manifest  as  either  inhibited  or  disinhibited  subtypes.    
¬ It  is  more  common  in  poverty-­‐‑stricken  and  socially  disrupted  environments.  

©  SPMM  Course   23  
¬ Causes:  It  occurs  as  a  direct  result  of  severe  parental  neglect,  abuse  and  serious  mishandling.  Other  
contributory  factors  include  young,  isolated,  inexperienced,  and/or  depressed  caretaker.    
¬ Features:  Fearfulness  and  hypervigilance  that  do  not  respond  to  comforting  are  characteristic.  Poor  
social  interaction  with  peers  is  typical;  aggression  towards  self  &  others  is  also  common;  growth  
failure  occurs  in  some  cases.  

B.  Disinhibited  attachment  disorder:  

¬ Disinhibited  attachment  disorder  of  childhood  is  characterised  by  a  particular  pattern  of  abnormal  
social  functioning  that  arises  during  the  first  5  years  of  life.  
¬ In  the  early  stages,  it  is  usually  manifest  by  clinging  and  diffuse  non-­‐‑selectively  focused  attachment  
behaviour.    
¬ By  the  age  of  4  years,  diffuse  attachment  remains  but  clinging  tends  to  be  replaced  by  attention  
seeking  and  indiscriminately  friendly  behaviour.    
¬ During  middle  and  later  childhood  this  behaviour  often  persists  and  depending  on  circumstances,  
there  may  also  be  associated  emotional  or  behavioural  disturbance.  

Sibling rivalry disorder

¬ Onset  is  within  6  months  of  the  birth  of  an  immediately  younger  sibling.  Duration  of  the  disorder  is  at  
least  4  weeks.    Emotional  disturbance  that  is  abnormal  in  degree  and/or  persistence  
¬ Emotional  disturbance  is  shown  by  anxiety,  regression,  tantrums,  and  dysphoria;  sleep  difficulties,  
oppositional  behaviour,  or  attention-­‐‑seeking  behaviour  with  one  or  both  parents  (two  or  more  of  these  
must  be  present).  Behaviour  can  range  from  strong  reluctance  to  share  and  a  lack  of  positive  regard  to,  
in  severe  cases,  overt  hostility,  physical  trauma  and/or  maliciousness  towards,  and  undermining  of,  
the  sibling  (ICD-­‐‑10).  

School refusal
¬ Refusal  to  go  to  school  or  stay  in  school,  even  when  under  pressure  from  parents  and  school  
authorities.  This  is  not  a  psychiatric  disorder  per  se  -­‐‑  it  can  have  many  causes.  
¬ School  refusal  is  considered  as  a  problem  rather  than  a  diagnosis.  It  is  a  condition  that  can  co-­‐‑occur  
with  anxiety  and  depressive  disorders.    Significant  difficulty  attending  school,  resulting  in  prolonged  
absence  and/or  severe  emotional  upset  in  children,  characterizes  school  refusal.  
¬ These  children  often  display  excessive  fearfulness,  temper  outbursts,  or  complaints  of  feeling  ill  when  
faced  with  the  prospect  of  going  to  school.  The  complaint  is  more  of  physical  symptoms  such  as  
headaches,  abdominal  pain,  nausea,  palpitations  etc.  
¬ The  nature  of  the  anxiety  associated  with  school  refusal  behaviour  is  likely  to  change  with  age,  as  is  
the  nature  of  the  precipitating  events.  For  example,  fear  of  separation  is  more  common  in  younger  
school  refusers,  while  in  older  children  social-­‐‑evaluative  fears,  such  as  fears  of  teachers  or  peers,  are  
more  commonly  reported.  
¬ Incidence  in  children  and  adolescents  reported  as  1-­‐‑5%.  Prevalence  uncertain.  Sex  distribution-­‐‑equal  
¬ Three  main  incidence  peaks  by  age:  
o 5-­‐‑7  years:  School  entry.  Possible  separation  anxiety  
o Age  11:  Commonest  age  of  presentation.  May  be  triggered  by  transition  to  secondary  school.    
©  SPMM  Course   24  
 o Age  14  years  and  older:  Possibly  partly  due  to  first  presentations  of  depressive  or  anxiety  
features/disorders.  Also  need  to  consider  bullying,  pressure  of  exams  or  any  specific  stressors  in  
individual  cases.  

School  Refusers   Truants  

1.  Presence  of  emotional  symptoms   Presence  of  antisocial  symptoms  
2.  Family  history  of  neurosis   Family  history  of  antisocial  behaviour  
3.  Over-­‐‑protective  parenting   Inconsistent  discipline  
4.  Satisfactory  academic  achievement   Poor  academic  achievement  
5.  Small  family  or  the  youngest  member   Large  family  size  
6.  Parents  aware  of  child’s  absence   Child  is  neither  at  home,  nor  at  school  
7.  No  gender  difference     Male  predominance  
¬ In  terms  of  outcome,  70%  will  successfully  reintegrate  into  school,  but  a  significant  minority  will  not.  
Social  anxiety  and  communication  problems  may  persist.  

Selective mutism
¬ Characterized  by  a  persistent  failure  to  speak  in  specific  settings,  such  as  school  (where  there  is  an  
expectation  to  speak),  despite  full  use  of  language  at  home  or  with  family.  Normally  begins  between  
ages  of  3-­‐‑5  years,  after  normal  speech  has  been  acquired.  
¬ Rates  of  associated  psychiatric  disorder,  especially  social  phobia,  high.  A  child  with  selective  mutism  
may  remain  completely  silent  or  near  silent,  in  some  cases  whispering  instead  of  speaking  out  loud.      
¬ Rare-­‐‑  affecting  about  3-­‐‑8/10,000  in  the  UK.  Prevalence  varies  with  age,  with  younger  children  at  
increased  risk  for  the  disorder.  Persistent  mutism  affects  less  than  1  per  1000  children.    
¬ Slightly  more  common  in  girls.    
¬ Some  cases  will  last  for  months  to  years.  No  evidence  that  any  particular  treatment  is  generally  
effective.  A  behavioural  approach  with  positive  reinforcement  techniques  aimed  at  increasing  the  
frequency  of  talking  and  decreasing  the  frequency  of  non-­‐‑communication  will  be  helpful.  It  is  
important  to  ascertain  what  communication  is  like  at  home.  

ANXIETY  DISORDERS  IN  CHILDREN-­‐‑  KEY  CHARACTERISTICS  

Separation  anxiety   Excessive  anxiety  concerning  separation  from  loved  one    

disorder  (SAD)   Possible  risk  factor  for  development  of  panic  disorder  or  agoraphobia  in  adulthood  
Social  phobia  (social   Persistent  fear  of  social  or  evaluative  situations    
anxiety  disorder)   Behavioural  inhibition  may  be  a  temperamental  predictor  of  social  phobia  in  childhood  or  
adulthood  
Generalized  anxiety   Excessive  and  uncontrollable  worry  about  multiple  issues    
disorder  (GAD)   At  least  one  somatic  complaint    
Close  genetic  link  with  depression  
Specific  phobia   Extreme  fear  of  a  specific  situation  or  object    
Five  types  of  phobias,  some  corresponding  to  evolutionary  dangers  (snakes,  blood)  
Panic  disorder  with  or   Unexpected  panic  attacks  accompanied  by  worry  about  future  attacks    
without  agoraphobia   Agoraphobia  is  diagnosed  if  individual  avoids  places  in  which  escape  would  be  difficult  or  
embarrassing    
 
Panic  attacks  can  be  caused  by  medical  conditions  (hyperthyroidism,  cardiac  abnormalities)  
(Adapted  from:    Lewis'ʹs  Child  and  Adolescent  Psychiatry:  A  Comprehensive  Textbook,  4th  Edition)  

©  SPMM  Course   25  
Treatment
¬ Cognitive  Behavioural  Therapy  (CBT)  has  proven  to  be  effective  at  treating  anxiety  disorders  in  children  
and  adolescents.  Most  CBT  interventions  were  initially  developed  for  adult  anxiety  and  phobic  
disorders.  The  techniques  for  child  and  adolescent  populations  are  conceptually  and  structurally  
similar  but  modified  according  to  the  developmental  level.    
¬ CBT  technique  focuses  on  relaxation  training  and  cognitive  restructuring.  Individual  CBT  plus  the  
family  component  was  shown  to  effectively  reduce  anxiety  symptoms  and  may  have  some  added  
benefits,  particularly  for  female  children.  Group  CBT  interventions  have  been  shown  to  be  effective  for  
the  treatment  of  socially  phobic  children  and  adolescents.  
¬ Psychoeducation  and  parent  training  are  also  useful.  
¬ Psychodynamic  therapies  include  group,  family,  and  individual/play  techniques  
¬ Pharmacological  interventions:  SSRIs  are  first-­‐‑line  agents.  Overall,  efficacy  and  safety  data  support  the  
use  of  selective  serotonin  reuptake  inhibitors  (SSRIs)  to  treat  childhood  social  phobia,  separation  
anxiety  disorder  and  generalised  anxiety  disorder.  Recent  studies  have  demonstrated  the  efficacy  of  
SSRIs  for  specific  anxiety  disorders.    Benzodiazepines  are  not  indicated  as  a  routine  treatment  in  
children  due  to  their  potential  adverse  effects.  There  is  also  little  or  no  evidence  for  the  efficacy  of  
other  anxiolytics,  such  as  buspirone  or  beta-­‐‑blockers.  

©  SPMM  Course   26  
 7. Other anxiety-related disorders
Post traumatic stress disorder:
¬ When  PTSD  as  a  diagnosis  was  first  formulated  in  1980,  it  was  initially  believed  that  this  would  not  be  
relevant  to  children!  But  it  is  now  known  that  PTSD  occurs  frequently  in  children  and  adolescents  with  
up  to  6  percent  of  young  people  meeting  criteria  for  this  diagnosis  at  some  point.  The  British  National  
Survey  of  Mental  Health  reported  that  0.4%  of  children  aged  11-­‐‑15  was  diagnosed  with  PTSD,  girls  
showing  twice  the  rate  for  boys  [Nice  Guidelines].    
¬ Most  common  traumatic  exposures  for  children  and   DSM-­‐‑5  AND  PTSD  IN  CHILDREN  
adolescents  include  physical  or  sexual  abuse  [can  be  chronic  
Diagnostic  threshold  is  lowered  for  
stress];  domestic,  school  or  community  violence;  being  
children.  In  addition,  a  separate  PTSD  
kidnapped;  terrorist  attacks;  motor  vehicle  or  household  
criterion  has  been  added  for  children  less  
accidents;  or  disasters,  such  as  floods,  hurricanes,  tornadoes,   than  age  6.  
fires,  explosions  etc.  The  child'ʹs  response  must  involve  
intense  fear,  terror,  helplessness,  horror,  or  disorganized  or  agitated  behaviour  
¬ Classification  of  childhood  trauma  
o Type  1:  Classic  single,  acute,  traumatic  event;  the  most  common  form  in  children.  Symptoms:  Full,  
detailed  memories,    ‘omens’  or  ‘cognitive  reappraisal’,  misperceptions.    
o Type  2:    Follows  longstanding  or  repeated  exposure  to  extreme  external  events,  (e.g.  chronic  
abuse).    Symptoms:  Denial  and  psychic  numbing,  self-­‐‑hypnosis,  depersonalisation,  and  
dissociation  and  rage,  self-­‐‑harm,  and/or  extreme  passivity  

Treatment  

¬ Trauma-­‐‑Focused  Cognitive-­‐‑Behaviour  Therapy:  Several  randomized  clinical  trials  have  provided  evidence  
for  the  efficacy  of  trauma-­‐‑focused  cognitive-­‐‑behaviour  therapy  (CBT)  in  the  treatment  of  PTSD  in  
children  and  adolescents.  This  treatment  is  generally  administered  over  8  to  12  treatment  sessions,  
including  a  number  of  components.  Group  treatments  are  preferred  for  large  number  of  people,  with  
separate  groups  for  girls  and  boys.      
¬ Crisis  intervention/psychological  debriefing  has  been  adapted  for  groups  of  children  following  trauma.  
Role  of  crisis  intervention  with  adults  is  being  called  into  question.  This  involves  structured  sessions  
with  group  leaders  discussing  the  trauma  with  a  group  of  children  to  share  feelings  and  knowledge  
and  process  it.  Single  session  debriefing  for  children  is  not  supported  by  evidence.    
¬ NICE  guidelines  advise  that  medications  should  not  be  routinely  prescribed  for  children  and  young  
people  with  PTSD.  Serotonin  reuptake  inhibitors  (SSRIs)  are  frequently  used  in  children  with  PTSD  in  
the  absence  of  evidence  demonstrating  efficacy.  Citalopram  from  20  mg  to  40  mg  has  been  reported  to  
be  helpful  in  the  management  of  PTSD  in  children  and  adolescents  according  to  results  of  an  open  trial  
over  an  8-­‐‑week  period.  
¬ EMDR  –  no  controlled  trials  –  one  unpublished  trial  with  inconclusive  results.  
¬ Families  should  be  involved,  where  appropriate.    

©  SPMM  Course   27  
¬ No  good  evidence  for  efficacy  of  other  treatments,  including  play  therapy,  art  therapy,  or  family  
therapy.  

Obsessive compulsive disorder

OCD  in  children:  

¬ Obsessive-­‐‑compulsive  disorder  (OCD)  is  characterized  by  the  presence  of  recurrent  intrusive  thoughts  
(obsessions)  associated  with  anxiety  or  tension  and/or  repetitive  purposeful  mental  or  physical  actions  
(compulsions)  aimed  at  reducing  fears  and  tensions  caused  by  obsessions.  It  has  become  increasingly  
evident  that  the  majority  of  cases  of  OCD  begin  in  childhood  or  adolescence.  
¬ The  clinical  presentation  of  OCD  in  childhood  and  adolescence  is  similar  to  that  in  adults  and  the  only  
alteration  for  children  is  that  they  do  not  necessarily  demonstrate  awareness  that  their  thoughts  or  
behaviours  are  unreasonable.  Childhood  OCD  is  characterised  by  secrecy  i.e.  –  they  understand  that  
their  OCD  behaviour  is  unusual,  and  so  try  to  hide  it.  40%  children  with  OCD  do  not  have  obsessive  
thoughts.    
¬ Rituals  and  habits  are  seen  in  2/3rd  of  children  but  they  are  less  frequent,  less  intense  and  do  not  cause  
distress.  
¬ Epidemiology:  Prevalence  of  OCD  in  children  and  adolescents  is  estimated  as  0.5%.    OCD  may  occur  as  
early  as  5  years  of  age,  thought  the  mean  age  of  onset  is  10  years.    Childhood  onset  OCD  has  a  ratio  of  
2  boys  to  every  girl.  The  onset  of  OCD  post-­‐‑pubertal  is  more  common  in  girls.  
¬ Aetiology:  Increased  incidence  in  1st  degree  relatives  and  in  monozygotic  twins  (80%  compared  to  40%  
in  monozygotic  twins);  possible  autoimmune  process;  reduced  volume  of  caudate  nucleus;  
hyperactive  orbitofrontal  circuits  (SPET);  5HT/serotonin  receptor  dysfunction  (clinical  response  to  
SSRI’s  in  both  children  and  adults),  and  dopaminergic  dysfunction  [high  dose  stimulants  may  increase  
OCD  symptoms]  
¬ Symptoms:  Contamination  fears  with  ritualized  washing  and  avoidance;  repetitive  doubting  and  
checking  (e.g.  locks);  repetitive  counting,  arranging,  hoarding  or  touching.  
¬ Comorbidity:  70%  have  at  least  one  co  morbid  disorder.  OCD  is  commonly  found  to  be  comorbid  with  
other  psychiatric  disorders,  such  as  Tic  disorders  (17-­‐‑40%),  major  depression  (26%)  specific  
developmental  disabilities  (24%),  phobias  and  other  anxiety  disorders.  There  are  also  higher  than  
expected  rates  of  attention-­‐‑deficit/hyperactivity  disorder  (ADHD),  autism  spectrum  disorders,  and  tic  
disorders,  including  Tourette'ʹs  syndrome,  among  children  and  adolescents  with  OCD.    DSM  IV  allows  
a  diagnosis  of  OCD  in  the  presence  of  schizophrenia.  
¬ Treatment:  Results  from  multiple  randomised  placebo-­‐‑controlled  trials  of  both  medication  and  CBT  
interventions  in  children  and  adolescents  with  OCD  have  confirmed  the  most  evidence  for  successful  
treatment  of  this  disorder  compared  to  any  of  the  other  anxiety  disorders  of  childhood.  A  multi-­‐‑site  
National  Institute  of  Health  funded  investigation  of  Sertraline  and  CBT  each  alone,  and  then  in  
combination  for  the  treatment  of  childhood  onset  OCD-­‐‑the  Paediatric  OCD  Treatment  Study  (POTS)-­‐‑  
revealed  that  the  combination  was  superior  to  either  treatment  alone  
¬ Fluoxetine  and  Sertraline  are  licensed  for  the  treatment  of  OCD  in  children  and  adolescents,  and  
should  be  prescribed  as  per  BNF  guidelines.  (NICE  guidelines)  

©  SPMM  Course   28  
¬ Fluoxetine  is  recommended  for  OCD  in  young  people  with  significant  co-­‐‑morbid  depression.  
¬ Clomipramine  is  not  recommended  as  a  first  line  treatment  due  to  its  greater  potential  risks  compared  
to  other  SSRI  agents,  including  cardiovascular  risk  of  hypotension  and  arrhythmia,  and  seizure  risk  
¬ CBT  geared  toward  children  of  varying  ages  is  based  on  the  principle  of  developmentally  appropriate  
exposure  to  the  feared  stimulus  coupled  with  response  prevention,  leading  to  diminishing  anxiety  
over  time  experienced  upon  exposure  to  feared  situations  
¬ Most  treatment  guidelines  for  children  and  adolescents  with  mild  to  moderate  OCD  recommend  a  trial  
of  CBT  prior  to  initiating  medication.  However,  there  is  evidence  from  POTS  that  optimal  treatment  
includes  the  combination  of  both  SSRI  medication  and  CBT  
¬ Young  people  with  mild  functional  impairment  are  initially  offered  self  help  guides.  If  self  help  hasn’t  
worked,  or  for  those  with  mild  and  moderate  impairment,  CBT  [including  exposure  response  
prevention]  should  be  offered.  In  the  event  of  an  inadequate  response,  or  for  those  with  severe  
impairment,  supplement  psychotherapy  with  SSRI  should  be  considered.  

PANDAS syndrome
¬ Some  children  appear  to  develop  obsessive-­‐‑compulsive  symptoms  associated  with  beta  haemolytic  streptococcal  
infection  and  this  presentation  represents  a  minority  of  OCD  cases  in  this  population.  This  association  has  led  to  
the  studies  of  immune  responses  in  OCD.    Cases  of  infection  triggered  OCD  have  been  termed  paediatric  
autoimmune  neuropsychiatric  disorders  associated  with  streptococcus  (PANDAS)  and  believed  to  signify  an  
autoimmune  process  such  as  that  of  Sydenham'ʹs  chorea  during  rheumatic  fever.    It  is  associated  with  OCD  
and/or  Tic  Disorder.  
¬ Pre-­‐‑pubertal  onset  is  common.    
¬ 75%  of  children  and  young  people  with  Sydenham’s  chorea  also  have  OCD  symptoms.    Specific  characteristics  
include  episodic  or  ‘sawtooth’  course,  choreiform  movements.  Typically,  symptoms  arise  along  with  tics  and  this  
phenomenon  may  be  related  to  obsessive-­‐‑compulsive  symptoms  seen  in  Sydenham'ʹs  chorea.  It  is  very  common  
for  children  with  tic  disorders  and  perhaps  OCD  to  report  an  abrupt  onset  and  experience  exacerbation  of  
symptoms  with  infection.  Singer  and  co-­‐‑workers  reported  that  over  50%  of  clinic  patients  with  tic  disorders  
reported  this  finding  and  that  11%  reported  exacerbation  of  illness  within  6  months  of  streptococcal  infection  
¬ It  is  hypothesized  that  exposure  to  streptococcal  bacteria  activates  the  immune  system  leading  to  inflammation  
of  the  basal  ganglia  and  resulting  disruption  of  the  cortical-­‐‑striatal-­‐‑thalamo-­‐‑cortical  function.    
¬ Scanning  data  suggest  that  increased  basal  ganglia  volumes  are  associated  with  PANDAS;  just  as  they  are  in  
OCD,  tic  disorders  and  Sydenham'ʹs  chorea.  MRI  has  documented  a  proportional  relationship  between  the  size  of  
the  basal  ganglia  and  the  severity  of  OCD  symptoms.    

Elimination Disorders
Enuresis
¬ Enuresis  is  the  repeated  voiding  of  urine  into  a  child'ʹs  clothes  or  bed;  the  voiding  may  be  involuntary  
or  intentional.  For  the  diagnosis  to  be  made,  a  child  must  exhibit  a  developmental  or  chronological  age  
of  at  least  5  years.  Duration  of  disorder  is  at  least  3  months.  
¬ Voluntary  control  of  micturition  does  not  begin  until  15-­‐‑18  months.  Most  children  are  reasonably  dry  
by  day  at  18  months.    By  2  years  50%  are  dry  at  night,  by  3  years  75%  are  dry  at  night.    By  5  years,  only  
1%  of  children  have  problems  with  daytime  wetting.  However,  nocturnal  enuresis  can  still  affect  15-­‐‑
©  SPMM  Course   29  
 22%  boys  and  7-­‐‑15%  girls  at  the  age  of  7  years.  A  small  minority  continues  to  have  problems  into  
adulthood.  
¬ Enuresis  can  occur  as  a  psychiatric  complication  of  stressful  life  events  or  emotional  disturbance;  it  is  
not  always  accompanied  by  encopresis.  It  is  twice  as  common  in  boys  than  girls.  Types:  Primary  or  
secondary,  nocturnal  or  diurnal  or  mixed.  
¬ Reported  prevalence:  2-­‐‑5%  among  school-­‐‑aged  children.  
¬ Nocturnal  enuresis:  Most  important  predictor  of  primary  nocturnal  enuresis  is  a  family  history  of  
enuresis.  70%  of  children  with  nocturnal  enuresis  have  a  parent  or  sibling  who  was  late  in  becoming  
dry.  Secondary  enuresis  is  predicted  by  delay  in  control  over  bedwetting,  and  experiencing  a  high  rate  
of  adverse  life  events.  There  is  also  a  reduced  sensitivity  to  vasopressin  [antidiuretic  effect]  in  the  
kidneys.      
¬ Daytime  enuresis  is  likely  to  be  related  to  structural  abnormalities.  Sexual  abuse  is  associated  with  
secondary  wetting.  Enuresis  is  diagnosed  only  if  the  behaviour  is  not  caused  by  a  medical  condition.  It  
is  important  to  rule  out  organic  factors,  such  as  the  presence  of  urinary  tract  infections,  obstructions,  
genitourinary  pathology,  neurological  conditions  like  spina  bifida  occulta;  other  organic  disorders  that  
can  cause  polyuria  and  enuresis,  such  as  diabetes  mellitus  and  diabetes  insipidus.  
¬ Association  of  enuresis  has  been  made  with  a  high  rate  of  stressful  life  events,  UTI,  constipation,  and  
with  children  from  low  socioeconomic  backgrounds,  living  in  large  families  or  overcrowded  
conditions.    
¬ Enuresis  is  often  self-­‐‑limited,  and  a  child  with  enuresis  may  have  a  spontaneous  remission  without  
psychological  sequelae.    The  significant  emotional  and  social  difficulties  of  these  children  usually  
include  poor  self-­‐‑image,  decreased  self-­‐‑esteem,  social  embarrassment  and  restriction,  and  intrafamilial  
conflict.  Children  with  enuresis  are  at  higher  risk  for  ADHD  compared  with  the  general  population.  
They  are  also  more  likely  to  have  comorbid  encopresis  

Treatment  

¬ Rule  out  organic  causes  of  urinary  dysfunction  –e.g.:    UTI  may  lead  to  obstruction.  The  first  step  in  any  
treatment  plan  is  to  review  appropriate  toilet  training.  
¬ Psychoeducation:  Child  with  nocturnal  enuresis  is  not  being  lazy.  Avoid  punishments.  
¬ Record  keeping  is  helpful  in  determining  a  baseline  and  following  the  child'ʹs  progress  and  may  itself  
be  a  reinforcer.    
¬ Behavioural  interventions  are  the  first  line  of  treatment  for  bed-­‐‑wetting.  Ball  and  pad,  or  enuresis  alarm.  
Classic  conditioning  with  the  bell  and  pad  apparatus  is  generally  the  most  effective  treatment  for  
nocturnal  enuresis,  with  dryness  resulting  in  more  than  60  percent  of  cases.  A  star  chart  may  be  
particularly  helpful.    
¬ Medications:  Imipramine  is  efficacious  and  has  been  approved  for  use  in  treating  childhood  enuresis,  
primarily  on  a  short-­‐‑term  basis.    Desmopressin,  an  antidiuretic  compound  that  is  available  as  an  
intranasal  spray,  has  shown  some  initial  success  in  reducing  enuresis.  Adverse  effects  that  can  occur  
with  Desmopressin  include  headache,  nasal  congestion,  epistaxis,  and  stomachache.  One  case  of  
hyponatraemic  convulsion.  Reboxetine  a  norepinephrine  reuptake  inhibitor  with  a  non  cardiotoxic  

©  SPMM  Course   30  
 side  effect  profile  has  recently  been  investigated  as  a  safer  alternative  to  Imipramine  in  the  treatment  
of  childhood  enuresis.  Oxybutynin  is  an  anticholinergic,  which  increases  bladder  capacity  though  
rarely  employed  in  clinical  practice.  

Encopresis  

¬ Voluntary  or  involuntary  soiling  of  normally  formed  stools  in  inappropriate  places  in  a  child  of  4  years  
(mental  age)  or  older,  in  the  absence  of  a  sufficient  organic  cause.  Soiling  occurs  at  least  once  a  month  
for  6  months.  
¬ Males  are  found  to  be  about  six  times  more  likely  to  have  encopresis  than  females.  Approximately  5%  
children  will  be  soiling  over  4  years  of  age.    
¬ Parents  present  more  often  to  paediatrics  than  child  psychiatric  services.  Although  encopresis  is  
considered  a  nonorganic  disorder,  more  than  three  quarters  of  children  with  encopresis  may  show  
evidence  of  chronic  constipation,  leading  to  infrequent  defecation,  withholding  of  bowel  movements,  
which  then  leads  to  impaction  and  eventual  overflow  soiling.  However,  it  is  important  to  exclude  
organic  cause  such  as  Hirschprung'ʹs  disease,  anorectal  pathology,  neurological  problems;  nutritional  
disorders  and  medication  side  effects.  
¬ Encopresis  has  been  demonstrated  to  occur  with  significantly  greater  frequency  among  children  with  
known  sexual  abuse  compared  with  a  normal  sample  of  children.    This  can  be  seen  as  possible  defense  
against  further  abuse,  or  retention  due  to  pain.  
¬ It  occurs  with  greater  frequency  among  children  with  a  variety  of  psychiatric  disturbances  compared  
with  controls  and  some  evidence  indicates  that  encopresis  in  children  is  associated  with  measures  of  
maternal  hostility,  and  harsh  and  punitive  parenting.  
¬ Encopresis,  in  some  children,  can  be  considered  secondary,  that  is,  emerging  after  a  period  of  normal  
bowel  habits.  Family  patterns  such  as  an  unhappy  child  in  a  family  with  clear  ongoing  difficulties  
[abuse,  domestic  violence],  recent  acute  stress  in  the  family  [death,  birth  of  sibling  etc.],  and  over  
tolerant  parents  have  been  found  in  half  the  families  studied  in  an  audit  [Silver,1996].    

Treatment  

¬ Initial  paediatric  assessment,  including  imaging  of  the  gut  if  indicated.  First  line  of  treatment  is  to  
evacuate  any  stool.  Laxatives  may  be  used  to  prevent  further  retention.  
¬ Education  of  the  family  and  correction  of  misperceptions  that  a  family  may  have  about  soiling  must  
occur  before  treatment    
¬ Psychological  treatment:  Behavioural  approach  –  operant  training  with  rewards  and  positive  
reinforcement.    
¬ Family  support/therapy.  It  is  important  to  reduce  the  family  tensions  about  the  symptom  and  a  
nonpunitive  atmosphere  is  established.  Randomised  control  trials  show  that  biofeedback  adds  nothing  
to  laxative  treatment.  
¬ In  many  cases,  encopresis  is  self-­‐‑limiting,  and  it  rarely  continues  beyond  middle  adolescence.  Most  
soiling  stops  by  the  age  of  16  years.  

©  SPMM  Course   31  
Pica
¬ This  condition  is  characterised  by  persistent  (>1month)  eating  of  non-­‐‑nutritive  substances  at  a  
developmentally  inappropriate  age  (>1  year)  and  it  occurs  at  least  twice  a  week.  
¬ It  typically  occurs  during  the  2nd  and  3rd  years  of  life  and  common  substances  are:  dirt,  stones,  plastic,  
paper,  hair,  faeces,  wood  etc.  It  is  common  in  people  with  developmental  disability.    
¬ Consequences  may  include  toxicity,  infection,  or  GIT  ulceration/obstruction.  
¬ Hypothesized  causes  include:  hunger,  malnutrition,  nutritional  deficiencies,  psychosocial  stressors  
and  brain  disorders  such  as  lesions  in  the  hypothalamus  

8. Developmental disorders
Pervasive developmental disorders (PDD)
¬ Pervasive  developmental  disorders  include  several  that  are  characterized  by  impaired  reciprocal  social  
interactions,  communication  difficulties,  aberrant  language  development,  and  restricted  behavioural  
repertoire.  They  typically  emerge  in  young  children  before  the  age  of  3  years.  Parents  often  become  
concerned  about  a  child  by  18  months  if  language  development  does  not  occur  as  expected.PDD  is  an  
umbrella  term,  which  includes  disorders  such  as  childhood  autism,  Asperger’s  syndrome  and  Rett’s  
syndrome.  
¬ PDD’s  frequently  involve  a  triad  of  deficits  in  social  skills,  communication/language,  and  behaviour.  
The  feature  that  all  have  in  common  is  a  difficulty  with  social  behaviour.  
¬ DSM-­‐‑IV  categorised  PDDs  as  follows:  Autism,  Asperger'ʹs  syndrome,  Rett'ʹs  syndrome,  Childhood  
disintegrative  disorder  and  PDD-­‐‑NOS. In  DSM-­‐‑5,  Autism  Spectrum  Disorder  is  a  new  description  that  
will  now  include  autism,  Asperger’s,  Childhood  Disintegrative  Disorder,  and  Pervasive  
Developmental  Disorder  (not  otherwise  specified)  in  a  single  category.  ASD  is  characterized  by  1)  
deficits  in  social  communication  and  social  interaction  and  2)  restricted  repetitive  behaviors,  interests,  
and  activities  (RRBs).  If  no  RRBs  are  seen,  then  a  diagnosis  of  social  communication  disorder  can  be  
applied.

Autism
¬ Childhood  autism  (previously  called  early  infantile  autism,  Kanner'ʹs  autism)  is  characterized  by  
features  from  the  following  three  symptom  domains:  
o Qualitative  impairment  in  social  interaction
o Impairment  in  communication  [language  delay  is  most  common  cause  for  initial  referral]
o Restricted  repetitive  and  stereotyped  patterns  of  behaviour  or  interests.
¬ The  failure  of  those  with  autism  to  understand  others’  situations  or  feelings  if  often  refererred  to  as  a  
lack  of  theory  of  mind.
¬ By  definition,  the  onset  of  childhood  autism  is  before  the  age  of  3  years.  In  some  cases,  a  diagnosis  is  
not  made  until  a  child  is  much  older  (sometimes  in  adulthood).    
¬ Autism  is  four  times  more  frequent  in  boys  than  in  girls.  There  has  been  an  apparent  increase  in  
prevalence  rates  over  the  years.  

©  SPMM  Course   32  
Aetiology and Pathogenesis
Genetic  Factors

¬ Family  studies:  Increased  risk  of  austistic  spectrum  disorder  in  siblings  of  those  with  ASD,  compared  
to  general  population.  The  recurrence  rate  in  siblings  of  affected  children  is  2-­‐‑8%.  The  risk  of  atusitic  
disorder  in  a  sibling  of  2  autistic  children  is  25-­‐‑30%.  
¬ Autistic  spectrum  disorders  are  subject  to  a  significant  degree  of  heritability  (overall  90%  heritability).  
The  concordance  rate  of  autistic  disorder  in  the  two  largest  twin  studies  was  36%  vs.  0%  in  
monozygotes  vs.  dizygotes  in  one  study  and  about  96%  vs.    27%  in  another.  
¬ It  now  appears  that  multiple  genes  are  involved  in  the  development  of  autism  and  linkage  analyses  
have  demonstrated  that  regions  of  chromosomes    2,  4,7,  13,15,and  19  are  likely  to  contribute  to  the  
genetic  basis  of  autism.  Likely  locations  for  autism-­‐‑related  genes  were  also  found  on  chromosomes  16  
and  17,  although  the  strength  of  the  correlation  was  somewhat  weaker.  Some  analyses  have  implicated  
genes  such  as  NRXN1  and  NLGN3  (Short  Oxford  Textbook  of  psyhiatry,  3rd  Edn).
¬ Fragile  X  syndrome,  a  genetic  disorder  in  which  a  portion  of  the  X  chromosome  fractures,  appears  to  
be  associated  with  autistic  disorder.  Approximately  1-­‐‑4  percent  of  children  with  autistic  disorder  also  
have  fragile  X  syndrome.  Tuberous  sclerosis,  a  genetic  disorder  characterized  by  multiple  benign  
tumours,  with  Autosomal  dominant  transmission  is  found  with  greater  frequency  among  children  
with  autistic  disorder.  Up  to  2  percent  of  children  with  autistic  disorder  may  also  have  tuberous  
sclerosis.
¬ Autistic  disorder  is  also  associated  with  neurological  conditions,  notably  congenital  Rubella  and  
phenylketonuria

Biological  Factors

¬ About  10%  of  children  with  autism  (1  in  10  cases)  have  a  medical  condition  of  some  type  (Shorter  
Oxford  Textbook  of  Psychiatry,  6th  edn).  The  high  rate  of  intellectual  disability  among  children  with  
autistic  disorder  and  the  higher-­‐‑than-­‐‑expected  rates  of  seizure  disorders  further  support  the  biological  
basis  for  autistic  disorder.  
¬ Approximately  80%  of  people  with  childhood  autism  have  learning  disability.  About  one  third  of  
these  children  have  mild  to  moderate  intellectual  disability.  In  contrast,  about  80%  of  people  with  
Autism  Spectrum  Disorders  more  generally  have  intellectual  abilities  within  the  normal  range.
¬ MRI  findings  include  larger  brain  volumes  and  early  acceleration  in  brain  growth;  increase  in  the  size  
of  the  lateral  and  4  ventricles;  frontal  lobe  and  cerebellar  abnormalities  (hypoplasia  of  cerebellar  
th

vermal  lobules  VI  and  VII).  The  greatest  average  percentage  increase  in  brain  size  occurred  in  the  
occipital  lobe,  parietal  lobe,  and  temporal  lobe.  No  differences  were  found  in  the  frontal  lobes.  The  
increased  volume  can  arise  from  three  different  possible  mechanisms:  increased  neurogenesis,  
decreased  neuronal  death,  and  increased  production  of  nonneuronal  brain  tissue,  such  as  glial  cells  or  
blood  vessels.  Brain  enlargement  has  been  suggested  as  a  possible  biological  marker  for  autistic  
disorder.
¬ Cerbellar  pathology:  abnormal  purkinje  cells  in  cerebellar  vermis;  abnormal  limbic  architecture.  An  
autopsy  study  revealed  fewer  Purkinje'ʹs  cells.
©  SPMM  Course   33  
¬ A  number  of  studies  have  demonstrated  that  about  one  third  of  patients  with  autistic  disorder  have  
high  plasma  serotonin  concentrations.  In  some  autistic  children,  a  high  concentration  of  homovanillic  
acid  in  cerebrospinal  fluid  (CSF)  is  associated  with  increased  withdrawal  and  stereotypes.  

Prenatal  and  postnatal  factors:  

¬ There  are  various  associations  between  autistic  spectrum  disorder  and  congenital  rubella  infection  
during  pregnancy.  Most  associations  are  with  first  trimester  exposure,  suggesting  that  an  impact  on  
early  brain  development  is  of  particular  significance.  Obstetric  complications  are  currently  not  thought  
to  represent  a  causative  factor  
¬ Child  rearing  practices  do  not  account  for  autism.  
¬ MMR  vaccination  was  hypothesised  to  be  related  to  a  regressive  form  of  autism.  These  links  arose  due  
to  the  findings  of  a  single  methodologically  flawed  study.  Other  studies  that  aimed  to  replicate  these  
findings  were  unable  to  do  so.  (Ref:  The  Handbook  of  Child  and  adolescent  Psychiatry-­‐‑pg  132)  

Course  and  Prognosis  

¬ Autism  is  a  neurodevelopmental  disorder  that  persists  lifelong.  Predictors  of  good  prognosis  include  
communicative  speech  by  the  age  of  6  years  and  higher  IQ  (>50)  and  having  a  skill  that  is  consistent  
with  a  secure  employment.  A  significant  proportion  of  people  with  autism  (at  least  60%)  will  be  
unable  to  lead  an  independent  life,  and  some  will  require  long  term  residential  care  (Shorter  Oxford  
Textbook  of  Psychiatry,  6th  edn).
¬ Findings  of  long  term  follow  up  studies  into  adult  life-­‐‑  12%  very  good  outcome,  10%  as  good,  19%  as  
fair,  46%  as  poor,  12%  as  very  poor.  Communication,  reading  and  spelling  were  impaired  in  most.  
Steretypies  and  restricted  interests  remained  for  most.  (Ref:  The  Handbook  of  Child  and  adolescent  
Psychiatry-­‐‑pg  140)  

Treatment    

¬ There  is  no  cure  or  treatment  for  autism.  Early  and  effective  management  is  desirable  for  a  better  
outcome,  and  involves  a  comprehensive  assessment  of  the  child  and  family’s  needs.  There  are  many  
management  models,  aimed  at  helping  the  family,  providing  vocational  training  and  support  to  the  
person,  addressing  health  requirements  etc.    Psychotherapy  with  the  individual  may  be  in  the  form  of  
specific  CBT  techniques  for  those  with  verbal  skills,  and  behaviour  management  programmes.  
However,  young  people  with  autism  can  find  CBT  dfficult  due  to  their  tendency  to  sometimes  have  
literal  understanding  and  rigid  thinking.      
¬ Two  specific  intervention  programmes  are  
o Applied  Behavioural  Analysis  program:  an  intense  program  [40  hours  a  week  for  3  years]  based  
on  operant  conditioning,  imitation  and  reinforcement.
o TEACCH  –  Treatment  and  Education  for  Autistic  and  related  Communication  Handicapped  
Children  program  is  based  on  the  belief  that  children  are  motivated  to  learn  language.  Successful  
in  reducing  self  injurious  behaviour,  and  enhancing  life  skills.  

©  SPMM  Course   34  
¬ Pharmacotherapies  are  commonly  used  in  individuals  with  autistic  spectrum  disorder  (ASD)  as  
adjuncts  to  psychological  interventions.  SSRIs  have  become  the  most  widely  prescribed  medications  to  
treat  restricted  repetitive  behaviours  in  paediatric  ASD  populations.  However  the  evidence  supporting  
the  effectiveness  of  SSRIs  in  ameliorating  these  symptoms  remains  limited.  When  using  SSRIs  to  treat  
repetitive  behaviour  in  ASD  patients,  it  has  been  found  that  lower  doses  are  required  than  the  
therapeutic  antidepressant  dose.    Second  generation  antipsychotics  are  the  first  line  pharmacological  
treatment  for  children  and  adolescents  with  ASD  and  associated  irritability.  The  only  licensed  
medication  in  UK  is  risperidone.  It  is  indicated  for  the  treatment  of  autism  with  aggressive  behaviour  
in  children  and  adolescents.  Weight  gain,  somnolence  and  hyperglycemia  require  monitoring.  
Melatonin  has  been  shown  in  several  small  studies  to  be  beneficial  in  children  with  ASD  with  
reductions  in  sleep  latency  as  well  as  efficiency.    

Asperger’s syndrome
¬ Individuals  with  Asperger’s  syndrome  have  same  type  of  qualitative  abnormalities  in  reciprocal  social  
interaction  that  typify  autism  with  a  restricted,  stereotyped  and  repetitive,  repertoire  of  
behaviour/interests.  IQ  and  language  are  ususally  within  normal  limits.
¬ Unlike  in  childhood  autism/autistic  disorder,  there  were  in  Asperger'ʹs  disorder  no  significant  delays  
occur  in  relation  to  language  development.,  cognitive  development,  and/or  age-­‐‑appropriate  self-­‐‑help  
skills.
¬ Mild  motor  clumsiness  and  a  family  history  of  autism  may  be  present,  as  is  the  case  for  other  autism  
spectrum  disorders.
¬ Epidemiology:  Global  prevalence  rate  is  uncertain.  Estimated  to  be  about  a  third  as  common  as  autism  
with  a  prevalence  of  about  6  in  10,000  (Shorter  Oxford  Textbook  of  Psychiatry,  6thedn).
¬ The  factors  associated  with  a  good  prognosis  are  a  normal  IQ  and  high-­‐‑level  social  skills.  Psychiatric  
comorbidity  is  high  with  depression  most  common.  BPAD  and  schizophrenia  are  more  common  than  
in  the  general  population.

Rett's syndrome
¬ Rett'ʹs  syndrome  is  a  rare  X  linked  dominant  disorder  of  arrested  neurodevelopment  associated  with  
mutations  in  the  MeCP2  gene.  It  almost  exclusively  affects  females.    
¬ Head  circumference  normal  at  birth  and  developmenatal  milestones  are  unremarkable  in  early  life.  
Between  6  and  18  months,  head  growth  begins  to  decelerate  and  produces  microcephaly.  Other  signs  
often  include  the  loss  of  purposeful  hand  movements,  which  are  replaced  by  stereotypic  motions,  such  
as  hand  wringing;  the  loss  of  previously  acquired  speech;  psychomotor  retardation;  and  ataxia.  
¬ Other  stereotypical  hand  movements  may  occur,  such  as  licking  or  biting  the  fingers  and  tapping  or  
slapping.  Language  skills  are  lost,  and  both  receptive  and  expressive  communicative  and  social  skills  
seem  to  plateau  at  developmental  levels  between  6  months  and  1  year.  Poor  muscle  coordination  and  
an  apraxia  gait  with  an  unsteady  and  stiff  quality  develop.  
¬ Associated  features  include  seizures  in  up  to  75  percent  of  affected  children  and  disorganized  EEGs  
with  some  epileptiform  discharges  in  almost  all  young  children  with  Rett'ʹs  disorder,  even  in  the  
absence  of  clinical  seizures.  

©  SPMM  Course   35  
¬ An  additional  associated  feature  is  irregular  respiration,  with  episodes  of  hyperventilation,  apnoea,  
and  breath  holding.  The  disorganized  breathing  occurs  in  most  patients  while  they  are  awake;  during  
sleep,  the  breathing  usually  normalizes.  Many  patients  with  Rett'ʹs  disorder  also  have  scoliosis  and  
spasticity.  
¬ Developmental  arrest  plateaus  and  many  may  reach  adulthood,  although  disability  is  great  and  
prognosis  poor.  

Childhood disintegrative disorder (CDD)

¬ Childhood  disintegrative  disorder  (CDD)  also  called  Heller’s  disease  and  disintegrative  psychosis  is  
characterized  by  marked  regression  in  several  areas  of  functioning  after  at  least  2  years  of  apparently  
normal  development.    
¬ There  is  normal  development  for  2-­‐‑3  years,  followed  by  a  loss  of  acquired  motor,  language,  and  social  
skills  between  ages  3  and  4  years.  Stereotypies  and  compulsions  are  common  
¬ To  receive  the  diagnosis,  a  child  must  exhibit  loss  of  skills  in  two  of  the  following  areas:  language,  
social  or  adaptive  behaviour;  bowel  or  bladder  control;  play;  and  motor  skills.  Abnormalities  must  be  
present  in  at  least  two  of  the  following  categories:  reciprocal  social  interaction,  communication  skills,  
and  stereotyped  or  restricted  behaviour.  The  main  neurological  associated  feature  is  seizure  disorder  
¬ Male  predominance  is  noted.  Cause  is  unknown  and  prognosis  is  poor.  Most  patients  are  left  with  at  
least  moderate  mental  retardation  

©  SPMM  Course   36  
 9. Learning and communication disorders
¬ Learning  disorders  are  problems  that  make  educational  achievement  difficult.  Specific  learning  
difficulties  can  be  underachievement  in  reading,  written  expression,  or  mathematics  in  comparison  
with  the  overall  intellectual  ability  of  the  child.  
¬ The  most  recent  revised  version  of  the  DSM-­‐‑IV  (DSM-­‐‑IV-­‐‑TR)  includes  four  diagnostic  categories  of  
learning  disorders:  reading  disorder,  mathematics  disorder,  disorder  of  written  expression,  and  
learning  disorder  not  otherwise  specified
¬ Genetic  predisposition,  perinatal  injury,  and  neurological  and  other  medical  conditions  can  contribute  
to  the  development  of  learning  disorders,  but  many  children  and  adolescents  with  learning  disorders  
have  no  specific  risk  factors
¬ Learning  disorders  affect  at  least  5%  of  school-­‐‑age  children.  They  are  associated  with  higher  than  
average  risk  of  a  variety  of  co  morbid  disorders,  including  attention-­‐‑deficit/hyperactivity  disorder  
(ADHD),  communication  disorders,  conduct  disorders,  and  depressive  disorders.
¬ DSM-­‐‑IV  groups  together  a  number  of  learning  disorders  that  share  the  following:
o Performance  significantly  below  that  expected  for  IQ  or  age
o A  discrete  developmental  disability  in  the  absence  of  learning  disability
o Commonly  present  as  emotional  or  behavioural  problems
o 50%  have  a  comorbid  psychiatric  disorder  and  many  have  other  LLDs
o Most  show  strong  evidence  of  heritability
¬ Communication  disorders  are  among  the  most  common  disorders  in  childhood.  They  include  
language  disorders  such  as  expressive  and  mixed  receptive-­‐‑expressive  language  disorder,  and  speech  
disorders  such  as  phonological  disorder  and  stuttering.

Reading disorder (dyslexia)

¬ Reading  disorders  are  present  in  approximately  75%  of  children  and  adolescents  with  learning  
disorders.  Reading  disorder  is  characterized  by  an  impaired  ability  to  recognize  words,  slow  and  
inaccurate  reading,  and  poor  comprehension.  Children  who  have  reading  disorder  can  usually  be  
identified  by  the  age  of  7  years  (second  grade).  
¬ Reading  comprehesion  skill,  reading  word  recognition,  oral  reading  skill,  and  performance  of  task  
requiring  reading  may  all  be  affected.  Children  with  reading  disorders  make  many  errors  in  their  oral  
reading.  The  errors  are  characterized  by  omissions,  additions,  and  distortions  of  words.  Such  children  
have  difficulty  in  distinguishing  between  printed  letter  characters  and  sizes,  especially  those  that  differ  
only  in  spatial  orientation  and  length  of  line.  The  child'ʹs  reading  speed  is  slow,  often  with  minimal  
comprehension.  Difficulty  with  reading,  in  most  cases  involving  a  deficit  in  phonological-­‐‑processing  
skills.  
¬ 4%  of  school-­‐‑age  children  are  affected.  Male  predominance  [4:1].  There  is  often  a  family  history  of  
dyslexia.  Approximately  20%  of  children  with  reading  disorder  have  comorbid  CD  or  ADHD  (Oxford  
Handbook  of  Psychiatry,  3rd  Edn.).  Conversely,  it  is  estimated  that  between  15  and  30  percent  of  
children  diagnosed  with  ADHD  have  a  learning  disorder.

©  SPMM  Course   37  
¬ Tools  used  to  measure  reading  ability  are  WORD  (Weschler  objective  reading  dimension)-­‐‑  a  single  
word  rreading  test  commonly  used  in  Bristish  schools,  TOWRE  (Test  of  word  reading  efficiency)-­‐‑  
measures  word  reading  rate  &  accuracy,  WISC  (Wescler  intelligence  sacle  for  children)-­‐‑  measures  
overall  cognitive  ability  of  the  child
¬ Management  includes  1:1  remedial  teaching  and  parent  involvement  improves  long-­‐‑term  outcome.

Disorder of written expression

¬ Disorder  of  written  expression  is  characterized  by  writing  skills  that  are  significantly  below  the  
expected  level  for  a  child'ʹs  age  and  intellectual  capacity.  These  difficulties  impair  the  child'ʹs  academic  
performance  and  writing  in  everyday  life.  
¬ Common  features  of  the  disorder  are  spelling  errors,  grammatical  errors,  punctuation  errors,  poor  
paragraph  organization,  and  poor  handwriting.  Often  coexists  with  dyslexia  and  manifests  as  
difficulties  with  spelling,  syntax,  grammar,  and  composition.  
¬ Occurs  in  2-­‐‑8%  of  school-­‐‑age  children  with  a  3:1  male  predominance.  
¬ ADHD  occurs  with  greater  frequency  in  children  with  writing  disorders  than  in  the  general  
population.
¬ Remedial  treatment  for  writing  disorder  includes  direct  practice  in  spelling  and  sentence  writing  as  
well  as  a  review  of  grammatical  rules.  Intensive  and  continuous  administration  of  individually  
tailored,  one-­‐‑on-­‐‑one  expressive  and  creative  writing  therapy  appears  to  effect  favourable  outcome.

Mathematics disorder
¬ Epidemiological  studies  have  indicated  that  up  to  6  percent  of  school  age  children  have  some  difficulty  
with  mathematics.  It  is  reported  more  commonly  in  females.  
¬ Often  associated  with  visuo-­‐‑spatial  deficits  and  attributed  to  right  parietal  dysfunction.
¬ Common  features  of  mathematics  disorder  include  difficulty  with  various  components  of  
mathematics,  such  as  learning  number  names,  remembering  the  signs  for  addition  and  subtraction,  
learning  multiplication  tables,  translating  word  problems  into  computations,  and  doing  calculations  at  
the  expected  pace.  A  Child  with  mathematics  disorder  generally  has  significant  problems  with  
concepts,  such  as  counting  and  adding  even  one-­‐‑digit  numbers,  compared  with  classmates  of  the  same  
age
¬ Currently,  the  most  effective  treatments  for  mathematics  disorder  combine  teaching  mathematics  
concepts  with  continuous  practice  in  solving  math  problems.  Flash  cards,  workbooks,  and  computer  
games  can  be  a  viable  part  of  this  treatment

Learning Disorder Not Otherwise Specified:

¬ Learning  disorder  not  otherwise  specified-­‐‑  It  does  not  meet  the  criteria  for  any  specific  learning  
disorder,  but  causes  impairment  and  reflects  learning  abilities  below  those  expected  for  a  person'ʹs  
intelligence,  education,  and  age.  An  example  of  a  disability  that  could  be  placed  in  this  category  is  a  
spelling  skills  deficit.
¬ The  ICD-­‐‑10  classifies  specific  developmental  disorders  of  scholastic  skills  learning  disorders  that  
include  specific  reading  disorder;  specific  spelling  disorder;  specific  disorder  of  arithmetic  skills;  
©  SPMM  Course   38  
 mixed  disorder  of  scholastic  skills;  other  developmental  disorders  of  scholastic  skills;  and  
developmental  disorder  of  scholastic  skills,  unspecified  

Expressive language disorders

¬ Expressive  language  disorder  is  diagnosed  when  a  child  demonstrates  a  selective  deficit  in  expressive  
language  development  relative  to  receptive  language  skills  and  nonverbal  intelligence.  
¬ A  child  with  expressive  language  disorder  is  likely  to  function  below  the  expected  levels  of  acquired  
vocabulary,  correct  tense  usage,  complex  sentence  constructions,  and  word  recall.  A  child  with  an  
expressive  language  disorder  exhibits  the  following  features:  limited  vocabulary,  simple  grammar,  
and  variable  articulation.  Language  understanding  (decoding)  skills  remain  relatively  intact.
¬ Prevalence:  a  rate  of  between  3-­‐‑5%  of  children  has  been  suggested  (Shorter  Oxford  Textbook  of  
Psychiatry,  6th  Edn).  The  disorder  is  two  to  three  times  more  common  in  boys  than  in  girls  and  is  most  
prevalent  among  children  whose  relatives  have  a  family  history  of  phonological  disorder  or  other  
communication  disorders.
¬ The  most  common  co  morbid  disorders  were  attention-­‐‑deficithyperactivity  disorder  (ADHD),  anxiety  
disorders,  oppositional  defiant  disorder,  and  conduct  disorder.
¬ Management  includes  special  education,  speech  therapy  and  treating  any  comorbidity,  if  applicable.

Mixed receptive-expressive language disorder

¬ The  essential  clinical  feature  of  the  disorder  is  significant  impairment  in  both  language  comprehension  
and  language  expression.  In  the  mixed  disorder,  the  expressive  impairments  are  similar  to  those  of  
expressive  language  disorder,  but  can  be  more  severe.
¬ Children  with  mixed  receptive-­‐‑expressive  language  disorder  show  markedly  delayed  and  below-­‐‑
normal  ability  to  comprehend  (decode)  verbal  or  sign  language,  although  they  have  age-­‐‑appropriate  
nonverbal  intellectual  capacity.  In  most  cases  of  receptive  dysfunction,  verbal  or  sign  expression  
(encoding)  of  language  is  also  impaired.
¬ Mixed  receptive-­‐‑expressive  language  disorder  tends  to  persist  in  approximately  3  percent  of  school-­‐‑
age  children  and  is  believed  to  be  at  least  twice  as  prevalent  in  boys  as  in  girls.

Phonoogical disorder
¬ Children  with  phonological  disorder  are  delayed  in,  or  incapable  of,  producing  speech  sounds  that  are  
expected  for  their  age,  intelligence.  Their  inability  to  produce  clear  speech  is  not  due  to  physical  
problems  as  may  be  seen  in  dysarthria.
¬ Phonological  disorder  can  be  recognized  in  early  childhood.  In  severe  cases,  the  disorder  is  first  
recognized  at  about  3  years  of  age.
¬ Omissions,  distortions,  and  substitutions  also  occur  normally  in  the  speech  of  young  children  learning  
to  talk.  But,  whereas  young,  normally  speaking  children  soon  replace  these  misarticulations,  children  
with  phonological  disorder  do  not.
¬ Children  with  phonological  disorder  cannot  articulate  certain  phonemes  correctly  and  may  distort,  
substitute,  or  even  omit  the  affected  phonemes.  With  omissions,  the  phonemes  are  absent  entirely  for  
example  ca  for  car,  or  whaa?  for  what'ʹs  that?  With  substitutions,  difficult  phonemes  are  replaced  with  

©  SPMM  Course   39  
 incorrect  ones  for  example,  wabbit  for  rabbit.  With  distortions,  the  correct  phoneme  is  approximated  
but  is  articulated  incorrectly.  

Stuttering
¬ Stuttering  is  a  condition  in  which  the  normal  flow  of  speech  is  disrupted  by  involuntary  speech  motor  
events.  Stuttering  can  include  a  variety  of  specific  disruptions  of  fluency,  including  sound  or  syllable  
repetitions,  sound  prolongations,  dysrhythmic  phonation,  and  complete  blocking  or  unusual  pauses  
between  sounds  and  syllables  of  words.  Usually  struggle  with  initial  syllables.  
¬ Male  predominance  of  3:1  is  noted.  The  prevalence  of  stuttering  is  about  1%  in  the  general  population.  
Stuttering  tends  to  be  most  common  in  young  children  and  has  often  resolved  spontaneously  by  the  
time  the  child  is  older.  The  typical  age  of  onset  is  2  to  7  years  of  age  with  a  peak  at  age  5  years.  Of  all  
children  who  stutter,  mostly  those  with  mild  cases,  50  to  80  percent  recover  spontaneously.  Most  
children  grow  out  of  it  but  stuttering  affects  1-­‐‑2%  of  adults.  
¬ Preschoolers  and  school-­‐‑age  children  who  stutter  exhibit  an  increased  incidence  of  social  anxiety,  
school  refusal,  and  other  anxiety  symptoms.  When  stuttering  persists  into  adolescence,  social  isolation  
occurs  at  higher  rates  than  in  the  general  adolescent  population.  
¬ Stuttering  is  also  associated  with  a  variety  of  abnormal  motor  movements,  upper  body  tics,  and  facial  
grimaces.  Other  disorders  that  coexist  with  stuttering  include  phonological  disorder,  expressive  
language  disorder,  mixed  receptive-­‐‑expressive  language  disorder,  and  ADHD.
¬ However,  stuttering  is  not  normally  associated  with  a  psychiatric  disorder  (Shorter  Oxford  textbook  of  
Psychiatry,  6th  edn.).  Majority  of  cases  are  developmental  but  occasionally  there  are  acquired  cases  (e.g.  
head  injury).  Aetiology:  genetic;  incomplete  cerebral  dominance;  hyperdopaminergic  state.
¬ Management:  speech  therapy.

10. Tic disorders

Tourette syndrome
¬ Characterised  by  multiple  motor  and  one  or  more  vocal  tics,  present  for  at  least  a  year,  causing  distress  
and  impaired  function.  
¬ The  tics  occur  many  times  a  day  (usually  in  bouts)  nearly  every  day  or  intermittently  throughout  a  
period  of  more  than  1  year,  and  during  this  period  there  was  never  a  tic-­‐‑free  period  of  more  than  3  
consecutive  months.
¬ Facial  tics:eye  blinks  or  head  jerks  are  often  the  initial  symptoms,  but  tics  involving  the  neck,  
shoulders,  and  upper  extremities  are  also  common.
¬ Vocal  tics  begin  1-­‐‑2  yrs  after  the  onset  of  motor  symptoms  and  range  from  meaningless  sounds  to  clear  
words.  The  vocal  tics  are  crucial  for  diagnosis  and  may  be  barks,  hisses,  hoots  and  not  necessarily  
obscene  blasphemous  utterances  (Coprolalia),  echolalia,  or  palilalia(repeating  ones  own  speech)
¬ Approximately  10%  exhibit  echolalia  or  echopraxia.  About  1/3  exhibit  coprolalia  (but  most  of  these  are  
not  children)(Shorter  Oxford  Textbook  of  Psychiatry,  6th  edn).
¬ Typically,  tics  vary  over  time  with  more  complex  tics  emerging  after  some  years.

©  SPMM  Course   40  
¬ Wax  and  wane  in  frequency  with  periods  of  remission.  The  periods  of  exacerbations  are  often  related  
to  physical  and  emotional  stress.  These  are  known  to  be  exacerbated  by  external  factors  such  as  stress,  
anxiety  and  fatigue
¬ The  onset  is  before  age  18  years.  Suggested  prevalence  in  children  of  1%.  Monozygotic  twin  
concordance  50%,  dizygotic  10%.  Mean  age  of  onset  is  7  years.  It  is  3-­‐‑4  times  more  likely  in  males  than  
females  (Shorter  Oxford  Textbook  of  Psychiatry,  6th  edn).

Aetiology

¬ Genetic  factors:  Autosomal  dominant  and  polygenic  common  (with  increase  in  Monozygotic  twins  and  
first  degree  relatives).  Family  history  very  common.  Overlap  with  genetic  liability  for  OCD.
¬ Neurotransmitter  abnormalities  thought  to  underlie  tic  disorders.  Functional  excess  of  dopamine  system  
is  a  popular  speculation  as  antipsychotics  reduce  symptoms.  The  effectiveness  of  Clonidine  suggests  
the  role  of  Noradrenaline
¬ Neuroimaging  studies  implicate  circuits  involving  the  basal  ganglia,  premotor  and  motor  cortex.
¬ Post-­‐‑infectious  autoimmune  mechanisms:  It  is  well  established  that  group  A  beta  haemolytic  streptococci  
(GABHS)  can  trigger  immune-­‐‑mediated  disease  in  genetically  predisposed  individuals.  Speculation  
concerning  a  post-­‐‑infectious  (or  at  least  a  post-­‐‑rheumatic  fever)  etiology  for  tic  disorder  symptoms  
dates  from  the  late  1800s.    An  increased  proportion  of  GABHS  infections  (odds  ratio  =  3.1)  is  found  in  
the  preceding  3  months  in  children  with  newly  diagnosed  TS  compared  to  well  matched  controls.  
Larger  odds  ratio  (OR  =  12.1  for  TS)  is  demonstrated  when  subjects  were  required  to  have  multiple  
GABHS  infections  in  the  previous  year,  suggesting  a  dose-­‐‑dependent  effect  of  exposure.  There  was  
also  a  statistically  significant  positive  association  between  preceding  streptococcal  infection  and  a  new  
diagnosis  of  OCD  and  tic  disorders.
¬ Comorbidity:  OCD  [1/3rd  to  2/3rd  of  children  and  adolescents  exhibit  OCD  symptoms)  and  ADHD  
[upto  50%]  common;  depression,  anxiety,  impulse  and  conduct  disorders  and  other  behavioural  
problems.  These  are  more  prevalent  than  would  be  expected  by  chance  association  alone.  1/3rd  of  
adults  with  Tourettes  have  persistent  OCD  into  adulthood.  

Management:  

¬ Psychoeducation  for  the  individual,  family  and  the  people  they  interact  with,  especially  schools  is  
crucial.  Both  tics  and  OCD  symptoms  may  improve  with  CBT,  if  succesful  exposure-­‐‑response  
prevention  can  be  acheived.  Techniques  include  a)  Relaxation  b)  Exposure-­‐‑response  prevention  c)  
massed  practice  (forced  reptition  of  the  tic)  d)  Habit  reversal  (movements  incompatible  with  the  tic)    
(Ref:  The  Oxhord  handbook  of  child  and  adolescent  psychiatry;  pg  198)  

¬ Medications  can  be  used  if  tics  are  disabling  and  non-­‐‑responsive  to  other  therapies.Medications  used  
to  treat  Tourette’s  disorder  include  Haloperidol,  Pimozide,  Sulpiride,  Risperidone  and  Clonidine  at  
low  doses.  All  these  drugs  have  been  shown  to  be  more  effective  than  placebo  in  a  number  of  small-­‐‑
randomised  studies.    
¬ Clonidine  (adrenergic  alpha  2  agonists)  should  be  tried  first.It  helps  to  reduce  the  severity  and  
frequency  of  tics.  Main  side  effects  are  sedation  and  postural  hypotension.  Guanfacine  also  an  

©  SPMM  Course   41  
 adrenergic  alpha  2  agonists  has  been  shown  to  lead  to  a  30%  reduction  in  tic  rating  scales.  These  drugs  
are  more  acceptable  in  terms  of  adverse  effects.  
¬ Antipsychotics  like  Risperidone,  Haloperidol  and  sulpiride  are  effective  in  alleviating  tics  but  their  
side  effects  may  outweigh  benefits  and  should  not  be  tried  as  first  line  drugs.  

Transient Tic Disorder

¬ Transient  tic  disorder  is  characerised  by  single  or  multiple  motor  and/or  vocal  tics  (sudden,  rapid,  
recurrent,  nonrhythmic,  stereotyped  motor  movements  or  vocalizations)  affecting  usually  face,  nose,  
throat  are  involved  (grimaces,  blinks,  frowns,  grunts,  throat  clearing,  sniffs).  The  tics  occur  many  times  
a  day,  nearly  every  day  for  at  least  4  weeks,  but  for  no  longer  than  12  consecutive  months
¬ The  onset  is  before  age  18  years.  The  disturbance  is  not  due  to  the  direct  physiological  effects  of  a  
substance  (stimulants)  or  a  general  medical  condition  (Huntington'ʹs  disease  or  post  viral  encephalitis).  
¬ Criteria  should  have  never  been  met  for  Tourette'ʹs  Disorder  or  Chronic  Motor  or  Vocal  Tic  Disorder.
¬ Note:  Transient  tics  occur  in  5-­‐‑20%  of  children.  80%  of  children  with  tics  will  have  outgrown  them  by  
adult  life.

Chronic Tic disorder:

¬ Persists  for  more  than  one  year  and  often  shows  relapses  and  remissions  throughout  childhood.  May  
be  one  or  several  tics  are  simultaneously  present.  Motor  or  vocal  tics  but  not  both  (so  it  is  a  form  of  
partial  Tourette  syndrome).  Over  time,  one  form  fades  to  be  replaced  by  another.  It  is  a  rarer  form  of  
tic  disorder.    

11. Miscellaneous topics

Substance abuse in the early life
¬ Alcohol  is  the  most  commonly  abused  substance  by  adolescents.    ~  30%  of  13-­‐‑  year  olds  admitting  to  
the  use  of  alcohol  at  least  once  a  week.    Binge  drinking  pattern  is  more  common  than  other  patterns  of  
abuse  among  the  adolescents  
¬ Tobacco  use  (cigarette  smoking)  in  young  people  is  decreasing  in  the  West  due  to  legislative  measures  
and  changing  public  perception  
¬ Cannabis:  ~  5%  of  11-­‐‑16  year  olds  in  the  UK  had  used  cannabis  at  least  once  previously,  with  rates  
increasing  significantly  in  the  late  teens.  
¬ Heroin  use  in  under  18’s  has  increased  in  the  past  decade  in  many  countries  including  the  UK.  At  least  
15%  of  users  will  switch  to  IV  use  within  1  year,  with  its  attendant  additional  risks.  
¬ 2.4%  of  the  12-­‐‑17  year  old  age  group  used  cocaine  at  some  point  in  their  life.  (US  national  survey)  
whereas  0.5%  of  11-­‐‑15  year  olds  in  the  UK  admitted  to  using  cocaine.    
¬ Party  drugs  like  MDMA  (ecstasy),  GHB,  ketamine,  rohypnol)  do  not  account  for  a  large  proportion  of  
child  and  adolescent  substance  problems,  but  are  being  experimented  with  at  increasingly  young  ages.  
¬ There  is  a  downward  trend  of  life-­‐‑time  methamphetamine  use  (speed)  from  1999  to  2005  (4.7%  rate  
reduced  to  2.5%  lifetime  rate  now)  

©  SPMM  Course   42  
¬ In  terms  of  steroid  use,  in  the  US,  4  and  12%  of  male  adolescents  have  used  anabolic  steroids  to  
improve  performance  at  sport  or  alter  body  size.  No  UK  data  is  available,  but  the  rates  are  often  
reported  to  be  less  than  the  US.  
¬ Use  of  LSD/hallucinogens  is  down  since  a  peak  in  the  1990s  and  now  used  only  by  a  small  minority.    

(Ref:  The  Oxford  handbook  of  Child  and  Adolescent  Psychiatry:  382-­‐‑383)

Rating scales in Children and Adolescents

Scale   Properties  
Connor’s  questionnaire   It  is  widely  used  to  obtain  information  from  parents  and  schoolteachers  on  
ADHD  symptoms.  There  are  parent  and  teacher  versions.    
 
Autism  diagnostic   It  is  a  structured  interview  mainly  used  in  research  to  obtain  a  thorough  
interview-­‐‑  Revised  (ADI-­‐‑R)   assessment  of  individuals  suspected  of  having  autism.  It  is  useful  for  formal  
diagnosis  as  well  as  treatment  and  educational  planning.  It  is  composed  of  93  
items  focusing  on  3  areas;  language  &  communication,  reciprocal  social  
interactions,  restricted  &  stereotyped  interests  and  behaviours.  
 
Wechsler  intelligence  scale   It  is  useful  to  assess  intelligence  for  children  aged  less  than  sixteen.  It  has  a  
for  children  (WISC)   verbal,  performance  subscales  that  yield  a  verbal,  performance  and  full-­‐‑scale  IQ.  
  WAIS  is  for  adults.    
 
Strength  and  difficulties   It  is  a  generic  rating  scale,  helpful  to  obtain  information  on  a  variety  of  
questionnaire  (SDQ)   psychiatric  symptoms  like  emotional,  behavioural  and  prosocial  problems.  It  is  
  validated  in  a  number  of  different  populations  of  children  aged  between  4-­‐‑16.  It  
is  quick  to  complete.    
 
The  Child  Behavior   The  Child  Behavior  Checklist  (CBCL)  assesses  a  broad  range  of  symptoms  that  
Checklist  (CBCL)   relate  to  academic  and  social  competence  of  children  aged  4  through  16.  Mainly  
used  in  children  with  oppositional  defiant  disorder  and  conduct  disorder.  CBCL  
is  completed  by  the  parents  or  others  (e.g.,  teachers)  who  know  a  child  well.    The  
checklist  is  composed  of  113  items  in  a  Likert  fashion.  This  scale  can  be  helpful  in  
the  evaluation  of  a  child  with  multiple  behavioural  problems,  especially  if  the  
child  presents  with  different  symptoms  in  different  settings  such  as  at  school  and  
home.    There  is  a  parent  and  a  teacher  version  so  that  the  reports  of  these  two  
observers  may  be  compared.    
 
The  Child  &  Adolescent   It  is  a  rating  scale  to  assess  the  degree  of  impairment  in  functioning  due  to  
Functional  Assessment   emotional,  behavioural,  or  psychiatric  problems.  It  is  completed  by  a  clinical  staff  
Scale   and  takes  about  10  minutes.  It  measures  aggression  and  conduct  problems  
especially  in  age  between  7  to  17  years.    
 
Children’s  Depression   It  is  a  scale  used  to  measure  severity  of  depressive  symptoms  between  7  to  17  
Inventory   years.    

©  SPMM  Course   43  
Beck  Depression  Inventory   It  could  be  used  for  screening  of  children  with  depression  only  after  the  age  of  
  14.    

CY-­‐‑BOCS   It  is  the  paediatric  version  of  Y-­‐‑BOCS  (Yale  Brown  Obsessive-­‐‑Compulsive  Scale)  
useful  to  measure  symptoms  of  childhood  OCD  
 

In-patient psychiatric care

(excerpt  from  Blanz  &  Schmidt  2000)  

¬ In  general,  psychiatric  hospitalization  is  not  a  preferred  option  for  the  assessment  and  treatment  of  
most  childhood-­‐‑onset  and  adolescent  psychiatric  disorders,  as  this  is  seen  as  disruptive  to  the  normal  
developmental  context  provided  by  a  child’s  home  and  school  environments.    
¬ Dalton  et  al.  (1989)  cited  the  following  factors  to  argue  against  hospitalisation:  
o Disruption  of  the  child’s  family  and  community  relationships  
o  Expense  s  incurred  by  the  family  and  health  services  
o Reinforcement  of  parental  denial  or  guilt    
o Sibling’s  confused  and  distorted  perception  of  the  issues  treated  
o Removal  of  the  child  from  the  continuum  of  education  
o Predictable  noxious  stigmata  and  labeling    
o potential  for  unresolved  transference  and  institutionalisation  
¬ Hersov  (1994)  proposed  a  set  of  admission  criteria  that  specify  the  need  for  hospitalisation  (numbers  
1–3)  and  the  need  to  remove  a  child  from  its  home  (numbers  4  and  5):  
1. For  diagnostic  work  that  cannot  be  obtained  on  an  outpatient  basis    
2. A  severe  psychiatric  disorder  with  need  for  treatment  by  a  multiprofessional  team  in  a  safe  setting    
3. Impaired  physical  status  of  the  child  that  requires  skilled  medical  and  nursing  care    
4. Adverse  environmental  circumstances  that  preclude  the  child’s  improvement  within  the  home  or  
severely  distorted  family  interaction  that  leads  to  progressive  interference  with  the  child’s  progress    
5. Gross  overprotection  by  parents  after  a  trauma/injury  that  precludes  recovery.    

 
 
DISCLAIMER: This material is developed from various revision notes assembled while preparing for
MRCPsych exams. The content is periodically updated with excerpts from various published
sources including peer-reviewed journals, websites, patient information leaflets and books. These
sources are cited and acknowledged wherever possible; due to the structure of this material,
acknowledgements have not been possible for every passage/fact that is common knowledge
in psychiatry. We do not check the accuracy of drug-related information using external sources;
no part of these notes should be used as prescribing information

©  SPMM  Course   44  
Notes prepared using excerpts from:
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! Canadian  Paediatric  Society,  Maternal  depression  and  child  development.  (2004).  Paediatrics  &  Child  Health,  
9(8),  575–583;      
! Coghill,  D.,  et  al  (2009).  Child  and  Adolescent  Psychiatry  (Oxford  Specialist  Handbooks  in  Psychiatry  series).  
! Geddes  et  al.,  Shorter  Oxford  Textbook  of  Psychiatry,  6th  Edition  
! Johnstone,  E.  C.,  Owens,  D.  C.,  &  Lawrie,  S.  M.  (2010).  Companion  to  psychiatric  studies.  Elsevier  Health  
Sciences.  
! Kessler  RC,  McLaughlin  KA,  Green  JG,  et  al.  Childhood  adversities  and  adult  psychopathology  in  the  WHO  
World  Mental  Health  Surveys.  The  British  Journal  of  Psychiatry.  2010;197(5):378-­‐‑385.  doi:10.1192/bjp.bp.110.080499.  
! Lewis,  M.  (Ed.).  (2002).  Child  and  adolescent  psychiatry:  A  comprehensive  textbook.  Philadelphia:  Lippincott  
Williams  &  Wilkins.  
! Murray,  L  &  Cooper,  PJ.  Effects  of  postnatal  depression  on  infant  development.    Arch  Dis  Child  1997;77:99-­‐‑101;  
http://adc.bmj.com/content/77/2/99.full  
! Rutter,  M.,  Bishop,  D.,  Pine,  D.,  Scott,  S.,  Stevenson,  J.  S.,  Taylor,  E.  A.,  &  Thapar,  A.  (2011).  Rutter'ʹs  child  and  
adolescent  psychiatry.  John  Wiley  &  Sons.  
! Sadock,  B.  J.,  &  Sadock,  V.  A.  (2011).  Kaplan  and  Sadock'ʹs  synopsis  of  psychiatry:  Behavioral  sciences/clinical  
psychiatry.  Lippincott  Williams  &  Wilkins.  
!  Semple,  D.,  &  Smyth,  R.  (2013).  Oxford  handbook  of  psychiatry.  Oxford  University  Press.  
! Taylor,  D.,  Paton,  C.,  &  Kapur,  S.  (2015).  The  Maudsley  prescribing  guidelines  in  psychiatry.  John  Wiley  &  Sons.  
 

©  SPMM  Course   45