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Autism and Dopamine

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Delays or abnormal functioning in one of the above major areas before the age of ... chorea (i.e. jerky, nonrhythmic), athetosis (i.e. slow, writhing), or dystonia ... – PowerPoint PPT presentation

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Title: Autism and Dopamine


1
Autism and Dopamine
  • Shannon Vettor

2
Symptoms
  • Qualitative impairment in social interaction
  • Qualitative impairment in communication
  • Restricted, stereotyped interest and activities
  • Delays or abnormal functioning in one of the
    above major areas before the age of three

3
Repetitive Behaviours
  • Stereotypy repetitive and apparently
    purposeless body movements (i.e. rocking), body
    part movements (i.e.. hand flapping, head
    rolling), or use of the body to generate object
    movements (i.e.. plate spinning, string twirling)
  • Compulsions repetitive, intentional behaviours
    that appear to follow certain rules
  • Obsessions repetitive persistent thoughts,
    impulses, or images that are experienced as
    intrusive and inappropriate and that cause marked
    anxiety or distress
  • Sameness insistence on sameness involves
    overall repetitive routines and preferences
    rather than discrete repeated acts or thoughts
  • Echolalia repetitive use of speech in either an
    immediate manner or delayed manner
  • Self-injury repetitive motor movements that
    result in injury to the person or have the
    potential to inflict injury
  • Tics brief, rapid, explosive or shock-like
    movements which can be simple or complex
  • Dyskinesia repetitive, involuntary movements
    expressed as chorea (i.e. jerky, nonrhythmic),
    athetosis (i.e. slow, writhing), or dystonia
    (i.e. slow, sustained, tensing)
  • Akathisia repetitive restless movements and
    hyperkinetic restless states

4
Epidemiology
  • Prevalence 4-5/10,000
  • Males females 3-41
  • At least one third have no speech
  • Cognitive impairments only 20-25 score within
    normal or near normal ranges on IQ tests
  • Comorbidity
  • -Seizure Disorders 30
  • -Fragile X syndrome 2-5
  • -Tuberous Sclerosis 1-3
  • -Separation Anxiety approx. 73

5
Etiology
  • Family
  • -risk of autism in the siblings of people with
    the disorder is about 75 times greater
  • Twin
  • -60-91 concordance for autism between MZ
    compared with DZ at 0-20
  • -other studies suggest that autism is linked
    genetically to a broader spectrum of deficits in
    communicative and social areas -higher CSF HVA
    levels in more severely impaired twin

6
Neuroanatomy
  • Frontal Lobes
  • ? Medial PFC memory functions (i.e. visual
    recognition)
  • Cerebellum
  • ? attention
  • Limbic System
  • ?amygdala social behaviours
  • Brain Stem

7
Neurochemistry
  • Serotonin
  • Dopamine
  • Norepinephrine
  • Opioids
  • Glutamate

8
Dopamine
  • Primarily found in the limbic system, parts of
    the hypothalamus, the frontal cortex, and the
    forebrain
  • Three pathways
  • Mesostriatal
  • -increases ? stereotypies/repetitive behaviours
  • Mesolimbic
  • -increases ? increased locomotor activity
  • Mesocortical
  • Modulates motor activity, attentional skills,
    social behaviour, and perception of the outside
    world, all of which are abnormal in autism

9
DA contd
  • Hypothesis hyperfunction of dopaminergic
    pathways arising in the brain-stem and projecting
    rostrally to mesolimbic structures in the
    temporal and frontal lobes might be crucial in
    the pathogenesis of certain symptoms of autism
  • Early social deprivation ? loss of DA innervation
    of key brain regions with consequent DA receptor
    supersensitivity

10
DA contd
  • Equivocal Findings Higher levels of CSF HVA vs.
    decreased levels
  • Stereotyped behaviours can be induced in animals
    by increasing central DA levels
  • Self-injurious behaviour can be induced by a DA
    agonist in monkeys

11
PET
  • PET FDOPA levels are reduced (39) in the
    anterior medial PFC
  • -may contribute to the cognitive impairment given
    the importance of DA in prefrontal function

12
Treatment
  • Most drug studies are only of a short duration
    and potiental long term impacts are not
    adequately considered.
  • 1) Agonists/Stimulants (i.e. bromocriptine,
    LDOPA, amphetamine)
  • -release DA from the presynaptic terminal and
    block its reuptake and degradation
  • -Amphetamines they exacerbate the symptoms ?
    increased activity, aggression, stereotypes, and
    general disorganization of behaviour
  • -Bromocriptine some efficacy in reversing
    repetitive behaviours associated with DA
    depletion
  • -(hypothesized) chronic administration should
    reverse the DA receptor supersensitivity ? down
    regulates DA receptors

13
Treatment contd
  • 2) Antagonists (i.e. Haloperidol,
    trifluoperazine, pimozide)
  • -Dopaminergic antagonists are the only drugs with
    consistent clinical efficacy in controlled trials
    in autism
  • -effective in improving motor stereotypies,
    anger/uncooperativeness, interpersonal
    withdrawal, speech deviance
  • -Haloperidol no adverse effect on IQ or on
    learning in a computerized laboratory
  • -older children greater response
  • -superior in decreasing levels of stereotypy and
    withdrawal
  • -long-term continued reductions in levels of
    maladaptive behaviours
  • -drawback development of tardive or withdrawal
    dyskinesias, sedation

14
Treatment contd
  • 3) Atypical Antipsycotics (i.e. risperidone,
    olanzepine)
  • -block D2 receptors and 5-HT2 receptors
  • -lower rates of extrapyramidal symptoms
  • -animal studies increase in social interaction
  • -risperidone repetitive behaviour disorders
  • -drawback weight gain

15
Future Directions
  • Pharmacological studies target specific core or
    comorbid symptoms of autism
  • Interaction between behavioural and
    pharmacological treatments
  • Further study into the interactions between
    neurotransmitter systems
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