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Chapter 6

Ch. 6 - Autism.docx

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PSYC 208
Paul Wehr

Autism 10/19/2012 9:55:00 AM Autism Symptomatology  Symptom Triad: o Communication deficits o Impaired social interaction  Lack of facial exploration, avoidance of eye contact, inability to monitor gaze, no joint attention  Deficits in “theory of mind,” lack of empathy, ignore presence of others, impaired imitation and symbolic play o Stereotyped behaviors and interests  Meaningless imitation of actions (echopraxia) or speech (echolalia)  Symptom severity: o Milder forms: Asperger syndrome and high-functioning autism (preserved verbal communication)  Asperger syndrome: difficulties in social interaction, with restricted and repetitive patterns of behavior and interests; preserves linguistic and cognitive development o Severe forms: Kanner Autism (mental retardation or epilepsy)  Social interaction problems (can’t make friends), communication deficits (lack development of speech, repetitive language), apathy of activity (do not play like typical children) o Normal intellectual functioning: superior technical intelligence o Savants (e.g. math, music) usually intellectually impaired  People with neurodevelopmental disorders demonstrate profound and prodigious capacities and/or abilities  Autistic Spectrum Disorder: experience deficits in only one of the three symptom groups  Restrict interests: inflexible preoccupation with an object or activity Epidemiology and Genetic Risk Factors  Epidemiology: onset occurs in early infancy, but diagnosis doesn’t occur until 18 to 24 months o Autism: 5.2/10,000 before 1980s; 7.2/10,000 after 1980s o Autism Spectrum: 3-6/1,000 individuals o Male:female (4:1)  Genetic Risk o 10-20 different alleles involved (polygenic disorder) Pathophysiological Mechanisms  Chemical messengers: o Elevated levels of endorphins and brain-derived neurotrophic factor (BDNF)  BDNF: stimulates neuron growth o Serotonin levels elevated in blood but reduced in CNS o Oxytocin is down-regulated o Elevated fetal testosterone/increased number of androgen receptors?  Neurological abnormalities o Reduced apoptosis (selective cell death) o Increased density of neurons except in mirror neuron system  Impaired imitation  Mirror neuron system is in parts of the prefrontal and temporal cortex  Mirror neuron system involved in observational learning and theory of mind o Increased white matter but reduced inter- and intra-hemispheric connectivity o “Mentalizing” center hypoactive  Impaired theory of mind o Enlarged amygdala at birth, but underdeveloped later on  Impaired social emotion Evolutionary Synthesis  Psychological mechanisms affected are those associated with social brain functioning (behavioral, cognitive, and emotional) o Deficits in theory of mind reflect selective impairment of social information processing o Not a reflection of low general intelligence  Mirror Neurons: linked with learning by imitation beginning early in life (bridge between two minds o Active during observation and also imitation of action o Connection between observing and performing behavior also important for “mentalizing”  Self-other discrimination  Take perspective of another individual o Cortical thickness reduced in autistic individuals Extreme Variation of “Male Brain” Traits  Excessive fetal testosterone and increased number of androgen receptors masculinize the brain? o Technical understanding is a male trait? Social functioning if a female trait?  Evidence: o Girls with congenital adrenal hyperplasia display boyish behavior and more autistic traits  Adrenal hyperplasia: abnormality in the adrenal gland leading to excess androgen (and male traits) in boys or girls (deeper voice, lack of menstruation) o Low 2D/4D ratio in autistic individuals  2D: second digit finger, 4D: fourth digit finger  High 2D:4D: index finger is longer than the ring finger  Equal 2D:4D: both fingers are the same length  Low 2D:4D: index finger is shorter than the ring finger  Women with Low 2D:4D are more likely to have athletic skills o Precocious puberty in autistic boys o Fetal testosterone in non-autistic children inversely related to eye-to-eye contact, shared attention, speech development, social functioning, and restricted range of interests Genomic Imprinting  Genes compete to be expressed by silencing other genes: paternal genes can silence maternal genes or vice-versa o Autism reflects over-expression of paternal genes?  Too much silencing or maternal genes  Exaggeration of male traits; impaired functioning of female traits  Exaggera
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