Childhood Learning And Neuropsychiatric Disorders Flashcards
What are primary determinants of dyslexia?
Disruptions to posterior regions
What are the two models of dyslexia?
*Visual processing model Surface: -word reading impaired/sounding out unimpaired -impairment if orthographic skills -visual and visuo-perceptual problems
Deep:
- sounding out words impaired
- impaired auditory/language skills
- phonological skills impaired
*Phonological loop
PM: what is impaired and what is intact with dyslexia?
Difficulty with: Word-decoding Slow & non-automatic reading Identifying and comprehending words Phonological processing (+ naming speed deficit)
Preserved:
Syntax, intelligence, reasoning, vocab
Listening comprehension
PM: what are the 3 aspects and the model’s hypothesis?
- Phonological processing
- Word-decoding
- Naming speed
Double deficit hypothesis: reading disabilities are deficits in either phonological or naming speed
What two working memory systems are thought to be involved with dyslexia?
Articulatory phonological loop: temp buffer for maintaining + manipulating verbal + auditory behavior
Visuospatial sketchpad: temp buffer for visuo and visuo-spatial info
What are the 3 proposed reading-related systems?
Left dorsal P-T areas
Left ventral O-T region
Left Broca’s area
What are the differences between a reading-spelling disability and nonverbal learning disability?
- Psycholinguistic skills: RS=weak, NVLD=strong
- Visual and tactile perception, psychomotor and non-verbal/novel problem solving: RS=preserved; NVLD=poor
- Academics: RS=poor reading/spelling, mechanical arithmetic competent but below avg; NVLD=poor basic arithmetic, sight word reading intact
- Arithmetic performance: RS=poor because of verbal deficits; NVLD=poor due to visual-perceptual and non-verbal
- Dysfx: RS=LH; NVLD=RH
What neurological areas are involved in Dyslexia?
Genetics (‘chromes’ 6 and 15)
Planum temporale of L post. temp. lobe (phonological processing)
Regional abnormality (less activation in LPT and T-P cortices)
CBF to region surrounding planum temporale (Wernicke’s & angular gyrus) = reading performance
Abnormal development of L planum temporale (neuronal ectopias & cytoarchitectonic dysplasia)
NVLD: Neuropsychological pathogenesis
RH (posterior, possibly anterior - mental flexibility, white matter tracts connecting F and RH)
RH organization
diffuse
more association regions
greater inter-regional integration of info
more adept at processing complex, novel or ambiguous info
Pervasive developmental disorders (4 criteria)
Must show impairment in 1 or more:
- Social interactions
- flexibility in behaviour
- verbal and non-verbal language
- range of interests and activities
Autism: are males more affected than females?
Male 2:1 - 6:1
- *Males naturally have more vasopressin and low oxytocin (females have more oxytocin - more likely to bond with others/make eye-contact)
- *Males externalize symptoms (commonly co-morbid with ADHD); females internalize (more comorbid with anxiety/depression)
Autism: 3 core deficits
- Ability to relate to others
- Deficits in communication
- Unusual behaviour patterns
Autism: Ability to relate to others
"autistic aloneness" Often exhibit: joint attention deficits (inability to see from someone else's PoV) poor conversational skills lack of eye contact inappropriate facial expressions
Autism: Deficits in communication
Minimal development in symbolic play
Delayed-onset of language
Restricted
Issues understanding/utilizing non-verbal
could see: echolalia, pronoun reversal, neologisms
Autism: Unusual behaviour patterns
Preoccupation
Specificity
Routine NB
Stereotypic body movements (rocking, hand-flipping etc)
Autism: pathogenesis
- Environ: perinatal complications, NOT vaccine
- Genetic: 20 possible genes (15q11-13) sib. study
- Bigger head circumference
- Growth profile = warning sign (small brain, accelerated 1-2 & 6-14, declines)
- Neural substrates (Social mind network; atypical white-to-grey; hyperserotonaemia)
Autism: What neural substrates are implicated?
- Hyperseratonemia (25-50%) increased seratonin
- Cortical and subcortical regions
- Social brain network (theory)
- Atypical white-to-grey matter ratio
Autism: Social brain network
O and medial PF cortices Anterior cingulate Amygdala Superior temporal sulcus Fusiform face area
What are explanatory theories of autism?
Theory of Mind
Executive Dysfunction theory (‘stuck in set’ perseveration)
Controversy regarding Disruptive Behavioural disorders
Overprescription of ritalin (kinds are naturally very energetic, should not be used in place of parenting/discipline)
- difference between not understanding and not WANTING to understand
ADHD: clinical presentations
Chronic, age-inappropriate inattention, impulsivity & hyperactivity
- across situations
- developmental origin (before school and typically persists)
ADHD: What happens when conduct disorder persists into adulthood?
Now fits into category of antisocial personality disorder
Theory for why more boys diagnosed with ADHD?
(3:1-9:1)
Boys more likely to externalize; might be because socially regarded as more acceptable for boys to play ‘rough’ (remember by word boisterous)
ADHD: ODD?
Oppositional defiant disorder: chronic age-inapprop angry mood and resistant, stubborn behaviours
ADHD: CD?
Conduct disorder: repeated violations of rights of others + societal norms
ADHD: pathogenesis
frontal lobes not symmetrical (R>L)
disruption in frontal-BG circutry
Smaller cerebellum
Major cortical/subcortical regions (4 foci in research/disruptions of transmission)
ADHD: tx
Behavioural intervention
Pharmacology
Multimodal (tailored, targets impulsivity, inattention, hyperactivity, more difficult when comorbid, continuity across contexts of intervention is NB for its success - teachers, parents etc)
Tic disorders and its 2 classifications
Repetitive, stereotypic, non-rhythmic, recurring motor movements or vocal responses in brief duration (<1sec)
- Simple: more reflexive (blinking, face twitch)
- Complex: appears more coordinated/purposeful (repeating others’ speech, obscene words)
Tic: 3 classifications of clinical presentation
Transient: motor OR vocal tics (1-12m)
Chronic: m OR v (>1y)
Tourette’s (GTS): 1 m AND v AND clinically significant impairment
GTS: clinical presentation
Copropraxia: obscene gestures
Echopraxia: repeat other’s movements
Coprolalia: inappropriate/obscene speech
Echolalia: repeat other’s words
GTS: pathogenesis
Genetics
Changes in NT intrinsic to frontostriatal pathways (Da) frontal=disinhibition issues (dopamine, specifically in substantia nigra)
Environment has been found as etiological factor (toxic exposure in mining areas)
Alterations to brain structure/metabolic activity
GTS: tx
-Behav mod: trigger identification (CBT)
habit reversal training (smile/frown)
-Pharmacology: dopamine agonists prescribed (but side effects)
contraindicated meds for GTS and adhd (antipsychotics, anti-epileptic, ADHD meds)
GTS: prevalence and co-morbidity
Boys (4:1), no ethnic preference, school 1/1000
ADHD and OCD, behavioural problems, anxiety, mood disorders (depression), learning and sleeping difficulties
ADHD: developmental course
Infancy: active, overly responsive, low adaptability, anger
Toddler-preschool: constantly busy/shifting activities, failure to follow/listen, disregard for consequences, diff to handle (esp. defiant)
High school: interferes with learning, frustration, peer & family judgement
Adult: greater regulatory control = reduction of symptoms of inattention, impulsivity, hyperactivity: but could persist
