Neurodevelopmental Disorders
Here are your **comprehensive flashcards for Chapter 17 – Neurodevelopmental Disorders**. Each card is designed for **long answer, short essay, and case study preparation** – not just recognition.
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## CHAPTER 17 – NEURODEVELOPMENTAL DISORDERS
### Section A: Specific Learning Disorder
**Card 1 (Definition & DSM-5 Criteria)**
**Q:** Define specific learning disorder. List the 4 DSM-5 criteria.
**A:** Difficulties learning and using academic skills for ≥6 months despite targeted interventions.
Criteria:
A. At least one symptom (inaccurate reading, poor spelling, number sense deficits, etc.) for ≥6 months
B. Skills substantially and quantifiably below age/expected level, interfering with academics or daily living
C. Onset during school‑age years (may not fully manifest until demands exceed capacity)
D. Not better explained by intellectual disability, uncorrected vision/hearing, other mental/neurological disorders.
**Card 2 (Dyslexia – Definition & Aetiology)**
**Q:** What is dyslexia? What causes it?
**A:** Specific learning disorder affecting word recognition, reading, and spelling. Prevalence 3–17.5% of school‑age children; 60–80% are boys.
Aetiology:
- Genetic – runs in families (80% of dyslexic children have affected relatives); MZ concordance > DZ
- Cognitive – phonological deficit (difficulty differentiating phonemes and associating them with letters) – independent of general intelligence
- Brain – less activation in left hemisphere reading areas (inferior frontal, superior temporal, parieto‑temporal, middle occipital gyri); temporo‑parietal abnormalities.
**Card 3 (Dyscalculia – Definition & Aetiology)**
**Q:** What is dyscalculia? Describe its three forms.
**A:** Mathematical ability significantly below expected for age, IQ, and education.
Three forms:
1. Deficit in memorising/retrieving arithmetic facts
2. Developmentally immature problem‑solving strategies
3. Impaired visuo‑spatial skills (errors aligning numbers, decimal points)
Aetiology: familial component, genetic transmission, prenatal factors; brain abnormalities in left parietotemporal, inferior prefrontal cortex, and intraparietal sulcus.
**Card 4 (Communication Disorders – 3 types)**
**Q:** Name and describe the three communication disorders under specific learning disorder.
**A:**
1. Language disorder – problems acquiring/using language (limited vocabulary, short sentences, slow development, word‑finding difficulty). Often comorbid with speech sound disorder.
2. Speech sound disorder – persistent difficulty with speech sound production (articulation), interfering with social/academic/occupational achievement. May have physical causes.
3. Childhood‑onset fluency disorder (stuttering) – problems with fluency and time‑patterning of speech (repetitions, prolongations, pauses, word substitutions, physical tension). Peak onset ~5 years; good prognosis.
**Card 5 (Aetiology & Treatment of Communication Disorders)**
**Q:** What causes stuttering and other communication disorders? How are they treated?
**A:**
Aetiology:
- Speech sound disorder: abnormal development of speech apparatus (hearing impairment, cleft palate, cerebral palsy)
- Stuttering: genetic (heritability up to 71%), basal ganglia‑thalamo‑cortical motor circuit abnormalities; emotional factors exacerbate but not cause.
Treatment:
- Educational interventions (specialised teaching methods)
- Stuttering: auditory feedback (AAF), prolonged speech training
- Controversial placement: clinical vs. educational setting.
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### Section B: Intellectual Disability (ID)
**Card 6 (Definition & DSM-5 Criteria)**
**Q:** Define intellectual disability. What are the 3 DSM-5 criteria?
**A:** Disorder with impairment in both intellectual and adaptive functioning, onset during developmental period (<18 years).
Criteria:
1. Deficits in intellectual functioning (e.g., reasoning, problem‑solving, abstract thinking) – typically IQ <70
2. Deficits in adaptive functioning (conceptual, social, practical skills) – failure to meet developmental/sociocultural standards
3. Onset during developmental period.
Severity specifiers: mild, moderate, severe, profound (based on adaptive functioning, not IQ alone).
**Card 7 (Prevalence & Alternative Approaches)**
**Q:** How common is intellectual disability? What are alternative approaches to definition?
**A:** Prevalence ~1% total; severe ID ~0.6%. Some UK studies show 5–10% of 13‑15 year olds have IQ <70.
Alternative approaches (AAIDD): individualised assessment of skills and needs; recognise strengths and limitations; UK inclusion strategy emphasises accessibility.
**Card 8 (Aetiology – Chromosomal Disorders)**
**Q:** Name two chromosomal causes of intellectual disability. Describe each.
**A:**
1. Down syndrome (trisomy 21) – extra chromosome 21; risk increases with maternal age; identified prenatally via amniocentesis. Accounts for 25–30% of ID cases.
2. Fragile X syndrome – X chromosome appears bent/broken; prevalence 0.04–0.08% of births; mild to moderate ID, language impairment, behavioural problems; more severe in males (only one X).
**Card 9 (Aetiology – Metabolic Disorders)**
**Q:** Describe PKU and Tay‑Sachs syndrome as causes of intellectual disability.
**A:**
PKU (phenylketonuria): deficiency of liver enzyme phenylalanine 4‑hydroxylase → buildup of phenylalanine and phenylpyruvic acid → brain damage (prevents myelination). Recessive gene on chromosome 12; 1 in 70 carriers. Results in severe ID and hyperactivity. Preventable by diet.
Tay‑Sachs: recessive gene, common in Eastern European Jewish ancestry; absence of hexosaminidase A → neuron death. Degenerative: onset ~5 months (exaggerated startle, poor motor development); only 17% live beyond 4 years; rapid cognitive/verbal decline.
**Card 10 (Aetiology – Perinatal & Childhood Causes)**
**Q:** What perinatal and childhood factors cause intellectual disability?
**A:**
Perinatal: congenital disorders – maternal diet (cretinism), infection (syphilis, rubella, HIV), substance use (FAS – foetal alcohol syndrome), anoxia (oxygen deprivation).
Childhood: accidents (shaken baby syndrome – differentiate from abuse), toxins (lead exposure → IQ drop up to 10 points), poverty/deprivation (intergenerational cycle: teenage motherhood, poor parenting, cognitive disadvantage).
**Card 11 (Interventions for Intellectual Disability)**
**Q:** How is intellectual disability managed? Describe prevention, training, inclusion.
**A:**
Prevention: predictive testing, genetic counselling, family support programmes, avoid FAS.
Training: applied behaviour analysis (ABA), functional analysis; skills taught – self‑help, language, daily living, anger control, adaptive skills.
Inclusion: deinstitutionalisation; mainstream schooling (accessibility strategies); supported employment, sheltered workshops; pursuit of social/educational/occupational goals.
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### Section C: Autism Spectrum Disorder (ASD)
**Card 12 (Definition & DSM-5 Criteria)**
**Q:** Define autism spectrum disorder. List the 4 DSM-5 criteria.
**A:** Neurodevelopmental disorder with persistent deficits in social communication and restricted, repetitive patterns of behaviour.
Criteria:
A. Persistent deficits in social communication/interaction across multiple contexts (social‑emotional reciprocity, nonverbal communication, developing/maintaining relationships)
B. Restricted, repetitive patterns of behaviour, interests, or activities (stereotyped movements, insistence on sameness, fixated interests, sensory hyper/hypo‑reactivity)
C. Symptoms present in early developmental period
D. Clinically significant impairment.
**Card 13 (Core Characteristics – The Old Triad)**
**Q:** Describe the three classic impairments in autism spectrum disorder.
**A:**
1. Impairments of reciprocal social interaction – inability to use nonverbal behaviours, rarely approaches others, no spontaneous greeting, no eye contact; cannot understand others' intentions/emotions (Theory of Mind deficit).
2. Impairments in communication – delayed spoken language; half never speak; echolalia and pronoun reversal common; inability to sustain conversation.
3. Impairments in imagination/flexibility – restricted, repetitive, stereotyped behaviours; distress with routine changes; strong attachments to inanimate objects; stereotyped body movements.
Also: 80% have intellectual disability (IQ <70); better visuo‑spatial than verbal; savant syndrome possible.
**Card 14 (Prevalence & Demographics of ASD)**
**Q:** How common is autism spectrum disorder? What demographic patterns exist?
**A:** Older studies: 5–13 per 10,000 (0.05%). Recent UK studies: ~1.1% (approx 695,000 people). 80% are boys. Equal across socioeconomic classes and racial groups. Diagnostic changes may affect rates. No association with MMR vaccine (refuted).
**Card 15 (Aetiology – Genetic Factors)**
**Q:** What genetic evidence exists for autism spectrum disorder?
**A:** Strong familial aggregation: sibling recurrence risk 2–14%. Co‑occurs with PKU, Fragile X, tuberous sclerosis. Twin studies: MZ concordance 60‑91%, DZ 0‑20%. Polygenic – as many as 15 genes involved.
**Card 16 (Aetiology – Brain & Biochemical Factors)**
**Q:** What brain abnormalities and biochemical factors are associated with ASD?
**A:**
Brain: aberrant development – limbic system and cerebellum abnormalities; overly large brain size, enlarged ventricles; anatomical/functional differences on fMRI, EEG, ERP.
Biochemical: inconclusive – methodological problems (small samples, contradictory findings, poor controls).
Perinatal: weak evidence – maternal infections, intrauterine drug exposure, bleeding, depressed immune function. MMR controversy – **refuted, no causal link**.
**Card 17 (Cognitive Theories – Theory of Mind)**
**Q:** Explain the Theory of Mind deficit in autism spectrum disorder. How is it tested?
**A:** Theory of Mind = ability to infer others' mental states (beliefs, intentions, emotions). Individuals with ASD fail to develop this.
Tested using Sally‑Ann False Belief Task – child must predict where Sally will look for her marble (understanding that Sally has a false belief). ASD children fail, indicating they cannot take another's perspective. Explains social/communication impairments but not non‑social features (narrow interests, need for sameness).
**Card 18 (Cognitive Theories – Executive Dysfunction & Empathizing‑Systematizing)**
**Q:** What are executive dysfunction and Baron‑Cohen's empathizing‑systematizing theory?
**A:**
Executive dysfunction: difficulty with problem‑solving, planning, initiating, organising, monitoring, inhibiting complex behaviours. Not all domains affected (cognitive inhibition and semantic fluency may be intact).
Empathizing‑systematizing theory (Baron‑Cohen): ASD = superior systematizing (analysing/constructing rule‑based systems) but deficient empathizing (understanding others' emotions and responding appropriately). Explains narrow interests, attention to detail, difficulty generalising.
**Card 19 (Treatment – Difficulties & Drug Treatments)**
**Q:** What difficulties arise in treating ASD? What medications are used?
**A:**
Difficulties: resistance to change, oblivious to outside world, limited interests, over‑selective attention, praise ineffective as reinforcer.
Drugs (mainly for problem behaviours):
- Antipsychotics: haloperidol, risperidone
- Opioid antagonist naltrexone – reduces hyperactivity and self‑injurious behaviour.
**Card 20 (Treatment – Behavioural Training & Inclusion)**
**Q:** What behavioural and inclusion strategies are used for ASD?
**A:**
Behavioural training: conditioning‑based (ABA – applied behaviour analysis), modelling, parent‑implemented early intervention. Develops self‑help, social, communication skills. Time‑consuming.
Inclusion: supported employment, structured transitions, help with life transitions (finding/keeping a job). Mainstream schooling with accessibility strategies.
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## CASE STUDY CUES FOR NEURODEVELOPMENTAL DISORDERS
| Disorder | Case features to look for |
|:---|:---|
| **Dyslexia** | Normal intelligence, but poor reading, difficulty sounding out words, family history of reading problems, avoids reading aloud. |
| **Dyscalculia** | Normal intelligence, cannot memorise times tables, misplaces decimal points, trouble with number sense, poor maths grades despite good reading. |
| **Language disorder** | Limited vocabulary, short sentences, slow language development, trouble finding words, grammatical errors. |
| **Speech sound disorder** | Substitutes sounds (e.g., "wabbit" for "rabbit"), intelligibility poor, no grammar/vocabulary issues. |
| **Stuttering** | Repetitions ("b-b-b-ball"), blocks, prolonged sounds, onset around 5 years, worse under pressure. |
| **Intellectual disability** | IQ <70 + adaptive deficits (dressing, feeding, money, social safety). May have known genetic syndrome (Down: flat face, single palmar crease; Fragile X: long face, large ears). |
| **Autism spectrum disorder** | No eye contact, delayed speech, echolalia, hand‑flapping, lining up toys, meltdowns with routine change, fails Sally‑Ann task, may have savant skill. |
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## ESSAY SKELETON FOR NEURODEVELOPMENTAL CASE
**1. Diagnosis** – name the specific disorder (e.g., Autism Spectrum Disorder, level 1)
**2. Evidence from case** – match DSM-5 criteria using exact features described
**3. Differentiation** – rule out similar disorders (e.g., "Not solely Intellectual Disability because social‑communication deficits are specific to ASD and non‑verbal problem‑solving is intact")
**4. Aetiology** – mention relevant factor (genetic, brain, cognitive – e.g., Theory of Mind deficit, phonological deficit, perinatal cause)
**5. Intervention** – behavioural training (ABA), inclusion strategies, parent training, medication if indicated, educational supports.
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