Source: Abnormal Psychology, University of Florida
Tags: ADHD, autism spectrum disorder, ASD, intellectual disability, neurocognitive disorder, dementia, Alzheimer's disease, delirium, learning disorders, Tourette's, Down syndrome, fragile X
Difficulty: Intermediate-Advanced | Prerequisites: Basic neuroscience (neurotransmitters, brain anatomy), genetics fundamentals
This chapter covers two broad categories of brain-based disorders. Neurodevelopmental disorders (ADHD, autism spectrum disorder, intellectual disability, learning and motor disorders) typically arise in childhood and reflect abnormal brain development. Neurocognitive disorders (major and mild NCD, delirium) typically arise later in life and involve acquired cognitive decline. Understanding these conditions requires knowledge of genetics, brain development, neurotransmitter systems, and the social contexts in which affected individuals live and are treated.
Neurodevelopmental disorders like ADHD and autism have their roots in abnormal brain development and strong genetic contributions, with treatment combining medication and behavioural interventions. Neurocognitive disorders (dementia, delirium) involve progressive or acute cognitive decline in adulthood, most commonly caused by Alzheimer's disease or vascular events. Early intervention matters enormously for childhood disorders, and the prognosis for most neurocognitive disorders remains poor despite available symptom management.
ADHD (Attention-Deficit/Hyperactivity Disorder)
Difficulty paying attention, controlling impulses, and organising behaviour. Three presentations: combined, predominantly inattentive, and predominantly hyperactive/impulsive.
Autism Spectrum Disorder (ASD)
Impairments in social interaction and communication, combined with restricted, repetitive patterns of behaviour, interests, and activities. DSM-5 collapsed the previous PDD subtypes (including Asperger's) into one spectrum diagnosis.
Intellectual Disability
Significant deficits in conceptual, social, and practical domains of daily living, with onset during development. Four severity levels: mild, moderate, severe, profound.
Major Neurocognitive Disorder (Dementia)
Cognitive decline severe enough to impair daily functioning, involving memory, language, executive function, and/or recognition.
Mild Neurocognitive Disorder
Modest cognitive decline from previous functioning, not yet severe enough to significantly impair daily life.
Delirium
Acute state of disorientation, memory loss, and impaired attention. Onset is sudden, duration short, and symptoms fluctuate (often worse at night, a phenomenon called sundowning).
Echolalia
Repeating words or phrases just heard. Seen in both autism and neurocognitive disorders.
Tardive Dyskinesia
(Cross-reference to Chapter 8.) Involuntary movements from long-term antipsychotic use.
DSM-5 raised onset age from 7 to 12 years (95% of eventual cases develop by 12)
Boys more likely to develop ADHD; girls tend to present primarily with inattentive features and less disruptive behaviour, leading to underidentification
Children with ADHD typically do poorly in school, have poor peer relationships, and may be intrusive, irritable, and demanding
20 to 25% also have a specific learning disorder
45 to 60% with combined presentation develop conduct disorder, substance abuse, or legal problems
Symptoms persist into young adulthood in approximately 50%; adults at increased risk for antisocial personality disorder, substance abuse, mood and anxiety disorders
Brain abnormalities: smaller cerebral cortex, abnormal prefrontal cortex, striatum, and cerebellum activity; reduced connectivity between frontal areas and motor, memory, and emotion regions
Cortex may continue growing into adolescence, supporting the "neurological immaturity" hypothesis
Catecholamine neurotransmitters (dopamine, norepinephrine) function abnormally
Strongly genetic; genes affecting dopamine, norepinephrine, and serotonin implicated
Associated with prenatal complications, low birth weight, maternal substance use during pregnancy, lead exposure
Treatment:
Stimulant medications (Ritalin, Dexedrine, Adderall) effective in 70 to 85% of cases. Work by increasing dopamine. Side effects: reduced appetite, insomnia, edginess, possible growth effects.
Non-stimulant alternatives: atomoxetine, clonidine, guanfacine (affect norepinephrine)
Behavioural therapy: reinforcing attentive and prosocial behaviour, teaching parents to break escalation cycles, teaching children to anticipate consequences and interact appropriately
Combined treatment (medication + behaviour therapy) produces the strongest short-term improvement: 68% vs. 56% for medication alone, 34% for behaviour therapy alone, 25% for community care
Two core domains: (1) deficits in social interaction and communication, (2) restricted, repetitive behaviours and interests
Social deficits may appear in infancy: absence of smiling, cooing, joint attention, eye contact
50% do not develop useful speech; those who do may show echolalia
Routines extremely important; disruption causes distress
Self-stimulatory behaviours (e.g. head banging) are common
50% show moderate intellectual disability, but some score well on non-verbal tests
Savants: rare cases with extraordinary specific abilities
More common in boys; IQ above 50 and communicative speech before age 6 are the best prognostic indicators
DSM-5 Changes:
Collapsed previous PDD categories (autism, Asperger's, Rett's, childhood disintegrative disorder, PDD-NOS) into one autism spectrum disorder
Changes motivated by difficulty making reliable distinctions between subtypes and evidence of shared causes
Approximately 50 to 60% of children diagnosed under DSM-IV captured under DSM-5 criteria; 91% in more recent analysis
Concerns about loss of diagnosis and services for higher-functioning individuals (previously Asperger's)
Causes:
Not caused by poor parenting (Kanner's original theory discredited)
Genetics: siblings 50% more likely to have autism; MZ concordance ~60%, DZ 0 to 10%
No single gene; abnormalities in several genes associated
Neurological: 30% develop seizure disorder; greater head and brain size; structural abnormalities in cerebellum, cerebrum, amygdala, hippocampus; fusiform gyrus deficits (facial recognition)
Prenatal and birth complications; differences in serotonin and dopamine levels
Treatment:
Medications improve specific symptoms (SSRIs for repetitive behaviours and aggression; atypical antipsychotics for self-control; stimulants for attention) but do not alter core features
Behavioural therapy: operant conditioning to reduce excessive behaviours and build communication and social skills; structured educational settings; parent training. Strong improvements when administered comprehensively and from an early age.
Deficits in conceptual (language, reasoning, memory), social (awareness, communication, judgement), and practical (self-care, job skills, organisation) domains
Four levels: mild (some academic and vocational success), moderate (second-grade academic level, assisted employment), severe (very limited vocabulary, cannot travel alone), profound (fully dependent, co-occurring sensory and motor impairments)
DSM-5 de-emphasises IQ scores and focuses on adaptive functioning across domains
IQ of 70 or below typically indicates intellectual disability; estimated 1 to 3% prevalence
Causes:
Genetic: 300+ genes implicated. PKU (treatable with diet), Tay-Sachs (untreatable, fatal), Down syndrome (trisomy 21, varies from mild to profound, accelerated ageing, Alzheimer's-like changes after 40), Fragile X syndrome (broken tip of X chromosome, primarily affects males, severe to profound ID)
Prenatal: maternal viral infection, chronic maternal disorders (e.g. high blood pressure), fetal alcohol syndrome
Postnatal: brain injury (including shaken baby syndrome), exposure to toxins, lead poisoning
Sociocultural: poverty, lack of prenatal care, poorly funded schools, less parental involvement
Treatment: medications for seizures and aggression; behavioural strategies for skill building; early intervention programmes (e.g. Infant Health and Development Program showed IQ gains and fewer behavioural problems); mainstreaming vs. specialised education; group homes and vocational training; community-based programmes
Specific learning disorder: deficits in reading (dyslexia, most common), mathematics, or written expression. Does not result from intellectual disability.
Communication disorders: language disorder, speech sound disorder, childhood-onset fluency disorder (stuttering), social communication disorder (deficits in pragmatic language use; cannot be diagnosed alongside ASD)
Motor disorders: Tourette's disorder (multiple motor tics + at least one vocal tic, persisting over a year), persistent motor or vocal tic disorder, stereotypic movement disorder, developmental coordination disorder
Tic disorders highly comorbid with OCD, share genetic factors and dopamine system dysfunction; treated with habit reversal therapy and dopamine-regulating medications
Symptoms of Major NCD (Dementia):
Progressive memory loss (does not return with cues or reminders)
Aphasia (deterioration of language, difficulty naming objects or people)
Apraxia (inability to execute common actions despite intact motor function)
Agnosia (failure to recognise objects or people)
Loss of executive functions (planning, initiating, monitoring complex behaviours)
Personality changes, impaired judgement, depression, paranoia, violent outbursts
Alzheimer's Disease (Most Common Cause):
Begins with mild memory loss, progresses to profound disorientation
Psychiatric symptoms: agitation, dysphoria, apathy, hallucinations, delusions
Usually after age 65; early-onset type progresses more quickly
Death typically within 8 to 10 years of diagnosis
Brain: neurofibrillary tangles (twisted tau protein filaments impeding cell nutrition), amyloid plaques (neurotoxic beta-amyloid deposits), cortex shrinkage, ventricle enlargement
Genetics: MZ concordance 44 to 58%, DZ 25 to 45%. ApoE gene (chromosome 19) regulates cholesterol transport and beta-amyloid; e4 allele increases risk. Chromosome 21 linked to some forms (connection to Down syndrome).
Neurotransmitter deficits: acetylcholine, norepinephrine, serotonin
Vascular NCD: caused by stroke or cerebrovascular disease; declines in processing speed, attention, executive function
Other causes: Parkinson's disease (dopamine cell death), Lewy body disease, HIV, Huntington's disease (single dominant gene, chromosome 4), prion disease, chronic substance abuse, traumatic brain injury
Gender, Culture, and Education:
More elderly women than men with NCD (longer lifespan)
Blacks diagnosed more often (higher rates of hypertension and cardiovascular disease)
Lower education associated with increased risk
Treatment:
Cholinesterase inhibitors (donepezil, rivastigmine, galantamine): prevent acetylcholine breakdown; modest effects
Memantine: regulates glutamate
Antidepressants, antianxiety meds, antipsychotics for secondary symptoms
Behavioural therapies for anger and emotional instability; family training
Aerobic exercise and cognitive activity may reduce risk
Acute onset (hours to days), short duration (rarely over a month), symptoms fluctuate (sundowning)
Progression: fatigue and decreased concentration, then mild cognitive impairment, then disrupted orientation, then memory loss
Often the first sign of a serious medical condition; treatable if underlying cause is addressed
Causes: NCD, medical disorders, drugs, fluid/electrolyte imbalances, toxins, surgery
Risk factors: older age, male sex, pre-existing brain damage, black race
Treatment: treat underlying medical condition, discontinue offending drugs, antipsychotics for confusion, reassuring environment
"Children with ADHD just need more discipline." ADHD reflects abnormal brain development and neurotransmitter function, not a failure of willpower or parenting.
"Autism is caused by vaccines." This has been extensively debunked. Autism has strong genetic and neurological roots.
"A low IQ score automatically means intellectual disability." DSM-5 de-emphasises IQ and focuses on adaptive functioning in conceptual, social, and practical domains.
"Dementia is a normal part of ageing." Dementia is a disease process, not an inevitable consequence of growing older.
⚠️ Know the three ADHD presentations and the DSM-5 age-of-onset change (7 to 12).
⚠️ DSM-5 changes to autism: collapsing PDD subtypes into one spectrum, and the implications for diagnosis.
⚠️ Alzheimer's brain pathology: neurofibrillary tangles (tau), amyloid plaques (beta-amyloid), and the ApoE e4 allele.
⚠️ Distinguish delirium from dementia: delirium is acute, fluctuating, and often reversible; dementia is chronic and progressive.
⚠️ Combined treatment for ADHD (stimulants + behavioural therapy) produces the best short-term outcomes.
⚠️ Down syndrome connection to Alzheimer's (chromosome 21).
True or False: The DSM-5 raised the ADHD onset age from 7 to 12.
Fill in the blank: __________ tangles and amyloid __________ are the two hallmark brain abnormalities in Alzheimer's disease.
True or False: Delirium is usually chronic and irreversible.
Fill in the blank: The ApoE __________ allele is associated with increased risk of Alzheimer's disease.
True or False: DSM-5 retained Asperger's syndrome as a separate diagnosis from autism.
Q: What evidence supports the neurological immaturity hypothesis of ADHD?
A: Children with ADHD have smaller cerebral cortex volume and reduced connectivity between frontal brain areas and regions controlling motor behaviour, memory, and emotion. The cortex continues to grow into adolescence, and symptoms (especially hyperactivity) often decline with age as the brain matures.
Q: Why did the DSM-5 collapse the PDD subtypes into a single autism spectrum disorder?
A: Distinctions between the subtypes were difficult to make reliably, and the conditions appeared to share common causes. The spectrum label captures the range of severity and presentation within a single diagnosis.
Q: What are neurofibrillary tangles and amyloid plaques?
A: Neurofibrillary tangles are twisted filaments of tau protein within nerve cells that impede nutrient transport and eventually cause cell death. Amyloid plaques are deposits of beta-amyloid protein (a neurotoxin) in the spaces between brain cells. Both accumulate in the cortex, hippocampus, and amygdala in Alzheimer's disease.
Q: How does delirium differ from major neurocognitive disorder?
A: Delirium has sudden onset (hours to days), short duration, and fluctuating symptoms; it is often reversible if the underlying cause is treated. Major NCD (dementia) has gradual onset, chronic and progressive course, and is usually irreversible.
Q: What was the outcome of the combined treatment study for ADHD?
A: 68% of children receiving combined treatment (stimulants + behaviour therapy) showed reduced or discontinued ADHD behaviours, compared to 56% for medication alone, 34% for behaviour therapy alone, and 25% for community care alone.
ADHD connects to antisocial personality disorder (Cluster B personality disorders) and substance use disorders through its long-term trajectory. Autism connects to intellectual disability and communication disorders. Alzheimer's connects to Down syndrome (chromosome 21) and to Parkinson's disease and Lewy body disease. Delirium connects to substance use disorders (withdrawal-induced delirium). The dopamine system is a recurring theme across ADHD, tic disorders, schizophrenia, and Parkinson's.
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