3.5 Neuropsychology
Week 3
Neurodegenerative &
Neurodevelopmental
Disorders
,Kolb & Wishaw (2015) → Chapter 24:
Neurodevelopmental Disorders
Fetal alcohol spectrum disorder
● Pattern of physical malformation and intellectual impairment observed in children born of
alcoholic mothers
● Umbrella term → fetal alcohol spectrum disorder (FASD)
● Symptoms
○ Irregular facial features → smooth philtrum, thin upper lip, short palpebral
fissures
○ Brain irregularities → small brains with abnormal gyri, abnormal clusters of cells,
misaligned cortex
○ Small stature, tendency to be thin
○ Behavioral symptoms → learning disabilities, lowered intelligence scores,
hyperactivity, social problems
● Pronounced FASD is found in approx 6% of alcoholic mothers
○ Incidence varies depending on geographic regions
○ Appears in about 1 in 100-700 newborns in the US
○ Especially high prevalence in child care settings and in prison populations
● The diagnosis is not all-or-none → abnormalities can range from hardly noticeable
physical & psychological effects to full blown
○ Severity is related to when how much and how frequently alcohol was consumed
during the pregnancy and individual factors
○ Worst if drinking occurs in first 3 months (often women do not know they are
pregnant) and if caused by binge drinking, poor maternal nutrition, use of other
drugs
● When is alcohol too much → many factors involved
○ Best not to drink at all to be safe → can lead to decreased intelligence scores,
also for males because it could produce epigenetic changes in sperm
○ In FASD babies mothers alcohol problems often predate pregnancy and there is
little access to prenatal care
● Mechanisms of alcohol
, ○ Effects on cell division & maturation and epigenetic effects
○ Possibly linked to potassium channel Kir2.1 that allows potassium to move freely
across cell membrane and thus is important to normal resting potential of cells
■ Support for this in mice studies, alcohol has an inhibitory effect on Kir2.1
channels
Kolb & Wishaw (2015) → Chapter 26: Neurological
Disorders
Multiple sclerosis
● Disorder of myelinated motor fibers → loss of myelin largely in motor but also in
sensory tracts
○ Loss is not uniform, lost in patches, causes small hard scars (sclerotic plaques)
in which the myelin sheath and sometimes the axons are destroyed
● Produces strange symptoms that usually appear in adulthood
○ Loss of sensation of face, limbs, body
○ Blurring of vision
○ Loss of sensation or control in one or more limbs
○ Often early symptoms go into remission and may not appear again for years but
in some cases disease progresses rapidly in just a few years
● Cause remains unknown
○ Possibly bacterial infection, virus, environmental factors, immune response of
CNS
○ Often multiple cases in a family (genetic predisposition)
● Prevalence
○ Most prevalent in northern Europe, then less so in north America and rare in
Japan and more southerly or tropical areas
○ 50 per 100 000 when prevalent makes it one of the most common structural
nervous system diseases (only Parkinson’s is as common)
○ Female to male ratio = 3:2, often progresses more rapidly in females
● The geographical prevalence issue has raised the question of being related to vitamin D
deficiency
○ Vitamin D is obtained from sunlight and oily fish → reduced sources in northern
latitudes
○ Vitamin D may be important to myelin development in childhood and its
maintenance in adulthood
○ But vitamin D plays many roles in the nervous system so it remains uncertain
● Drug treatment → alemtuzumab (lemtrada) destroys a class of immune cells that attack
healthy body treatment
○ Shows promise for MS treatment
○ Advances in brain computer interface technology are also promising for aiding
mobility
, Kolb & Wishaw (2015) → Chapter 27: Psychiatric
and Related Disorders
Motor disorders
● General
○ Clinical symptoms marked by abnormalities in movement and posture referable
to dysfunctions of basal ganglia
○ Most obvious symptom is motor affliction but cognitive changes can also be
made especially with progression of the disorder (schizophrenia like)
○ Two groups of motor symptoms
■ Loss of movement → hypokinetic-rigid syndrome (eg Parkinson’s)
■ Increased motor activity → hyperkinetic-dystonic syndrome (eg
Tourette’s)
● Hyperkinetic disorders
○ Huntington’s disease
■ Intellectual deterioration and personality changes and abnormal
movements (choreas)
■ First symptoms usually appear around 30-50 but can come earlier
■ First behavioral symptoms and within a year
involuntary movements occur
● Begins with fidgeting and become incessant,
irregular and patternless
■ Behavioral symptoms → impairment of recent
memory, defective ability to manipulate acquired
knowledge, slowed information processing
■ Emotional changes → anxiety, depression, mania,
schizophrenia like psychosis
● Suicide is common in younger onset patients →
disease progresses faster
■ After disease onset patients live for 12 years on
average
■ Rare disease → 1.6 per million die per year
■ Often affects white Europeans
■ Transmitted genetically → autosomal dominant allele
with complete penetrance (half of the offspring will
develop the disease)
● The location of the gene is now known and in
utero there is the ability to determine if a family
member will develop Huntington’s
■ Autopsy results → cortical shrinkage and thinning,
gross atrophy of the basal ganglia and neuronal loss
Week 3
Neurodegenerative &
Neurodevelopmental
Disorders
,Kolb & Wishaw (2015) → Chapter 24:
Neurodevelopmental Disorders
Fetal alcohol spectrum disorder
● Pattern of physical malformation and intellectual impairment observed in children born of
alcoholic mothers
● Umbrella term → fetal alcohol spectrum disorder (FASD)
● Symptoms
○ Irregular facial features → smooth philtrum, thin upper lip, short palpebral
fissures
○ Brain irregularities → small brains with abnormal gyri, abnormal clusters of cells,
misaligned cortex
○ Small stature, tendency to be thin
○ Behavioral symptoms → learning disabilities, lowered intelligence scores,
hyperactivity, social problems
● Pronounced FASD is found in approx 6% of alcoholic mothers
○ Incidence varies depending on geographic regions
○ Appears in about 1 in 100-700 newborns in the US
○ Especially high prevalence in child care settings and in prison populations
● The diagnosis is not all-or-none → abnormalities can range from hardly noticeable
physical & psychological effects to full blown
○ Severity is related to when how much and how frequently alcohol was consumed
during the pregnancy and individual factors
○ Worst if drinking occurs in first 3 months (often women do not know they are
pregnant) and if caused by binge drinking, poor maternal nutrition, use of other
drugs
● When is alcohol too much → many factors involved
○ Best not to drink at all to be safe → can lead to decreased intelligence scores,
also for males because it could produce epigenetic changes in sperm
○ In FASD babies mothers alcohol problems often predate pregnancy and there is
little access to prenatal care
● Mechanisms of alcohol
, ○ Effects on cell division & maturation and epigenetic effects
○ Possibly linked to potassium channel Kir2.1 that allows potassium to move freely
across cell membrane and thus is important to normal resting potential of cells
■ Support for this in mice studies, alcohol has an inhibitory effect on Kir2.1
channels
Kolb & Wishaw (2015) → Chapter 26: Neurological
Disorders
Multiple sclerosis
● Disorder of myelinated motor fibers → loss of myelin largely in motor but also in
sensory tracts
○ Loss is not uniform, lost in patches, causes small hard scars (sclerotic plaques)
in which the myelin sheath and sometimes the axons are destroyed
● Produces strange symptoms that usually appear in adulthood
○ Loss of sensation of face, limbs, body
○ Blurring of vision
○ Loss of sensation or control in one or more limbs
○ Often early symptoms go into remission and may not appear again for years but
in some cases disease progresses rapidly in just a few years
● Cause remains unknown
○ Possibly bacterial infection, virus, environmental factors, immune response of
CNS
○ Often multiple cases in a family (genetic predisposition)
● Prevalence
○ Most prevalent in northern Europe, then less so in north America and rare in
Japan and more southerly or tropical areas
○ 50 per 100 000 when prevalent makes it one of the most common structural
nervous system diseases (only Parkinson’s is as common)
○ Female to male ratio = 3:2, often progresses more rapidly in females
● The geographical prevalence issue has raised the question of being related to vitamin D
deficiency
○ Vitamin D is obtained from sunlight and oily fish → reduced sources in northern
latitudes
○ Vitamin D may be important to myelin development in childhood and its
maintenance in adulthood
○ But vitamin D plays many roles in the nervous system so it remains uncertain
● Drug treatment → alemtuzumab (lemtrada) destroys a class of immune cells that attack
healthy body treatment
○ Shows promise for MS treatment
○ Advances in brain computer interface technology are also promising for aiding
mobility
, Kolb & Wishaw (2015) → Chapter 27: Psychiatric
and Related Disorders
Motor disorders
● General
○ Clinical symptoms marked by abnormalities in movement and posture referable
to dysfunctions of basal ganglia
○ Most obvious symptom is motor affliction but cognitive changes can also be
made especially with progression of the disorder (schizophrenia like)
○ Two groups of motor symptoms
■ Loss of movement → hypokinetic-rigid syndrome (eg Parkinson’s)
■ Increased motor activity → hyperkinetic-dystonic syndrome (eg
Tourette’s)
● Hyperkinetic disorders
○ Huntington’s disease
■ Intellectual deterioration and personality changes and abnormal
movements (choreas)
■ First symptoms usually appear around 30-50 but can come earlier
■ First behavioral symptoms and within a year
involuntary movements occur
● Begins with fidgeting and become incessant,
irregular and patternless
■ Behavioral symptoms → impairment of recent
memory, defective ability to manipulate acquired
knowledge, slowed information processing
■ Emotional changes → anxiety, depression, mania,
schizophrenia like psychosis
● Suicide is common in younger onset patients →
disease progresses faster
■ After disease onset patients live for 12 years on
average
■ Rare disease → 1.6 per million die per year
■ Often affects white Europeans
■ Transmitted genetically → autosomal dominant allele
with complete penetrance (half of the offspring will
develop the disease)
● The location of the gene is now known and in
utero there is the ability to determine if a family
member will develop Huntington’s
■ Autopsy results → cortical shrinkage and thinning,
gross atrophy of the basal ganglia and neuronal loss
