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Bryan Kolb & Ian Q.

Whishaws

Fundamentals of

Human Neuropsychology,
Sixth Edition
Chapter 27
Lecture PPT

Prepared by Gina Mollet, Adams State College

Chapter 27

Psychiatric and
Related Disorders

Portrait: Losing Touch with Reality


Mrs. T.
Symptoms of schizophrenia beginning at age
16
Began with self-consciousness and progressed
to delusions and hallucinations
Hallucinations led to bizarre and dangerous
behavior

PET scans of schizophrenia indicate


abnormal blood flow in the prefrontal cortex

The Brain and Behavior


The mind-body problem
Dualists
Monists

Psychiatric or behavioral disorders have a


biological, anatomical, or genetic basis

Schizophrenia
DSM-IV R
Delusions or beliefs that distort reality
Hallucinations
Disorganized speech, senseless rhyming
Disorganized, agitated behavior
Blunted emotions, loss of interest and drive

Structural Abnormalities in
Schizophrenic Brains
Less than average weight
Enlarged ventricles
Reduction in the number of neurons in the
prefrontal cortex
Abnormal cellular structure in the
prefrontal cortex and hippocampus
Hypofrontality during card sorting

Biochemical Abnormalities in
Schizophrenic Brains
Dopaminergic function
Anti-psychotics
Act on the dopamine synapse

Glutamate
GABA

Types of Schizophrenia
Type I: Acute Schizophrenia
Positive symptoms
More responsive to neuroleptics (antipsychotics)

Type II: Chronic Schizophrenia


Negative symptoms
Structural abnormalities in the brain

Schizophrenia As a Disorder of
Development
Develops during late adolescence
Slow emergence of brain abnormalities
Combination of genetics and environment
No single gene
More likely to have experienced a
combination of adverse events

Neuropsychological Assessment
Poor performance on long-term verbal and
nonverbal memory
Poor frontal-lobe functioning
May not perform well on any test

Mood Disorders
Clinical Depression
Prolonged feelings of worthlessness and guilt
Behavioral slowing
Disrupted eating and sleeping

Mania
Excessive euphoria
Hyperactivity

Bipolar disorder
Periods of depression and mania

Neurochemical Aspects of
Depression
Reduction of monoamines
Brain-derived neurotrophic factors (BDNF)
Downregulated by stress
May affect functioning of monoamine
synapses

Hypothalamic-Adrenal system (HPA-axis)


Oversecretion of cortisol; chronic stress
Widespread influence on cerebral functioning
Kills granule cells in the hippocampus

Neurochemical Aspects of
Depression
Fluoxetine
SSRI
Stimulates BDNF and neurogenesis in the
hippocampus

Blood Flow and Metabolic


Abnormalities in Depression
Decreased activity in:
Dorsolateral and medial prefrontal regions
Reduced memory and attention

Increased activity in:


Orbital regions
An attempt to inhibit amygdala activity
An attempt to break persistent negative thoughts

Amygdala
May increase HPA-axis activity

Medial thalamus

Blood Flow and Metabolic


Abnormalities in Depression
Sleep-cycle
May be altered due to lowered serotonin
levels

Thyroid-hormone
Decrease in production may influence mood

Neurobiological Aspects of Bipolar


Disorder
Decrease in gray matter in the temporal
lobe and cerebellum
Decrease correlates with number of episodes

Sensitization Model
Bipolar patients are sensitive to stress and
drugs
Episodes of mood disorder change the brain

Snapshot: Cortical Metabolic and


Anatomical Abnormalities in Mood Disorders
Drevets and colleagues
PET images of unipolar and bipolar patients
12% decrease in blood flow to the subgenual area
Bipolars exhibit an increase in blood flow during
the manic phase

MRI images of unipolar and bipolar patients


Reduction in gray matter volume in the left
subgenual area

Neurobiological Aspects of Bipolar


Disorder
Sensitization Model
Genetically predisposed individuals may be
more sensitive
There is a link between psychomotorstimulants and mania
Bipolars are at high risk for drug abuse and
may be especially sensitive to the effects

Vitamins, Minerals, and Food


Kaplan and colleagues
Mood symptoms may be related to:

Inborn errors in metabolism


Alterations in gene expression
Epigenetic alterations in genes
Long-latency effects of nutritional abnormalities

Psychiatric Symptoms of Cerebral


Vascular Disease
Post-stroke patients
25-50% experience depression
About 25% experience generalized anxiety
disorder
Catastrophic reactions
11-50% experience pathological affect

Psychosurgery
Destruction of a region of the brain to
alleviate psychiatric symptoms
Neurosurgery
Brain surgery intended to repair damage to
alleviate symptoms

Egas Moniz
Prefrontal lobotomy

Psychosurgery
Modern Psychosurgery
13 targets
Smaller lesions
Rarely performed
Does not replace abnormal activity with
normal activity

Motor Disorders
Hyperkinetic
Increase motor activity

Hypokinetic
Loss of movement

Hyperkinetic Disorders
Huntingtons chorea
Genetic disorder
Intellectual deterioration and abnormal
movements
Begins as a reduction of activity and a
restriction of interest
Involuntary movements begin about a year
later

Hyperkinetic Disorders
Huntingtons chorea
Movements
Entail whole limbs
Irregular, no pattern
Affect head, face, trunk and limbs

Behavioral Symptoms
Personality changes
Cognitive impairments
Anxiety, depression, mania, and schizophrenic-like
psychoses

Hyperkinetic Disorders
Huntingtons chorea
Brain abnormalities
Shrinkage of the cortex
Atrophy of the basal ganglia
Imbalance among the various neurotransmitter
systems
Death of GABA and ACh neurons in the basal ganglia

Poor performance on memory and frontal-lobe


tests

Tourettes Syndrome
Three stages
1. Multiple tics
2. Inarticulate cries are added to the tics
3. Articulate words
Echolalia: Repeating what others say
Coprolalia: Obscene or lewd speech

Age of onset: 2-15


Not associated with neuroses, psychoses,
or other disorders

Tourettes Syndrome
Subcortical origin
Small cells in the basal ganglia

Treatment
Antidopaminergic drugs
Norepinephrine receptor agonists

Abnormalities in cognitive functions


supported by the right hemisphere

Hypokinetic Disorders
Parkinsons Disease
Degeneration of the substantia nigra
Loss of dopamine
Variety of symptoms that vary from patient to
patient
Symptoms resemble changes in motor activity
that occur with age

Hypokinetic Disorders
Parkinsons Disease
Rigidity
Tremor
Akinesia
Postural disturbances

Hypokinetic Disorders
Parkinsons Disease: Positive Symptoms
Resting tremor
Muscular rigidity
Cogwheel rigidity

Involuntary movements
Akathesia
Cruel restlessness

Oculogyric crisis
Involuntary turns of the head and eyes to the side

Hypokinetic Disorders
Parkinsons Disease: Negative Symptoms
Disorders of posture
Disorder of fixation
Disorder of equilibrium

Disorders of righting
Disorders of locomotion
Festination

Disorders of speech
Akinesia

Hypokinetic Disorders
Progression of Parkinsonism
Begins with tremors in the hand
Face becomes masklike and movement slows
10-20 years of progression
On-again-off-again quality

Causes of Parkinsonism
Idiopathic
Familial
Part of the aging process
Viral origin

Postencephalitic
Occurs after encephalitis

Causes of Parkinsonism
Drug Induced
Ingestion of major tranquilizers
Contaminant of synthetic heroin (MPTP)
Environmental toxins

Depletion of dopamine

Treatment of Parkinsons Disease


Physical therapy
Pharmacological therapy
Increase dopamine function
Block cholinergic system

Stem-cell research
Deep brain stimulation (DBS)

Psychological Aspects of
Parkinsons Disease
Cognitive functions
Generalized behavior slowing
Show symptoms similar to individuals with
frontal lobe or basal ganglia lesions
Impaired on the WAIS

Dementia
DSM-IV-R
Memory and other cognitive deficits
Impairment in social and occupational
functioning

Degenerative dementias
Intrinsic to the nervous system
Affects the CNS selectively

Nondegenerative dementias
Diverse etiologies

Dementia
Alzheimers disease
Most prevalent form of dementia
Neuritic Plaques
Found in the cortex
Positively correlated with cognitive decline
Amyloid surrounded by degenerative cellular
fragments

Paired Helical Filaments


Found in the cortex and hippocampus

Dementia
Alzheimers disease
Neocortical Changes
Shrinkage of the cortex; not uniform

Dementia
Alzheimers Disease
Paralimbic cortex changes
Degeneration of the limbic system and entorhinal
cortex

Cell changes
Shrinking of neurons
Loss of dendritic aborizations

Dementia
Alzheimers Disease
Neurotransmitter changes
Reduction in two or more transmitter systems
ACh, Noradrenaline, DA, 5-HT, and glutamate
receptors

Putative Causes of Alzheimers


Disease
Genetics
Trace Metals
Increased concentration of aluminum

Immune Reactions
Antibrain antibodies that cause neuronal
degeneration

Putative Causes of Alzheimers


Disease
Blood Flow
Decrease in blood flow to the brain

Abnormal Proteins
Increased production of abnormal proteins
that accumulate in the brain

Clinical Symptoms and the


Progression of Alzheimers Disease
Gradual progression
Recent memory
Remote memory
Ability to recognize family members

Impairments on the WAIS


Impaired on nearly all tests of memory
Names of objects and distinguishing among
objects in a category

Language impairments

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