Fundamentals of Human Neuropsychology,Sixth Edition

Chapter 27Lecture PPT

Prepared by Gina Mollet, Adams State College

Bryan Kolb & Ian Q. Whishaw’s

Cha

pter

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 (anti-

psychotics)

• 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 psychomotor-

stimulants 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

• Huntington’s 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

• Huntington’s 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

• Huntington’s 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

Tourette’s 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

Tourette’s 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

• Parkinson’s 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

• Parkinson’s Disease– Rigidity– Tremor– Akinesia– Postural disturbances

Hypokinetic Disorders

• Parkinson’s 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

• Parkinson’s 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 Parkinson’s Disease

• Physical therapy

• Pharmacological therapy– Increase dopamine function– Block cholinergic system

• Stem-cell research

• Deep brain stimulation (DBS)

Psychological Aspects of Parkinson’s 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

• Alzheimer’s 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

• Alzheimer’s disease– Neocortical Changes

• Shrinkage of the cortex; not uniform

Dementia

• Alzheimer’s Disease– Paralimbic cortex changes

• Degeneration of the limbic system and entorhinal cortex

– Cell changes• Shrinking of neurons• Loss of dendritic aborizations

Dementia

• Alzheimer’s Disease– Neurotransmitter changes

• Reduction in two or more transmitter systems• ACh, Noradrenaline, DA, 5-HT, and glutamate

receptors

Putative Causes of Alzheimer’s Disease

• Genetics

• Trace Metals– Increased concentration of aluminum

• Immune Reactions– Antibrain antibodies that cause neuronal

degeneration

Putative Causes of Alzheimer’s 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 Alzheimer’s 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