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219 Cards in this Set

  • Front
  • Back
Posttraumatic stress disorder (PTSD)
Syndrome characterized by prolonged
physiological arousal symptoms related to
recurring memories and dreams linked to a
traumatic event and continuing for months
or years after the event.
Neuropsychoanalysis
Movement within
neuroscience and psychoanalysis to
combine the insights of both to yield a
unified understanding of mind and brain.
id.
Primitive functions, including “instinctual drives” such as sex and aggression, are
located in the part of the mind that Freud thought to be operating on an
unconscious level and called the
superego
aspect of mind acts to repress the id and to mediate the ongoing
interaction between the ego and the id.
ego
The rational part of the mind he called the ego. Much of the ego’s activity Freud
also believed to be unconscious, although experience (to him, our perceptions of
the world) is conscious.
The aim of psychoanalysis
, the original talking therapy,
is to trace symptoms back to their unconscious roots and thus expose them to rational
judgment.
In a contemporary brain-imaging and
lesioning studies map, the brainstem and
limbic system correlate
with Freud’s
depiction of the id, the ventral frontal and
posterior cortex with the ego, and the dorsal
frontal cortex with the superego
At present, however, neurologists treat
organic disorders of the nervous system such as Parkinson’s disease and stroke
Psychiatrists
treat
behavioral disorders such as schizophrenia and depression.
Behavioral studies by their very
nature
are investigations of the whole organism.
Later behavioral studies
used groups of patients or laboratory animals with brain
injuries.
typical causes of neurological disorders
1. Genetic errors, as in Huntington’s disease
2. Progressive cell death resulting from a variety of neurodegenerative causes, as in
Parkinson’s or Alzheimer’s disease
3. Rapid cell death, as in stroke or traumatic brain injury
4. Loss of neural connections seen in disorders such as multiple sclerosis
Genetic error
Tay-Sachs disease
Negative experience
Developmental delays among Romanian orphans
Stress
Anxiety disorders
Poor nutrition
Korsakoff’s syndrome
toxins
MPTP poisoning
infection
encephalitis
injurty
traumatic brain injury
developmental anomaly
schizophrenia
Phenylketonuria (PKU)
Behavioral
disorder caused by elevated levels of the
amino acid phenylalanine in the blood and
resulting from a defect in the gene for the
enzyme phenylalanine hydroxylase; the
major symptom is severe mental
retardation.
hormonal abnormality
androgenital syndrome
challenges to diagnosis
1) reporting bias
2) identifying specific symptoms is difficult
3) diagnostician bias
Genetic Inborn error of metabolism;
autosomal recessive defective gene
treatment
Restrict dietary intake of phenylalanine
social disability
Loss of meaningful, productive life; significant social and economic cost
Behavioral symptoms
For 95 percent of patients, IQ below 50
Neurological findings
Severe mental retardation, slow growth, abnormal EEG
Histological abnormality
Decreased neuron size and dendritic length, and lowered spine density; abnormal cortical lamination
Other receptor systems, such as the activating systems for acetylcholine, dopamine,
and serotonin,
are equally diffuse, with little specificity between biochemistry and behavior.
Biochemical pathogenesis
Impairment in the hydroxylation of phenylalanine to tyrosine, causing elevated blood levels of
phenylalanine and its metabolite
Nigrostriatial Dopamine Pathways.
Axons of neurons in the midbrain substantia nigra project to the basal ganglia, supplying dopamine to maintain normal motor behavior. Loss of dopamine is related to the
muscle rigidity and dyskinesia seen in Parkinson’s disease.
Just as obvious brain lesions do not always produce
behavioral symptoms, behavioral
symptoms are not always linked to obvious neuropathology.
Rats with specific lesions of the nigrostriatal dopamine system
are used as a
model of Parkinson’s disease.
DSM
Abbreviation for Diagnostic and
Statistical Manual of Mental Disorders,
the American Psychiatric Association’s
classification system for psychiatric
disorders.
Neurobiological investigations of behavioral disorders are based on the assumption
that a direct link ought to exist between brain abnormalities and
disordered behavior. In most cases, however, the relation is far from direct.
Discrete biological markers are difficult to identify, except in the best-studied
disorders.
✔ Brain pathology can exist without
obvious clinical symptoms and clinical symptoms without obvious pathology.
✔ The general causes of behavioral disorders range from
genetic factors to negative
experiences, including injuries, toxins, and stress. It will be some time before a
unified science of brain and behavior can fully explain the disordered mind.
behavioral and neurological disorders
are the leading cause of disability after
age 15.
Epidemiology
is the study of the distribution and causes of diseases in human populations.
We
can categorize psychiatric disorders by three general types—
disorders of psychoses,
mood, and affect.
Disorders usually first diagnosed in infancy, (such as autism),
Tend to emerge and sometimes dissipate before adult life: pervasive developmental disorders(such as autism), learning disorders, attention-deficit hyperactivity disorder, conduct disorder, SAD
Delirium, dementia, amnesia,
and other cognitive disorders
Dominated by impairment in cognitive functioning: Alzheimer’s disease, Huntington’s disease
Mental disorders due to a
general medical condition condition
Caused primarily by a general medical disorder: mood disorder due to a general medical condition
Substance-related disorders
Brought about by the use of substances that affect the central nervous system: alcohol-use
disorders, opioid-use disorders, amphetamine-use disorders, cocaine-use disorders,
hallucinogen-use disorders
anxiety disorders.
Anxiety: generalized anxiety disorder, phobias, panic disorder, obsessive-compulsive disorder,
acute stress disorder, posttraumatic stress disorder
mood disorders
Severe disturbances of mood resulting in extreme and inappropriate sadness or elation for
extended periods of time: major depressive disorder, bipolar disorder
schizophrenia and other psychotic disorders
Functioning deteriorates toward a state of psychosis, or loss of contact with reality
Fictitious disorders
Intentional production or feigning of physical or psychological symptoms
Somatoform disorders
Physical symptoms that are apparently caused primarily by psychological rather than
physiological factors: conversion disorder, somatization disorder, hypochondriasis
Dissociative disorders
Significant changes in consciousness, memory, identity, or perception, without a clear physical
cause: dissociative amnesia, dissociative fugue, dissociative identity disorder (multiple
personality disorder)
Eating disorders
Abnormal patterns of eating that significantly impair functioning: anorexia nervosa, bulimia
nervosa
sexual disorders
Chronic disruption in sexual functioning, behavior, or preferences: sexual dysfunctions,
sexual-identity disorder paraphilias, sexual-identity disorder
sleep disorders
Chronic sleep problems: primary insomnia, primary hypersomnia, sleep-terror disorder,
sleepwalking disorder
Impulse-control disorders
Chronic inability to resist impulses, drives, or temptations to perform certain acts that are
harmful to the self or others: pathological gambling, kleptomania, pyromania, intermittent
explosive disorder
adjustment disorders
Maladaptive reaction to a clear stressor, such as divorce or business difficulties, that first occurs
within 3 months after the onset of the stressor
Other conditions that may be disorders, and psychophysiological disorders
Conditions or problems that are worth noting because they cause significant impairment, such
a focus of clinical attention as relational problems, problems related to abuse or neglect, medication-induced movement
between the ages of 13 and 18,
the children who
developed schizophrenia showed a remarkable loss of gray matter in the cerebral cortex.
To be useful, imaging tests must be sensitive enough to detect
unique features of brain disorders but specific enough to rule out similar conditions.
This feature is problematic, inasmuch as many behavioral disorders display similar abnormalities.
Enlarged ventricles may appear in schizophrenia, Alzheimer’s disease, alcoholism,
or head trauma, for example.
The abnormality was found
throughout the brain but was greater in the frontal lobes,
delayed growth rate in children with schizophrenia compared to
healthy children
metabolic changes in adult-onset schizophrenia,
showing an obvious abnormality in activity in the prefrontal cortex.
An inclusive list of brain and behavioral disorders
would consist of some 2000 entries.
Organic abnormalities
include genetic disorders (such as Huntington’s
chorea), developmental disorders (such as autism), infectious diseases (such as meningitis),
nervous system injuries (such as brain or spinal-cord trauma), and degenerative
dementias (such as Alzheimer’s disease).
biochemical abnormalities
disordered proteins in cell membrane channels, abnormal number of neuroreceptors, abnormal number of molecules, especially neurotransmitters or hormones
Treatments fall into four general categories:
neurosurgical,
electrophysiological, pharmacological, and behavioral
More recent neurosurgical approaches aim to
alter brain activity to alleviate some behavioral disorder.
The surgery either damages
some dysfunctional area of the brain or stimulates dysfunctional areas with electrodes.
neurosurgical treatment for Parkinson's
In the first technique, an electrode is placed into
the motor thalamus and an electric current is used to damage neurons that are responsible
for producing the tremor characteristic of Parkinson’s.
DBS and depression
Following the onset of stimulation,
an acute shift in brain activity induces a change similar to long-term potentiation in
baseline neural activity. This change in activity appears to make the brain more plastic
and receptive to other treatments.
Experimental work with laboratory monkeys has shown that DBS
in the striatum
induces neurogenesis in the hippocampus.
In laboratory rats, for example, stem cells can be induced by neurotrophic factors
to generate new cells that can migrate to the site of an injury.
difficulty with use bone marrow stem cells
The challenge is getting the cells to differentiate appropriately
and develop the correct connections.
stem cell transplant
stroke victims from teratocarcinoma.

The tumor cells were chemically altered to develop a neuronal
phenotype, and then between 2 million and 6 million cells were transplanted
into regions around the stroke
TMS
transcranial magnetic stimulation (TMS), uses magnetic
rather than electrical stimulation. To date, its only widespread and FDA-approved
clinical application is as a treatment for depression

very precise

broad applications
The development of phenothiazines (neuroleptics) as a treatment for
schizophrenia stemmed from a drug
used to premedicate surgical patients. In the next 50 years, neuroleptic drugs became increasingly more selective, and they
remain effective.
anxiolytics
Medications such as Valium quickly became—and remain—the most widely
prescribed drugs in the United States.
L-dopa,
provided the first treatment for a
serious motor dysfunction in Parkinson’s disease.
L-dopa,
provided the first treatment for a
serious motor dysfunction in Parkinson’s disease.
neuroleptics.
These antipsychotic drugs act on the mesolimbic
dopamine system, which probably is functioning abnormally in the schizophrenia patient.

The side effect emerges because the drugs also act on the nigrostriatal dopaminergic
system that controls movement.

Patients who take neuroleptics for a prolonged
period commonly have motor disturbances.
neuroleptics.
These antipsychotic drugs act on the mesolimbic
dopamine system, which probably is functioning abnormally in the schizophrenia patient.

The side effect emerges because the drugs also act on the nigrostriatal dopaminergic
system that controls movement.

Patients who take neuroleptics for a prolonged
period commonly have motor disturbances.
Tardive dyskinesia
Inability to stop the
tongue from moving; motor side effect of
neuroleptic drugs.
Tardive dyskinesia
Inability to stop the
tongue from moving; motor side effect of
neuroleptic drugs.
psychotherapy
Talking therapy derived
from Freudian psychoanalysis and other
psychological interventions.
psychotherapy
Talking therapy derived
from Freudian psychoanalysis and other
psychological interventions.
cogntive therapy
Psychotherapy based
on the perspective that thoughts intervene
between events and emotions, and thus the
treatment of emotional disorders requires
changing maladaptive patterns of thinking.
Behavioral therapy
Treatment that
applies learning principles, such as
conditioning, to eliminate unwanted
behaviors.
cogntive therapy
Psychotherapy based
on the perspective that thoughts intervene
between events and emotions, and thus the
treatment of emotional disorders requires
changing maladaptive patterns of thinking.
Real-time fMRI (rtfMRI)
Behaviormodification
technique where, to change
their behavior, individuals learn to control
their own patterns of brain activation.
Virtual-reality therapy is usually
combined
with behavioral therapies to offer patients an opportunity to talk about
their virtual experiences.
Behavioral therapy
Treatment that
applies learning principles, such as
conditioning, to eliminate unwanted
behaviors.
Real-time fMRI (rtfMRI)
Behaviormodification
technique where, to change
their behavior, individuals learn to control
their own patterns of brain activation.
Therapies for brain and behavioral disorders, , range from the
ery invasive (neurosurgery) to the moderately invasive
(pharmacological) to the noninvasive (electrophysiological) and indirect
(cognitive rehabilitation and other behavioral therapies).
Virtual-reality therapy is usually
combined
with behavioral therapies to offer patients an opportunity to talk about
their virtual experiences.
Therapies for brain and behavioral disorders, , range from the
ery invasive (neurosurgery) to the moderately invasive
(pharmacological) to the noninvasive (electrophysiological) and indirect
(cognitive rehabilitation and other behavioral therapies).
✔ Little is known about the relation between behavioral disorders and specific
biological pathologies
Classification schemes such as the DSM are essentially
checklists of likely symptoms.
✔ Little is known about the relation between behavioral disorders and specific
biological pathologies
Classification schemes such as the DSM are essentially
checklists of likely symptoms.
Traumatic brain injury (TBI)
is a common result of head impacts with other objects—
as can occur in automobile and industrial accidents—and of sporting injuries. Cerebral
trauma, or injury from a blow to the head, is the most common form of brain
damage in people under age 40.
TBI stats
Children and elderly people are more likely to suffer head injuries from falls than are
others, and males between 15 and 30 are very likely to incur brain injuries, especially
from automobile and motorcycle accidents (Figure 16-5). A child’s chance of suffering
significant traumatic brain injury before he or she is old enough to drive is 1 in 30.
TBI in athletes and soldiers
Sports account for about 20 percent
of TBIs, and the U.S. Army Institute of Surgical Research reports that traumatic
brain injury affects 22 percent of U.S. soldiers wounded in the Iraq war
Preliminary examination of four brains of professional football
players who had a history of concussion and severe postconcussion symptoms, such as depression, have revealed
have revealed an alarming diffuse loss of cerebral tissue.
The disruption in blood supply tends to
be brief,
but a parallel disruption of energy production
by the mitochrondria in the brain can
persist for weeks and is no doubt related to many
postconcussion behavioral symptoms.
Two kinds of behavioral effects result from
TBI:
(1) impairment of the specific functions mediated
by the cortex at the coup (the site of impact)
or countercoup (opposite side) lesion, as illustrated
in Figure 16-6, and (2) more generalized impairments
from widespread trauma throughout the
brain.
Magnetic resonance spectroscopy
(MRS)
Modification of MRI to identify
changes in specific markers of neuronal
function; promising for accurate diagnosis
of traumatic brain injuries.
Ischemia
Lack of blood to the brain as a
result of stroke.
Traumatic brain injuries that .
damage the frontal and temporal lobes also tend to
have significant effects on personality and social behavior
People
with traumatic brain injuries show a chronic decrease in NAA, which
correlates
with the severity of the injury
recovery from head trauma may continue for
2 to 3 years
and perhaps longer, there is little doubt that the bulk of the cognitive recovery occurs
in the first 6 to 9 months
Findings from numerous studies support the conclusions that
the quality of life—
in regard to social interactions, perceived stress levels, and enjoyment
of leisure activities—is significantly reduced after TBI and that this reduction is
chronic.
A cascade of events
takes place after blood flow is
blocked as a result of stroke.
Within seconds, ionic changes
at the cellular level spur
changes in second-messenger
molecules and RNA production.
Changes in protein production
and inflammation follow and
resolve slowly, in hours to days.
Recovery begins within hours
to days and continues from
weeks to months or years.
Diaschisis
Neural shock that follows brain
damage in which areas connected to the site
of damage show a temporary arrest of
function.
Idiopathic seizure
Appears
spontaneously and in the absence of other
diseases of the central nervous system.
Symptomatic seizure
Identified with a
specific cause, such as infection, trauma,
tumor, vascular malformation, toxic
chemicals, very high fever, or other
neurological disorders.
Neuroprotectant
Drug used to try to
block the cascade of poststroke neural
events.
tissue plasminogen activator (t-PA).
The difficulty is that t-PA must be administered within 3 hours to be effective. Only a
small percentage of stroke patients currently arrive at the hospital soon enough, in large
part because stroke is often not considered to be an emergency
When the course of the stroke has led to dead brain tissue, the only treatments that
can be beneficial are those that facilitate
plastic changes in the brain. Examples are speech
therapy or physical therapy.
constraint-induced therapy
Its logic confronts a problem in poststroke recovery related to learned nonuse.

the intact limb is held in a sling for several hours
per day, forcing the patient to use the impaired limb.
The bulk of the evidence suggests that .
patients with small gray
matter strokes are most likely to show benefits of these treatments, whereas those with
large strokes including white matter show little benefit
TMS
The idea is to induce
plasticity in regions adjacent to the dead tissue with the goal of enhancing the efficiency
of the residual parts of the networks.
In epilepsy,
a person suffers recurrent seizures that register on an electroencephalogram
(EEG) and are associated with disturbances of consciousness.
seizures do have a consistent
feature:
the brain is most epileptogenic when it is inactive and the patient is sitting
still.
seizure symptoms
1. An aura, or warning, of impending seizure may take the form of a sensation—an
odor or a noise—or it may simply be a “feeling’’ that the seizure is going to occur.
2. Loss of consciousness ranges from complete collapse in some people to simply
staring off into space in others. The period of lost consciousness is often
accompanied by amnesia, including forgetting the seizure itself.
3. Seizures commonly have a motor component, but as noted, the movement
characteristics vary considerably. Some people shake; others exhibit automatic
movements, such as rubbing the hands or chewing.
Complex partial seizures, another focal type, originate most commonly
in the temporal
lobe and somewhat less frequently in the frontal lobe.
Complex partial seizures
are characterized by three common manifestations:
1. Subjective experiences—for example, forced, repetitive thoughts, alterations in
mood, feelings of déjà vu, or hallucinations—before the attack
2. Automatisms—repetitive stereotyped movements such as lip smacking or chewing
or activities such as undoing buttons during the attack
3. Postural changes, such as when the person assumes a catatonic, or frozen, posture,
during the attack
Focal seizure
Begins locally (at a focus)
and then spreads out to adjacent areas.
Petit mal seizure
Seizure of brief
duration, characterized by loss of awareness
with no motor activity except for blinking,
turning the head, or rolling the eyes.
Postictal depression
Postseizure state
of confusion and reduced affect.
Grand mal seizure
Seizure characterized
by loss of consciousness and stereotyped
motor activity.
Catatonic posture
Rigid or frozen pose
resulting from a psychomotor disturbance.
automatism
Unconscious, repetitive,
stereotyped movement characteristic of
seizure.
stages of grand mal seizures
(1) a tonic stage, in which the body stiffens and breathing stops, (2) a clonic stage, in
which there is rhythmic shaking, and (3) a postseizure postictal depression during
which the patient is confused. About 50 percent of grand mal seizures are preceded by
an aura.
The treatment of choice for epilepsy is an
anticonvulsant drug such as diphenylhydantoin
(DPH, Dilantin), phenobarbital

no alcohol

they presumably inhibit the discharge of abnormal neurons by stabilizing the
neuronal membrane, especially in inhibitory neurons.
If medication fails to alleviate the seizure problem satisfactorily,
surgery can be performed
to remove the focus of abnormal functioning in patients with focal seizures.
The abnormal tissue is localized by the surgeon by both EEG and cortical stimulation.
In multiple sclerosis (MS),
myelin is damaged, and the functions of the neurons whose
axons it encases are disrupted. Multiple sclerosis is characterized by the loss of myelin,
Proposed causes of MS include
bacterial infection, a
virus, environmental factors including pesticides, and an immune response of the central
nervous system.
known as horror autotoxicus.
And here is the problem
for the human immune system: a foreign microbe may have proteins that are very
similar to the body’s own proteins. If the microbe and human have a common gene sequence,
the immune system can mistakenly attack itself,

Many microbial protein sequences are homologous with structures found in
myelin, which leads to an attack against the microbe and a person’s own myelin.
Autoimmune disease
Illness resulting
from the loss of the immune system’s ability
to discriminate between foreign pathogens
in the body and the body itself.
Dementia
Acquired and persistent
syndrome of intellectual impairment
characterized by memory and other
cognitive deficits and impairment in social
and occupational functioning.
In 1900, about 4 percent of the population had attained 65 years of age.
By
2030, about 20 percent of the population will be older than 65—about 50 million in
the United States alone.
Currently, about 6 million people
in the United States are diagnosed with dementia.
This number is projected to rise to
about 15 million by 2050, at which time there will be 1 million new cases per year
Nondegenerative dementias
are a heterogeneous group of disorders with diverse etiologies,
including diseases of the vascular or endocrine systems, inflammation, nutritional
deficiency, and toxic conditions,
degenerative dementias
Parkinson's Alzheimer's
arkinson’s disease seems related to the degeneration of the substantia nigra and to
the loss of the neurotransmitter dopamine produced there and released in the
striatum. The disease is therefore is the source
he source of an important insight into the role of
this brainstem nucleus and its dopamine in the control of movement.
• Many symptoms of Parkinson’s disease strikingly resemble changes in motor
activity that take place as a consequence of aging. Thus the disease is a source of
indirect insight into the more general problems of neural changes in aging.
• Although Parkinson’s disease is described as a disease entity, symptoms vary
enormously among people, thus illustrating the complexity in understanding a
behavioral disorder.
A well-defined set of cells degenerates in Parkinson’s disease,
yet the symptoms are not the same in every sufferer.
tremor at rest
Tremor at rest. Tremor consists of alternating movements of the limbs when they
are at rest; these movements stop during voluntary movements or during sleep. The
tremors of the hands often have a “pill rolling’’ quality, as if a pill were being rolled
between the thumb and forefinger.
muscular rigidity
Tremor at rest. Tremor consists of alternating movements of the limbs when they
are at rest; these movements stop during voluntary movements or during sleep. The
tremors of the hands often have a “pill rolling’’ quality, as if a pill were being rolled
between the thumb and forefinger.
involuntary movements
Involuntary movements. Small movements or changes in posture, sometimes
referred to as akathesia or “cruel restlessness,” may be concurrent with general
inactivity to relieve tremor and sometimes to relieve stiffness but often occur for no
apparent reason. Other involuntary movements are distortions of posture, such as
occur during oculogyric crisis (involuntary turns of the head and eyes to one side),
which last for periods of minutes to hours.
Akathesia
Small, involuntary movements
or changes in posture; motor restlessness.
festination
Tendency to engage in a
behavior, such as walking, at faster and
faster speeds.
Disorders of posture.
A disorder of fixation presents as an inability or difficulty
in maintaining a part of the body in its normal position in relation to other
parts. Disorders of equilibrium create
difficulties in standing or even sitting unsupported. In less severe cases, people
Positive symptoms are behaviors not seen
in normal people or seen only so rarely—
and then in such special circumstances—
that they can be considered abnormal.
disorders of righting
Disorders of righting. A person has difficulty in achieving a standing position from
a supine position. Many advanced patients have difficulty even in rolling over.
disorders of locomotion
Disorders of locomotion. Normal locomotion requires support of the body against
gravity, stepping, balancing while the weight of the body is transferred from one
leg to the other, and pushing forward. Parkinson patients have difficulty initiating
stepping, and when they do walk, they shuffle with short footsteps on a fairly wide
base of support because they have trouble maintaining equilibrium when shifting
weight from one leg to the other. On beginning to walk, Parkinson patients often
demonstrate festination: they take faster and faster steps and end up running
forward.
akinesia
5. Akinesia. Poverty or slowness of movement may also manifest itself in a blankness
of facial expression or a lack of blinking, swinging the arms when walking,
spontaneous speech, or normal fidgeting. Akinesia is also manifested in difficulty
in making repetitive movements, such as tapping, even in the absence of rigidity.
People who sit motionless for hours show akinesia in its most striking
manifestation.
speech disturbances
Speech disturbances. One symptom most noticeable to relatives is the almost
complete absence of prosody (rhythm and pitch) in the speaker’s voice.
possible causes of Parkinson's
MPTP exposure, encephalitis, syphilis, insecticides, herbicides, enviornmental pollutants
A drawback of drug therapies is that,
as the disease progresses, they become less effective
and the incidence of side effects increases.
L-Dopa is converted into dopamine in the brain and enhances effective dopamine transmission,
as do drugs
such as amantadine, amphetamine, monoamine oxidase inhibitors,
and tricyclic antidepressants.
surgical treamtns for Parkinson'
Lesioning
the internal part of the globus pallidis (GPi) has been found to reduce rigidity and
tremor. Hyperactivity of GPi neurons can also be reduced neurosurgically by electrically
stimulating the neurons via deep brain stimulation
A newer course of treatment for Parkinson's proposes to increase the number of dopamine cells
either by transplanting stem cells
that could then be induced to take a dopaminergic
phenotype or by stimulating the production of endogenous stem cells and their migration
to the basal ganglia.
Alzheimer's disease
accounts for 65% of dementias
possible causes of Alzheimer's
including genetic predisposition, environmental
toxins, high levels of trace elements such as aluminum in the blood, an
autoimmune response, a slow-acting virus, and reduced blood flow to the cerebral hemispheres.
Alzheimer brain changes
Nonetheless, it became clear that widespread changes take
place in the neocortex and limbic cortex and associated changes take place in a number
of neurotransmitter systems.
areas unaffected by alzheimer's
most of the brainstem, cerebellum, and spinal cord are
relatively spared its major ravages.
The principal neuroanatomical change in Alzheimer’s disease is the emergence of
neuritic (amyloid) plaques,
chiefly in the cerebral cortex. Increased plaque concentration
in the cortex has been correlated with the magnitude of cognitive deterioration
Another anatomical correlate of Alzheimer’s disease
is neurofibrillary tangles—paired helical (spiral) filaments found in both the cerebral cortex and the hippocampus. The posterior half of the hippocampus is affected more severely than the anterior half.

has been observed in patients w/ Down syndrome, Parkinson's, & other dementias
areas unaffected by alzheimer's
the primary sensory and motor areas of the
cortex, especially the visual cortex and the sensory–motor cortex, are spared.
areas most affected by alzheimer's
posterior parietal areas, inferior temporal cortex, and limbic cortex.
The entorhinal cortex is t
he major relay through which information
from the neocortex gets to the hippocampus and related structures
and is then sent back to the neocortex.
similarity between Parkinson's and Alzheimer's
The Parkinsonian brain suffers a larger loss, but the brains of Alzheimer
patients also have nigral cell loss

Lewy bodies
Noninvasive imaging studies reveal that aging is correlated with a
decrease in whitematter
volume probably related to myelin loss.
older participants tend to activate larger regions
of their attentional and executive networks (parietal and prefrontal cortex)
when
they perform complex cognitive and executive tasks.
Both hypertension and obesity were related to decreased cortical thickness in the
frontal lobe, which was correlated with decreased performance
on tests of frontal
lobe function. In contrast, high cholesterol was associated with temporal lobe cortical
thickening and impaired temporal lobe functioning.
Lewy body
Circular fibrous structure
found in several neurodegenerative
disorders; forms within the cytoplasm of
neurons and is thought to result from
abnormal neurofilament metabolism.
✔ Normal aging is associated with neurological and behavioral changes that are
preventable or reversible by stimulating
neural plasticity.
Stroke results from an interruption of blood supply to the brain, leading to
damage to
gray and/or white matter; treatments are more effective if there is
limited involvement of white matter.
Epilepsy is a chronic neurological syndrome of
recurrent seizures

it can be treated with antiepileptic drugs or in extreme cases
with neurosurgery
Multiple sclerosis is an autoimmune disease in which the
body’s immune system attacks
the myelin in the central nervous system; there is
no known cure for MS
nearly 50 percent of the U.S. population
is experiencing behavioral disorder
schizophrenia
Schizophrenia—1.1%
Characterized by delusions, hallucinations,
disorganized speech, inappropriate or
blunted emotional responses, loss of
motivation, and cognitive effects.
major depression
Major depression—6.7%
Episodes during which the patient feels sad or empty nearly every day; loses
interest or pleasure in hobbies and activities; experiences changes in appetite,
weight, energy levels, or sleeping patterns; harbors thoughts of death or suicide.
dysthymia
Dysthymia—1.5%
Similar to major depression but symptoms are less severe and more chronic
(years). Also includes low self-esteem, fatigue, and poor concentration.
bipolar disorder
Bipolar—2.6%
Episodes of abnormally elevated or irritable mood. In the elevated
mood, the person feels inflated self-esteem, needs less sleep, talks
more than usual, or engages excessively in pleasureable but unwise
activities. These manic periods alternate with depressive episodes.
generalized anxiety
Generalized anxiety—5%
Unrealistic, excessive, long-lasting worry; motor tension,
restlessness, irritability, and difficulty sleeping.
panic disorder
Panic disorder—3%
Brief, recurrent, unexpected episodes of terror, sympathetic
crises, and shortness of breath.
ptsd
Posttraumatic stress—3.5%
Recurrent episodes of fear triggered by reminders of a previous
extremely stressful event.
social phobia
Social phobia—13%
Aversion, fear, autonomic arousal in unfamiliar social settings.
Specific phobias—11%
Aversion, fear, autonomic arousal in specific situations (exposure to
animals, blood, and so on).
OCD
Recurrent obsessions (persistent, intrusive, inappropriate thoughts that cause anxiety) and
compulsions (repetitive acts performed to reduce anxiety).
6 symptoms of schizophrenia
The DSM lists six diagnostic symptoms of schizophrenia:
1. Delusions—beliefs that distort reality
2. Hallucinations—distorted perceptions—such as hearing voices
3. Disorganized speech, such as incoherent statements or senselessly rhyming talk
4. Disorganized behavior or excessive agitation
5. The opposite extreme: catatonic behavior
6. Negative symptoms, such as blunted emotions or loss of interest and drive, all
characterized by the absence of some normal response
Type I schizophrenia
Disorder
characterized predominantly by positive
symptoms (e.g., behavioral excesses such
as hallucinations and agitated movements)
likely due to a dopaminergic dysfunction
and associated with acute onset, good
prognosis, and a favorable response to
neuroleptics.
Type II schizophrenia
Disorder
characterized by negative symptoms
(behavioral deficits) and associated with
chronic affliction, poor prognosis, poor
response to neuroleptics, cognitive
impairments, enlarged ventricles, and
cortical atrophy, particularly in the frontal
cortex.
structural abnormalities associated with schizophrenia
Broca's area (associated with AH)
Wernicke's area (associated w/ thought disorders)
large ventricles and thinner cortex in the medial temporal regions

hippocampal neurons in the
schizophrenic brain have a haphazard (memory deficits)

Another correlation is frequently seen in schizophrenia between an abnormally low
blood flow in the dorsolateral prefrontal cortex and deficits in executive functions,
organization
neurochemical correlates of schizophrenia
dopamine
glutamate
GABA
Mania
mental state
characterized by excessive euphoria.
Bipolar disorder
Mood disorder
characterized by alternating periods of
depression and mania.
The main symptoms
of major depression
are prolonged feelings of worthlessness and guilt, disruption
of normal eating habits, sleep disturbances, a general slowing of behavior, and frequent
thoughts of suicide.
systems involved in depression
that monoamine systems, particularly both the norepinephrine
and the serotonin systems, have roles in depression.
antidepressant drugs acutely increase
the synaptic levels of norepinephrine and serotonin.
(BDNF)
is down-regulated by stress and up-regulated by
antidepressant medication.

acts to enhance the growth and survival of cortical neurons and
synapses, BDNF dysfunction may adversely affect noreprinephrine and serotonin systems
through the loss of either neurons or synapses
HPA axis
HPA axis Hypothalamic-pituitary-adrenal
circuit that controls the production and
release of hormones related to stress.

The best-established abnormality in the HPA-axis modulation is an oversecretion
of cortisol from the adrenal gland.
If the cortisol release is too large,
the norepinephrine
neurons fail to regulate it.
Chronic stress can lead to
the oversecretion of cortisol, an imbalance associated
with depression in adulthood. Nemeroff found, for example, that 45 percent
of adults with depression lasting 2 years or more had experienced abuse, neglect, or
parental loss as children.
Abused suicide victims showed decreased
gene expression for cortisol
receptor relative to the other people. These results, derived from epigenetics, confirm
that early neglect or abuse alters the HPA axis.
HPA axis.
(A) In this
medial view of the stress-activating system,
the locus coeruleus contains the cell bodies
of norepinephrine (noradrenaline) neurons
(top), and cell bodies of the serotonergic
activating system emanate from the Raphé
nuclei (bottom). (B) When activated, the
HPA system affects mood, thinking, and
indirectly, secretion of cortisol by the
adrenal glands. HPA deactivation begins
when cortisol binds to hypothalamic
receptors.
But independent of serotonin production,
fluoxetine stimulates
both BDNF production and neurogenesis in the hippocampus,
resulting in a net increase in the number of granule cells
depression is accompanied by increased blood
flow and glucose metabolism
in the orbitofrontal cortex, the anterior cingulate cortex,
and the amygdala. Blood flow drops as the symptoms of depression remit when a patient
takes antidepressant medication
CBT
Although we have emphasized the biological cause of depression, once again we
must emphasize that the best treatment need not be a direct biological intervention.
Cognitive-behavioral therapy (CBT) focuses on challenging the reality of the patient’s
beliefs and perceptions. The objective is to identify dysfunctional thoughts and beliefs
that accompany negative emotions and replace them with more realistic ones.
Simply pointing out to a person that the person’s beliefs are faulty is not likely to
be effective, however, because it probably took months or years to develop the beliefs.
The neural circuits underlying the beliefs must be changed, just as the strategies of developing
new ones must be changed. In a real sense, CBT is effective if it can induce
neural plasticity and change brain activity. And in fact, CBT is at least as effective as
medication as a treatment for depression.
prevalence of anxiety disorders
37.5%
Imaging studies of people with anxiety disorders record
increased baseline activity
in the cingulate cortex and parahippocampal gyrus and an enhanced response to anxiety-
provoking stimuli in the amygdala and prefrontal cortex.
Researchers hypothesize that, because drugs
that enhance the inhibitory transmitter GABA are particularly effective in reducing anxiety,
excessive excitatory neurotransmission may enhance anxiety. But
Pups raised by mothers
that display low levels of licking and grooming
show more anxiety-related behaviors,
including an enhanced corticosterone response in response to mild stressors

show this behavior toward their infants even if they had adoptive mothers
In the case of anxiety disorders, CBT
focuses on challenging the reality of the patients’
obsessions and the behavioral necessity for their compulsions.

The most effective
behavioral therapies expose and reexpose patients to their fears.
It is likely that anxiety disorders are related to GABA systems and abnormally high
levels of blood flow
in the cingulate cortex, amygdala, and parahippocampal
cortex. Treatments aim to reverse the GABAergic abnormalities and to help people
learn to modify their behaviors.
The monoamine systems are abnormal in mood disorders,
cingulate cortex and in the amygdala.
particularly in signal
transduction in postsynaptic cells.
And in depression, abnormally high levels of
blood flow and glucose utilization show up in the
prefrontal and anterior
cingulate cortex and in the amygdala.
Antidepressant treatments aim largely at
normalizing the
monoaminergic systems, which in turn normalizes glucose
utilization.
Schizophrenia is correlated with
abnormalities in dopamine, GABA, and
glutamate systems.
schizophrenia structural abnormalities
Structural abnormalities and low blood-glucose utilization are
observed in both the prefrontal cortex and the temporal cortex.
treatments for schizophrenia
Treatments
emphasize normalizing the dopaminergic abnormalities.
Neurocognitive enhancement
Brainfunction
enhancement by pharmacological,
physiological, or surgical manipulation.