Chapter 17

Anxiety Disorders, Autistic Disorder,

Attention-Deficit/Hyperactivity Disorder,
and Stress Disorder
 Anxiety Disorders
 Panic Disorder

 Anxiety disorder: >25% of population

• A psychological disorder characterized by
unrealistic fear and anxiety.
Panic disorder
generalized anxiety
obsessive compulsive behavior
 Panic Disorder:
• A disorder characterized by episodes of intense
fear accompanied by symptoms such as
shortness of breath and irregularities in
heartbeat.
Copyright © 2004 Allyn and Bacon
 Anxiety Disorders
 Panic Disorder

 Anticipatory anxiety:
• A fear of having a panic attack; may lead to the
development of agoraphobia.

 Agoraphobia:
• An unrealistic and intense fear of being away
from home or other protected places.
• In severe cases people will not leave home!
 Anxiety Disorders

 Panic Disorder
Possible Causes:
 Genetic origins:
• Evidence supports some anxiety disorders may be
inherited.
Associated with joint hypermobility.
• Lactate-induced panic appears heritable
 Neurotransmitters:
• Serotonin and GABA receptors may be involved in
anxiety disorders. GBIs induce severe anxiety.
• Serotonin depletion increases susceptibility to panic
• Treated with benzodiazepines and occasionally SSRIs
 Brain Structures:
• Imaging studies suggest that the cingulate gyrus,
prefrontal, and anterior temporal cortices are involved in
panic attack.
 Anxiety Disorders

 Brain Mechanisms
• fMRI reveals lower activity in frontal cortex during
panic attack in panic subjects compared to
controls
• Decreased frontal activity may inhibit one’s ability
to control reactions to panic inducing stimuli
 Anxiety

 Generalized Anxiety
• Often a result of Pavlovian conditioning
• Role of Central Nucleus of the Amygdala
Essential for identifying fear and anxiety stimuli
Initiating emotional responses
• Hypothalamus
Hypothalamus>pituitary>adrenal gland responses
Sympathetic responses
• Cortex
Cingulate and orbitofrontal cortex for feelings of anxiety
Frontal cortex for “control” of anxiety
 Treatment for Anxiety

• Historically, barbiturates were used to treat

severe cases of anxiety
• Benzodiazapines (valium, ativan, librium) had
less severe side effects
• Other GABA agonists
Gabapentin
• Serotonin agonists
 Anxiety Disorders
 Obsessive-Compulsive Disorder
(2-3%) of population)

 Obsessive-compulsive disorder:
• A mental disorder characterized by obsessions and
compulsions.

 Obsession:
• An unwanted thought or idea with which a person is
preoccupied.
• e.g., “I left the doors unlocked!”
 Compulsion:
• The feeling that one is obliged to perform a behavior,
even if one prefers not to do so.
• Checking behaviors (keep checking the doors)
 Anxiety Disorders

 Examples of obsessions:
 Concern for order and constancy
 Cleanliness (body or living space)
 Forbidden sexual thoughts

 Examples of compulsions:
 Hand washing
 Checking
 Collecting
 Repeating behaviors (in and out of a door)
 Arranging things
 Cleaning
 Anxiety Disorders
 Obsessive-Compulsive Disorder
 Possible Causes:

 Genetic Origin:
• Evidence is beginning to accumulate suggesting
that OCD might have a genetic origin. Appears
with Tourette’s syndrome
 Brain Damage (from trauma)
• Basal ganglia, cingulate, frontal cortex
 Anxiety Disorders

 Treatment
 Serotonin's involvement in impulse control via
orbitofrontal cortex and basil ganglia (both receive
SE input)
• SSRIs are most effective
• Serotonin antagonists worsen symptoms
 Anxiety Disorders
 Obsessive-Compulsive Disorder
 Possible Causes:

 Tourette’s syndrome:
• A neurological disorder characterized by tics and
involuntary vocalizations and sometimes by
compulsive uttering of obscenities and repetition
of the utterances of others.

• Treatment with antipsycolics (dopamine

antagonists, D2)
 Anxiety Disorders
 Obsessive-Compulsive Disorder
 Possible Causes:

 Cingulotomy:
• The surgical destruction of the cingulum bundle,
which connects the prefrontal cortex with the
limbic system; helps to reduce intense anxiety
and the symptoms of obsessive-compulsive
disorder.
• Only used on patients who are unresponsive to
drug treatment.
 Autistic Disorder
 Description:

 Autistic Disorder:
• A chronic disorder whose symptoms include
failure to develop normal social relations with
other people, impaired development of
communicative ability, lack of imaginative ability,
and repetitive, stereotypical movements.
 Autistic Disorder
 Possible Causes:

 Biological:
• Research and mental health professionals are
convinced autism is caused by biological factors.

• Between 2 and 3 percent of siblings of people

with autism are themselves autistic.

• There is a 70 percent concordance rate for

monozygotic twins.
Copyright © 2004 Allyn and Bacon
 Autistic Disorder
 Possible Causes:

 Phenylketonuria (PKU):
• A hereditary disorder caused by the absence of
an enzyme that converts the amino acid
phenylalanine to tyrosine; causes brain damage
unless a special diet is implemented soon after
birth.
 Autistic Disorder
 Possible Causes:

 Brain pathology:
• Heritable aspect of autism suggests the disorder
is a result of structural or biochemical
abnormalities in the brain.

• Researchers have found evidence for structural

abnormalities in the brains of autistics, but so far
we cannot point to any single abnormality as the
cause of the disorder.
 Attention-Deficit/Hyperactivity Disorder

 Attention-deficit/hyperactivity disorder (ADHD):

• The principal characteristics of ADHD are
inattention, hyperactivity, and impulsivity.
These symptoms appear early in a child's life.
• There are three patterns of behavior that indicate
ADHD. People with ADHD may show several
signs of being consistently inattentive. They may
have a pattern of being hyperactive and
impulsive. Or, they may show all three types of
behavior.
 Attention-Deficit/Hyperactivity Disorder

 Inattention

• Often becoming easily distracted by irrelevant

sights and sounds (hyper vigilant)
• Often failing to pay attention to details and
making careless mistakes
• Rarely following instructions carefully and
completely losing or forgetting things like toys, or
pencils, books, and tools needed for a task
• Often skipping from one uncompleted activity to
another.
 Attention-Deficit/Hyperactivity Disorder

 Hyperactivity-Impulsivity

• Feeling restless, often fidgeting with hands or

feet, or squirming while seated
• Running, climbing, or leaving a seat in
situations where sitting or quiet behavior is
expected (lack of impulse control)
• Blurting out answers before hearing the
whole question (lack of impulse control)
• Having difficulty waiting in line or taking
turns.
 Attention-Deficit/Hyperactivity Disorder
 Possible causes

• There is strong evidence from family and twin studies for hereditary
factors in a person’s likelihood of developing ADHD.
• Thirty-six percent of all findings were positive (P< 0.05), 17% were
trends (0.05 <P < 0.15), and 47% were negative (P > 0.15).
• Genetic investigations have supported the role of both dopamine D4
receptor gene (DRD4) and dopamine transporter gene (DAT1) in the
vulnerability to the disorder.
• The DRD4 gene has been postulated as a candidate gene for
attention-deficit-hyperactivity disorder
Lower DA binding in basal ganglia
Increased DA transport in frontal lobes
 Attention-Deficit/Hyperactivity Disorder

 Other causes
 Possible correlation between the use of cigarettes
and alcohol during pregnancy.
 Lead paints?
 Sugar sensitivities?
 Head injuries?
 Attention-Deficit/Hyperactivity Disorder
 Brain structure involvement:
• Studies of brain structure of people with ADHD
do not reveal any localized abnormalities,
though the total volume of their brains is
approximately 4% smaller than normal.
• Candidates:
Frontal lobes
Medial temporal lobes
Caudate nucleus
 Attention-Deficit/Hyperactivity Disorder

 NIMH Child Psychiatry Branch studied 152 boys

and girls with ADHD, matched with 139 age- and
gender-matched controls without ADHD. The
children were scanned at least twice, some as
many as four times over a decade. As a group, the
ADHD children showed 3-4 percent smaller brain
volumes in all regions—the frontal lobes, temporal
gray matter, caudate nucleus, and cerebellum.
 Attention-Deficit/Hyperactivity Disorder

 The Reticular Activating System

• Decreased NE activity in RAS

• Poor attention, learning difficulties, memory deficits, lack
of behavior control
• Treatment with amphetamines increase RAS activity

• Increased RAS activity

• Hyperactivity, restlessness, hyper vigilant
• Treatment may include Clonadine (NA Antagonist)
 Attention-Deficit/Hyperactivity Disorder
 Drug Treatment
• Adderall amphetamine
• Concerta methylphenidate
• Cylert pemoline*
• Dexedrine dextro-amphetamine
• Ritalin methylphenidate

* DA agonist? Mechanism not well described

 Stress Disorders

 Stress:
• A pattern of physiology that results from a
stressor
 Stressor:
• A stimulus (or situation) that produces a
generalized stress response.
 Stress Disorders

 Fight-or-flight response:
• First stage of the stress response where
organism is mobilized.
• Changes in hormonal and sympathetic activity in
preparation for response.
 Stress Disorders
 Physiology of Stress

 Corticotropin-releasing hormone (CRH):

• A hypothalamic hormone that stimulates the
anterior pituitary gland to secrete ACTH.

 Adrenocorticotropic hormone (ACTH):

• A hormone released by the anterior pituitary
gland in response to CRH; stimulates the adrenal
cortex to produce glucocorticoids.
 Stress Disorders

 Physiology of Stress

• Sympathetic activation of adrenal cortex

• Results in release of EP and NE from adrenal
medulla
Epinephrine causes increased HR, respiration,
increased glucose metabolism
Norepinephrine increases blood flow to muscles
& BP. These increases are mediated through
the central n. of amygdala, RAS, and frontal
cortex.
 Stress Disorders
 Physiology of Stress

 Glucocorticoid (cortisol)
• One steroid hormone of the adrenal cortex that is
important in protein and carbohydrate
metabolism, secreted especially in times of
stress.
• Immunosuppressive
• Neurotoxic to several brain regions including
cortex and hippocampus
Copyright © 2004 Allyn and Bacon
 Stress Disorders
 Immunology

 Antigen:
• A protein present on a microorganism that permits the
immune system to recognize the microorganism as an
invader.
 Antibody:
• A protein produced by a cell of the immune system that
recognizes antigens present on invading microorganisms.
 Lymphocytes (White Blood Cells)
• B-Cell: A white blood cell that originates in the bone
marrow; part of the immune system.
• T-Cell: A wbc that originates in the thymus
T lymphocytes recognize surface markers on other cells in
the body that label those cells for destruction.
Immunology

 Macrophage (big eater)

• A wbc that engulfs and destroys weakened
bacterial or viral material.
 Natural Killer Cell:
• A wbc that identifies and engulfs abnormal cells--
typically cancer cells.
 Immunoglobulin:
• An antibody released by B-lymphocytes that bind
with antigens and help to destroy invading
microorganisms.
• Found in blood and saliva
A macrophage ingests bacteria
as part of the immune
response to infection.
 Natural killer cells burst forth from the the tonsils, lymph nodes
and spleen, and destroy infected and cancerous cells while the
immune system's T and B cells are still mobilizing,
 Stress Disorders
 Immunology

 Cytokine:
• A category of chemicals released by certain white
blood cells when they detect the presence of an
invading microorganism; causes other white
blood cells to proliferate and mount an attack
against the invader.
• Stimulate cell division
• Neurotoxic