Definition

Anxiety is an emotional state commonly caused by

the perception of real or perceived danger that
threatens the security of an individual.
Anxiety can produce uncomfortable and potentially
debilitating psychologic (e.g., worry or feeling of
threat) and physiologic arousal (e.g., tachycardia or
shortness of breath) if it becomes excessive
EPIDEMIOLOGY
in the United States, the 1-year prevalence rate for
anxiety disorders was 18.1% in persons aged 18
years and older.
Specific phobias were the most common anxiety
disorder, with a 12- month prevalence of 8.7%.
The 1-year prevalence of generalized anxiety
disorder (GAD) was 3.1%, that of panic disorder was
2.7%, and that of social anxiety disorder (SAD) was
6.8%
ETIOLOGY
The differential diagnosis of anxiety disorders
includes medical and psychiatric illnesses and
certain drugs
PATHOPHYSIOLOGY
abnormal function in several neurotransmitter
systems, including norepinephrine (NE), -
aminobutyric acid (GABA), serotonin (5-HT),
 The amygdala, a temporal lobe structure, plays a
critical role in the assessment of fear stimuli and
learned response to fear. The locus ceruleus (LC),
located in the brain stem, is the primary NE-
containing site, with widespread projections to
areas responsible for implementing fear responses
(e.g., vagus, lateral and paraventricular
hypothalamus)
The hippocampus is integral in the consolidation of
traumatic memory and contextual fear
conditioning. The hypothalamus is the principal
area for integrating neuroendocrine and autonomic
responses to a threat
NEUROCHEMICAL THEORIES

Noradrenergic Model

GABA Receptor Model

Serotonin Model
Noradrenergic Model

The basic premise of the noradrenergic theory is

that the autonomic nervous system of anxious
patients is hypersensitive and overreacts to
various stimuli. Many anxious patients clearly
display symptoms of peripheral autonomic
hyperactivity.
In response to threat or fearful situations, the LC
serves as an alarm center, activating NE release
and stimulating the sympathetic and
parasympathetic nervous system
GABA Receptor Model
There are two superfamilies of GABA
protein receptors: GABA-A and GABA-B.
Drugs to reduce anxiety and produce
sedation target the GABA receptor
GABA, the major inhibitory
neurotransmitter in the CNS, has a strong
regulatory or inhibitory effect on the 5-HT,
NE, and dopamine (DA) systems.
When GABA binds to the GABA-A receptor,
neuronal excitability is reduced.
Serotonin Model
Although there are data suggesting that the 5-HT
system is dysregulated in patients with anxiety
disorders, definitive evidence that shows a clear
abnormality in 5-HT function is lacking. 5-HT is
primarily an inhibitory neurotransmitter that is used
by neurons originating in the raphe nuclei of the
brain stem and projecting diffusely throughout the
brain (e.g., cortex, amygdala, hippocampus, and
limbic system
1) GENERALIZED ANXIETY DISORDER
2) PANIC DISORDER
3) SOCIAL ANXIETY DISORDER
4) PHOBIC DISORDERS
5) OBSESSIVE-COMPULSIVE
DISOERDERS
6) POST TRAUMATIC DISORDERS
GENERALIZED ANXIETY DISORDER

The diagnostic criteria for GAD require

persistent symptoms for most days for at
least 6 months. The essential feature of
GAD is unrealistic or excessive anxiety
and worry about a number of events or
activities.
GAD has a gradual onset with an
average age of 21 years. Most patients
present between the ages of 35 and 45
years
 The majority of patients with GAD
eventually will develop another mental
disorder. GAD is usually the primary
disorder in patients with comorbid
anxious depression
PANIC DISORDER
Panic disorder begins as a series of
unexpected (spontaneous) panic attacks
involving an intense, terrifying fear similar
to that caused by life-threatening danger.
The unexpected panic attacks are followed
by at least 1 month of persistent concern
about having another panic attack, worry
about the possible consequences of the
panic attack, or a significant behavioral
change related to the attacks. During an
attack, patients describe at least four
physiologic and physical symptoms
 Because panic symptoms mimic those present in
several medical conditions, patients often are
misdiagnosed, and multiple referrals are common.

Panic disorder has an adverse impact on the

patients quality of life (QOL), including a
significant degree of social and work impairment.
Complications include depression (10% to 65%
have major depressive disorder), alcohol abuse,
and high use of health services and emergency
rooms. Patients with panic disorder have a high
lifetime risk for suicide attempts compared with the
general population
SOCIAL ANXIETY DISORDER
SAD is characterized by an intense, irrational, and
persistent fear of being negatively evaluated or
scrutinized in at least one social or performance
situation

Differentiating SAD from other anxiety disorders

can be difficult. Panic attacks occur in both SAD
and panic disorder, but the distinction between the
two is the rationale behind fear; fear of anxiety
symptoms is characteristic of panic disorder,
whereas fear of embarrassment from social
interaction typifies SAD
DESIRED OUTCOME
The goals of therapy in the acute
management of anxiety are to reduce
the severity and duration of the anxiety
symptoms and to improve overall
functioning.
The long-term goal in anxiety is
remission with minimal or no anxiety
symptoms, no functional impairment and
increased QOL
NONPHARMACOLOGIC THERAPY
Nonpharmacologic treatment modalities in
GAD include psychoeducation, short-term
counseling, stress management,
psychotherapy, meditation, or exercise
Psychoeducation includes information on
the etiology and management of GAD.
Anxious patients should be instructed to
avoid caffeine, nonprescription stimulants,
diet pills, and excessive use of alcohol
 Most patients with GAD require psychologic
therapy, alone or in combination with antianxiety
drugs, to overcome fears and to learn to manage
their anxiety and worry.

Cognitive behavioral therapy (CBT) is the most

effective psychologic therapy in GAD patients
Panic disorders
Patients should be educated to avoid substances
that can precipitate panic attacks, including
caffeine, drugs of abuse, and nonprescription
stimulants.

CBT is associated with short-term improvement in

80% to 90% of patients and 6-month improvement
in 75% of patients. A course of CBT for panic
disorder is 16 to 20 hours in length conducted over
a period of 4 months
SAD
Patients should be educated about SAD
and effective therapeutic options. Support
groups are helpful for some patients. Self-
help group programs that focus on effective
communication can benefit people with
public-speaking phobia
CBT for SAD consists of exposure therapy,
cognitive restructuring, relaxation training
techniques, and social skills training
EVALUATION OF
THERAPEUTIC OUTCOMES
Initially, anxious patients should be
monitored once every 2 weeks for a
reduction in the frequency, duration, and
severity of anxiety symptoms and
improvement in functioning
The clinician should assess the patient
for response to treatment by asking
about specific target symptoms of
anxiety and emergence of adverse
events
 If a patient has only a partial response,
the dose should be increased after 4 to
6 weeks of antidepressant therapy (or 2
weeks of acute therapy with
benzodiazepines)
The length of therapy should be
individualized, with some patients
requiring up to 1 year of antidepressant
therapy