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Anxiety Disorders - Article (long) - excellent overview, IMO

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Dec 16, 2003, 5:26:15 PM12/16/03
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For informational purposes only. Gain from this what you will.

Elliott

===========
Anxiety Disorders

M. Katherine Shear, M.D.

WebMD Scientific American® Medicine 2003.
Posted 12/08/2003
Introduction and Approach to Management
Introduction

Anxiety disorders are the most common mental disorders in the community. Anxiety
disorders include panic disorder, agoraphobia, specific phobia, social phobia,
generalized anxiety disorder, obsessive-compulsive disorder, and acute and
posttraumatic stress disorder. Shared features of these disorders are prominent
somatic symptoms, panic attacks, anticipatory worry or fear, and avoidance or
compulsive rituals. Persistent nagging health concerns are common and frequently
cause patients with these disorders to seek medical treatment, where their
anxiety disorders may go unrecognized. In addition to producing serious
impairment in functioning, anxiety disorders can worsen the course of medical
illnesses. Moreover, untreated anxiety symptoms lead to ineffective utilization
of health care resources. Anxiety disorders frequently occur together with
depression, a condition known to presage poorer medical outcomes. In addition to
their similarities, the anxiety disorders have distinct clinical and
neurobiologic features and typical presentations (see Table 1).
Approach to Management

Anxiety disorders are best managed through a systematic approach to diagnosis,
treatment, and, when necessary, referral. To facilitate accurate detection of
anxiety symptoms, physicians should be vigilant for the behavioral, physiologic,
and cognitive features of anxiety and know the key criteria for different
disorders. Anxiety disorders should be included in the differential diagnosis in
many cases of apparently medical illness.

When taking the history in a patient who may have an anxiety disorder, direct
and sensitive questioning is required. Phobic responses can be cognitive as well
as behavioral, leading patients to neglect to mention anxiety. Fear of stigma
may also lead to patient reticence.

Therapy for patients with anxiety can be initiated by the primary care physician
or, in some cases, by a consulting physician. It is a truism in medicine that
the first step in treatment is accurate diagnosis. Thus, upon recognition of
anxiety disorder symptoms, the physician should identify the condition and
provide the patient with information about its treatment and course. Such
information is readily available on the Internet (see Sidebar: Internet
Resources for Anxiety Disorders). In addition, information on panic disorders
can be obtained from the Institutes of Mental Health by calling 1-800-64-PANIC.

Treatment by physicians usually entails the use of medication. Although drug
treatment is certainly an appropriate intervention, the majority of patients
with anxiety disorder prefer nonpharmacologic treatment. Highly effective
cognitive-behavioral treatments are available. It is best if physicians discuss
treatment preferences with their patients and are prepared to provide
appropriate referrals if the patient so wishes.

When medications are used, effective management techniques include monitoring
patients' responses to treatment by using one or more target symptoms. General
rules for pharmacologic treatment of anxiety include the following: (1)
serotonin-active medications are effective for every disorder except specific
phobias, (2) patients with panic disorder are highly sensitive to medication, so
drugs should be started at a very low dose and gradually increased to a
therapeutic level, (3) barring adverse effects, a medication trial should be
continued for 4 weeks before one declares the agent ineffective and changes
medications, and (4) failure to respond to an initial trial of a selective
serotonin reuptake inhibitor (SSRI) does not mean that another agent of this
class will not work.

Referral to a mental health specialist is indicated for the following reasons:
(1) uncertainty about the diagnosis, (2) presence of multiple concomitant
psychiatric conditions, (3) acute suicidal ideation or a past history of serious
suicide attempt or other serious behavioral disturbances, and (4) failure to
respond to two trials of normally effective medications. Referral information is
available at many Web sites devoted to anxiety disorders (see Sidebar: Internet
Resources for Anxiety Disorders).

Panic Disorder with or without Agoraphobia

The pathognomonic feature of panic disorder is unexpected panic attacks, which
are characterized by sudden onset and rapid escalation of somatic symptoms
referable to the autonomic nervous system (e.g., chest pain, shortness of
breath, heart palpitations, and dizziness) along with fear or apprehension (see
Tables 1 and 2). Panic attacks typically last 10 to 20 minutes, but they can be
shorter. Persons with panic disorder have recurrent panic attacks; between
attacks, they are beset by fear of the attacks and their consequences or
implications. For example, the patient may believe that the panic attacks
reflect underlying heart disease or schizophrenia.

Agoraphobia is a fear of situations in which the person would feel trapped or
alone should a panic episode occur. Such situations typically include travel far
away from home, on public transportation, or via bridges or tunnels; crowded
places such as supermarkets, restaurants, theaters, churches, or shopping malls;
standing in line; and being alone. Agoraphobia is characterized by avoidance of
these situations. In its most severe form, sufferers can be housebound.
Epidemiology

The lifetime prevalence rates of panic disorder are about 3.5%.[1] Up to 10% of
the population experience sporadic panic attacks. Panic disorder is more common
in women and has an average-age-group onset of early adulthood. Persons with
panic disorder are at risk for developing major depression, with over half
meeting lifetime criteria for major depression.

Lifetime prevalence rates for agoraphobia are estimated at 6.7%, with a mean age
of onset of 29 years.[2] Agoraphobia can occur when the panic attacks include
frightening physical symptoms, such as those suggesting a medical disorder.
Pathophysiology

In laboratory studies, paniclike symptoms have been provoked with pharmacologic
agents such as carbon dioxide, sodium lactate, and cholecystokinin (CCK).
Several neurotransmitter systems have been implicated in these symptoms,
including serotonin (5-HT), norepinephrine, and G-aminobutyric acid (GABA),
along with the neuromodulatory CCK system. Theories involving 5-HT in panic
disorder focus on opposing actions in the dorsal raphe nucleus (DRN) and the
median raphe nucleus (MRN).[3] The MRN modulates fear and anticipatory anxiety,
along with autonomic symptoms of panic, whereas the DRN modulates the behavioral
aspects of panic, such as the fight-or-flight response. Both systems are
involved in a feedback loop that also includes the locus coeruleus and lateral
hypothalamus.[4]

Yohimbine, an a2-adrenergic antagonist, can trigger anxiety or panic in
susceptible patients,[5] which suggests that norepinephrine also has a role in
panic disorder. The locus coeruleus has projections to brain structures thought
to play a role in anxiety, including the amygdala, the bed nucleus of the stria
terminalis (BNST), the periaqueductal gray area (PAG), the paraventricular
nucleus of the hypothalamus, the lateral hypothalamus, and the nucleus of the
tractus solitarius (NTS). Norepinephrine projections from the locus coeruleus
also interact with corticotropin-releasing factor (CRF), which may play a role
in anxious responses to stress.[6]

GABA has been implicated in the pathophysiology of panic disorder, perhaps as a
nonspecific mechanism related to anxiety. Persons with panic disorder
demonstrate decreased GABA ligand binding in the right orbitofrontal cortex and
right insula.[7] Decreased platelet benzodiazepine receptor binding has also
been observed in patients with panic disorders and other anxiety disorders. On
magnetic resonance spectroscopy, patients with panic disorder have been shown to
have decreased GABA function and lower levels of GABA in the occipital
cortex.[8] GABA interacts with CCK in the amygdala, cortex, and hippocampus, and
this interaction has been postulated to play a role in mediating anxious states.

Other models focus on the ethologic roots of panic disorder. In his
false-suffocation alarm theory, Klein hypothesized a brain stem abnormality
causing dysregulation and heightened sensitivity to carbon dioxide. Respiratory
abnormalities have been consistently documented in patients with panic
disorder[9]; these patients exhibit unstable respiratory patterns and high
respiratory variability even when not experiencing panic.[10] The respiratory
stimulant doxapram induces panic in many patients with panic disorder, as well
as in some control subjects; a simple cognitive intervention can reduce the
panic response to doxapram. Decreased heart rate variability related to
decreased vagal tone has been documented in panic disorder.[11] Decreased vagal
tone may play a role in the migraine and irritable bowel syndrome associated
with some cases of panic disorder.[12]
Diagnosis

Clinical Features
Panic attack is diagnosed when at least four of 13 symptomatic criteria occur
unexpectedly and peak within 10 minutes (see Table 3). The diagnosis of panic
disorder requires recurrent panic attacks accompanied by significant worry or
concern about panic, its consequences or implications, or a change in usual
behavior.[13] Agoraphobia is diagnosed when the patient fears and avoids
situations in which escape would be difficult or help would be unavailable if a
panic attack were to occur.

Fear and hyperawareness of bodily sensations are hallmarks of panic
disorder.[14] These patients misinterpret benign bodily sensations (e.g.,
dizziness, palpitation) as indications of serious medical illness.

Presentation in Medical Settings
Persons with panic disorder are more likely to present for medical treatment
than for mental health treatment. The majority of cases of panic disorder seen
in primary care practices and emergency departments go unrecognized.[15,16]

Panic disorder has four common clinical presentations in general medicine: (1)
physical symptoms (e.g., heart palpitations, chest pain, shortness of breath,
gastrointestinal complaints, headache, dizziness), (2) anxiety and tension, (3)
hypochondriacal concerns, and (4) certain diagnosed medical conditions, such as
migraine, asthma, chronic obstructive pulmonary disease (COPD), and labile
hypertension.[17]

Panic disorder is often seen in patients referred for cardiologic complaints,
especially atypical chest pain or chest pain despite angiographically normal
coronary arteries. Patients with microvascular angina may have panic disorder.
Because of prominent cardiovascular symptoms during panic attacks, this disorder
should be considered in patients with intractable cardiac symptoms. Several
studies have shown that men with phobic anxiety are at higher risk of
cardiovascular mortality from fatal myocardial infarction and sudden cardiac
death.[18] Idiopathic clinical and subclinical cardiomyopathies have been
associated with panic disorder,[19] possibly related to increased adrenergic
activity. Panic attacks are associated with transient increased blood
pressure,[20] so this diagnosis should be considered in patients with labile
hypertension. Panic disorder has been found in about 16% of patients with
implantable cardioverter defibrillators.[21]

There is an association of respiratory illness with panic disorder. Patients
with asthma have a higher incidence of panic disorder, and the presence of panic
disorder predicts a poorer clinical course in asthma. A history of childhood
respiratory illness is more common in patients with panic disorder than in those
with other psychiatric disorders.[22] In adults, COPD is associated with panic
disorder.

Panic disorder is frequently associated with other mood and anxiety disorders.
Prognosis is poorer in such cases.
Treatment

Pharmacotherapy
Drug therapy can be markedly effective for patients with panic disorder (see
Table 4). However, the fear of bodily sensations in these patients may lead to
difficulty taking medications, medication refusal, or poor adherence to
prescribed medicine. Many patients with panic disorder believe they are allergic
to medication. Physicians should convey understanding of this medication
sensitivity. Whenever possible, medication for any purpose should be started at
a very low dosage and then gradually increased. This is especially important
when using medication to treat the panic disorder itself. If the initial dose is
too high, the patient may not tolerate the medication and a potentially
effective treatment will be rendered useless. There is a psychological
intervention of proven efficacy for fear of bodily sensations, so referral
should be considered for patients in whom this fear complicates drug therapy.

Imipramine. A tricyclic antidepressant with serotoninergic activity, imipramine
was the first medication used for panic disorder. This drug has well-documented
efficacy in controlling panic disorder and can prevent relapse with continued
use.[23] The efficacy and tolerability of imipramine are similar to those of
SSRIs, so patients who are responding well to imipramine need not necessarily be
switched to an SSRI. However, most experts now start drug therapy for panic
disorder with an SSRI.

Selective serotonin reuptake inhibitors. SSRIs are the first-line
pharmacotherapy for panic disorder. Every medication in this class has been
proved effective. The Food and Drug Administration has approved paroxetine and
sertraline for use in panic disorder, but citalopram, fluoxetine, and
fluvoxamine also have well-documented beneficial effects[24] that are often
lasting, even after discontinuance of the medication. However, several studies
with different SSRIs show that continuing the medication for up to 80 weeks
lowers relapse rates. There is a tendency for side effects to decrease over
time.[25] Different SSRIs have different chemical structures and somewhat
different side-effect profiles, so patients who do not respond to one agent or
who fail to tolerate it may do well on a different drug in this class. Standard
practice dictates trying several SSRIs before moving to another class of
medication.

Other antidepressants. Antidepressants with mixed neurotransmitter effects, such
as venlafaxine or mirtazapine, can be used to treat panic disorder. It is less
clear whether selective noradrenergically active medications are effective for
panic disorder. Studies of nortriptyline suggest it may be therapeutic. Studies
of bupropion have showed mixed results. Reboxetine has demonstrated efficacy in
the treatment of panic disorder.

Benzodiazepines. Although benzodiazepines are not first-line agents for the
treatment of panic disorder, they provide relief for some patients who do not
respond to other medications. Alprazolam is approved by the FDA for the
treatment of panic disorder; clonazepam and lorazepam also have proven efficacy.
When used, benzodiazepines should be prescribed on a daily basis rather than on
an as-needed basis.

Many physicians are wary of prescribing benzodiazepines because these agents are
potentially addictive. Certainly, benzodiazepines should be avoided if possible
in patients with a personal or family history of alcohol or substance-abuse
disorders. Patients without such a history are unlikely to abuse
benzodiazepines, however.

Discontinuance of a benzodiazepine should be accomplished by very slow tapering.
In patients who have difficulty being weaned from the drug, cognitive-behavioral
therapy can be used to promote discontinuance.[26]

Psychological Treatment
Targeted cognitive-behavioral psychotherapy is as effective as medication in
treating panic disorder.[27] Gains are maintained at 1-year follow-up, and a
naturalistic follow-up study found that in some cases, the effects endured for
as long as 14 years after treatment. A brief psychological intervention in the
emergency department can reduce future visits by panic disorder patients.[28]
Simple instructions advising patients not to avoid situations in which they
experienced panic or feared the onset of panic, along with educational support
about panic disorder, is helpful in an emergency setting.

When to Refer
Most cases of panic disorder, with or without agoraphobia, respond readily to
drug therapy or targeted cognitive-behavioral treatment. Referral to a
psychiatrist is indicated for patients whose panic disorder is relatively
treatment resistant, those with comorbid depression (especially bipolar illness)
or other psychological disorders, and those who are suicidal.
Complications

In part because clinicians fail to recognize the condition, persons with panic
disorder are heavy utilizers of health care services and have significant
disability, with high rates of unemployment and substance abuse.[29] Panic
disorder is associated with suicide risk, even in the absence of concomitant
depression.

Acute and Posttraumatic Stress Disorders

Acute and posttraumatic stress disorders (ASD and PTSD) are conditions that
follow exposure to violence. ASD is diagnosed up to 4 weeks after a traumatic
episode. PTSD is a highly debilitating condition that is not apparent until at
least 1 month after trauma exposure.
Epidemiology

Lifetime exposure to violence is common in the general population. In a recent
large United States survey, 51% of women and 61% of men reported having a
traumatic experience at some time in their lives.[30] Lifetime prevalence rates
for PTSD are estimated at 7.8%, with women twice as likely to have the disorder
as men (10.4% versus 5.0%). Approximately 9% to 25% of persons who experience a
trauma eventually develop posttraumatic stress symptoms. Nearly 80% of those
with ASD subsequently develop PTSD, compared with only 4.3% of persons who
experience a trauma but do not qualify for an ASD diagnosis.
Pathophysiology

Acute stress stimulates the hypothalamic-pituitary-adrenal (HPA) axis, leading
to secretion of CRF and adrenocorticotropic hormone (ACTH). Increased levels of
CRF have been found in the cerebrospinal fluid of patients with PTSD, as
compared with CSF levels in control subjects.[31] Chronic stress has been shown
to suppress development of granule neurons in the dentate gyrus of the
hippocampus,[32] and patients with chronic PTSD have lower hippocampal volumes
than control subjects[33]; this may result in reduced hippocampal inhibition of
CRF. Increased CRF secretion then leads to greater CRF interaction with
noradrenergic projections from the locus coeruleus, producing further increases
in both CRF and norepinephine. Locus coeruleus activity increases with chronic
uncontrollable stress. Patients with PTSD have higher urinary norepinephrine and
epinephrine levels than nonanxious control subjects, and urinary catecholamine
levels correlate with intrusive recollection of trauma in combat veterans.[34]
Catecholamines are responsible for alertness and vigilance, and sympathetic
arousal enhances memory encoding.

Alterations in benzodiazepine receptors may contribute to PTSD. Reduction in
peripheral benzodiazepine receptor density has been documented in combat
veterans with PTSD, and a single-photon emission computed tomography (SPECT)
study showed reduced affinity for benzodiazepine receptor binding in the
prefrontal cortex. On functional MRI studies, PTSD patients have an exaggerated
amygdala response to threatening stimuli.[35]
Diagnosis

Clinical Features
Diagnostic criteria for PTSD include exposure to an event that posed a risk of
death or serious physical injury, along with subsequent symptoms that cluster in
three areas: (1) reexperiencing the event (e.g., recurrent thoughts, images,
dreams, illusions, and flashback episodes), (2) avoidance of trauma reminders,
and (3) arousal (e.g., restlessness, insomnia, hypervigilance, difficulty
concentrating, and irritability). Dissociative symptoms (e.g., numbing or
detachment, reduced awareness of surroundings, depersonalization, derealization,
and dissociative amnesia) may also be present, especially in the early period
after a trauma. These reactions are predictive of PTSD, as is increased heart
rate during the acute-trauma phase.

Presentation in Medical Settings
Evidence suggests that a patient with PTSD is more likely to present for
treatment in a primary care setting than in a mental health setting. However,
primary care physicians recognize anxious symptoms in these patients only about
50% of the time and often fail to make the diagnosis.[36]

Patients who present to a trauma or emergency service are at risk for PTSD, as
are combat veterans and victims of rape or domestic violence. Frightening or
painful medical illness or procedures also can trigger PTSD. Assisted
ventilation for acute respiratory distress syndrome, cardiac defibrillation,
cardiac and lung transplantation,[37] cancer diagnosis or treatment,[38]
stillbirth,[39] and patient awareness during surgical procedures because of
inadequate anesthesia[40] have all reportedly triggered PTSD. It is likely that
any life-threatening medical event (e.g., cardiac arrest, diabetic coma,
myocardial infarction, pulmonary embolism, or massive organ failure) could
trigger these symptoms, especially in patients with a history of anxiety or
depressive illness.

Physicians and other medical staff in the emergency department should provide
patients with support and information about PTSD in the early aftermath of
trauma; such measures can help with quick recognition of the disorder if it
should develop. Early recognition may prevent the development of full-blown PTSD
and its negative consequences for illness course.
Treatment

Acute Stress Disorder
No pharmacologic treatment has proved effective in acute stress disorder,
although beta blockers are currently under investigation. Studies of
cognitive-behavioral therapy in patients with acute stress disorder suggest that
it might prevent PTSD in patients who have experienced trauma and seem to be
struggling with their reaction to the event.[41]

Posttraumatic Stress Disorder
Pharmacotherapy. SSRIs are effective in the treatment of PTSD. Sertraline and
paroxetine have FDA approval for this indication: studies of sertraline show
about a 50% reduction in symptoms in each symptom cluster, and response rates
with paroxetine range from 54% to 62%. As with other anxiety disorders, however,
every SSRI tested has been found to work. At least one study showed nefazodone
to be helpful.

Psychological treatment. An intensive form of cognitive-behavioral therapy that
requires patients to imagine themselves being exposed to the traumatic event is
highly effective for rape-related PTSD.[41] This technique produces significant
reduction in all symptom clusters of the disorder in most patients. The
limitations of the treatment are that it requires a skilled therapist and
courage on the part of the patient. However, if a qualified therapist is
available and the patient is willing to participate, cognitive-behavioral
therapy is the treatment of choice.
Complications

Traumatic stress reactions are associated with debilitating psychosocial and
physical impairment,[42] including increased length of hospital stay for medical
conditions, independent of severity of medical illness or medical comorbidity.
PTSD also contributes to prolongation of recovery from medical illness. PTSD is
associated with nonadherence to medication regimens after myocardial
infarction[43] and independently predicts mortality in heart transplant
patients. PTSD frequently coexists with substance-abuse disorder or mood
disorder.

Generalized Anxiety Disorder

The defining characteristic of generalized anxiety disorder (GAD) is persistent,
excessive, and uncontrollable worry about everyday life situations. GAD can be
highly debilitating and may predispose to the development of other mood or
anxiety disorders.[44]
Epidemiology

Lifetime prevalence rates of GAD range from 4% to 7%, with nearly a 10%
prevalence in women older than 40 years.[45] Onset is sometimes early in life
but is also common in middle to late adulthood, with a large increase in
incidence at 35 to 45 years of age. Once established, GAD often becomes a
chronic condition lasting 20 years or longer. GAD is the most common anxiety
disorder in the elderly.
Pathophysiology

Patients with GAD exhibit reductions in heart rate variability. Heart rate
variability-as measured by beat-to-beat changes in the R-R interval on ECG-is
considered a measure of autonomic nervous system function, reflecting the net
effect of sympathetic versus parasympathetic (vagal) stimulation. In studies of
heart rate variability during experimentally induced periods of worry and
periods of calmness, normal control subjects had lower heart rate variability
during periods of worry than during periods of calmness, whereas patients with
GAD showed little change in variability between the two states. Although
worrying is potentially adaptive if it is specific and limited to problem
solving, chronic emotional restraint and inhibition could lead to a reduced
range in physiologic response in persons with GAD.[46]

Muscle tension is a criterion symptom for GAD. Electromyographic activity
correlates with right hemispheric brain activity in patients with GAD,
suggesting that right hemisphere activity may control muscle tension symptoms in
this population.[47] The muscle tension in GAD patients does not reflect
autonomic arousal, however; rather, GAD is characterized by decreased autonomic
arousal and activity.[46] GAD patients react to stressors with less autonomic
flexibility than nonanxious control patients do and have inaccurate perceptions
of physiologic changes.

SPECT and MRI studies show decreased benzodiazepine receptor binding in the left
temporal pole in patients with GAD.[48] Vagally mediated heart rate variability
is positively correlated with blood flow to the medial prefrontal cortex during
emotional processing tasks.[49]
Diagnosis

Clinical Features
Worry is the key pathognomonic feature of GAD. Other diagnostic features include
restlessness, fatigue, irritability, difficulties with concentration, muscle
tension, and insomnia. The diagnosis of GAD is made when patients report at
least 6 months of persistent worry accompanied by at least three of these
associated clinical features.

Presentation in Medical Settings
GAD is the most common anxiety disorder seen in primary care settings,[50] often
presenting as sleep disturbance or somatic symptoms such as muscle aches and
tension headaches.[51] GAD is associated with chronic medical conditions, poor
general health, frequent hospital admissions, and high health care costs and
utilization.[52] Like other anxiety disorders, GAD often goes undiagnosed and
untreated, especially when accompanied by physical illness. GAD patients are as
likely to seek treatment from a cardiologist as are patients with panic
disorder.[53]
Treatment

Pharmacotherapy
The FDA has approved venlafaxine for use in GAD, and most experts consider this
agent to be the first-line treatment. Venlafaxine also relieves anxious and
depressive symptoms in GAD patients with comorbid major depressive disorder.
SSRIs have also been found to be effective in GAD.[54]

Benzodiazepines have been used to treat GAD, and at least one study suggests
that their use does not lead to tolerance.[55] However, these drugs are
generally not used as first-line treatment. Many patients with GAD also have
depression, which benzodiazepines do not relieve.

Psychological Treatment
Cognitive-behavioral therapy for GAD has been less well studied than that for
other anxiety disorders.[56] However, this approach appears promising. An
intervention that targets worry has shown good results that were maintained at
6-month and 12-month follow-up. Because of the chronic nature of GAD, the
efficacy of combining psychodynamic therapy with cognitive-behavioral techniques
has been suggested, and a preliminary evaluation of psychodynamic treatment of
GAD found positive results. A randomized trial of integrated interpersonal and
cognitive-behavioral therapy, which is currently under way, suggests improved
efficacy over either therapy alone.

Social Anxiety Disorder (Social Phobia)

Social phobia, or social anxiety disorder, is characterized by fear or avoidance
of negative evaluation by others. Patients with this condition expect
embarrassment or humiliation in a wide range of social encounters. Social phobia
may occur in a specific form, with fear of one situation (most often, public
speaking), or in a generalized form that is debilitating and chronic.
Epidemiology

In large, community-based studies, the lifetime prevalence of social phobia
ranges from 7.2% to 9.5%.[57] The disorder is more common in women, normally
begins in adolescence or early adulthood, and is characterized by a chronic
course. One study suggests that only 30% of patients experience remission.[58]
Pathophysiology

A recent review posits some interesting possibilities for amygdala involvement
in social behavior and social anxiety, suggesting that study of social primates,
such as the macaque, may be informative for human anxiety.[59] Hypothetically,
the amygdala may act as a behavioral brake mechanism, functioning to support
adaptive evaluation of a novel situation. Social or other anxiety disorders may
be associated with enhanced braking and, consequently, too little exposure and
learning. A recent study of functional MRI in patients with social phobia has
extended this idea by showing that these patients are hypersensitive to human
facial displays of emotion, particularly anger, threat, or fear, and exhibit
exaggerated amygdala responses to such facial expressions.[60] Patients with
generalized social phobia have also been found to have low density of platelet
peripheral benzodiazepine receptors, as occurs in other anxiety disorders.
Diagnosis

Clinical Features
Persons with social phobia have persistent fear or avoidance of situations in
which they expect to be scrutinized by others or to do something that is
humiliating or embarrassing. Common examples are public speaking, eating in
restaurants, writing in public (e.g., signing checks or sales slips), urinating
in public bathrooms, talking with people in authority, or conversing in other
situations of scrutiny, such as parties or social gatherings. Generalized social
phobia can be very debilitating, because the person has persistent fear of
almost any social situation, including speaking to a supervisor or teacher or
even a physician, going to parties, or asking for assistance.

Persons with social phobia have a tendency toward negative interpretation of
social events, self-focused attention, and negative-outcome-based cognitive
processes (e.g., rumination and anticipatory anxiety). They have a memory bias
for negative emotions in others' faces and expressions.[61] Normal individuals
tend to blame negative social interactions on others while taking credit for
positive experiences. Persons with social phobia often reverse this so-called
self-serving bias, blaming themselves for negative experiences and crediting
others when interactions are positive.[62]

Presentation in Medical Settings
A person with social phobia who fears urinating in a public bathroom can present
with urinary retention. I have treated such a patient, who was serving in the
military and thus had minimal privacy, and whose urinary retention was so severe
that it resulted in hospitalization. Although there are few specific
presentations of social phobia in medical settings, physicians should be alert
to this condition. As is the case with other anxiety disorders, persons with
social phobia frequent primary care settings[63] and are often not
diagnosed.[64] A recent study found that only 2% of persons with social phobia
who present to primary care clinicians are diagnosed and that fewer are
effectively treated.[65]
Treatment

Pharmacotherapy
SSRIs are first-line pharmacotherapy for social phobia. Paroxetine and
sertraline have FDA approval, but other SSRIs are also effective. Paroxetine
response rates range from 55% to 70%. Fluvoxamine and sertraline response rates
are similar.

High-potency benzodiazepines, especially clonazepam, are effective in the
treatment of social phobia. Although benzodiazepines are not first-line
treatment for social phobia, they can be a highly useful tool in the treatment
of this disorder. Monoamine oxidase inhibitors are effective but are rarely used
because of the risk of hypertensive crisis and the availability of other, less
toxic choices.

Psychological Treatment
Cognitive-behavioral treatments are effective in social phobia,[66] although the
disorder presents some special challenges for this approach. Several successful
strategies have been developed and tested.[67] As with all the anxiety
disorders, delivery of this treatment requires special training and expertise.
Complications

Social phobia is one of the most disabling anxiety disorders, because it can
affect virtually every area of potential achievement. Patients with social
phobia tend to have less education, lower occupational functioning, and lower
health-related quality of life; and they utilize health care resources
significantly more than nonanxious persons.[68] Comorbid mood disorders, other
anxiety disorders, and substance-abuse disorders are common. Patients with
social phobia are as likely to commit or attempt suicide as patients with major
depressive disorder.

Obsessive-Compulsive Disorder

Obsessive-compulsive disorder (OCD) is characterized by repeated intrusive
thoughts, ideas, or images (obsessions) and by repeated ritualistic behaviors
(compulsions). Afflicted persons recognize the irrationality of their thoughts
but are powerless to control them. Similarly, compulsive rituals are seen as
senseless but frequently take many hours a day to perform. Obsessions have
stereotyped content involving fear of contamination or aggression, persistent
doubting, increased religiosity, or the need for symmetry. Associated
compulsions often entail cleaning, checking, touching, or counting or other
mental activities.
Epidemiology

OCD is relatively rare in comparison with other anxiety disorders, but it can be
one of the most debilitating of psychiatric disorders. The estimated lifetime
prevalence is approximately 1% to 3%, with monthly prevalence ranging from 0.6%
to 3.3%. Mean age of onset is 24 years. The disorder is often chronic, lasting
up to 40 years.[69]
Pathophysiology

There is converging evidence for abnormal activity in the orbitofrontal
basal-ganglia thalamocortical circuit in patients with OCD.[70] Positron
emission tomography (PET) in these patients has shown that improvement after
treatment with an SSRI is associated with decreased metabolism in the right
caudate and putamen, the bilateral orbitofrontal cortex and thalamus, and parts
of the prefrontal cortex. Functional MRI scans show increased metabolism in
frontal subcortical regions after clinical improvement.

A possible autoimmune etiology of OCD has recently been suggested. The antibody
D8/17, which is found in rheumatic fever and Sydenham chorea, is elevated in
patients with OCD and Tourette syndrome; this elevation predicts larger basal
ganglia volume. In childhood, OCD sometimes occurs as a poststreptococcal
syndrome known as PANDAS (pediatric autoimmune neuropsychiatric disorders
associated with streptococcal infections).[71]
Diagnosis

Clinical Features
OCD is diagnosed when obsessions, compulsions, or both are present for at least
1 hour a day or present at a level that interferes with functioning. Chronicity
is the rule, although symptoms may change in focus over time.

Presentation in Medical Settings
A patient with OCD may present to any of several types of specialists, depending
on the form the disorder takes. Approximately half of OCD patients partake in
washing compulsions[72] in response to obsessive fears relating to germs and
contamination. Repetitive hand washing is associated with increased risk for
nonspecific dermatitis, which can result in these patients seeking dermatologic
treatment.[73] OCD patients may also be seen by dermatologists for excoriation,
or excessive picking and scratching of the skin. Those patients with
contamination obsessions may present for treatment at an infectious disease
practice as a result of their irrational fears.[73] OCD patients may be seen by
rheumatologists for physical symptoms resulting from somatization. Many of those
with contamination fears are hypochondriacal, fearing a wide range of illnesses.
The result is increased utilization of health care resources and time spent with
physicians. Primary care physicians may encounter patients with OCD. However,
many patients with OCD feel considerable shame about their disorder and may be
reluctant to reveal its existence. Like other psychiatric conditions, OCD is
clinically recognized by primary care physicians in only 10% to 30% of cases.
Treatment

Pharmacotherapy
Serotonin-active antidepressants are the clear first-line pharmacotherapy for
OCD. Clomipramine, a serotonin-active tricyclic antidepressant, was the first
drug to receive FDA approval for treatment of OCD. Nearly 60% of patients
improve substantially with clomipramine, compared with only 3% of those persons
who receive placebo. Fluoxetine, sertraline, fluvoxamine, paroxetine, and
citalopram have demonstrated comparable degrees of efficacy and tolerability in
the treatment of OCD.[74]

Psychological Treatment
Cognitive-behavioral therapy focusing on exposure and response prevention is
highly effective for OCD,[75] with over 85% of participants demonstrating
clinical improvement in the hands of experts. Adding clomipramine therapy to
cognitive-behavioral therapy does not result in improved outcome, whereas the
addition of cognitive-behavioral therapy to pharmacotherapy does improve
outcome. However, OCD patients with significant comorbid depression might
benefit from SSRI treatment before beginning cognitive-behavioral therapy.
Complications

OCD is associated with significant social and occupational impairment,
unemployment, and burden to family members.[76]

Specific Phobia in Medical Settings

Specific phobias are irrational fears, usually accompanied by avoidance of the
feared stimulus. Physicians should be especially aware of phobias regarding
blood and injections. Patients with such phobias may have syncopal episodes on
exposure to blood or even to hypodermic needles. Because of their phobias, these
patients may avoid obtaining needed tests or even seeking proper medical care;
this can result in serious illnesses going undiagnosed and untreated.

Patients with blood-injury phobia may experience significant emotional distress
if the medical staff is dismissive or unsympathetic about this problem.
Blood-injury phobia differs from other anxiety and phobic reactions in that
heart rate slows, rather than accelerates, on exposure to the phobic stimulus.
These patients often have a family history of this condition, and it is
considered to be a neurobiologic illness rather than a deficit in self-control.
Studies document that short-term treatment for blood-injury phobia can be
accomplished by trained therapists. Patients who receive effective treatment
experience tremendous relief.

Other medically relevant phobias include dental phobia and phobia of childbirth
(also called tokophobia). Persons with dental phobia experience extreme
apprehension and may avoid dental treatment completely. Psychological
intervention in the form of one-session exposure and stress management can be
effective. Fear of childbirth can also be a clinically significant condition. At
times, it may be so intense that a woman terminates a pregnancy, despite a
desire to have children. Even in its milder form, this condition causes
considerable emotional distress during pregnancy, and it is desirable to reduce
such distress for the benefit of both mother and fetus. Again, referral to a
trained therapist is indicated in such cases. No pharmacotherapy has proved
effective, but cognitive-behavioral treatments are simple and beneficial.

For more information, visit tellme.

setup to WebMD Scientific American® Medicine.

Tables
Table 1. Key Symptoms of Anxiety Disorders

Disorder Symptoms
Panic disorder Recurrent unexpected panic attacks; fear of panic or its
consequences
Agoraphobia Fear and avoidance of places where it may be difficult to get help
or easily leave (e.g., bridges, tunnels, restaurants, supermarkets, public
transportation)
Posttraumatic stress disorder Exposure to a life-threatening or physically
threatening event, followed by (1) disturbing images, flashbacks, nightmares;
(2) avoidance of trauma reminders; (3) hyperarousal (e.g., easy startle,
irritability, difficulty concentrating, insomnia)
Generalized anxiety disorder Excessive uncontrollable worries about everyday
things; fatigue, muscle tension, insomnia; restlessness, irritability,
difficulty concentrating
Social phobia Fear and avoidance of specific social situations (e.g., fear of
urinating in public bathrooms, fear of eating in restaurants, fear of public
speaking) or social situations in general
Obsessive-compulsive disorder Repeated intrusive throughts, impulses, or images,
recognized as irrational; compulsive ritualistic behaviors such as cleaning or
checking
Specific phobias Fear and avoidance of a specific place, activity, or situation
(e.g., fear of blood or needles, fear of dental procedures, fear of childbirth)

Table 2. Conditions Commonly Confused with Anxiety Disorders

Disorder Conditions
Panic disorder Heart palpitations, mitral valve prolapse, cardiac arrhythmias,
hyperthyroidism, irritable bowel syndrome, migraine
Posttraumatic stress disorder Insomnia, substance use disorders, unexplained
fears of medical procedures, or unexplained worsening of course of medical
illness
Generalized anxiety disorder Insomnia, migraine or tension headaches,
hypertension, peptic ulcer disease, irritable bowel syndrome
Social phobia Unexplained urinary retention, academic or occupational
underachievement, mood disorders, substance use disorders
Obsessive-compulsive disorder Tourette syndrome, other tic disorders, pediatric
autoimmune neuropsychiatric disorders associated with streptococcal infections
(PANDAS), excoriative dermatitis, unexplained fears of illness

Table 3. Diagnostic Criteria for Panic Attack*

Palpitations, pounding heart, or accelerated heart rate
Sweating
Trembling or shaking
Sensations of shortness of breath or smothering
Feeling of choking
Chest pain or discomfort
Nausea or abdominal distress
Feeling dizzy, unsteady, light-headed, or faint
Derealization (feelings of unreality) or depersonalization (being detached from
oneself)
Fear of losing control or going crazy
Fear of dying
Paresthesias
Chills or hot flushes

Table 4. FDA-Approved Drugs for Anxiety Disorders

Disorder Drugs Daily Dosages
Starting Target
Panic disorder Imipramine 10-25 mg 150-200 mg
Paroxetine 10 mg 10-60 mg
Sertraline 25-50 mg 50-200 mg
Alprazolam 0.25-0.50 mg b.i.d. or t.i.d. 0.5-2.0 mg b.i.d. or t.i.d.
Posttraumatic stress disorder Sertraline 50 mg 50-200 mg
Paroxetine 10 mg 10-60 mg
Generalized anxiety disorder Venlafaxine 75 mg in two or three divided doses
150-300 mg in two or three divided doses
Social anxiety disorder (social phobia) Paroxetine 10-20 mg 10-60 mg
Sertraline 50 mg 50-200 mg
Obsessive-compulsive disorder Clomipramine 25-50 mg 150-300 mg
Fluoxetine 5-10 mg 20-80 mg
Fluvoxamine 50 mg h.s. 100-300 mg in two divided doses
Paroxetine 10-20 mg 40-60 mg

References

1. Kessler RC, McGonagle KA, Zhao S, et al: Lifetime and 12-month prevalence of
DSM-III-R psychiatric disorders in the United States: results from the National
Comorbidity Survey. Arch Gen Psychiatry 51:8, 1994 [PMID 8279933]
2. Magee WJ, Eaton WW, Wittchen HU, et al: Agoraphobia, simple phobia, and
social phobia in the National Comorbidity Survey. Arch Gen Psychiatry 53:159,
1996 [PMID 8629891]
3. Bourin M, Baker GB, Bradwejn J: Neurobiology of panic disorder. J Psychosom
Res 44:163, 1998 [PMID 9483472]
4. Coplan JD, Lydiard RB: Brain circuits in panic disorder. Biol Psychiatry
44:1264, 1998 [PMID 9861469]
5. Sullivan GM, Coplan JD, Kent JM, et al: The noradrenergic system in
pathological anxiety: a focus on panic with relevance to generalized anxiety
disorder and phobias. Biol Psychiatry 46:1205, 1999 [PMID 10560026]
6. Abelson JL, Glitz D, Cameron OG, et al: Endocrine, cardiovascular, and
behavioral responses to clonidine in patients with panic disorder. Biol
Psychiatry 32:18, 1992 [PMID 1391293]
7. Malizia AL, Cunningham VJ, Bell CJ, et al: Decreased brain
GABA(A)-benzodiazepine receptor binding in panic disorder: preliminary results
from a quantitative PET study. Arch Gen Psychiatry 55:715, 1998 [PMID 9707382]
8. Marazziti D, Rotondo A, Martini C, et al: Changes in peripheral
benzodiazepine receptors in patients with panic disorder and
obsessive-compulsive disorder. Neuropsychobiology 29:8, 1994 [PMID 8127425]
9. Sinha S, Papp LA, Gorman JM: How study of respiratory physiology aided our
understanding of abnormal brain function in panic disorder. J Affective Disord
61:191, 2000
10. Abelson JL, Weg JG, Nesse RM, et al: Persistent respiratory irregularity in
patients with panic disorders. Biol Psychiatry 49:588, 2001 [PMID 11297716]
11. McCraty R, Atkinson M, Tomasino D, et al: Analysis of twenty-four hour heart
rate variability in patients with panic disorder. Biol Psychol 56:131, 2001
[PMID 11334700]
12. Walker EA, Gelfand AN, Gelfand MD, et al: Psychiatric diagnoses, sexual and
physical victimization, and disability in patients with irritable bowel syndrome
or inflammatory bowel disease. Psychol Med 25:1259, 1995 [PMID 8637955]
13. Diagnostic and Statistical Manual of Mental Disorders (DSM IV). American
Psychiatric Association: Washington, DC, 1994
14. Schmidt NB, Lerew DR, Jackson RJ: Prospective evaluation of anxiety
sensitivity in the pathogenesis of panic: replication and extension. J Abnorm
Psychol 108:532, 1999 [PMID 10466277]
15. Ballenger JC, Davidson JR, Lecrubier Y, et al: Consensus statement on panic
disorder from the International Consensus Group on Depression and Anxiety. J
Clin Psychiatry 59(suppl 8):47, 1998
16. Yingling KW, Wulsin LR, Arnold LM, et al: Estimated prevalences of panic
disorder and depression among consecutive patients seen in an emergency
department with acute chest pain. J Gen Intern Med 8:231, 1993 [PMID 8505680]
17. Zaubler TS, Katon W: Panic disorder in the general medical setting. J
Psychosom Res 44:25, 1998 [PMID 9483462]
18. Kawachi I, Colditz GA, Ascherio A, et al: Prospective study of phobic
anxiety and risk of coronary heart disease in men. Circulation 89:1992, 1994
[PMID 8181122]
19. Kahn JP, Drusin RE, Klein DF: Idiopathic cardiomyopathy and panic disorder:
clinical association in cardiac transplant candidates. Am J Psychiatry 144:1327,
1987 [PMID 3310671]
20. Shear MK, Kligfield P, Harshfield G, et al: Cardiac rate and rhythm in panic
patients. Am J Psychiatry 144:633, 1987
21. Godemann F, Ahrens B, Behrens S, et al: Classic conditioning and
dysfunctional cognitions in patients with panic disorder and agoraphobia treated
with an implantable cardioverter/defibrillator. Psychosom Med 63:231, 2001 [PMID
11292270]
22. Zandbergen J, Bright M, Pols H, et al: Higher lifetime prevalence of
respiratory disease in panic disorder? Am J Psychiatry 148:1583, 1991 [PMID
1928478]
23. Mavissakalian MR, Perel JM: 2nd year maintenance and discontinuation of
imipramine therapy in panic disorder with agoraphobia. Ann Clin Psychiatry
13:63, 2001 [PMID 11534926]
24. Otto MW, Tuby KS, Gould RA, et al: An effect-size analysis of the relative
efficacy and tolerability of serotonin selective reuptake inhibitors for panic
disorder. Am J Psychiatry 158:1989, 2001 [PMID 11729014]
25. Rapaport MH, Wolkow R, Rubin A, et al: Sertraline treatment of panic
disorder: results of a long-term study. Acta Psychiatr Scand 104:289, 2001 [PMID
11722304]
26. Bruce TJ, Spiegel DA, Hegel MT: Cognitive-behavioral therapy helps prevent
relapse and recurrence of panic disorder following alprazolam discontinuation: a
long-term follow-up of the Peoria and Dartmouth studies. J Consult Clin Psychol
67:151, 1999 [PMID 10028220]
27. Barlow DH, Gorman JM, Shear MK, et al: Cognitive-behavioral therapy,
imipramine, or their combination for panic disorder: a randomized controlled
trial. JAMA 283:2529, 2000 [PMID 10815116]
28. Dyckman JM, Rosenbaum RL, Hartmeyer RJ, et al: Effects of psychological
intervention on panic attack patients in the emergency department.
Psychosomatics 40:422, 1999 [PMID 10479947]
29. Leon AC, Portera L, Weissman MM: The social costs of anxiety disorders. Br J
Psychiatry Suppl (27):19, 1995
30. Kessler RC, Sonnega A, Bromet E, et al: Posttraumatic stress disorder in the
National Comorbidity Survey. Arch Gen Psychiatry 52:1048, 1995 [PMID 7492257]
31. Bremner JD, Licinio J, Darnell A, et al: Elevated CSF
corticotropin-releasing factor concentrations in posttraumatic stress disorder.
Am J Psychiatry 154:624, 1997 [PMID 9137116]
32. Gould E, Tanapat P: Stress and hippocampal neurogenesis. Biol Psychiatry
46:1472, 1999 [PMID 10599477]
33. Bremner JD, Randall P, Vermetten E, et al: Magnetic resonance imaging-based
measurement of hippocampal volume in posttraumatic stress disorder related to
childhood physical and sexual abuse-a preliminary report. Biol Psychiatry 41:23,
1997
34. Yehuda R, Southwick S, Giller EL, et al: Urinary catecholamine excretion and
severity of PTSD symptoms in Vietnam combat veterans. J Nerv Ment Dis 180:321,
1992 [PMID 1583475]
35. Rauch SL, Whalen PJ, Shin LM, et al: Exaggerated amygdala response to masked
facial stimuli in posttraumatic stress disorder: a functional MRI study. Biol
Psychiatry 47:769, 2000 [PMID 10812035]
36. Taubman-Ben-Ari O, Rabinowitz J, Feldman D, et al: Post-traumatic stress
disorder in primary-care settings: prevalence and physicians' detection. Psychol
Med 31:555, 2001 [PMID 11305864]
37. Dew MA, Kormos RL, DiMartini AF, et al: Prevalence and risk of depression
and anxiety-related disorders during the first three years after heart
transplantation. Psychosomatics 42:300, 2001 [PMID 11496019]
38. Mundy EA, Blanchard EB, Cirenza E, et al: Posttraumatic stress disorder in
breast cancer patients following autologous bone marrow transplantation or
conventional cancer treatments. Behav Res Ther 38:1015, 2000 [PMID 11004740]
39. Turton P, Hughes P, Evans CD, et al: Incidence, correlates and predictors of
post-traumatic stress disorder in the pregnancy after stillbirth. Br J
Psychiatry 178:556, 2001 [PMID 11388974]
40. Osterman JE, Hooper J, Heran WJ, et al: Awareness under anesthesia and the
development of posttraumatic stress disorder. Gen Hosp Psychiatry 23:198, 2001
[PMID 11543846]
41. Foa EB, Dancu CV, Hembree EA, et al: A comparison of exposure therapy,
stress inoculation training, and their combination for reducing post traumatic
stress disorder in female assault victims. J Consult Clin Psychol 67:194, 1999
[PMID 10224729]
42. Zayfert C, Dums AR, Ferguson RJ, et al: Health functioning impairments
associated with posttraumatic stress disorder, anxiety disorders, and
depression. J Nerv Ment Dis 190:233, 2002 [PMID 11960084]
43. Shemesh E, Rudnick A, Kaluski E, et al: A prospective study of posttraumatic
stress symptoms and nonadherence in survivors of a myocardial infarction (MI).
Gen Hosp Psychiatry 23:215, 2001 [PMID 11543848]
44. Kessler RC, Keller MB, Wittchen HU: The epidemiology of generalized anxiety
disorder. Psychiatr Clin North Am 24:19, 2001 [PMID 11225507]
45. Wittchen HU, Hoyer J: Generalized anxiety disorder: nature and course. J
Clin Psychiatry 62(suppl 11):15, 2001
46. Thayer JF, Friedman BH, Borkovec TD: Autonomic characteristics of
generalized anxiety disorder and worry. Biol Psychiatry 39:255, 1996 [PMID
8645772]
47. Hoehn-Saric R, Hazlett RL, Pourmotabbed T, et al: Does muscle tension
reflect arousal? Relationship between electromyographic and
electroencephalographic recordings. Psychiatry Res 71:49, 1997 [PMID 9247981]
48. Tiihonen J, Kuikka J, Rasanen P, et al: Cerebral benzodiazepine receptor
binding and distribution in generalized anxiety disorder: a fractal anaylsis.
Mol Psychiatry 2:463, 1997 [PMID 9399689]
49. Thayer JF, Lane RD: Perseverative thinking and health: neurovisceral
concomitants. Psychol Health 17:685, 2002
50. Goldberg DP, Lecrubier Y: Mental Illness in General Health Care: An
International Study. John Wiley & Sons, New York, 1995
51. Hidalgo RB, Davidson JR: Generalized anxiety disorder: an important clinical
concern. Med Clin North Am 85:691, 2001 [PMID 11349480]
52. Newman MG: Recommendations for a cost-offset model of psychotherapy
allocation using generalized anxiety disorder as an example. J Consult Clin
Psychol 68:549, 2000 [PMID 10965629]
53. Logue MB, Thomas AM, Barbee JG, et al: Generalized anxiety disorder patients
seek evaluation for cardiological symptoms at the same frequency as patients
with panic disorder. J Psychiatric Res 27:55, 1993
54. Davidson JR: Pharmacotherapy of generalized anxiety disorder. J Clin
Psychiatry 62(suppl 11):46, 2001
55. Rickels K, Schweizer E: Panic disorder: long-term pharmacotherapy and
discontinuation. J Clin Psychopharmacol 18(6 suppl 2):12S, 1998
56. Borkovec TD, Ruscio AM: Psychotherapy for generalized anxiety disorder. J
Clin Psychiatry 62(suppl 11):37, 2001
57. Stein MB, Torgrud LJ, Walker JR: Social phobia symptoms, subtypes, and
severity: findings from a community survey. Arch Gen Psychiatry 57:1046, 2000
[PMID 11074870]
58. Yonkers KA, Dyck IR, Keller MB: An eight-year longitudinal comparison of
clinical course and characteristics of social phobia among men and women.
Psychiatric Services 52:637, 2001 [PMID 11331798]
59. Amaral DG: The primate amygdala and the neurobiology of social behavior:
implications for understanding social anxiety. Biol Psychiatry 51:11, 2002 [PMID
11801227]
60. Birbaumer N, Grodd W, Diedrich O, et al: fMRI reveals amygdala activation to
human faces in social phobics. Neuroreport 9:1223, 1998 [PMID 9601698]
61. Foa EB, Gilboa-Schechtman E, Amir N, et al: Memory bias in generalized
social phobia: remembering negative emotional expressions. J Anxiety Disord
14:501, 2000 [PMID 11095543]
62. Hope DA, Gansler DA, Heimberg RG: Attentional focus and causal attributions
in social phobia: implications from social psychology. Clin Psychol Rev 9:49,
1989
63. Stein MB, McQuaid JR, Laffaye C, et al: Social phobia in the primary care
medical setting. J Fam Pract 48:514, 1999 [PMID 10428248]
64. Olfson M, Guardino M, Struening E, et al: Barriers to the treatment of
social anxiety. Am J Psychiatry 157:521, 2000
65. Ballenger JCL: Current treatment of the anxiety disorders in adults. Biol
Psychiatry 46:1579, 1999
66. Heimberg RG: Cognitive-behavioral therapy for social anxiety disorder:
current status and future directions. Bio Psychiatry 51:101, 2002
67. Shear MK, Beidel DC: Psychotherapy in the overall management strategy for
social anxiety disorder. J Clin Psychiatry 59(suppl 17):39, 1998
68. Katzelnick DJ, Stein MB, Helstad CP: Impact of generalized social anxiety
disorder in managed care. Psychosomatics 158:1999, 1999
69. Skoog G, Skoog I: A 40-year follow-up of patients with obsessive-compulsive
disorder. Arch Gen Psychiatry 56:121, 1999 [PMID 10025435]
70. Micallef J, Blin O: Neurobiology and clinical pharmacology of
obsessive-compulsive disorder. Clin Neuropharmacol 24:191, 2001 [PMID 11479390]
71. Swedo SE, Leonard HL, Garvey M, et al: Pediatric autoimmune neuropsychiatric
disorders associated with streptococcal infections: clinical description of the
first 50 cases. Am J Psychiatry 155:264, 1998 [PMID 9464208]
72. Rasmussen SA, Eisen JL: The epidemiology and differential diagnosis of
obsessive compulsive disorder. J Clin Psychiatry 55(suppl):5, 1994 [PMID
9464208]
73. Folks DG, Warnock JK: Psychocutaneous disorders. Curr Psychiatry Rep 3:219,
2001 [PMID 11353586]
74. Mundo E, Bianchi L, Bellodi L: Efficacy of fluvoxamine, paroxetine, and
citalopram in the treatment of obsessive-compulsive disorder: a single-blind
study. J Clin Psychopharmacol 17:267, 1997 [PMID 9241005]
75. Kozak MJ, Liebowitz MR, Foa EB: Obsessive-Compulsive Disorder: Contemporary
Issues in Treatment. Goodman WK, Rudorfer MV, Maser JD, Eds. Lawrence Erlbaum
Assoc., Inc. Mahwah, New Jersey, 2002
76. Koran LM, Thienemann ML, Davenport R: Quality of life for patients with
obsessive-compulsive disorder. Am J Psychiatry 153:783, 1996 [PMID 8633690]

The author has received grants for clinical research from Pfizer, Inc., and
Forest Pharmaceuticals, Inc., and has served as a consultant for and member of
the speakers' bureaus of Pfizer, Inc., and GlaxoSmithKline.
Sidebar: Internet Resources For Anxiety Disorders
Multipurpose Sites

Anxiety Disorders Association of America
http://www.adaa.org
http://www.anxieties.com

* General information, referral information, patient materials, screening
measures, and medication information

Anxiety Disorders Clinic, McMaster University Medical Centre
http://www.macanxiety.com

* General information, patient materials, and Canadian referral information

Freedom From Fear
http://www.freedomfromfear.com

* General information, patient materials, screening measures, and medication
information

National Institute of Mental Health-Anxiety
http://www.nimh.nih.gov/anxiety/anxietymenu.cfm

* General information, referral information, patient materials in English and
Spanish, screening measures, and medication information

General Information and Patient Materials

Lifeline Anxiety Disorder Newsletter
http://www.designandcopy.ca/lifeline

Mental Health: A Report of the Surgeon General
http://www.surgeongeneral.gov/library/mentalhealth/chapter4/sec2.html

Mental Health Net
http://mentalhelp.net/poc/center_index.php?id=1

Practice Guidelines

American Psychiatric Association
http://www.psych.org/clin_res/prac_guide.cfm

Psychotherapeutic Referral Sources

Academy of Cognitive Therapy
http://www.academyofct.org

American Board of Professional Psychology
http://www.abpp.org

American Psychiatric Association
http://www.psych.org/public_info/APA~1.HTM

Screening for Anxiety New York University School of Medicine-Psychiatry
http://www.med.nyu.edu/Psych/screens/anx.html

Generalized Anxiety and Other Anxiety Disorders

Generalized Anxiety Disorder (GAD) Study
http://www.bu.edu/anxiety/gad.html

Obsessive-Compulsive Disorder

Obsessive-Compulsive Foundation
http://www.ocfoundation.org

Posttraumatic Stress Disorder and Other Stress-Related Conditions

International Society for Traumatic Stress Studies (ISTSS)
http://www.istss.org

Social Anxiety Disorder

Madison Institute of Medicine
http://www.socialfear.com

The Social Anxiety Network
http://www.social-anxiety-network.com

Social Phobia/Social Anxiety Disorder: Effective Treatment 2003
http://www.socialfear.com

M. Katherine Shear, M.D., Professor of Psychiatry, University of Pittsburgh
School of Medicine, and Director, Panic, Anxiety and Traumatic Grief Program,
Western Psychiatric Institute and Clinic

=============

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Gigglz

unread,
Dec 16, 2003, 10:06:53 PM12/16/03
to
Thank you, Elliott! I printed this out!

Hugs,

Gigglz

"E" <sna...@ds2.domainspa.com> wrote in message
news:bro0n...@drn.newsguy.com...

Christina

unread,
Dec 17, 2003, 11:27:58 PM12/17/03
to
I had replied to this the day you posted it, but it didn't go through and I
don't feel like typing it all over again, but I wanted to thank you for
sending this because after reading it I realized that I have social
phobia....this article was so very informative....I have never EVER been
diagnosed with social phobia which is probably why I have never been treated
properly, other than the one time I was prescribed Paxil for depression and
it worked wonders!!!!!!!

Thank you so much for posting it for us....my mouth dropped when I read the
part about SP because everything that I deal with everyday was on that
list....even the "writing a check" part and "not being able to go to the
bathroom in public places"....I thought I was just weird, but now I realize
it's a phobia.....

Christina

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http://www.angelfire.com/la2/pets/
http://www.geocities.com/christinamarie29/ourpage.html


"E" <sna...@ds2.domainspa.com> wrote in message
news:bro0n...@drn.newsguy.com...

Dennis

unread,
Dec 18, 2003, 2:25:51 AM12/18/03
to
Thanks, Elliott!

I keep thinking. One of my abusive therapists kept talking about
how I couldn't relate to people, (never mind that I had a lot of friends,
and a really close friend), and talked like it was the greatest crime in
the universe. Now it's just called a social anxiety.

Dennis

Christina

unread,
Dec 18, 2003, 4:56:14 AM12/18/03
to
Dennis, nice to know it's not just me....

"Dennis" <lion_h...@yahoo.com> wrote in message
news:Xns9454EFB6BE3EDl...@130.133.1.4...

Dennis

unread,
Dec 19, 2003, 3:20:34 AM12/19/03
to
"Christina" <chr...@rtconline.com> wrote :

> Dennis, nice to know it's not just me....

Indeed.

I was really being sarcastic about my abusive therapist. Really,
plenty of people are shy. Is that the root of all evil?

It is good to know there is help for it, now.

purple...@clear.net.nz

unread,
Feb 5, 2004, 9:10:14 PM2/5/04
to
Hello Anna,

Prothiadon is also known as Dothiepin.

Yes the Zantac really does help with the nausea from my Efexor, I tried
stopping the Zantac but after one missed dose I had the awful nausea back
again, yuck!!

Smiles,
Jude.

>purple...@clear.net.nz wrote:
>> Hi,
>>
>> I'm on 75mg Efexor a day, 150mg Zantac twice a day to help with gastric
>> symptoms from Efexor (nausea and stomach ache) and 50mg Prothiadon
>> (Dothiepin)at night for anxiety.
>>
>> The Efexor is wonderful for my Depression but my anxiety and agoraphobia
>> are not too good, though the Prothiadon seems to be helping with the
>> anxiety.
>>
>> Jude.
>
>Hello Jude,I never heard of Prothiadon before. I will google it.
>maybe it has another name in Holland. Does the Zantac do the trick for you ?
>
>Love from Anna

anna

unread,
Feb 7, 2004, 5:33:14 PM2/7/04
to
purple...@clear.net.nz wrote:
> Hello Anna,
>
> Prothiadon is also known as Dothiepin.
>
> Yes the Zantac really does help with the nausea from my Efexor, I tried
> stopping the Zantac but after one missed dose I had the awful nausea back
> again, yuck!!
>
> Smiles,
> Jude.

Ahhhhhh,that is good ! It seems the Zantac works differently for
everyone. A girlfriend of mine also benefits from it :-)

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