NAME: Ayessa Camelle A.

Dumile SUBJECT: NCM 117

RELATED READINGS ABOUT ANXIETY AND ANXIETY DISORDERS

Anxiety is a normal reaction to stress and can be beneficial in some situations. It

can alert us to dangers and help us prepare and pay attention. Anxiety disorders differ
from normal feelings of nervousness or anxiousness and involve excessive fear or
anxiety. Anxiety disorders are the most common of mental disorders and affect nearly
30% of adults at some point in their lives. But anxiety disorders are treatable and a
number of effective treatments are available. Treatment helps most people lead normal
productive lives. In any given year the estimated percent of U.S. adults with various
anxiety disorders are: Specific Phobia: 8% - 12%, Social Anxiety Disorder: 7%, panic
disorder: 2% - 3%, Agoraphobia: 1-2.9% in Adolescents and Adults, Generalized
Anxiety Disorder: 2% and Separation Anxiety Disorder: 0.9% - 1.9%. Women are more
likely than men to experience anxiety disorders.

Anxiety refers to anticipation of a future concern and is more associated with muscle
tension and avoidance behavior. Fear is an emotional response to an immediate threat
and is more associated with a fight or flight reaction – either staying to fight or leaving to
escape danger. Anxiety disorders can cause people to try to avoid situations that trigger
or worsen their symptoms. Job performance, school work and personal relationships
can be affected. In general, for a person to be diagnosed with an anxiety disorder, the
fear or anxiety must: anxiety disorders can cause people to try to avoid situations that
trigger or worsen their symptoms. Job performance, school work and personal
relationships can be affected. In general, for a person to be diagnosed with an anxiety
disorder, the fear or anxiety must:

 Be out of proportion to the situation or age-inappropriate

 Hinder ability to function normally

There are several types of anxiety disorders, including generalized anxiety disorder,
panic disorder, specific phobias, agoraphobia, social anxiety disorder and separation
anxiety disorder.

Anxiety disorders are the most prevalent psychiatric disorders. There is a high
comorbidity between anxiety (especially generalized anxiety disorders or panic
disorders) and depressive disorders or between anxiety disorders, which renders
treatment more complex. Current guidelines do not recommend benzodiazepines as
first-line treatments due to their potential side effects. Selective serotonin reuptake
inhibitors and selective serotonin norepinephrine reuptake inhibitors are recommended
as first-line treatments. Psychotherapy, in association with pharmacotherapy, is
associated with better efficacy. Finally, a bio-psycho-social model is hypothesized in
anxiety disorders.

Anxiety disorders are the most prevalent psychiatric disorders (with a current
worldwide prevalence of 7.3% [4.8%-10.9%]—Stein et al, in this issue p 127). Among
them, specific phobias are the most common, with a prevalence of 10.3%, then panic
disorder (with or without agoraphobia) is the next most common with a prevalence of
6.0%, followed by social phobia (2.7%) and generalized anxiety disorder (2.2%).
Evidence is lacking as to whether these disorders have become more prevalent in
recent decades. Generally speaking, women are more prone to develop emotional
disorders with an onset at adolescence; they are 1.5 to 2 times more likely than men to
have an anxiety disorder (Bandelow et al. in this issue p 93). There is a high comorbidity
between anxiety (especially generalized anxiety disorders or panic disorders) and
depressive disorders. Additionally, anxiety disorders are often associated, which
renders treatment even more complex for nonspecialists. As a result, anxiety disorders
often remain underdiagnosed and undertreated in primary care.

Both psychotherapy and pharmacotherapy have been shown to be more effective

than placebo or waiting lists in the treatment of anxiety disorders. In a meta-analysis
published in 2015 by Bandelow et al, and based on 234 randomized controlled studies,
medications were associated with a significantly higher average pre-post effect size
(Cohen's d=2.02) than psychotherapies (d=1.22; P<0.0001); somehow, patients
included in psychotherapy studies were less severely ill. 4 This meta-analysis also
showed that psychotherapy in association with pharmacotherapy had a relatively high
effect size (d=2,12). Due to their good benefit/risk balance, selective serotonin reuptake
inhibitors and selective serotonin norepinephrine reuptake inhibitors were
recommended as first-line treatments. Current guidelines do not recommend
benzodiazepines as first-line treatments due to their potential side effects. In fact,
Parsaik et al, in a 2016 meta-analysis, have reported a higher mortality rate among
benzodiazepines users compared with nonusers. Underlying mechanisms need to be
further studied. In addition, the development of tolerance and an increased risk for
dependence were also reported in association with long-term use of benzodiazepine
(which generally means ≥6 months). An increased risk of dementia was also claimed by
several authors in long-term benzodiazepine users (pooled adjusted risk ratio for
dementia of 1.55) compared with never users (for review, see ref. Finally,
benzodiazepines do not treat depression, which is a common comorbid condition in
anxiety disorders, and benzodiazepines may be associated with a higher suicide risk in
case of comorbidity between anxiety and depressive disorders.

The current conceptualization of the etiology of anxiety disorders includes an

interaction of psychosocial factors such as childhood adversity or stressful events, and
a genetic vulnerability. Until now, there are few biomarkers available. Domschke et al (in
this issue, p 159) will summarize recent data about the genetic factors involved in
anxiety disorders. The serotonergic and catecholaminergic systems, and neurotrophic
signaling, are promising candidate genes in generalized anxiety disorders, even if the
genetic risk remains moderate (heritability of approximately 30%). In addition, gene-
environment studies have highlighted the importance of early developmental trauma
and recent stressful life events in interaction with molecular plasticity markers. Among
socio-environmental factors, parenting behavior may also play a role in the prevention
of anxiety disorders (Aktar et al, in this issue p 137).

TYPES OF ANXIETY DISORDERS

Generalized Anxiety Disorder

Generalized anxiety disorder involves persistent and excessive worry that

interferes with daily activities. This ongoing worry and tension may be accompanied by
physical symptoms, such as restlessness, feeling on edge or easily fatigued, difficulty
concentrating, muscle tension or problems sleeping. Often the worries focus on
everyday things such as job responsibilities, family health or minor matters such as
chores, car repairs, or appointments.

Panic Disorder

The core symptom of panic disorder is recurrent panic attacks, an overwhelming

combination of physical and psychological distress. During an attack several of these
symptoms occur in combination:

 Palpitations, pounding heart or rapid heart rate

 Sweating
 Trembling or shaking
 Feeling of shortness of breath or smothering sensations
 Chest pain
 Feeling dizzy, light-headed or faint
 Feeling of choking
 Numbness or tingling
 Chills or hot flashes
 Nausea or abdominal pains
 Feeling detached
 Fear of losing control
 Fear of dying

Because the symptoms are so severe, many people who experience a panic attack
may believe they are having a heart attack or other life-threatening illness. They may go
to a hospital emergency department. Panic attacks may be expected, such as a
response to a feared object, or unexpected, apparently occurring for no reason. The
mean age for onset of panic disorder is 20-24. Panic attacks may occur with other
mental disorders such as depression or PTSD.
Phobias, Specific Phobia

A specific phobia is excessive and persistent fear of a specific object, situation or

activity that is generally not harmful. Patients know their fear is excessive, but they can't
overcome it. These fears cause such distress that some people go to extreme lengths
to avoid what they fear. Examples are public speaking, fear of flying or fear of spiders.

Agoraphobia

Agoraphobia is the fear of being in situations where escape may be difficult or

embarrassing, or help might not be available in the event of panic symptoms. The fear
is out of proportion to the actual situation and lasts generally six months or more and
causes problems in functioning. A person with agoraphobia experiences this fear in two
or more of the following situations:

 Using public transportation

 Being in open spaces
 Being in enclosed places
 Standing in line or being in a crowd
 Being outside the home alone

The individual actively avoids the situation, requires a companion or endures with
intense fear or anxiety. Untreated agoraphobia can become so serious that a person
may be unable to leave the house. A person can only be diagnosed with agoraphobia if
the fear is intensely upsetting, or if it significantly interferes with normal daily activities.

Social Anxiety Disorder (previously called social phobia)

A person with social anxiety disorder has significant anxiety and discomfort about
being embarrassed, humiliated, rejected or looked down on in social interactions.
People with this disorder will try to avoid the situation or endure it with great anxiety.
Common examples are extreme fear of public speaking, meeting new people or
eating/drinking in public. The fear or anxiety causes problems with daily functioning and
lasts at least six months.

Separation Anxiety Disorder

A person with separation anxiety disorder is excessively fearful or anxious about

separation from those with whom he or she is attached. The feeling is beyond what is
appropriate for the person's age, persists (at least four weeks in children and six months
in adults) and causes problems functioning. A person with separation anxiety disorder
may be persistently worried about losing the person closest to him or her, may be
reluctant or refuse to go out or sleep away from home or without that person, or may
experience nightmares about separation. Physical symptoms of distress often develop
in childhood, but symptoms can carry though adulthood.

Risk Factors

The causes of anxiety disorders are currently unknown but likely involve a
combination of factors including genetic, environmental, psychological and
developmental. Anxiety disorders can run in families, suggesting that a combination of
genes and environmental stresses can produce the disorders.

Diagnosis and Treatment

The first step is to see your doctor to make sure there is no physical problem
causing the symptoms. If an anxiety disorder is diagnosed, a mental health professional
can work with you on finding the best treatment. Unfortunately, many people with
anxiety disorders don't seek help. They don't realize that they have an illness for which
there are effective treatments.

Although each anxiety disorder has unique characteristics, most respond well to
two types of treatment: psychotherapy or "talk therapy," and medications. These
treatments can be given alone or in combination. Cognitive behavior therapy (CBT), a
type of talk therapy, can help a person learn a different way of thinking, reacting and
behaving to help feel less anxious. Medications will not cure anxiety disorders, but can
provide significant relief from symptoms. The most commonly used medications are
anti-anxiety medications (generally prescribed only for a short period of time) and
antidepressants. Beta-blockers, used for heart conditions, are sometimes used to
control physical symptoms of anxiety.

Self-Help, Coping, and Managing

There are a number of things people do to help cope with symptoms of anxiety
disorders and make treatment more effective. Stress management techniques and
meditation can be helpful. Support groups (in-person or online) can provide an
opportunity to share experiences and coping strategies. Learning more about the
specifics of a disorder and helping family and friends to understand the condition better
can also be helpful. Avoid caffeine, which can worsen symptoms, and check with your
doctor about any medications.

Related Conditions

 Posttraumatic stress disorder (PTSD)

 Acute stress disorder
  Obsessive-compulsive disorder
 Adjustment disorder
 Selective mutism

Selective Mutism

Children with selective mutism do not speak in some social situations where they
are expected to speak, such as school, even though they speak in other situations.
They will speak in their home around immediate family members, but often will not
speak even in front of others, such as close friends or grandparents.

The lack of speech may interfere with social communication, although children
with this disorder sometimes use non-spoken or nonverbal means (e.g., grunting,
pointing, writing). The lack of speech can also have significant consequences in school,
leading to academic problems and social isolation. Many children with selective mutism
also experience excessive shyness, fear of social embarrassment and high social
anxiety. However, they typically have normal language skills.

Selective mutism usually begins before age 5, but it may not be formally
identified until the child enters school. Many children will outgrow selective mutism. For
children who also have social anxiety disorder, selective mutism may disappear, but
symptoms of social anxiety disorder may remain.

Physician Review

Philip R. Muskin, M.D., M.A.

June 2021

REFERENCE: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5573565/

https://www.psychiatry.org/patients-families/anxiety-disorders/what-
are-anxiety-disorders
 RELATED READINGS ABOUT OBSESSIVE COMPULSIVE

Obsessive-compulsive disorder (OCD) was described as early as the

seventeenth century, when the Oxford Don, Robert Burton, reported a case in his
compendium, The Anatomy of Melancholy (1621). Modern concepts of OCD began to
evolve in France and Germany in the nineteenth century. In the late twentieth century
we have begun to understand the biology of this mental disorder, as neurochemical
assay and brain imaging techniques have become available.

Age at Onset

OCD usually begins before age 25 years and often in childhood or adolescence.
In individuals seeking treatment, the mean age of onset appears to be somewhat earlier
in men than women. According to Swedo et al.'s report in 1989, in a series of 70
children and adolescents seen at the National Institute of Mental Health, the mean age
of onset was 9.6 years for boys and 11.0 for girls. In a series of 263 adult and child
patients, Lensi et al. in 1996 reported that the mean age at onset was 21 years for men
and 24 years for women. Still, in another series reported by Rasmussen and Eisen in
1992, the means were 21 years for men and 22 years for women -- in this series, major
symptoms began before age 15 years in about one-third, before age 25 in about two-
thirds, and after age 35 in less than 15%.

In one series of 200 patients reported by Rasmussen and Eisen in 1988, 29% felt
that an environmental precipitant had triggered their illness, most frequently increased
responsibility, such as the birth of a child, or significant losses, such as a death in the
family, while Williams and Koran reported in 1997 that of 100 women in their study, 62%
reported premenstrual worsening.

In community surveys, the results are mixed. The Epidemiological Catchment

Area survey (ECA), which utilized lay interviewers (trained non-professionals) to
examine more than 18,500 individuals in five cities reported a similar mean age of onset
for men and women identified as OCD cases (22.4 and 23.0 years). A similar study in
Edmonton, Canada reported a slightly later median age of onset for males (age 20
years) than females (age 19 years). Among 56 individuals in their mid-20s with
obsessive-compulsive syndrome identified in a Zurich survey, the mean age of onset
was 17 years for males and 19 years for females.

Course and Prognosis

For most adult patients who come to treatment, OCD appears to be a chronic
condition. In their series of 560 patients in 1988, Rasmussen and Eisen reported that
85% had a continuous course with waxing and waning symptoms, 10% a deteriorative
course and only 2% an episodic course marked by full remissions lasting six months or
more. An Italian series by Lensi et al. in 1996 reported more patients with episodic or
deteriorative courses in which 26% were episodic, 9% were deteriorative, and 64%
were chronic. The conclusions drawn from studies that predate current diagnostic
criteria, effective treatments and current patterns of health care utilization should not be
applied to today's patients.

The prognosis of children and adolescents who present for treatment appears to
be good for half or more. Leonard et al. reported in 1993, that a little more than half of
54 children and adolescents were only mildly affected when evaluated two- to seven-
years after vigorous treatment with medications, and less often with behavior therapy.
Only six patients (11%) were symptom free, however, and only three of these were
taking no medication. A 9 -to 14 -year follow-up study reported that 8 of 14 adolescents
who had received medication treatment were medication free and did not meet OCD
criteria; the other six had experienced a chronic, or a relapsing and then chronic course,
reported Bolton, Luckie and Steinberg in 1995. Finally, Thomsen and Mikkelsen
reported in 1995 that a 1.5 to 5 year follow-up of 23 children and adolescents who had
recieved drug treatment found that four were free of OCD, eight had subclinical
symptoms and the remaining 11 had chronic or episodic OCD. Larger studies from
multiple sites are needed to establish accurately the prognosis associated with modern
treatment methods.

In community-identified cases, remission, or a course marked by long, symptom-

free periods, seems to be the rule. The apparent frequency of this benign course is
probably due to the limited diagnostic validity of interviews conducted by lay
interviewers and to the large proportion of milder cases in community sample.
According to Nelson and Rice in 1997, only 19% (56 of 291 subjects) meeting OCD
criteria during their first lay inerview met these criteria duing a lay interview conducted
one year later.

Comorbidity

Patients with OCD are at high risk of having comorbid (co-existing) major
depression and other anxiety disorders. In a series of 100 OCD patients who were
evaluated by means of a structured psychiatric interview, the most common concurrent
disorders were: major depression (31%), social phobia (11%), eating disorder (8%),
simple phobia (7%), panic disorder (6%), and Tourette's syndrome (5%). In Koran et
al.'s 1998 Kaiser Health Plan study, 26% of patients had no comorbid psychiatric
condition diagnosed during the one year study period -- 37% had one and 38% had two
or more comorbid conditions. These proportions did not differ substantially between
men and women. The most commonly diagnosed comorbid conditions were major
depression, which affected more than one-half, other anxiety disorders, affecting one-
quarter, and personality disorders, diagnosed in a little more than 10%. Panic disorder
and generalized anxiety disorder were the most common anxiety disorders. Bipolar
mood (manic-depressive) disorder was uncommon, but schizophrenia was rare. Except
for eating disorders, which were diagnosed in 1 in 20 women, the rates of specific
comorbid conditions were not strkingly different between men and women.

OCD seems to be associated with a mildly increased risk for alcohol abuse and
dependence. Rates of OCD observed among alcoholic patients admitted to inpatient
and outpatient treatment programs exceed the rate in the general population, but not to
the extent suggested by Karno et al.'s study in 1988, which attributed alcohol abuse or
dependence to 24% of OCD subjects.

Reports of the lifetime rate of body dysmorphic disorder (fear of imagined

ugliness) in OCD patients are also prevalent, as well as findings by Barsky in 1992
indicating that patients with hypochondriasis have an elevated lifetime prevalence rate
of OCD compared to medical outpatients from the same clinic. Eating disorders may be
more common in OCD patients than in the general population, but the data are sparse.
According to Rothenberg in 1990, OCD symptoms are common in patients with
anorexia nervosa, second only to depressive disorders. Trichotillomania (compulsive
hair pulling with bald spots) is another comorbidity of OCD, as is Tourette's syndrome
(the combination of behavioral and vocal tics).

Quality of Life

OCD impairs patients' quality of life. In a study of 60 patients, Koran,

Thienemann and Davenport reported in 1996 that medication-free patients with
moderate to severe OCD reported worse social functioning and performance in work
and other activities than the general population and than patients with diabetes. The
more severe the OCD, the more impaired the patients' social functioning, even after
controlling for effects of concurrent depression. Moreover, Rasmussen and Eisen noted
in 1992 that another indicator of reduced quality of life is lower likelihood of OCD
patients marrying.

The high personal cost of OCD is mirrored in high social costs. The estimated
1990 direct costs of OCD to the United States economy were $2.1 billion, and the
indirect cost (i.e., lost productivity) $6.2 billion, reported Dupont et al. in 1995. If a
greater proportion of individuals with OCD were in treatment, the direct costs would
have been considerable higher. For example,according to Nestadt et al. in 1994, among
a random sample of the Baltimore study participants, only 1 of 15 individuals (7%)
whom a psychiatrist judged to need treatment was receiving it. Rasmussen and Eisen
reported in 1988 that the delay between symptom onset and first seeking care is often
prolonged by a mean of seven years, while Marks in 1992 reported 10 years. Even with
much treatment foregone, OCD accounted for almost 6% of the estimated 1990 cost of
all mental illness. High social costs are also reflected in the high rates of unemployment
in OCD patients and receipt of disability and welfare payments, reported Leon, Portera
and Wissman in 1995. Family members suffer as well. Many studies indicate that
patients' symptoms may create disharmony, angry or anguished demands for
participating in rituals, a draining dependency, restricted access to rooms or living
space, difficulty in taking holidays and intereference with work obligations.
 OCD is a common mental disorder, and is often disabling. The past few decades,
however, have seen the emergence of many effective treatments, both pharmacological
and psychotherapeutic. The challenges for the 21st century are two-fold: first, to make
these effective treatments available to all sufferers; and, second, to unravel the biology
of this disorder sufficiently so that we can cure its symptoms, and ultimately, prevent its
occurrence. In order to tackle these challenges, it is essential that we understand the
etiology of OCD.

Prevailing theories indicate that OCD is a biological disease. Functional brain

imaging studies have produced a model for pathophysiology of OCD which involves
hyperactivity in certain subcortical and cortical regions. On the basis of imaging studies,
Insel has proposed that inappropriately increased activity in the head of the caudate
nucleus inhibits globus pallidus fibers that ordinarily dampen thalamic activity. The
resulting increase in thalamic activity produces increased activity in orbitofrontal cortex,
which, via the cingulate gyrus, completes the circuit to the caudate and produces
increased activity in the head of the caudate. Hypothetically, primitive cleaning and
checking behaviors are "hard-wired" in the thalamus. Insel's hypothesis is supported by
evidence from MRI (magnetic resonance imaging) studies, which have found an
abnormally small caudate in some OCD patients, and by positron emission tomography
(PET scan) studies, which have found increased metabolism in orbital frontal cortex,
cingulate gyrus, and caudate, with decreases following successful treatment. The
association of OCD with Tourette's syndrome and Sydenham's chorea, which are
believed to involve basal ganglia pathology, is also consistent with this model.

In the section below, we have outlined a more detailed description of the various
theories and hypotheses involved in the biological basis of OCD. As will be noted by
many readers, the information provided here is more suited for clinicians, medical
professionals, or others who are more familiar with medical terminalogy. For this
reason, readers are encouraged to seek further information from their
physicians/psychiatrists and/or other OCD resources.

Etiology: Biological Models

Functional Neuroanatomy

Many investigators have contributed to the hypothesis that OCD involves

dysfunction in a neuronal loop running from the orbital frontal cortex to the cingulate
gyrus, striatum (cuadate nucleus and putamen), globus pallidus, thalamus and back to
the frontal cortex. Organic insult to these regions can produce obsessive and
compulsive symptoms. The results of neurosurgical treatment of OCD strongly support
this hypothesis. Surgical interruption of this loop by means of cingulotomy, anterior
capsulotomy or subcaudate tractotomy brings about symptomatic improvement in a
large proportion of patients unresponsive to all other treatments. Cingulotomy interrupts
this loop at the anterior cingulate cortex, thereby disrupting frontal cortical input into the
Papez circuit and limbic system, which are believed to mediate anxiety and other
emotional symptoms. Anterior capsulotomy (lesions within the anterior limb of the
internal capsules) and subcaudate tractotomy (lesions in the substantia innominata, just
under the head of the caudate nucleus) interrupt fronto-thalamic fibers, which may
mediate the obsessive and compulsive components of OCD. Baxter et al. in 1992
hypothesized that the hyperactivity observed in this neuronal loop arises because of
imparied caudate nucleus function. The impariment allows "worry inputs" from the
orbitofrontal cortex to inhibit excessively the inhibitory output from the globus pallidus to
the thalamus. The resulting excess in thalamic output then impinges on various brain
regions involved in the experience of OCD symptoms, including the orbital frontal
region, thus reinforcing hyperactivity in the neuronal loop. However, Baxter et al. caution
that the abnormal neurophysiology underlying OCD symptoms may involve structures
as yet undetected. Decreased metabolic activity can be missed by current scanning
techniques. Alternately, the metabolic hyperactivity of small neuronal fields can be
missed when surrounding structures exhibit no change or mask the increase behind
compensatory decreases.

Serotonin and Other Neurotransmitters

The hypothesis that an abnormality in serotonergic neurotransmission underlies

OCD arose out of the observation that clomipramine, which inhibits both serotonin and
norepinephrine reuptake, relieved symptoms, whereas noradrenergic reuptake inhibitors
did not. The unique efficacy of clomipramine and the SSRIs remains the strongest
support for this hypothesis. Studies of peripheral markers of serotonergic function in
blood and cerebrospinal fluid have not conclusively demonstrated an abnormality.
Pharmacological challenge studies with serotonergic agonists have suggested
dysregulation within the serotonin system, with behavioral hypersensitivity and
neuroendocrinological hyposensitivity to the activation of serotonin receptors, but
numerous inconsistencies remain to be resolved. The beneficial effects of enhanced
serotonergic neurotransmission do not prove that abnormalities in this system are the
root cause of OCD symptoms. Serotonergic neurons modulate the function of many
other systems, where the primary cause or causes may lie. In patients with comorbid
Tourette's syndrome, tics and schizotypal personality disorder, treatment studies
indicate a role for dopaminergic neurons.

Genetic Contributions

Twin studies and family studies strongly suggest that vulnerability to OCD can be
inherited, but a positive family history is absent in many patients. Older studies of
monozygotic twins show a 65% concordance for OCD, but no control groups were
included. One study found an 87% concordance for "obsessional features" (OCD
symptoms that may not have caused significant distress or social impairment) in
monozygotic twins; the concordance of dizygotic twins was only half as large. On the
other hand, none of eight monozygotic twin pairs in another study were concordant for
OCD, according to Andrews et al. in 1990. A recent review notes that in Pauls' study in
1992, 10% of the parents of children and adolescents with OCD themselves had the
disorder, and in another study, OCD was present in 25% of fathers and 9% of mothers.
The symptoms of parents and children usually differed, arguing aginst social or cultural
transmission. A study by Black et al. in 1992 however, found no increase in OCD
prevalence in first degree relatives of OCD patients compared to those of control group.
The recent finding, by Murphy et al. in 1997 and Swedo et al. in 1997, that an antigen
which is a genetic marker for rheumatic fever susceptibility is also a marker for
susceptibility to an autoimmune form of childhood onset OCD will undoubtedly spur
progress in unraveling genetic contributions to the pathogenesis of OCD.

The goals of therapy are to diminish symptoms and to ameliorate or reverse their
effects on the patient's interpersonal, work place and social functioning. A modest
proportion of patients will achieve freedom from significant symptoms. The clinician can
use the Y-BOCS symptom checklist to obtain a record of the patient's current and past
symptoms. Patients may not reveal embarrassing symptoms or symptoms that they
believe may suggest they are "crazy" until a trusting therapeutic relationship has been
established. If completing a Y-BOCS severity rating is impractical, a useful gauge of
severity is how much time obsessions and, separately, compulsions, are occupying "an
average day in the past week."

Treatment planning depends on careful evaluation. As noted earlier, comorbid

depressive and anxiety disorders will commonly be present. These comorbid conditions
may not respond to the particular serotonin reuptake inhibitor (SRI) prescribed for the
patient's OCD. Treatment approaches to such cases, including several kinds of
psychotherapy, are also available. If a patient is abusing alcohol to reduce anxiety, this
problem must be addressed. The presence of a tic disorder, schizotypal or borderline
personality disorders, or a personal or family history of hypomania or mania should be
explored, since these would influence therapy choices.

A comprehensive treatment plan evolves as one gets to know the patient.

Experienced clinicians will exercise their clinical judgement in tailoring the plan to their
patients' needs, preferences, capacities, situation and history. For a patient with
isolated, mild to moderate OCD, a combination of an SRI and exposure and response
prevention in vivo is a reasonable initial strategy in most cases. In certain situations,
such as the patient with low motivation or anergia secondary to major depression,
medications alone may be preferable. In still other cases, medications may be needed
to decrease the intensity of symptoms so that the patient can subsequently comply with
behavioral treatment. There is insufficient data to draw any conclusions about the
relative efficacy of medications alone, exposure and response prevention alone, and
their combination, but many experienced clinicians believe that the combination offers
more rapid improvement and greater protection against relapse. All patients should be
guided to educate themselves through various OCD related resources.

REFERENCE: https://med.stanford.edu/ocd/treatment.html
 RELATED READINGS ABOUT PERSONALITY DISORDERS

Personality disorders are mental disorders characterized by unhealthy patterns of

behavior, thought, and/or daily function. Because these patterns deviate from what is
considered the societal norm, individuals with personality disorders often experience
internal and social problems.

There are 10 personality disorders divided into three clusters: A, B, and

C. Cluster A includes paranoid personality disorder, schizotypal personality disorder,
and schizoid personality disorder. Cluster B personality disorders include histrionic,
narcissistic, borderline, and antisocial. Finally, cluster C includes obsessive-compulsive,
dependent, and avoidant personality disorders.

Treatment for personality disorders can include intensive, long-term

psychotherapy. Sometimes, medication can help. Anyone with signs or symptoms of a
personality disorder should speak with a primary care provider or mental health
professional to determine their risk factors and medical history. Without treatment,
personality disorders have the potential to cause disruptions in patients' and their loved
ones’ lives and could lead to social isolation, drug or alcohol abuse, or other social or
medical problems.

What Causes Personality Disorders?

There is no single cause that leads to personality disorders. Factors that may
contribute to the development of personality disorders include:
 Changes in the brain and neurobehavioral activity, such as structural or
functional differences in the amygdala
 Genetics
 Cultural factors
 Early life experiences and childhood trauma, such as verbal or sexual abuse

Genetic and external factors may play a role in the onset of personality disorders,
with early environmental influences being one consideration. Some personality
disorders are less common in certain parts of the world and more prominent in others.
Researchers believe that genetic deviations may impact the development of obsessive-
compulsive disorder, while stressful experiences and trauma may factor into other types
of personal disorders. For example, one study determined that subjects with borderline
personality disorder had higher-than-usual rates of childhood sexual trauma. Those with
paranoid personality disorder had higher rates of verbal abuse in the past. It's likely that
most personality disorders are the result of a combination of internal and external
factors, and researchers continue to investigate potential causes.

What Are the Symptoms of Personality Disorders? Signs to Know

Since most personality disorders emerge or become symptomatic in the teen years or
early adulthood, it's crucial for individuals and their families to be aware of common
personality disorder symptoms and know when to get professional support.
The symptoms will depend on the personality disorder but may include: (2)
 Problems with relationships
 Poor self-awareness
 Problems with a sense of self
 Seeming detached, irresponsible, or overemotional

People with personality disorders can have difficulty forming bonds and stable
relationships with others because of troubling and otherwise non-typical behaviors.
Some individuals with personality disorders may seek excessive attention or have too
few boundaries. They may have a hard time understanding how their behaviors or
thought patterns are dangerous or upsetting. People living with personality disorders
may have poor self-esteem, excessive self-esteem, or a muddled image of themselves.
Additionally, while not all people with personality disorders are dangerous or abusive,
some may have abusive tendencies toward themselves or others. To determine if a
loved one has a personality disorder, they will require an assessment from a qualified
healthcare professional.

Do I Have a Personality Disorder? How Are They Diagnosed?

Speaking to a professional is the best way to get a formal personality disorder

diagnosis. There are 10 personality disorders in the DSM-5-TR, each with its own
hallmarks. Using the DSM-5-TR as a guide, mental health professionals and specialists
check to see if patients' symptoms or behaviors match the specific criteria required for
diagnosis. Healthcare professionals look at a patient’s long-term health history, patterns
of behavior, physical functions, and persistent symptoms. Those under 18 may not
receive a formal personality disorder diagnosis because they are still growing and
developing.

What Is the Best Treatment for Personality Disorders?

The right personality disorder treatment depends on the diagnosis and severity of
the condition. Psychotherapy is the most common treatment, and it comes in forms
such as: (7)(11)
 Dialectical behavior therapy
 Cognitive-behavioral therapy
 Group therapy
 Psychoanalytic therapy
 Psychoeducation
 Dialectical behavior therapy helps patients get to know their emotions and behaviors
for better emotional regulation. Cognitive-behavioral therapy encourages people to
recognize their thought patterns and work to change them in a positive way.
Psychoanalytic therapy is a type of talk therapy that helps patients gain insight into their
behaviors, while group therapy helps peers get to know each other and find support
while living with similar conditions. Psychoeducation teaches about these and other
possible treatment options.
Medications for personality disorders aren't usually the first treatment approach, but
mood stabilizing, anti-anxiety, or antidepressant medications may address some
symptoms, such as mood swings or depression. In some cases, a patient may work
with a team including social workers, psychologists, psychiatrists, family members,
primary care physicians, and other specialists, to address care from a multitude of
angles.

What Is the Best Treatment for Personality Disorders?

The right personality disorder treatment depends on the diagnosis and severity of
the condition. Psychotherapy is the most common treatment, and it comes in forms
such as:

 Dialectical behavior therapy

 Cognitive-behavioral therapy
 Group therapy
 Psychoanalytic therapy
 Psychoeducation

Dialectical behavior therapy helps patients get to know their emotions and behaviors
for better emotional regulation. Cognitive-behavioral therapy encourages people to
recognize their thought patterns and work to change them in a positive way.
Psychoanalytic therapy is a type of talk therapy that helps patients gain insight into their
behaviors, while group therapy helps peers get to know each other and find support
while living with similar conditions. Psychoeducation teaches about these and other
possible treatment options.

Medications for personality disorders aren't usually the first treatment approach, but
mood stabilizing, anti-anxiety, or antidepressant medications may address some
symptoms, such as mood swings or depression. In some cases, a patient may work
with a team including social workers, psychologists, psychiatrists, family members,
primary care physicians, and other specialists, to address care from a multitude of
angles.

How to Help Someone With a Personality Disorder

Family members and friends of those with personality disorders can help by
being patient and trying not to judge their loved one. Setting boundaries and planning
for triggers can help reduce conflicts. It’s also essential for friends and family to avoid
labeling their loved ones or assuming how the condition may impact them. Learning
about the disorder can be beneficial for all involved. Family therapy or couples therapy
can also be helpful when symptoms of a personality disorder impact the family or
relationship dynamic.

Sources:
1. https://www.mayoclinic.org/diseases-conditions/personality-disorders/symptoms-
causes/syc-20354463
2. https://my.clevelandclinic.org/health/diseases/9636-personality-disorders-
overview#symptoms-and-causes
3. https://www.nhs.uk/mental-health/conditions/personality-disorder/
#:~:text=Causes,such%20as%20abuse%20or%20neglect
4. https://www.apa.org/topics/personality-disorders/causes
5. http://www.ncbi.nlm.nih.gov/pubmed/12193835?
ordinalpos=35&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu
bmed_RVDocSum
6. https://www.apa.org/topics/personality-disorders/causes
7. https://www.psychiatry.org/patients-families/personality-disorders/what-are-
personality-disorders
8. https://my.clevelandclinic.org/health/diseases/9636-personality-disorders-
overview#management-and-treatment
9. https://www.mayoclinic.org/diseases-conditions/personality-disorders/diagnosis-
treatment/drc-20354468
10. https://www.apa.org/topics/personality-disorders/help
11. https://www.nimh.nih.gov/health/topics/borderline-personality-disorder
12. https://www.sciencedirect.com/topics/neuroscience/psychoeducation

LINK OF SITE : https://www.mentalhelp.net/articles/personality-disorders/