MHP 3
MHP 3
MHP 3
Asna Anwer
05-171211-202
5D
15 June 14, 2023
Functional imaging studies in OCD have shown certain repeatable aberrant patterns. The
orbitofrontal cortex, limbic regions, caudate, and thalamus have increased blood flow and
metabolic activity, with a tendency towards right-sided predominance, according to magnetic
resonance imaging (MRI) and positron emission tomography (PET) scanning. After receiving
effective treatment with either SSRIs or cognitive-behavioral therapy (CBT), these areas of
over activity have been demonstrated in certain trials to return to normal.
These results support the idea that certain orbitofrontal-subcortical circuitry, which governs
strong emotions and the autonomic reactions to those emotions, has poor intracortical
inhibition, which underlies the symptoms of OCD. This circuit is broken by cingulotomy, a
neurosurgical procedure that is occasionally used to treat severe and treatment-resistant OCD
(see Treatment and Management).
Glutamatergic anomalies and potential glutamatergic therapies for OCD have also received
attention. The synapses in the cortico-striato-thalamo-cortical circuits thought to be centrally
engaged in the pathology of OCD mostly use glutamate and gamma-aminobutyric acid
(GABA); however they are also controlled by serotonin and other neurotransmitters.
Genetic influence in OCD
Strong heritability for OCD has been demonstrated by twin research, with a genetic
effect of 45–65% in studies of children and 27–47% in studies of adults. Compared to
dizygotic twins, which have a concordance of 47–50%, monozygotic twins can
exhibit extremely high levels of OCD (80–87%). Linkages to a number of
serotonergic, dopaminergic, and glutamatergic genes have been supported by
numerous genetic investigations.
Other genes that have been suggested to be associated with OCD include those that
code for catechol-O-methyl transferase (COMT), monoamine oxidase-A (MAO-A),
brain-derived neurotrophic factor (BDNF), myelin oligodendrocyte glycoprotein
(MOG), GABA-type B-receptor 1, and the mu opioid receptor. However, these
associations must currently be viewed as tentative. OCD, ADHD, and Tourette
disorder/tic disorders co-variate in some cohorts in an autosomal dominant manner
with varied penetrance.
Infectious disease and OCD
Case studies of OCD in children and young adults that developed after acute group A
streptococcal infections, both with and without tics, have been documented. Herpes
simplex virus is mentioned less frequently as the apparent triggering infectious event.
According to a theory known as pediatric autoimmune neuropsychiatric disorders
associated with streptococcal infections (PANDAS), these infections set off a CNS
autoimmune response that causes neuropsychiatric symptoms. Numerous post
streptococcal cases allegedly improved after receiving antibiotic therapy.
Other neurologic conditions
Occasionally, neurologic traumas such brain trauma, stimulant addiction, and carbon
monoxide poisoning can emerge as OCD.
PREVALENCE
the 12-month prevalence of OCD in the United States is 1.2%, with a similar prevalence
internationally (1.1%—1.8%). Females are affected at a slightly higher rate than males in
adulthood, although males are more commonly affected in childhood.
PROGNOSTIC FACTORS
OCD is a chronic disorder that can manifest in a variety of ways. Without therapy, symptoms
may increase and decrease in severity, but they seldom go away on their own. In general,
symptoms significantly improve for about 70% of individuals beginning treatment. OCD,
however, continues to be a chronic condition with symptoms that can wax and wane
throughout the course of a patient's life. Approximately 15% of individuals can demonstrate a
gradual worsening of their symptoms over time or a decline in functionality.in between
episodes of aggravation, 5% of patients get total symptom remission.
Although several suggestions have been put forth, the causes of body dysmorphic disorder
(BDD) have not yet been identified.
It is possible that this problem develops because of heredity. In first-degree relatives of BDD
patients, the prevalence of the disorder is four times higher than in relatives of probands
without the condition. Given that it regularly affects OCD patients and their family and reacts
to the same treatments, BDD appears to be linked to OCD.
Brain anomalies could be a major factor. Front striatal, limbic, and visual processing systems
have all been shown to function abnormally. A correlation between decreased insight (a
clinically significant trait) and fibre disorganization in pathways linking visual with
emotion/memory processing systems was suggested by diffusion-weighted magnetic
resonance imaging (MRI) of white matter. Another study discovered that those with BDD
have problems with the whole-brain's structural topologic organization. The scientists also
discovered indications of interhemispheric visual information transmission and aberrant
connection between regions engaged in lower-order visual processing and those involved in
higher-order visual and emotional processing, which may be related to anomalies in
information processing.
According to a study looking into the potential contribution of early-life sexual, physical, or
emotional abuse to the emergence of BDD, those with the disorder reported more recollected
memories of sexual and physical abuse in their formative years or adolescence than did the
healthy control individuals. [38] These results imply that misuse may be a possible risk factor
for BDD development.
PREVALENCE
The point prevalence among U.S. adults is 2.4% (2.5% in females and 2.2% in males).
Outside the United States (i.e., Germany), current prevalence is approximately 1.7%–1.8%,
with a gender distribution similar to that in the United States. The current prevalence is 9%–
15% among dermatology patients, 7%–8% among U.S. cosmetic surgery patients, 3%– 16%
among international cosmetic surgery patients (most studies), 8% among adult orthodontia
patients, and 10% among patients presenting for oral or maxillofacial surgery
PROGNOSTIC FACTORS
The symptoms of body dysmorphic disorder (BDD) include severe suffering, job difficulties,
or social ill health. Many BDD sufferers also struggle with comorbid mental health issues
such OCD, significant depression, delusions, or social anxiety.
BDD often has a fair prognosis when thoroughly and appropriately treated with both
medication and psychotherapy. According to a short prospective study on the progression of
BDD, the likelihood of complete recovery is rather high (0.76) and the likelihood of relapse
after remission is low (0.14 over 8 years). [49] The need for more comprehensive and
thorough therapy as well as follow-up care may arise from the presence of concomitant
disorders or a delusional intensity of belief. 30% of people with a primary diagnosis of BDD
also fit the OCD criteria. The two diseases share a number of characteristics, including
recurrent thoughts about a perceived fault and time-consuming efforts aimed at covering up
or confirming the defect. Poor insight, ideas of reference, inflated ideas, and delusions are far
more prevalent in BDD than in OCD.
About 60% of BDD patients also have major depression, which is a frequent comorbidity and
puts these patients at higher risk for suicide. 45-70% of people with BDD report having
suicidal thoughts, and 22-24% report having attempted suicide in the past. Different BDD
sufferers are more or less conscious of the mental nature of their condition. Even when they
are aware that their worries are unreasonable, many people nonetheless agonize over a
perceived flaw. Other BDD sufferers are thought to be delusional and unaware of their odd
behavioral habits.
People with BDD frequently exhibit severe social and vocational dysfunctions that can
worsen to the point of social isolation. Few people achieve functional remission, and
psychosocial functioning frequently remains poor over time. [53, 54]
In one study, nearly 50% of the patients who had an eating issue displayed BDD. [55]
Therefore, efforts should be made to identify BDD in patients with eating disorders,
particularly since its presence will influence treatment.
HOARDING DISORDER
ETIOLOGY:
Hoarding has no known cause. Despite the fact that many patients would mention a family
history of hoarding, genetic research has implicated a number of different genes. The intense
sentimental attachment that hoarding patients have to their things, [6] trouble starting and
finishing tasks, [7] indecision, and diminished memory confidence are all factors that have
been the subject of different psychological theories. Some individuals with late-onset
hoarding cite stressful life events as precipitants, including grief and loss.
PREVALENCE
PROGNOSTIC FACTORS.
Hoarding has a chronic and progressive pattern, with symptoms beginning in adolescence and
getting worse as people get older.
TRICHOTILLOMANIA
ETIOLOGY:
Trichotillomania's aetiology is mainly unknown, while both genetic and environmental
factors have been suggested as potential contributors. The following are some of the
explanations that have been put out for the development and maintenance of the hair-pulling
behaviour:
• Genetic susceptibility: According to the DSM-5, there is some evidence that genetic
predisposition plays a part [8]. Trichotillomania is more common in first-degree
relatives and in those with obsessive-compulsive disorder (OCD).
PREVALENCE
Prevalence In the general population, the 12-month prevalence estimate for trichotillomania
in adults and adolescents is 1%–2%. Females are more frequently affected than males, at a
ratio of approximately 10:1. This estimate likely reflects the true gender ratio of the
condition, although it may also reflect differential treatment seeking based on gender or
cultural attitudes regarding appearance (e.g., acceptance of normative hair loss among males).
Among children with trichotillomania, males and females are more equally represented.
PROGNOSTIC FACTORS
The prognosis is bright for very young children who pull their hair out; it could be more
accurate to refer to small children's hair pulling as a short-term habit issue. The prognosis for
alopecia in late childhood and adolescence is typically good, although caution should be
exercised because it frequently lasts for months or even years before relapsing at an
unpredictable period. The prognosis is dismal and permanent recovery is uncommon in adult
patients.
EXCORIATION DISORDER
ETIOLOGY:
Numerous factors can contribute to neurotic excoriations, including selecting as a coping
mechanism for stress or, as previously mentioned, underlying psychopathology. [7]
Obsessive-compulsive disorder (OCD) is seen by some to show physically itself in neurotic
excoriations.
PREVALENCE
In the general population, the lifetime prevalence for excoriation disorder in adults is 1.4% or
somewhat higher. Three-quarters or more of individuals with the disorder are female. This
likely reflects the true gender ratio of the condition, although it may also reflect differential
treatment seeking based on gender or cultural attitudes regarding appearance.
PROGNOSTIC FACTORS
The prognosis for recovery is dismal, with the exception of minor temporary cases brought on by an
abrupt stress. The patient's life circumstances tend to cause the disease to wax and wane. However,
if the underlying psychological condition is managed, excoriation disorder is frequently under
control. Patients require assistance, but it can be challenging to break the picking habit. Excoriation
illness typically persists for a long time without medical and mental intervention. Untreated
excoriations may cause scarring, an infection, or tissue damage that may call for antibiotics or
surgery. Rarely, wrist synovitis caused by persistent picking have been described.