Teaching 30 july

MRCPsych General Adult Psychiatry
(Eating Disorders, OCD and PTSD)
By: Yasir Hameed (MRCPsych)
Specialist Registrar
Norfolk and Suffolk NHS Trust
30 July 2014

Disclaimer
• SPMM and Birmingham notes
• BMJ learning
• Various MCQs from previous papers and online
courses

Eating disorders
1. Anorexia nervosa
2. Bulimia nervosa
3. EDNOS – atypical ED or ED not otherwise
specified

Important to note
• Binge eating disorders
• Amenorrhoea in Anorexia
• Food intake during binges
• Bulimia vs anorexia patients’ engagement
• Stability of the diagnosis

Epidemiology of bulimia and
anorexia
(adapted from Fairburn & Harrison, 2003)

Risk factors (adapted from Fairburn & Harrison, 2003)
• Female sex
• Adolescence and early adulthood
• Western cultural adaptation
• Family history of ED, depression
• Family history of substance misuse, especially alcoholism (bulimia
nervosa)
• Family history of obesity (bulimia nervosa)
• Adverse parenting (especially low contact, high expectations, parental
discord)

Risk factors (cont’d)
• Childhood sexual abuse
• Critical comments about eating, shape, or weight from family and
others
• Occupational and recreational pressure to be slim
• Low self-esteem
• Perfectionism (anorexia nervosa more than bulimia nervosa)
• Past history of being obese (bulimia nervosa)
• Early menarche (bulimia nervosa)

Binge eating disorder (BED)
• Recurrent episodes of binge eating in the absence of extreme
weight-control behaviour
• Association with obesity
• Patients typically present in their 40s, more males (25%)
• High spontaneous remission
• Stress associated overeating common phenomenon
• Self help, behavioural weight loss programmes and CBT/IPT
can help

Diagnostic features of bulimia
nervosa
The core diagnostic symptoms include :
• Extreme concerns about weight
• Regular binge eating
• Preoccupation with food and diet
• Extreme measures of weight control
• If there is also severe self maintained weight loss
(for example with a body mass index <18) a
diagnosis of anorexia nervosa of the “binge
eating and purging” type will apply.

Physical symptoms of EDs (adapted from
Fairburn & Harrison, 2003)
• Increased sensitivity to cold
• Gastrointestinal symptoms
• Dizziness and syncope
• Amenorrhoea
• Poor sleep with early morning wakening

Physical signs of EDs
• Emaciation; stunted growth and failure of breast
development (if pre-pubertal onset)
• Dry skin; fine downy hair (lanugo) on the back,
forearms, and side of the face; in patients with
• Hyper carotenaemia, orange discolouration of the skin
• Russell's sign – calluses in knuckles due to repeated
vomit induction
• Swelling of parotid and submandibular glands
(especially in bulimic patients)

Signs (cont’d)
• Erosion of inner surface of front teeth (peri-mylolysis) in
those who vomit frequently
• Cold hands and feet; hypothermia
• Bradycardia; orthostatic hypotension; cardiac
arrhythmias (especially in underweight patients and
those with electrolyte abnormalities)
• Dependent oedema (complicating assessment of
bodyweight)
• Weak proximal muscles (elicited as difficulty rising from
a squatting position)

Abnormalities on physical
investigation
Endocrine
• Low concentrations of LH, FSH and and
oestradiol
• Low T3, T4 in low normal range, normal
concentrations of TSH (low T3 syndrome)
• Mild increase in plasma cortisol
• Raised GH
• Severe hypoglycaemia (rare)
• Low leptin

Investigations (cont’d)
Cardiovascular
• ECG abnormalities
• Myopathy and fatal cardiomyopathy
Gastrointestinal
• Delayed gastric emptying
• Decreased colonic motility
• Acute gastric dilatation

Investigations (cont’d)
Haematological
• Moderate normocytic normochromic anaemia
• Mild leucopenia with relative lymphocytosis
• Thrombocytopenia
Other metabolic abnormalities
• Hypercholesterolaemia
• Raised serum carotene
• Hypophosphataemia
• Dehydration

Electrolyte disturbance
• metabolic alkalosis and hypokalaemia (vomiting)
• metabolic acidosis, hyponatraemia, hypokalaemia
(laxative abuse)
Other abnormalities
• Osteopenia and osteoporosis (with heightened
fracture risk)
• Enlarged cerebral ventricles and external
cerebrospinal fluid spaces (pseudo atrophy)

Effects on pregnancy (Human Reproduction
Update 2006 12(3):193-207)
• Decreased fertility
• May have more abortions
• Higher rates of hyperemesis gravidarum, anaemia,
impaired weight gain
• Compromised intrauterine foetal growth
• Premature delivery is more likely
• Rates of caesarean delivery is high
• Post-natal complications and post-partum
depression are higher
• Associated with low birth weight, microcephaly, low
APGAR scores.
• In actively anorexic mother, the neonate may have
hypoglycaemia

Managing bulimia
Cognitive behaviour therapy
• Typically involves about 20 individual treatment
sessions over 5 months
• 33-50% make a complete and lasting recovery
• Antidepressants
• Have an anti-bulimic effect
• Produce a rapid decline in the frequency of
binge eating and purging, and an improvement
in mood.

Managing anorexia
Major therapeutic goals:
1. Engagement
2. weight restoration
3. psychological therapy
4. if needed use of compulsion

Outpatient therapy for anorexia has best chance if
a. Illness is present for less than 6 months
b. No bingeing or vomiting
c. Have parents who cooperate and are willing to
participate in family therapy

Summary of NICE guidelines
Anorexia:
▫ Drugs should not be used as sole or primary
treatment for anorexia nervosa
▫ Consider Psychological therapies
▫ Individual and family interventions
▫ Dietary counselling should not be provided as sole
treatment for anorexia nervosa

Summary of NICE guidelines
Bulimia:
▫ Evidence-based self-help programme and/or
antidepressants
▫ SSRIs (specifically fluoxetine) are drugs of first
choice for bulimia nervosa
▫ Specifically adapted CBT
▫ Interpersonal psychotherapy should be considered
as alternative to CBT

What's the outlook? (BN)
• Up to 70% or more are in full or partial
remission
• What do patients want to know?
• Patients want to know where to go for help and
“what will work.”

Case vignette
• A 23 year old woman presents to your practice with
dizziness. On questioning you find out that she exercises
for two to three hours each day at a gym. You suspect
that she has bulimia nervosa. To confirm your suspicion
what should you ask her?
A. Are you sleeping badly and do you have a poor
appetite?
B. Do you have panic attacks?
C. Have you suffered from abuse?
D. Have you been binge eating?
E. Have you recently been dieting?

Case vignette 1
• A 23 year old woman presents to your practice with
dizziness. On questioning you find out that she exercises
for two to three hours each day at a gym. You suspect
that she has bulimia nervosa. To confirm your suspicion
what should you ask her?
A. Are you sleeping badly and do you have a poor
appetite?
B. Do you have panic attacks?
C. Have you suffered from abuse?
D. Have you been binge eating?
E. Have you recently been dieting?

• The woman tells you that as well as exercising
she is taking 40 Senokot (laxative) tablets a day
and vomiting twice a day after binge eating.
What tests should you order?
A. Liver function tests
B. Urea, creatinine, and potassium levels
C. A full blood count
D. Thyroid function tests
E. Serum calcium level

• You arrange an electrocardiogram. What
is this most likely to show?
A. Peaked T and flat P waves
B. Bradycardia
C. ST depression and tall U waves
D. QRS widening and QT prolongation
E. ST elevation and inverted T waves

• She asks you which treatments can best help people with
bulimia nervosa. What should you tell her?
A. No treatment has been found to be really effective
B. Most people improve without specific help after about
six months
C. There is good evidence supporting the use of cognitive
behavioural therapy, which is a form of psychotherapy
D. An antidepressant is best because bulimia nervosa is a
masked form of depression
E. She needs an analytic form of psychotherapy to find
out what is underlying her problems

• Your patient says she has heard that there is an
"epidemic of eating disorders." Which one of the
following should you advise her?
A. Although eating disorders are at epidemic levels there
is no need for alarm
B. The incidence of eating disorders is decreasing
C. There may have been an increase in the incidence of
eating disorders, but it is not large
D. It is only anorexia nervosa that is at epidemic levels
E. Eating disorders are increasing at the same rate as
weight disorders and obesity

• You advise her that cognitive behavioural therapy will
involve keeping a food diary. She says this won't be
necessary because she knows exactly what she eats and
can tell a therapist from memory at each session. What
would you reply?
A. OK, I'm sure that will work just as well
B. Keeping the diary is an important and essential first
step in the therapy
C. She could skip that part and come back to it later
D. Perhaps cognitive behavioural therapy isn't right for
her
E. If she takes antidepressants she will find it easier to
keep the diary

• She is worried that the cognitive behavioural therapy will
make her gain weight. What should you tell her?
A. She is likely to gain weight with cognitive behavioural
therapy, but it's better to be fat than to have bulimia
nervosa
B. She will definitely lose weight with cognitive
behavioural therapy
C. She might gain weight with cognitive behavioural
therapy, but you can prescribe her some tablets to help
D. Most people lose or gain only a few kilograms at most
E. She shouldn't gain weight with cognitive behavioural
therapy because it incorporates weight loss strategies,
such as restrictive dieting

• She confides that as well as binge eating and abusing
laxatives, she used to cut herself to relieve psychological
distress, she drinks heavily (more than eight standard
drinks daily at her local pub, mostly with friends), and
her moods go "up and down" all the time to the extent
that she can't remember ever feeling happy or relaxed
over a sustained period. What diagnosis should you now
consider?
A. Major depression
B. Borderline personality disorder
C. Social phobia
D. Bipolar disorder
E. A factitious disorder

Various MCQs
• A 30 year old man has bulimia nervosa. If he does have a
family history then which one of the following conditions
is one or both of his parents likely to have?
A. Schizophrenia
B. Pica
C. Obesity
D. Psychopathy
E. Depression
F. Bipolar disorder

Case vignette 2
• A 30 year old man has bulimia nervosa. If he does have a
family history then which one of the following conditions
is one or both of his parents likely to have?
A. Schizophrenia
B. Pica
C. Obesity
D. Psychopathy
E. Depression
F. Bipolar disorder

• The man says he is puzzled that he has an eating
disorder as he thought they only occurred in women.
Which one of the following should you advise him?
A. Eating disorders are extremely rare in men and are
usually secondary to some other problem
B. He's partly right - the only men who have eating
disorders are those who are also homosexual
C. About one in 10 people with bulimia nervosa is male,
and the presentation is similar to bulimia in females,
although excessive exercising is more common in men
than purging
D. Eating disorders are as common in men as in women,
it is just that they are not asked about them
E. Eating disorders are increasing in men at an alarming
rate

Case vignette 3
A 22-year-old man attends A&E department accompanied by very worried parents. They claim
that their son has lately become increasingly aggressive and unusually suspicious of them. He
is convinced that the neighbours are after him because they hate him. His parents are
convinced that these symptoms may be due to a very strict diet he is doing in order to take
part in a sport competition.
The patient is oriented to time, place and person. His past medical history is unremarkable
and he denies taking any medication. On examination, the patient is well built with no
abnormal findings except for nodulocystic acne on his face and back.
What is the most likely cause of this patient’s abnormal behaviour?
A. Anorexia nervosa
B. Paranoid schizophrenia
C. Bipolar disorder
D. Exogenous androgens
E. Corticosteroid abuse

Case vignette 4
• A15year old girl is admitted as an inpatient with anorexia
nervosa. She suddenly develops dizziness and shortness
of breath with chest pain. Which of the following is the
most likely complication that can explain her symptoms?
(Jan 2009)
A. Pulmonary embolism
B. First degree heart block
C. Sinus tachycardia
D. Cardiomyopathy
E. Myocarditis

Various MCQs
• With respect to epidemiological differences between
bulimia and anorexia, choose an incorrect statement:
A. Bulimia starts later than anorexia
B. Anorexia is excessively represented in lower social
classes
C. The prevalence of anorexia is around 0.5% to 1%
D. The prevalence of bulimia is around 2%
E. Stability of individual diagnoses of various eating
disorders is poor.

• Risk factors specific for bulimia rather than
anorexia include
A. Family history of obesity
B. Family history of alcoholism
C. Impulsivity
D. Early menarche
E. All of the above

• Which of the following is true with regard to the
diagnosis of eating disorders?
A. Anorexia is more prevalent than bulimia
B. Binge episodes are characteristic of anorexia
C. A typical binge can include 1000-2000 Cal
D. Anorexic patients seek treatment more often than
bulimic patients
E. Most patients with anorexia have a past history of
bulimia

• Which of the following is true with regard to the
diagnosis of eating disorders?
A. Anorexia is more prevalent than bulimia
B. Binge episodes are characteristic of anorexia
C. A typical binge can include 1000-2000 KCal
D. Anorexic patients seek treatment more often than
bulimic patients
E. Most patients with anorexia have a past history of
bulimia

• With respect to epidemiological differences between
bulimia and anorexia, choose an incorrect statement:
A. Bulimia starts later than anorexia
B. Anorexia is excessively represented in lower social
classes
C. The prevalence of anorexia is around 0.5% to 1%
D. The prevalence of bulimia is around 2%
E. Stability of individual diagnoses of various eating
disorders is poor.

• Monozygotic concordance rate in anorexia is
estimated to be around
A. 25%
B. 35%
C. 15%
D. 5%
E. 55%

• A 34 year old lady presents with recurrent episodes of
binge eating but has no weight control behaviour. She
has a general tendency to overeat and looks overweight.
Which of the following is correct regarding this
presentation?
A. Nearly a quarter of those suffering from this problem
are males
B. She has bulimia nervosa
C. She has anorexia nervosa
D. Her condition will not remit spontaneously
E. Stressful periods are associated with decline in binges

• Which of the following is a laboratory
abnormality seen in anorexia?
A. High oestrogen
B. Low cortisol
C. Hyperphosphataemia
D. Low tri-iodothyronine
E. Hyperkalaemia

• The babies of anorexic mothers
A. Are large for dates
B. Have lower APGAR scores
C. Are born post-term
D. Have a larger head circumference
E. Have diabetes

• Which of the following is not commonly
associated with bulimia?
A. Oesophageal tears
B. Dental decay
C. Peptic ulcer
D. Seizures
E. Parotid gland enlargement

• Which of the following modes of treatments is
not endorsed by evidence based guidelines for
managing anorexia?
A. Antidepressants
B. Cognitive analytical therapy
C. Cognitive behavioural therapy
D. Dialectic behavioural therapy
E. Family based interventions

• Which of the following is true with regard to use of
antidepressants in eating disorders?
A. Antidepressants do not have specific antibulimic effects
B. Antidepressants act slower in eating disorders than in
depression
C. Antidepressants are more effective than CBT in
anorexia
D. Antidepressant effects are often sustained even after
stopping the medications
E. Medications should not be used as sole treatment for
anorexia

• Focused family interventions are particularly
useful in which of the following subgroups with
eating disorders?
A. Late onset anorexia
B. Adolescents with bulimia
C. Adolescents with anorexia nervosa
D. Adults with co-morbid physical illnesses
E. Binge eating disorder

Further reading
• The Royal College of Psychiatrists
information site for eating disorders
• Includes leaflets, factsheets, books, and reports
on eating disorders, a primary care protocol for
managing adults with eating disorders, and
information about the eating disorders special
interest group and relevant events.
• https://www.rcpsych.ac.uk/members/sections/e
atingdisorders.aspx

OCD
• Introduction
• Obsessive-compulsive disorder is a prevalent and
disabling condition. Epidemiological surveys have
repeatedly shown a high lifetime prevalence, amounting
to 2-3% of the population worldwide. [ 2 ] [ 3 ] A recent
European study suggested a lower estimate, with a 12
month prevalence of 0.7% and a lifetime estimate of
0.8%. [ 4 ]
• Nevertheless, only a fraction of people with obsessive-
compulsive disorder present for treatment and the
diagnosis is often missed.
• The lifetime prevalence of obsessive-compulsive disorder
relative to other major mental disorders is given in Table
1.

Table 1. Lifetime prevalence of major mental disorders
Major depressive episode 6.7%
Obsessive-compulsive disorder 2.6%
Schizophrenia 1.9%

• The illness is more common in women than in men
(ratio 1.5:1). The mean age of onset is reported as 20
years, with bimodal peaks at ages 12-14 years and
20-22 years. [ 5 ]
• Untreated obsessive-compulsive disorder usually
runs a chronic, lifelong course: it fluctuates in
intensity but rarely disappears. In a seminal follow
up study spanning several decades, Skoog and Skoog
reported only a minority of patients had become free
from symptoms. [ 6 ]

How do I diagnose it?
• The International Classification of Diseases (10th revision,
ICD-10) and the Diagnostic Statistical Manual (4th edition,
DSM-IV) recognise obsessions or compulsions (or both) as
core symptoms of obsessive-compulsive disorder. [ 7 ] [ 8 ]
• To make the diagnosis:
• Obsessions or compulsions (or both) must be present on most
days for at least two weeks
• Obsessions and compulsions must share the following
features, all of which must be present:
▫ They must originate in the mind of the individual
▫ They must be repetitive and unpleasant
▫ At least one must be unsuccessfully resisted
▫ Carrying out the obsessive thought or compulsive act is not
intrinsically pleasurable.

• Obsessions are unwanted ideas, images, or impulses
that repeatedly enter a person's mind. Although
recognised to be generated by the person (unlike
"made thoughts" that characterise schizophrenic
delusions) they are out of character, unwanted, and
distressing.
• Compulsions are repetitive stereotyped behaviours
or mental acts that are driven by rules that must be
applied rigidly. They are not inherently enjoyable
and do not result in the completion of any useful
task. To qualify for the diagnosis the symptoms
must be experienced as disabling.

Table 2. Common symptoms of obsessive-compulsive disorder
Common obsessions Common compulsions
•Fear of causing harm to someone else
•Fear of self harm
•Fear of behaving unacceptably
•Fear of contamination
•Fear of making a mistake
•Need for symmetry or exactness
A. Behaviours
•Cleaning
•Hand washing
•Ordering and arranging
•Checking
•Asking for reassurance
B. Mental acts
•Making mental lists
•Counting
•Repeating words silently

• Most people with obsessive-compulsive disorder
endure a mixture of obsessions and compulsions.
• Common obsessions include unrealistic worries
about harm, such as being responsible for an
accident or the fear of contamination, accompanied
by avoidance of situations in which harm or
contamination may occur. These obsessions
generate compulsive behaviours aimed at avoiding
the feared event, such as excessive checking or
cleaning rituals. Other frequently occurring
obsessions include a need for symmetry or
orderliness and unwarranted fears and images about
committing aggressive or sexual acts.

• Other common compulsions include counting,
ordering, and arranging things. Symptoms are
distressing and embarrassing and patients may
be unwilling to discuss them for fear of censure.
They may involve family members in their
compulsions or persistently demand
reassurance.

• Excessive doubt, the need for completeness, shame, and
abnormal assessment of risk are thought to underlie
most obsessions.
• You need to be able to differentiate aggressive obsessions
from other forms of psychopathology, such as urges to
commit suicide or violence that occur in depression or
psychopathic disorder, respectively. People with pure
obsessive-compulsive disorder almost never carry out
the feared act and spend an excessive amount of time
and energy resisting and controlling their behaviour to
avoid the risk of harm. But people with obsessive-
compulsive disorder are not immune from the influences
of other complicating disorders that may occur in
addition, such as depression or personality disorder.

• OCD in children and young people
• OCD frequently commences in childhood or adolescence, with a prevalence
of 1% being quoted from population studies. [ 9 ] Undetected OCD in
children not only causes marked psychological distress, but also can lead to
an increased risk of morbidity and comorbidity in adulthood. [ 5
]Interestingly, some studies suggest that the juvenile onset form of OCD
seems more strongly related to a positive family history and may be more
associated with tic disorders. [ 10 ]
• You should consider guided self help for children and young people with
OCD with mild functional impairment, in conjunction with support and
information for the family or carers. Children and young people with OCD
with moderate to severe functional impairment, and those with OCD with
mild functional impairment for whom guided self help has been ineffective
or refused, should be offered CBT (including Exposure and Response
Prevention) involving the family or carers and adapted to suit the
developmental age of the child as the treatment of choice. Group or
individual formats should be offered depending upon the preference of the
child or young person and their family or carers.

• If psychological treatment is declined by children or
young people with OCD and their families or carers, or
they are unable to engage in treatment, an SSRI may be
considered with specific arrangements for careful
monitoring for adverse events. The coexistence of
comorbid conditions, learning disorders, persisting
psychosocial risk factors such as family discord, or the
presence of parental mental health problems, may be
factors if the child or young person’s OCD is not
responding to any treatment.
• Additional or alternative interventions for these aspects
should be considered. However, the child or young
person will still require evidence based treatments for
his or her OCD.

Comorbidity and the obsessive-
compulsive disorder spectrum
• A substantial lifetime comorbidity with other
disorders has been identified, including [ 11 ] :
• Depression (66%)
• Simple phobia (22%)
• Social phobia (18%)
• Eating disorder (17%)
• Alcohol dependence (14%)
• Panic disorder (12%)
• Tourette's syndrome (7%).

• There are also reports of an increased rate of obsessive-
compulsive disorder in people with schizophrenia.
Poyurovsky et al found a rate of 14% in 50 people
hospitalised with first episode schizophrenia. [ 12 ]
• Several disorders appear to be related to obsessive-
compulsive disorder by:
• The nature of their symptoms, which show similarities to
obsessions or compulsions, or
• Their frequent co-occurrence with obsessive-compulsive
disorder, or both.
• They have been termed obsessive-compulsive disorder
spectrum disorders. [ 13 ] Examples are listed in Table 3.

Table 3. Obsessive-compulsive disorder related disorders
•Autistic spectrum disorders
•Body dysmorphic disorder (dysmorphophobia)
•Trichotillomania
•Hypochondriasis
•Paraphilias
•Compulsive gambling
•Anorexia nervosa
•Gilles de la Tourette syndrome

• Hypochondriasis involving a preoccupation with health related fears
can be indistinguishable from obsessive-compulsive disorder. Body
dysmorphic disorder, which involves obsessional thoughts relating
to imagined or slight defects in appearance and frequent checking in
the mirror, can also be difficult to distinguish from obsessive-
compulsive disorder. However, in pure hypochondriasis and body
dysmorphic disorder obsessions and compulsions are restricted to
specific body related themes, unlike obsessive-compulsive disorder
in which a broader range of obsessive-compulsive symptoms are
usually manifested. Those with hypochondriasis do not regard their
preoccupations as senseless and try little to resist them.
• Tourette's syndrome, Huntington's disease, and Sydenham's chorea
are neurological disorders that are commonly associated with
obsessive-compulsive behaviours.

Non-psychiatric presentations of
obsessive-compulsive disorder
• Patients may present in a wide variety of ways. They may
present with:
• Chapped hands, eczema, or trichotillomania
• Fear of cancer
• Fear of HIV
• Vaginal discomfort from douching.
• People with obsessive-compulsive disorder frequently present
to nonpsychiatrists for treatment and there is a need for
greater awareness of obsessive-compulsive disorder in
nonpsychiatric healthcare settings.
• Patients with hypochondriacal obsessions, falsely believing
themselves to be unwell, often present to GPs or hospital
services seeking medical reassurance where their obsessive-
compulsive disorder may escape notice.

• A recent survey of 92 patients attending the dermatology clinic at a
general hospital revealed approximately 20% screened positive
either for obsessive-compulsive disorder or a clinically relevant
obsessive-compulsive disorder related disorder. In most cases the
obsessional symptoms had not been previously diagnosed. Patients
had a variety of dermatological problems, not simply sore hands
from excessive washing, most notably eczema and acne. [ 14 ]
• People with obsessive-compulsive disorder may also present to the
genitourinary clinic with obsessions concerning venereal disease;
previously syphilis, nowadays mainly HIV infection.
• Women may develop obsessive-compulsive disorder in pregnancy or
the puerperium. [ 15 ] Their illness may be mistaken for postnatal
depression. It is important to differentiate between severely
depressed women who may threaten the safety of their children
through infanticide and women with postnatal obsessive-
compulsive disorder, who obsessively worry about harming their
children but are most unlikely to do so.

Raising the profile of obsessive-
compulsive disorder
• Obsessive-compulsive disorder is a chronic condition, which, if untreated,
causes substantial social and emotional impairment. It is responsible for
people failing to achieve their academic or occupational potential, and
cripples personal relationships. The celibacy rate associated with obsessive-
compulsive disorder is unusually high. [ 16 ]
• Many patients hide their symptoms because they fear they are going mad or
because of the stigma attached to the illness. It can therefore take some
people many years before they are able to discuss their problems with a
professional.
• The diagnosis and treatment of obsessive-compulsive disorder by
healthcare practitioners is also less than satisfactory. Patients are reported
to wait roughly 17 years before receiving appropriate treatment, despite
surveys indicating that the time between the onset of symptoms and correct
diagnosis is shortening. [ 16 ] [ 17 ] Better recognition of obsessive-
compulsive disorder is important because the illness readily responds to
psychological or pharmacological treatments.

Table 4. The Zohar-Fineberg obsessive-compulsive screen
1.Do you wash or clean a lot?
2.Do you check things a lot?
3.Is there any thought that keeps bothering you that you would like to get rid of
but can't?
4.Do your daily activities take a long time to finish?
5.Are you concerned about orderliness or symmetry?

• Measuring obsessive-compulsive disorder
• People with obsessive-compulsive disorder are
notoriously poor at gauging their level of
impairment, particularly during treatment when
they may have difficulty recognising signs of
improvement. It can be helpful to ask a family
member to corroborate the patient's history.

• Psychological treatment
• Behavioural therapy
• Prolonged "graded exposure" to the feared situation combined with self
imposed "response prevention" has been shown to be effective for patients
with obsessions and overt compulsions.
• Graded exposure is based on the observation that an obsessional patient
who has an intense fear of a situation, such as contamination with dirt,
when confronted with the feared situation may escape or perform activities
(washing) to reduce or prevent the harm they fear might result. Escape and
compulsions reduce the unpleasant anxiety associated with their
obsessions. Consequently, these behaviours are reinforced and worsen after
each episode of brief exposure and escape.
• The reduction in anxiety produced by a compulsive ritual such as washing
tends to be small and the effect temporary. The aim of graded exposure
treatment is to produce prolonged periods of contact with the feared
situation until anxiety naturally reduces (habituation), producing more long
lasting remediation.

• During treatment the patient may be asked to dirty
their hand and remain in that situation until their
anxiety has decreased significantly. This can take
one or two hours. Patients are taught techniques to
help them endure and overcome the anxiety
associated with exposure.
• Although this appears to be a simple technique, the
therapist's skill is essential in accurately identifying
the appropriate fear provoking cues, educating the
patient about the therapy, and agreeing a level of
exposure that will cause a degree of anxiety that can
be tolerated.

• Response prevention - prevention of mental or physical compulsions (in this example by not washing
the dirt away) - is the essential second step following exposure. This can usually be achieved by
demonstrating to the patient how compulsions interfere with exposure.
• Exposure tasks are repeated by the patient at least daily (preferably three times a day) until there is little
anxiety even at the start of exposure. More difficult situations can then be tackled when the patient has
completed all the tasks on their individual hierarchy of anxiety.
• For exposure to be most effective, it should be:
• Prolonged rather than of short duration [ 18 ]
• In real life rather than in fantasy [ 19 ]
• Practised regularly with homework tasks. [ 20 ]
• Graded exposure and response prevention has been shown to be a quick and cost effective treatment. The
technique can be easily learnt through supervision from a trained therapist or from appropriate reading
material (for example Hawton et al and Stern and Drummond [ 21 ] [ 22 ] ).
• Some patients need 10 to 15 hours of therapist aided exposure time, while others need no more than
simple instruction in self exposure techniques.
• There are now several self help manuals (for example Veale [ 23 ] ). Computerised treatment packages
such as BT Steps (Marks et al) have also become popular. [ 24 ] But unless the disorder is mild, few
patients are able to complete self help programmes without some guidance from a
• professional.

• Cognitive behavioural therapy
• Cognitive behavioural therapy involves supplementing graded exposure and
response prevention with talking treatments aimed at remedying faulty
reasoning that may have developed with the disorder.
• For example, people may be encouraged to re-evaluate overvalued beliefs
about risk or personal responsibility to regain a more realistic perspective. [
25 ] [ 26 ] Although there is no clear evidence that cognitive therapy
produces better results than simple exposure and response prevention,
there is evidence in favour of using targeted cognitive techniques to
overcome specific problems with exposure and facilitate patient
engagement and concordance. [ 27 ] [ 28 ] [ 29 ] [ 30 ]
• In contrast to simple behavioural therapy, cognitive behavioural therapy
requires a greater level of therapist expertise. This is because poorly applied
cognitive therapy may make obsessive-compulsive disorder worse as the
patient can incorporate the process of looking for evidence to confirm or
refute obsessions into their rituals.

• Outcome of behavioural therapy and cognitive behavioural
therapy
• Controlled trials indicated that graded exposure and response prevention
was effective in many patients who completed treatment, with success rates
varying from 75% to 85%. [ 31 ] [ 32 ]However, these studies lacked
intention to treat data.
• Family involvement in treatment may improve outcome. [ 33 ] According to
an uncontrolled follow up survey, the improvements made during graded
exposure and response prevention can be maintained for at least four
years. [ 34 ]
• However, some patients are reluctant to engage in exposure treatments
even when accompanied by cognitive therapy, while others need booster
sessions because their symptoms return. Patients with compulsions appear
to respond better to behavioural therapy than patients with obsessions. [ 35
] Patients with psychiatric comorbidity, in particular depression of more
than moderate intensity, tend not to respond well to cognitive behavioural
therapy unless medication is added. [ 36 ]

• Other forms of psychotherapy
• There is no evidence to support psychodynamic
psychotherapy for patients with obsessional disorders. [
37 ] Indeed, there is a perception that insight oriented
therapy can make obsessive-compulsive disorder worse
by encouraging introspection. For this reason this form
of psychotherapy is not recommended for most patients
(see the NICE website at:http://www.nice.org.uk).
Moreover, there is no convincing evidence for the use of
psychoanalysis, transactional analysis, hypnosis, or
marital or couple therapy for treating obsessive-
compulsive disorder.

• Pharmacological treatment
• The weight of evidence shows that obsessive-compulsive disorder responds
preferentially to drugs that powerfully inhibit the synaptic reuptake of
serotonin. These are the:
• Tricyclic antidepressant clomipramine
• More highly selective serotonin reuptake inhibitors (SSRIs).
• Meta-analyses of randomised controlled trials have shown that these drugs
are effective in obsessive-compulsive disorder, both in the presence and
absence of comorbid depression. [ 38 ]
• Clomipramine
• Building on several small, positive trials, two seminal multicentre studies of
clomipramine, which included 238 and 263 nondepressed patients with
obsessive-compulsive disorder, were performed.[ 39 ] [ 40 ] Significant
differences between drug and placebo emerged in favour of clomipramine
as early as the first and second weeks of treatment. The benefits of
clomipramine, given in flexible doses, increased slowly and gradually up to
around 45% improvement by the 10 week endpoint of the studies.

• Clomipramine is associated with potentially dangerous side effects such as
cardiotoxicity and cognitive impairment, which occur substantially more
with clomipramine than with SSRIs. There is also an increased risk of
convulsions in patients taking clomipramine (up to 2%).
• The recommended maximum daily dose of clomipramine in the UK is 250
mg.
• Selective serotonin reuptake inhibitors
• The efficacy of fluvoxamine, sertraline, fluoxetine, paroxetine, and
citalopram in the treatment of obsessive-compulsive disorder has been
demonstrated in large scale studies. [ 41 ] [ 42 ] [ 43 ] [ 44 ] [ 45 ] [ 46 ] [ 47
] [ 48 ] [ 49 ] [ 50 ] [ 51 ] Like clomipramine the effect appears early but
takes several weeks to develop fully. Dose finding studies have suggested
that higher doses (60 mg citalopram, fluoxetine, paroxetine; 200 mg
sertraline) are more effective, although the evidence for higher doses of
sertraline and citalopram was less clear cut. [ 45 ] [ 47 ] [ 48 ] [ 51 ] [ 52 ]

• Which drug is the most clinically effective?
• Head to head studies show equivalent efficacy and better
tolerability for SSRIs compared with clomipramine. [ 50
] [ 53 ] Not only is the risk of dangerous side effects such
as convulsions, cardiotoxicity, and cognitive impairment
substantially lower with SSRIs, but clomipramine is also
associated with greater impairment of sexual
performance (up to 80% of patients) compared with
SSRIs (up to 30% of patients) and troublesome
anticholinergic effects. [ 54 ]
• On the other hand, SSRIs are associated with initially
increased nausea, nervousness, and insomnia.[ 55 ]

• Slow, gradual improvement characterises the response to
medication
• The treatment effect of SSRIs or clomipramine emerges within days
after treatment is started, and increases slowly and almost
imperceptibly for weeks and months. Gains continue to accrue for at
least six months and probably longer. Sometimes progress seems
remarkably slow, and people with obsessive-compulsive disorder
may find it difficult to acknowledge changes are occurring.
• Meanwhile, side effects such as nausea and agitation tend to emerge
early, before signs of improvement are consolidated, but usually
abate over time. [ 45 ] For these people it is important to allow
enough time for the treatment effect to develop and not to
discontinue or change the drug prematurely. A trial of at least 12
weeks at the maximum tolerated dose and careful assessment is
advisable before judging its effectiveness.

• Long term drug treatment
• Obsessive-compulsive disorder is a chronic illness and so treatment needs
to be tested to see whether it remains effective in the longer term. A small
number of double blind studies lasting up to 12 months have shown that
those who responded to acute treatment benefited from continuing with
medication with no evidence of tolerance developing. [ 45 ] [ 56 ] [ 57 ]
• In contrast, studies looking at the effects of discontinuing clomipramine or
SSRIs under double blind, placebo controlled conditions showed a
relatively rapid and incremental worsening of symptoms in people who
switched to placebo.
• This emphasises the importance of maintaining treatment with medication
long term, that is for at least 12 months (see the NICE website
at: http://www.nice.org.uk), and argues against discontinuation of
treatment even after one year. You should discuss the option of long term
medication with the patient. If medication is to be stopped, this may best be
done gradually over weeks and months to mitigate possible withdrawal
effects.

• Comparison of pharmacological and psychological treatments
• From available evidence, psychological and pharmacological treatments
appear equally effective and it is not clear whether the two forms of
treatment combined is superior to psychological or pharmacological
monotherapy.
• The lack of availability of psychological therapies, relative to
pharmacotherapy, means that drug treatment is started first for most
people.
• Treatment resistant obsessive-compulsive disorder
• Residual symptoms remain despite prolonged treatment in about 30% of
patients. If the patient has been receiving monotherapy with either
treatment as a first line strategy it may be appropriate to combine the two
forms.
• The evidence base for the management of treatment resistant obsessive-
compulsive disorder is slim, but a few treatment strategies are available
(Table 5).

Table 5. Evidence based strategies for resistant obsessive-
compulsive disorder
•Increase the dose
•Switch to another SSRI
•Change administration to intravenous (citalopram, clomipramine)
•Change to a selective noradrenaline reuptake inhibitor
•Add clomipramine and an SSRI
•Add an antipsychotic

• Some of these can be managed by the GP. Alternatively, it would be
reasonable to refer patients with refractory illness to the local
psychiatry service.
• Before changing from first line treatments it is important to check
concordance and review the diagnosis. In particular you should look
for evidence of Tourette's syndrome, which can easily masquerade
as obsessive-compulsive disorder and which responds preferentially
to the addition of antipsychotic agents.
• Increase the dose
• Uncontrolled case studies suggest that for some patients increasing
doses of SSRIs above formulary limits may produce a better effect. [
58 ] Doses of clomipramine up to 300 mg have been systematically
investigated in the US in large scale trials and found to be safe.
However, doses exceeding 250 mg should be prescribed with
caution because of the risk of seizures and cardiotoxicity.

• Switch to another SSRI
• Some people may be helped by switching drug. [ 59 ] [ 60 ]
• Change administration to intravenous (citalopram,
clomipramine)
• Although a single double blind study investigating refractory obsessive-
compulsive disorder has shown intravenous clomipramine to be more
effective than placebo, changing the mode of drug delivery from oral to
intravenous is impractical in many patients. [ 61 ]
• Change to a selective noradrenaline reuptake inhibitor
• Venlafaxine acts rather like SSRIs at higher dose levels. The evidence
supporting switching from SSRIs to venlafaxine is not strong. [ 62 ]
• Add clomipramine and an SSRI
• The combination of an SSRI with clomipramine has been suggested,
although controlled studies are lacking. Such a procedure may best be
managed by a clinician experienced in treating resistant obsessive-
compulsive disorder. It is advisable to monitor the patient's ECG and
clomipramine plasma level.

• Combining SSRIs and antipsychotic properties
• Obsessive-compulsive disorder does not respond to antipsychotics given as
monotherapy.
• Although evidence for adding antipsychotics is inconsistent, placebo
controlled studies suggest that atypical antipsychotics added in may have a
role in treatment resistant obsessive-compulsive disorder, particularly
risperidone, quetiapine, olanzapine, and haloperidol. [ 63 ]
• Doses used in these studies were at the lower range to minimise side effects.
Recent studies have been of short duration and small sample size, and were
therefore prone to type II errors. [ 64 ] [ 65 ]There is insufficient evidence
to prefer one antipsychotic over another.
• Other strategies for refractory obsessive-compulsive disorder
• The efficacy of several other treatments is not yet proved.
• Immune system modulating drugs, such as intravenous immunoglobulin
and plasmapheresis, may have a role in obsessive-compulsive disorder, for
example following streptococcal infections in children. [ 66 ]
• Electroconvulsive therapy may help treat comorbid depression but is not
thought to be effective for treating obsessive-compulsive disorder alone.

• Invasive treatments such as capsulotomy and
cingulotomy produce an effect in difficult to treat
obsessive-compulsive disorder, but the evidence is
limited. Stereotactic neurosurgery is recommended
only as a last option.
• Deep brain stimulation involves less intracerebral
neuronal damage and holds promise for future
investigation in highly specialised centres.
• NICE guidelines for obsessive-compulsive
disorder
• The NICE guidelines for obsessive-compulsive
disorder are summarised in Figure 1. [ 1 ]

• Mild functional impairment or patient
preference for low intensity approach
• Offer cognitive behavioural therapy (including
exposure and response prevention)

• If the patient cannot engage in cognitive
behavioural therapy (including exposure and
response prevention) or if cognitive behavioural
therapy (including exposure and response
prevention) is inadequate, or if the person has
mild functional impairment, offer a choice of
either
Treatment with an SSRI alone (12 weeks) or
cognitive behavioural therapy (including
exposure and response prevention) alone (>10
therapist hours)

• Inadequate response or severe functional
impairment
• Offer SSRI and cognitive behavioural therapy
(including exposure and response prevention)
combined

• Inadequate response after 12 weeks or no
response to SSRI alone, or patient has not
engaged in CBT (including exposure and
response prevention)
• Offer either a different SSRI or clomipramine

• No response to a full trial of at least one SSRI
alone, a full trial of combined SSRI + cognitive
behavioural therapy (including exposure and
response prevention), or a full trial of
clomipramine alone

• Refer to multidisciplinary mental health team
with specialist expertise in obsessive-compulsive
disorder
• Still no response

• Consider:
• Additional cognitive behavioural therapy
(including exposure and response prevention) or
cognitive therapy
• Adding an antipsychotic to an SSRI or
clomipramine
• The combination of clomipramine and
citalopram.

• What is the lifetime prevalence of
obsessive-compulsive disorder?
• 2%
• 5%
• 10%
• 15%

• Which one of the following statements
about obsessions in obsessive-compulsive
disorder is correct?
• They are enjoyable
• They are recognised to be generated by someone
else
• They are out of character, unwanted, and
distressing
• They are never sexual in nature

• What is the mean age of onset of
• 10 years
• 20 years
• 30 years
• 40 years

• In response prevention, when is exposure
most effective?
• When it is of short duration
• When undertaken in reality rather than in
fantasy
• When undertaken only in therapy sessions

• Which one of the following statements
about behavioural therapy is correct?
• Compulsions appear to respond better than
obsessions
• Patients with psychiatric morbidity respond
better than those without
• It is less effective than psychodynamic
psychotherapy in obsessive-compulsive disorder
• Comorbid depression has no effect on outcome

• Which one of the following statements about
the use of SSRIs in obsessive-compulsive
disorder is correct?
• They are more likely to cause seizures than
clomipramine
• A trial of at least 12 weeks is advisable before
judging response
• Signs of improvement appear before side effects
appear
• They are associated with a greater prevalence of
sexual side effects than clomipramine

• Which one of the following is an evidence
based strategy for people with obsessive-
compulsive disorder that is resistant to
treatment?
• Changing from SSRIs to venlafaxine
• Adding inositol as augmentation
• Combining SSRIs and an antipsychotic
• Electroconvulsive therapy

• Which one of the following statements about
antipsychotics in treatment resistant
obsessive-compulsive disorder is correct?
• They are effective as monotherapy
• Evidence for their use as add on treatment is very
strong
• Clozapine has been shown to be effective as add on
treatment
• Haloperidol has been shown to be effective as add
on treatment

• Which one of the following forms of
psychotherapy is recommended for treating
• Psychoanalysis
• Transactional analysis
• Marital or couple therapy
• Graded exposure and response prevention

• The lifetime prevalence of OCD is around
(August 2008)
• A. 10 - 20%
• B. 0.5 – 1%
• C. 2 – 3%
• D. 8 – 10%
• E. 1 to 2 in 1000

• Which of the following neuroimaging findings is
most consistent with OCD? (August 2008)
• A. Decreased metabolism at orbitocingulate
region
• B. Increased metabolism of orbitocingulate
region
• C. Decreased metabolism at dorsal prefrontal
cortex
• D. Increased metabolism at amygdala
• E. Decreased metabolism at amygdala

• Which of the following statements is true regarding anorexia nervosa?
• choice.
• A.
• Amenorrhoea precedes weight loss in 50% of patients
• B.
• Lack of sexual interest is usual
• C.
• High levels of T3 and T4 with low levels of thyroid-stimulating hormone (TSH) are a usual biochemical
finding
• D.
• Decreased growth hormone concentration occurs
• E.
• 25% of patients eventually develop schizophrenia
• The answer is: B
• Amenorrhoea precedes weight loss in 20% of patients; low levels of T3 and low normal T4 with normal
TSH is a usual biochemical finding; raised growth hormone concentration is seen. Anorexia does not
evolve into shizophrenia.#

• Which of the following statements is true regarding restoration of weight in
anorexia nervosa?
• choice.
• A.
• It is usually done as an outpatient
• B.
• The aim is to increase body weight by 0.5 kg a week
• C.
• It requires an extra 500–1000 calories per day
• D.
• The usual target weight is between a healthy weight and a weight the
patient thinks is ideal
• E.
• All of the above

• OCD (neuroimaging)
• •
• Studies utilizing 18Fluorodeoxyglucose PET (FDG-PET)
report increased glucose metabolism in the orbitofrontal
cortex (OFC), caudate, thalamus, prefrontal cortex, and
anterior cingulate among patients with OCD as compared
with nonpatients.
• Studies utilizing Technetium-99m (99mTc )-
hexamethylpropyleneamine-
• oxime SPECT (HMPAO-SPECT) have found both increased
and decreased blood flow to various brain regions including
the OFC, caudate, various areas of the cortex, and thalamus in
OCD patients as compared with normal controls.Odd speech
without being incoherent

• All of the following are licenced for obsessive
compulsive disorder except.
A. Paroxetine
• B. Sertraline
• C. Escitalopram
• D. Citalopram
• E. Fluoxetine

• What would you do for a patient with OCD and
no improvement after two months on 50mg of
• sertraline? (March 2008)
• A. Increase the sertraline
• B. Change to a different SSRI
• C. Add an antipsychotic
• D. Switch to venlafaxine
• E. Add sodium valproate

• A. The dose required to treat OCD is higher than dose
required for depression and initial response
• can take 10-12 weeks. (Maudsley.2007). If there is no
response to initial starting doses of SSRIs, dose
• should be gradually increased. (NICE.2005) Venlafaxine and
valproate are not indicated at this stage
• for OCD. Antipsychotics may be used as second line
augmenting agents.
• Maudsley prescribing guidelines, 9th edition, page
252
• NICE Guidelines. Obsessive-compulsive disorder:
Core interventions in the treatment of
• obsessive-compulsive disorder and body dysmorphic
disorder.2005

• A community health worker regularly sees a patient
with OCD. She wants to use a scale to
• screen for depression before asking the patient to
attend your clinic for an evaluation. Which scale
would you choose? (Jan 2009)
• a. Edinburgh depression scale
• b. Beck’s depression inventory
• c. Montgomery Asberg Rating Scale
• d. Calgary depression scale
• e. Schedule for clinical assessment in
Neuropsychiatry

• Ans:B. A community health worker can screen
for depression in a high risk group by using self
• rated Beck’s depression inventory. Other scales
mentioned here may not be useful for the given
• clinical scenario. A trained clinician could use
Hamilton Depression Rating Scale in OCD
patients
• to assess severity and presence of depression

• In OCD which of the following symptoms may be
specifically resistant to treatment?
• A. Washing
• B. Checking
• C. Hoarding
• D. Sexual obsessions
• E. Religious obsessions

• Which of the following is associated with
PANDAS?
• A. Panic disorder
• B. Agoraphobia
• C. Psychosis
• D. OCD
• E. Hypochondriasis

• The first line treatment in an adult with severe
OCD is
• A. SSRIs only
• B. Clomipramine
• C. CBT only
• D. A choice of either SSRI or CBT
• E. Antipsychotic augmentation

• Which of the following outcomes is often used as
treatment response in OCD trials?
• A. 35% reduction in YBOCS
• B. YBOCS scores fall below detectable levels
• C. 50% reduction in YBOCS
• D. 75% reduction in YBOCS
• E. 20% reduction in YBOCS

• In PANDAS which of the following tests is most
likely to be positive?
• A. Anti DNAse B
• B. Anti nuclear antibodies
• C. pANCA
• D. cANCA
• E. Anti Basal Ganglia antibodies

PANDAS
• Paediatric autoimmune neuropsychiatric
disorders associated with streptococcal
infection—PANDAS is thought
• to be secondary to streptococcal infection and
mediated by autoantibodies binding to basal
ganglia. This produces
• tics, fluctuating obsessive compulsive symptoms
and anxiety.

• National Institute of Mental Health Clinical Diagnostic
Criteria for PANDAS
• 1. Presence of OCD or a tic disorder.
• 2. Onset between 3 years of age and the beginning of
puberty.
• 3. Abrupt onset of symptoms or a course characterized
by dramatic exacerbations of symptoms.
• 4. The onset or the exacerbations of symptoms is
temporally related to infection with GABHS.
• 5. Abnormal results of neurologic examination
(hyperactivity, choreiform movements, and/or tics)
during an
• exacerbation.

• Note that the neuropsychiatric symptoms need not have
onset during streptococcal (group A beta hemolytic)
• infection; exacerbation correlated temporally is also
acceptable for a diagnosis.
• AntiDNAseB or Antistreptolysin O titres are likely to be
elevated in most with recent streptococcal infection. A
• fraction of these may have auto antibodies to neurons in
basal ganglia called anti basal ganglia antibodies. These
• are not established as diagnostic of PANDAS though
initial studies are encouraging.

OCD spectrum
• OCD spectrum disorders can be classified as
• 1. Those associated with somatic preoccupation
e.g.body dysmorphic disorder or anorexia nervosa.
• 2. Those associated with neurological disorders
(repetitive behaviours) e.g. Tourette syndrome,
Sydenham's
• chorea and autism.
• 3. Those associated with impulse control
disorders or with rousing or pleasurable repetitive
behaviours e.g.
• paraphilias, kleptomania, trichotillomania, and
pathological gambling. (Castle & Phillips, 2006)

• Various OCD spectrum disorders are
• 1. Anankastic personality
• 2. Anorexia nervosa
• 3. Asperger’s
• 4. Body dysmorphic disorder
• 5. Hypochondriasis
• 6. Kleptomania
• 7. Sydenham’s chorea
• 8. Tourette’s syndrome.
• 9. Trichotillomania

Obsessive compulsive disorder in
young people (NICE Guidelines)
• NICE suggest the following on the management of OCD in
young people
• Mild - Guided self help, if no improvement try CBT with ERP
• Moderate / severe - CBT with ERP (first), then SSRI's
•
NICE recommend using sertraline and fluvoxamine for OCD
in young people.
If the child also has depression then fluoxetine is suggested.
Clomipramine is suggested as second line.
Treatment should be continued for at least 6 months from the
beginning of remission.

Post Traumatic Stress Disorder
• Factors associated with post-traumatic stress disorder
(from Bisson, 2007):
• Pretraumatic factors
• • Previous psychiatric disorder
• • Sex (more prevalent in female patients than in male patients)
• • Personality (external locus of control greater than internal locus of
control)
• • Lower socioeconomic status
• • Lack of education
• • Race (minority status)
• • Previous trauma including childhood unresolved trauma
• • Family history of psychiatric disorders
• • Insecure childhood attachment
• • Personality disorders including ASPD, Borderline.

• Peritraumatic factors
• • Severity of trauma
• • Perceived threat to life
• • Peritraumatic emotions
• • Peritraumatic dissociation
• • Chronic pain
• Post-traumatic factors
• • Perceived lack of social support
• • Subsequent life stress
• Protective factors:
• ı High IQ
• ı High social class
• ı Viewing the dead body of friend/relative after trauma
• ı Male
• ı Psychopath

• The incidence varies across the world. Resilience to trauma is
a dynamic factor and so individuals who may not
• develop PTSD after one trauma may develop after another.
• Females suffer from more PTSD than males. It is unclear if
this is due to higher exposure to trauma or greater
• vulnerability to develop PTSD. Molestation is more common
in females than males. Mugging is more common in
• males than females. But in both instances women develop
more PTSD. The only trauma where men develop more
• PTSD may be rape.
• Hippocampus and amygdala show neuroimaging
abnormalities. Hypocortisolaemia is reported in PTSD. Strong
• avoidance features may predict chronicity in PTSD.

NICE guidelines for PTSD - summary
• Encourages primary care diagnosis and screening – it is probably
• underdiagnosed.
• Up to 30% of people exposed to trauma may develop PTSD.
• PTSD can also develop in children.
• Watchful waiting if symptoms are mild and present for less than 4 weeks after
• trauma.
• Trauma-focussed CBT - individual basis as outpatients to be offered to all with
• severe symptoms present for less than 3 months
• If present for more than 3 months (chronic) offer trauma focussed CBT or
• EMDR.
• If no improvement consider pharmacological treatment.
• Paroxetine, mirtazapine for general use; amitriptyline or phenelzine for
• specialist use.

• Few questions appeared in March 2008 paper 3
from Bisson, 2007 review in APT. Please see the
summary of this
• paper in the following table:

• Drug Evidence
• Paroxetine Good RCT evidence. NICE second line.
• Licenced for PTSD in UK
• Sertraline RCT evidence; but NICE appraisal did not show
• significance. Licensed for females not males with
• PTSD in UK!!
• Fluoxetine 1 RCT but not significant
• Imipramine &
• Amitriptyline
• Poor quality of evidence; but statistically
• significant result for Amitriptyline; not so for
• imipramine.
• Phenelzine Poor quality of evidence; but statistically
• significant result
• Mirtazapine One small strongly positive RCT. NICE second
• line.
• Venlafaxine One large RCT no benefit
• Olanzapine Monotherapy RCT negative; augmentation of
• SSRIs positive
• Risperidone Tested only as adjunct – no effect

Prevention of PTSD
• What are the effects of interventions to prevent post-
traumatic stress disorder (Bisson, Clinical evidence
• 2004)?
• Likely to be beneficial Multiple-session CBT to prevent PTSD in
people with acute stress
• disorder (reduced PTSD compared with supportive counselling)
• Unknown effectiveness Multiple-session CBT to prevent PTSD in all
people exposed to a
• traumatic event
• Propranolol to prevent PTSD
• Single-session group debriefing to prevent PTSD
• Temazepam to prevent PTSD
• Unlikely to be beneficial Single-session individual debriefing to
prevent PTSD
• Supportive counselling to prevent PTSD

Psychological treatments
• Categories:
• ı Individual trauma focussed:
• Trauma-focused cognitive–behavioural therapy
(TFCBT).
• Eye movement desensitisation and reprocessing
(EMDR).
• ı Individual non trauma focussed:
• Stress management and relaxation.
• Other therapies (including supportive therapy/non-
directive non-directive counselling,
• psychodynamic therapies and hypnotherapy).
• ı Treatments delivered in groups:
• Group cognitive–behavioural therapy.

Trauma focused CBT
• May include exposure therapy wherein repeated
confrontation of traumatic memories and
• repeated exposure to avoided situations take place together
with relaxation and anxiety reduction. In trauma
• focused cognitive component modification of
misinterpretations that lead to overestimation of current
threat and
• modification of other beliefs related to the traumatic
experience and the individual's behaviour during the trauma
• (for example, guilt and shame) are attempted via cognitive
restructuring process. Trauma focused psychological
• treatment should usually be given for eight to 12 sessions

Eye movement desensitisation and
reprocessing
• This was serendipitously discovered by a psychologist
called
• Shapiro when she first applied it to herself. It is based on
the theory that bilateral stimulation, in the form of eye
• movements, allows the processing of traumatic
memories. While the patient focuses on specific images,
negative
• sensations and associated cognitions, bilateral
stimulation is applied to desensitise the individual to
these
• memories and more positive sensations and cognitions
are introduced.

Post traumatic stress disorder
• Post traumatic stress disorder (PTSD) is an emotional reaction to a
traumatic event.
The ICD-10 diagnostic criteria are as follows:-
• Exposure to a traumatic event which would be likely to cause pervasive
distress in almost anyone.
• The event must be persistently remembered or relived, as evidenced by
flashbacks, vivid memories, or nightmares.
• The patient must actively avoid situations which remind them of the event.
•
In addition it stipulates that either of the following must be present
Partial amnesia for part of the event
• Persistent symptoms of psychological arousal such as, poor sleep, poor
concentration, hypervigilance, exaggerated startle response, irritability.

• The above symptoms must occur within 6 months of the event.
NICE guidelines make the following recommendations about the treatment of PTSD
• Debriefing should not be offered
• Where symptoms are mild and have been present for less than 4 weeks watchful waiting
should be considered (follow up given within 1 month)
• All people with PTSD should be offered a course trauma-focused cognitive behavioural
therapy (CBT) or eye movement desensitisation and reprocessing (EMDR).
• Drug treatments for PTSD should not be used as a routine first-line treatment for adults in
preference to a trauma-focused psychological therapy.
• Drug treatments (paroxetine or mirtazapine for general use, and amitriptyline or
phenelzine for initiation only by mental health specialists) should be considered for the
treatment of PTSD in adults who express a preference not to engage in trauma-focused
psychological treatment.

• With regard to PTSD which of the following is
true?
• A. it is overdiagnosed
• B. resilience is not a dynamic quality
• C. prevalence of PTSD is the same all over the
world
• D. prior trauma does not increase susceptibility
to PTSD
• E. Chronic pain is associated with PTSD.

• In PTSD which of the following statement is
true?
• A. refugees are at no more risk than the
indigenous population
• B. avoidance is associated with chronicity
• C. misdiagnosis as refractory depression does
not occur
• D. cortisol levels are high
• E. Securely attached individuals exhibit more
symptoms.

• In the aetiology of PTSD choose one correct
option:
• A. the hippocampus has no role
• B. locus of control has no role
• C. the sympathetic nervous system is not
involved
• D. lower level of education is protective
• E. Unresolved childhood trauma increases the
risk.

• Vulnerability factors for PTSD include:
• A. male gender
• B. middle age
• C. internal locus of control
• D. Personality disorders.
• E. good impulse control

• In PTSD there is confirmed effectiveness for all
of the following treatments except:
• A. EMDR
• B. Hypnotherapy
• C. Antidepressant
• D. Stress management
• E. Trauma focused therapy

• With respect to the recommended treatments for
PTSD which of the following are endorsed by
NICE guidelines for use in primary care
settings?
• A. Sertraline and fluoxetine
• B. Sertraline and paroxetine
• C. Mirtazapine and paroxetine
• D. Amitriptyline and phenelzine
• E. Mirtazapine and fluoxetine

Teaching 30 july

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