OBSESSIVE-COMPULSIVE DISORDER

 Obsessive-compulsive disorder (OCD) is described as an anxiety disorder. The condition has two main
parts: obsessions and compulsions.
 An obsession is a recurrent, persistent idea, thought, impulse, or image that is experienced as intrusive
and inappropriate and produces marked anxiety.
 A compulsion is defined as a repetitive behavior or mental act generally performed in response to an
obsession.
EPIDEMIOLOGY

 The lifetime prevalence of OCD is 2.3%,

 Although this may be an underrepresentation because often only patients with moderate to severe
symptoms seek help.
 The mean age of onset is 19.5 years, and it is rare for new cases of OCD to develop after the early 30s.
PATHOGENESIS

 The pathogenesis of OCD is a complex interplay between neurobiology, genetics, and environmental
influences.
 Historically, dysfunction in the serotonin system was postulated to be the main factor in OCD
pathogenesis, given the selective response to serotonergic medication.
 The role of glutamate, dopamine, and possibly other neurochemicals also play a role in pathogenesis.
CLINICAL PRESENTATION
Obsessions
• Repetitive thoughts (eg, feeling contaminated by germs, fears of harming others)
• Repetitive images (eg, recurrent sexually explicit pictures)
• Repetitive urges (eg, need for symmetry or putting things in specific order)
Compulsions
• Repetitive activities (eg, hand washing, need to ask, need to confess)
• Repetitive mental acts (eg, counting excessively, repeating words silently, praying)

DIAGNOSIS

 Obsessions are recurrent intrusive thoughts or images that cause marked distress.
 The thoughts are unwanted and inconsistent with the individual’s sense of self (ego dystonic), and
great effort is made to resist or suppress them.
 They can involve contamination; repeated doubts; or taboo thoughts of a sexual, religious, or
aggressive nature.
 Compulsions are repetitive behaviours or mental rituals performed to counteract the anxiety caused
by obsessions.
 Individuals feel strongly compelled to complete these actions, and the behaviours become
automatic over time.
 They can include hand washing, checking, ordering, praying, counting, and seeking reassurance.
NON PHARMACOLOGIC THERAPY

 CBT with behavioural techniques (eg, exposure and response prevention [ERP]) is the most
common initial nonpharmacologic treatment of choice in OCD and is largely considered to be
more efficacious than pharmacotherapy.
 CBT is preferred for motivated patients, particularly children and adolescents, with both mild
OCD symptoms and psychiatric comorbidities, and in those with a desire to avoid medications.
 Neuromodulator approaches (eg, deep brain stimulation [DBS], TMS, and electroconvulsive
therapy [ECT]) and ablative neurosurgery for severely symptomatic patients who have not
achieved sustained response to standard of care interventions.
PHARMACOLOGIC THERAPY
Antidepressant Therapy

 SSRIs and clomipramine are the main antidepressants used in OCD treatment.
 MOA- SSRIs and clomipramine inhibit 5-HT reuptake into the presynaptic neuron, making more
5-HT available to postsynaptic receptors and reducing formation of the 5-HT metabolite 5-
hydroxyindoleacetic acid.
 SIDE EFFECTS -SSRIs are less likely to cause cardiovascular, sedative, anticholinergic, and
weight-gain side effects, and to reduce the seizure threshold. Clomipramine, however, is less
likely than SSRIs to cause insomnia, akathisia, nausea, and diarrhoea.
 DOSE

Augmentation with Antipsychotics

 Augmentation of SSRI treatment with low-to-moderate doses of antipsychotics may be helpful,
and should be considered for patients with tic-related OCD, comorbid psychosis, and treatment-
refractory patients.
 One-third of treatment-refractory patients with OCD respond to antipsychotic augmentation and
perhaps with an earlier response (2-4 weeks) compared to antidepressants.
 First-generation antipsychotics, such as haloperidol, are less preferred given risk of
extrapyramidal symptoms. As the long-term use of second-generation antipsychotic
augmentation result in higher rates of adverse effects (eg, weight gain, increased blood glucose,
lipid abnormalities)