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OCD
1. Obsessive-Compulsive disorder
Definition:Obsessive-compulsivedisorder(OCD)ischaracterizedby distressing,
intrusiveobsessivethoughts and repetitive compulsive physical or mental acts.
Etiology:
1.Seratonin hypothesis:
Low levels of serotonin lead to hypersensitivity of postsynaptic receptors
Serotonin is a neurotransmitter that communicate between brain structures
and helps regulate vital process, such as mood, aggression, impulse control,
sleep, appetite, temperature and pain.
NOTE: Abnormalities in dopamine levels also
2.Structural hypothesis:
Impaired intracortical inhibition of specific orbitofrontal-subcortical circuitry
(modulated by serotonin, glutamate and GABA) that mediates strong emotions
and the autonomic responses to those emotions.
3.Genetic influence:
Genes putatively linked to OCD have included those coding for Catechol-O-
methyltransferase (COMT), monoamine oxidase-A (MAO-A), brain-derived
2. neurotrophicfactor (BDNF),myelin oligodendrocyteglycoprotein(MOG),GABA-
type B-receptor 1, and the mu opioid receptor.
4.Infections:
In responseto streptococcal infection, antibodies are produced and antibodies
produce inflammation of the basal ganglia. This leads to increased volumes of
the caudate, putamen, and the globus pallidus
5. Brain trauma, stimulant abuse, and carbon monoxide poisoning
Pathophysiology/ signs and symptoms:
Diagnosis:
Once OCD is suspected, the following should be performed:
1. Define the rangeand severity of OCD symptoms; the Yale-Brown
ObsessiveCompulsiveScale(Y-BOCS)is a good tool for this purpose
2. Complete Mental Status Examination; look for comorbid symptoms and
disorders
3. Treatment:
Goals:
-To reduce frequency and severity of obsessivethoughts and time spent
performing compulsiveacts
-Efforts should be made to minimize adverse drug events and prevent drug
interactions.
General approach to treatment:
Firstline treatment:
-Cognition behaviour therapy alone for 13-20 sessions
-SSRIs alone for 8-12 wk
-CBT+SSRIs if, inadequate response occurs
Second line treatment:
-Switch to another SSRIs or Clomipramine
-Augmentation with antipsychotics if, inadequate responseoccurs
Third line treatment:
-Augmentation of SSRIs with Clomipramine
- Switch to another antipsychotic augmenting agent
Nonpharmacological therapy:
1. Transcranialmagnetic stimulation (TMS),
2. Deep brain stimulation (DBS),
3. Ablative neurosurgery
Pharmacological therapy:
DRUG Initial dose Maximum dose
SSRIs
Fluoxetin 20mg/day 80mg/day
Paroxetine 20 60
Fluvoxamine 50 300
Citalopram 20 80
Escitalopram 10 40
Sertraline 50 200
4. TCAs
Clomipramine 25 250
1. Tricyclic Antidepressants:
MOA:
ο· Depression is associated with low levels of NA and 5-HT. Physiologically
largeamountsof theseneurotransmittersliberated atthe nerveterminals
are reabsorbed into storage sites making them less available for
transmission.
ο· TCAs inhibit the reuptake of monoamines into their respective neurons.
This causes an increase in monoamine concentration in the synaptic cleft
in the CNS and periphery leading to their enhanced neuro transmission.
ο· Thus inhibition of this 5-HT and NA reuptake produces antidepressant
effects.
ο· They also block alpha-adrenergic, H1 and Muscarinic receptors leading to
ADRs.
ADRs:
Antimuscarinic effects- Blurred vision, constipation, dry mouth and urinary
retention
CNS- Sedation, confusion and seizures
CVS- Postural hypotension, tachycardia and arrhythmias
Also Jaundice, weight gain, tremors and skin rash
Contraindication:
In epilepsy, narrow angle glaucoma and patients on MAO inhibitors
2. Selective serotonin reuptake inhibitors:
MOA:
ο· SSRIs selectively inhibits the neuronal uptake of serotonin, thereby
potentiates the action of serotonin by making it more available for
transmission.