OCD (ALL)

Define OCD:

a form of anxiety disorder which involves obsessions which lead to compulsions

Define obsessions:

recurring and persistent thoughts, and urges

Define Compulsions:

repetitive behaviours that the person feels driven to do because of their obsessive thoughts

what are the emotional characteristics of OCD?

• anxiety

• distress

what are the cognitive characteristics of OCD?

• involuntary obsessions

• intrusive thoughts

what are the behavioural characteristics of OCD?

• compulsive and repetitive behaviours

• irrational behaviours

Biological explanation of OCD - neurological

What is Serotonin?

a neurotransmitter implicated in many different behaviours and physiological processes, including aggression, sleep, and depression

Biological explanation of OCD - neurological

what is the serotonin hypothesis?

low levels of serotonin are associated with OCD

Biological explanation of OCD - neurological

Dopamine definition:

neurotransmitters in brain - effects motivation and drive

Biological explanation of OCD - neurological

What are Neurotransmitters?

Chemical substances that play an important part in the workings of the nervous system by transmitting nerve impulses

Biological explanation of OCD - neurological

what is the dopamine hypothesis?

high levels of dopamine are associated with OCD

Biological explanation of OCD - neurological
What is Noradrenaline?

a neurotransmitter found mainly in areas of the brain that are involved in governing autonomic nervous system activity (eg: blood pressure or heart rate)

Biological explanation of OCD - neurological

what are the neurological explanations for OCD?

Worry Circuit

• specific neural circuit involving the orbito-frontal cortex and thalamus

• this may be responsible for the obsessive thoughts and compulsive behaviours

Low serotonin/high dopamine

Biological explanation of OCD - neurological

how does the worry circuit work?

• orbito-frontal cortex = associated w/ decision making + reward behaviours

• perceives worry (eg: germs on hands) → sends worry signal to thalamus

• thalamus relays signals to different brain regions to deal w/ worry (eg: wash hands)

• caudate nucleus doesn’t act as ‘brake’ on the thalamus

• Thalamus becomes hyperactive + sends a signal back to the OFC

• the OFC ≠ rewarded by the action (eg: washing hands) → sends more worry signals to the thalamus

Biological explanation of OCD - neurological

Evaluation: Can’t establish if causational or correlational

numerous neurological factors that influence OCD - dopamine, serotonin, worry circuit - can’t establish if correlational, or causational bcs cannot isolate variables → weakness bcs limits understanding of OCD cause

Biological explanation of OCD - neurological

Evaluation: reductionist

Reduces cause of OCD to only neurological influences, when evidence for genetic, and psychological influences → bad bcs limits understanding, and important factors may be missed by reducing to just neurological influences → interactionist approach may be better

Biological explanation of OCD - genetics

what is a candidate gene?

a possible gene that could create genetic vulnerability to a disorder

Biological explanation of OCD - genetics

what is a polygenic disorder

• a disorder that is caused by a variety of genetic combinations, not a single gene

• 230 genes have been linked to OCD (Taylor)

Biological explanation of OCD - genetics

OCD is an aetiologically heterogeneous disorder - what does that mean?

the origins of the disorder vary between people

Biological explanation of OCD - genetics

what are the two most common candidate genes for OCD?

• SLITRK5

• COMT

Biological explanation of OCD - genetics

how does COMT relate to OCD?

• low activity variation of COMT may lead to build up of dopamine in synapses

• when dopamine is high an action is repeated

• explanation for repetitive compulsive behaviours

Biological explanation of OCD - genetics

how does SLITRK relate to OCD?

• Shmelkov took a group of mice and replaced the SLITRK gene of some of them with a reporter gene (lacZ)

• the mice without SLITRK exhibited less OCD behaviours (scratching, burying things)

Biological explanation of OCD - genetics

Evaluation: Supporting evidence

Billet et al (1998) - M-A of 14 twin studies → CR of MZ= 68%, DZ = 31% → suggests clear genetic basis for OCD, BUT bcs CRs never 100% → environmental factors must play a role too (the diathesis-stress model)

Biological explanation for OCD - Genetics

Evaluation: symptom over-lap + co-morbidity

Symptom overlap: obsessional behaviour also in: Tourette’s, anorexia nervosa, + children w/ autism (display stereotyped behaviours/rituals + compulsions) → Pauls + Leckman (1986) concluded OCD is one expression of same gene that determines Tourette’s

Co-morbidity: Rasmussen and Eisen (1992) - 2/3 patients with OCD also experience at least 1 episode of depression

supports the view that there isn’t one specific gene(s) unique to OCD, instead several act as vulnerability for obsessive-type behaviour

Biological explanation of OCD - neurological + genetics

Evaluation: genetic link to neurological + practical application

Menzies et al (2007) MRIs of OCD patients + close relatives = reduced grey matter in key regions of brain, including OFC (worry circuit) → supports view that anatomical differences = inherited and may lead to OCD in certain individuals → SO brain scans may be used to detect OCD risk

Biological explanations of OCD - genetic

Evaluation: practical use

Genetic screening to see vulnerability → gene therapy may produce means of turning certain genes 'off' so OCD isn’t expressed BUT same genes may have other benefits, also presumes there’s a relatively simple relationship b/w OCD + genes, which may not be the case → SO Applying, biological therapies (such as gene therapy) is therefore more complex

The biological approach of treating OCD

what are the possible biological treatments for OCD?

anti-depressant drugs

• SSRIs

• Tricyclics

Anti-anxiety drugs

• Benzodiazepines (BZs)

Treatments of OCD

How do SSRIs work?

Selective serotonin re-uptake inhibitors - type of anti-depressants that keeps serotonin levels in the synapse high by preventing re-uptake

Treatments of OCD

what are Tricyclics

• work the same as SSRIs

• TARGET SEROTONIN AND NORADRENALINE

The biological approach of treating OCD

What is GABA (gamma-aminobutyric acid)?

• a neurotransmitter that regulates excitement in the nervous system, thus acting as a natural form of anxiety reducer

• tells 40% of the neurons in the brain to 'slow down'/stop firing

Treatments of OCD

What are Benzodiazepines (BZs)?

• range of anti-anxiety drugs (eg: Valium and Diazepam)

• increase the NT GABA (gamma-aminobutyric acid)’s activity

• GABA tells around 40% neurons in the brain to ‘slow down’ and ‘stop firing’

• SO BZs have a general quietening influence on the brain → reduce anxiety (experienced as a result of obsessive thoughts)

Treatment of OCD

Evaluation: publication bias

Turner et al (2008) suggest publication bias towards studies showing positive outcome of antidepressant + studies that weren’t positive were often published in a way conveying positive outcome→ exaggerating benefits → Drug companies = strong interest in success of psychotherapeutic drugs + fund much of the research → selective publication can lead doctors to make inappropriate treatment decisions that may not be best interest of patients

Treatment of OCD

Evaluation: drugs = not lasting cure

Maina et al (2001) - patients relapse within a few weeks if medication is stopped, Koran et al (2007)’s M-A suggests psychotherapies (eg: CBT) should be tried first → suggests, while DT requires little effort + relatively effective in ST, doesn’t provide a lasting cure

Treatment of OCD

Evaluation: drugs side effects + addiction

SSRIs = Soomro et al (2008) - nausea, headache and insomnia → Although not always severe, often enough to make patient stop taking the drug

Tricyclic antidepressants (worse) = hallucinations, irregular heartbeat (so only used if SSRIs = not effective)

BZs = increased aggressiveness, LT memory impairment, + addiction issues - Ashton (1997) - BZ use should be maximum four weeks

SO limit usefulness of drugs treatment of OCD

Treatments of OCD

Evaluation: supporting research for drug therapy

Soomro et al (2008) M-A of 17 studies using SSRIs w/ OCD patients → found them more effective than placebos reducing symptoms of OCD up to three months after treatment BUT most studies on effectiveness = only three-four months duration (Koran et al (2007)) SO while drug treatments shown to be effective in ST, lack of LT data = limitation

Treatments of OCD

Evaluation: drug therapy = low time/effort commitments for patients + cheaper

vs CBT requires patient to attend regular meetings + put considerable thought into tackling their problems → Drug therapies = cheaper for health service bcs require little monitoring and cost less psychological treatments → patients may benefit simply from talking w/a doctor during consultations SO drug therapies = more economical than psychological therapies for health services