Biological and Cognitive Approaches to Obsessive-Compulsive Disorder - Term Paper Example

Describe and evaluate the contributions made by the biological and cognitive approaches to our understanding of obsessive compulsive disorder. Name: Affiliation: Date: Introduction: Obsessions are unnecessary, undesirable and intrusive recurring thoughts, ideas, images, urges or doubts that create distress as anxiety about some feared consequences. For example the patient doubts whether germs are present or he/she has made or may make some disastrous mistake. As a result persons with OCD seek safety strategy to overcome obsessional discomfort. Some of such strategies are compulsive. These strategies may be explicit stereotype repetitive rituals such as checking to prevent a probable threat or washing to remove existing one. Sometimes the strategies are covert, short and GO unnoticed. These various neuropsychiatric and psychological disorders are collectively referred as Obsessive Compulsive Spectrum Disorder (OCSDs) (Abramowitz, 2006 p37). Jakes (1996) has compiled diagnostic features of obsession from literature and provided nine criteria to identify these in OCD. Very similar definitions are provided in DSM-III-R and by Rachman and Hodgson (1980). I f these are combined with other definitions, the diagnostic features of obsession are as follows: A subjectively compulsive quality Unwanted and unacceptable thoughts Intrusiveness Repetitiveness Difficulty in controlling thoughts and actions Persistence Senselessness Resistance Recognising these as obsession as products of one's own mind. It is not necessary that all of these nine criteria would be shown by all OCD patients. Moreover many of these symptoms are present in cases of other phobias as well. Compulsions are the voluntary reactions to obsessions. It is necessary for a compulsion to be a part of OCD that it should occur in response to obsession. Biological understanding of OCD: Evidences support that OCD is linked to distinct patterns of brain dysfunction. Abramowitz (2006) also posits in a neuroanatomical hypothesis that obsession and compulsions are caused by structural and functional deformities in the brain. Antony & Stein (2008) have explained that altered activity was observed in brain, particularly in the orbitofrontal cortex, dorsal anterior cingulated cortex, the basal ganglia (mainly the caudate) and hippocampus. Many theories conclude that this dysfunction makes thoughts and stimuli to persist and become obsessions since brain fails to reset the state of thinking. These obsessions then become compulsion as actions become repetitive. The neuroanatomical explanation of development of OCD concerns orbitofrontal frontal cortex and basal ganglia especially the striatum. Kaplan (2009, 1) referred a number of researches showing the role of these parts of brain. The orbital cortex is responsible for stimulating a "worry circuit" consisting of the "caudate nucleus, a part of the basal ganglia that helps in switching gears from one thought to another; the cingulated gyrus, which jerks the gut with fear, and the thalamus, which processes the body's sensory inputs". The possible sequence of events in OCD may begin from thalamus processing the sensory images which are coming to the brain from the rest of the body, while the Caudate nucleus controls and filters the sensory information and thoughts. When these messages are being misinterpreted, the thinking part of the brain gets confused and responds chemically to a threat perceived by the primitive, non-reasoning part of the brain but with rational doubt of the threat's danger and a major need to respond in case the danger is real. The Caudate nucleus sends unnecessary thoughts and impulses to the cortex where the thoughts and emotions combine; and an over active cingulated nucleus at the brain's centre helps shift attention from one thought or behaviour to another normally but in OCD it becomes over active and gets stuck on certain behaviours, thoughts or ideas. The Cingulate is that part of the brain which tells the OCD victim that something terrible will happen if the compulsions are not carried out (Anxiety care, 2009) A number of findings point out that OCD is associated to neurodevelopmental deviation as nearly 80% cases onset in childhood or adolescence. Rosenberg and Keshavan (in Antony & Stein, 2001, p129) compared pediatric OCD patients with normal controls and found that pediatric OCD patients had larger anterior cingulate volume than the controls. The findings indicate a developmental rather than acquired degenerative process. However, the study was cross sectional and prospective studies are required for confirmation. A childhood streptococcal infection is also linked with early onset of OCD and there is considerable interest in 'paediatric autoimmune neuropsychiatric disorders associated with streptococcal infections' or PANDAS (Antony & Stein, p129). Other studies of the brain using magnetic resonance imaging showed that the subjects with OCD had notably less white matter than did normal control subjects, suggesting a highly dispersed brain abnormality in OCD" (http://www.nimh.nih.gov/publicat/ocd.htm as in Kaplan, 2009, p1). The white matter, found under the cerebral cortex contains axons which link neurons in the cerebral cortex to neurons in other parts of the brain. Less white matter content seemingly reduces intracranial communication in the brains of OCD patients. The neurochemical theory suggests that OCD is caused by abnormality in the serotonin system. Zohar and Insel (as cited in Abramowitz, 2006, p 55) reported hypersensitivity of post synaptic serotonergic receptors. Considerable evidences support the serotonin hypothesis. These are studies on medication outcome, biological marker and inducing OCD symptoms using serotonin agonists and antagonists. The pharmacotherapy finding provide most convincing proof in which serotonin reuptake inhibitor (SRIs i.e. fluoxetine and sertraline) medications are found more useful than other medications with different action mechanism viz. desipramine or imipramine in reducing OCD symptoms (Abramowitz, 2006.) Other explanations have also been put forth for serotonin deficiency in OCD patients. Evidence supporting this hypothesis comes from use of drugs that increase serotonin output reduces symptoms of OCD. Because serotonin is essential for nerve cell communication, perhaps its lower levels in OCD patients account for the fewer axons in their white matter (Kaplan, 2009). However studies provide inconclusive results of relationship between serotonin and OCD. Since SRIs work for a wide variety of neurological disorders so OCD's response to SRIs is no conclusive evidence that low serotonin is the culprit in OCD (Abramowitz, 2006). MacFarlane (2001) also stated that evidences support disturbances in the brain chemistry particularly associated with the neurotransmitters of serotonin group in causing OCD. Moreover the neuroimaging studies reveal structural differences between normal and OCD brains. The evidence for biological and genetic basis of OCD comes from the finding that OCD runs in families. In 20-25% cases, OCD is diagnosed in parents of the children with OCD. Billet et al (in MacFarlane 2001, p164-165) noted that there is evidence of involvement of a single gene in OCD. The biological understanding of OCD is helpful in psycho educational process of treating OCD persons (MacFarlane, 2001). Schwartz and Baxter of UCLA and the univ. of Alabama have proposed that the 3 brain parts involved in the "worry circuit" can become unlinked with either Prozac or 10 weeks of behavioral therapy ( From http://www.schizophrenia.com/ami/diagnosis/ocd.html in Kaplan, 2009, p1). In a new development to understand neurobiology of OCD, scientists at University of Cambridge's Department of Psychiatry used functional magnetic resonance imaging (fMRI) to evaluate brain activity in the lateral orbitofrontal cortex (OFC). It is located in the frontal lobes and helps in decision making and behaviour. The scientists have observed that people with OCD and their close family members show under-activation of brain areas responsible for preventing repetitive behaviour.. The normal controls and OCD patients participated in the study. They were asked to look at superimposed pictures of a house and a face. The participants were asked to employ trial and error to find out whether the house or face was the correct target. They pressed a button to indicate which image they believed to be the target and response as 'correct' or 'incorrect' flashed on the screen. After the correct target had been identified six times continuously, it changed so the participant had to learn again. The fMRI was used to monitor their patterns of brain activity throughout. Later comparison of fMRI images of their brain activity throughout showed under-activation in the lateral orbitofrontal cortex and other brain areas in both the OCD patients and their family members. The technique could be developed for early detection of risk of OCD development. Currently the methods used involve interviewing the patient and OCD is detected after its onset (Science Daily, 2008). Cognitive-behavioural approaches to OCD: Antony & Stein (2008) discuss two psychological models related to onset of OCD; these are behavioural and cognitive models. The Behavioural model is based on learning theory, applied principle of conditional reinforcement and punishment besides the two stage theory of fear and avoidance. The behaviour theory of OCD explains that normal intrusive thoughts, impulses and images become associated with anxiety that has failed to subside (Swinson, 2001). The behavioural theories hypothesise that a neutral event evokes fear when associated with offending stimulus. In the second stage of this model, compulsion provides relief from obsessional anxiety or discomfort which in fact negatively reinforce compulsions.. Thus the frequency of compulsive incidents is increased in the future which triggers an obsessional concern. Evidences also support that obsession increase discomfort and compulsion reduce it Cognitive theory: According to this theory the reaction to negative intrusive experiences in OCD people depends on underlying beliefs such as an exaggerated sense that one is responsible for protecting oneself and others so one must act. An intrusive thought such as " I will kill my baby" is interpreted as she will unless she counters the feeling by doing something such as not being alone with the baby, being reassured or performing some ritual. Such interpretation results in increased anxiety, discomfort and depression. While the neutralizing thoughts such as washing, checking results in reduction of discomfort but only temporarily since the probability of disturbing thoughts is increased in future (Antony & Stein, 2008, p130). Abramowitz (2006) explains the cognitive basis using Cognitive deficit models, the components of which are: Memory deficit: The OCD symptoms may result due to the dysfunction of some cognitive processes such as memory. Probably the compulsive checking occurs since person does not remember whether he has locked the door or washed the hands. In a meta-analysis of 22 studies, Woods et al (p59) found that compulsive checkers do not perform as well as the non-checkers on short term and long term intermittent memory. Though, the other variables such as extreme caution may be the reason rather than memory deficit. Since theorists state that persons with OCD have memory deficit only where their obsessional fears are concerned. For example, they will repeatedly check outside doors for fear of burglary however they are not same way inclined to check the bathroom or closet doors. Such a finding brings entirely new hypothesis which is opposite to memory deficit hypothesis: contrary to memory deficit theory, patient have enhanced memory for threat relevant (OCD- related) information. Radomsky and Rachman (in Abramowitz, 2006, 59) studied the responses of OCD and normal individuals in their experiment towards clean and dirty things. They found OCD patients recalled more incidents than healthy individuals when a thing is touched by a dirty cloth rather when it was touched by clean cloth. While the non-OCD controls recalled more things touched by clean cloths. Their experiment revealed that OCD patients have selectively better memory for anxiety related events. Thus it may be a different phenomenon of memory deficit, the reality monitoring deficit. The person with OCD is unable to discriminate between memory of real and imagined incidents. It is possible that ritualistic checking is prompted by thinking that action was imagined or really happened (Abramowitz, 2006, p60). Abed & de Pauw (2009) present the hypothesis of (Bradshaw, 1997) that the neurobiological system that generates the OCD phenomena has the function of generating risk scenarios without awareness and may thus function as an 'Involuntary Risk Scenario Generating System' (IRSGS). Compulsive rituals, the other component of OCD, are conceptualised as primitive harm avoidance behavioural routines that are under semi-voluntary control. It is suggested that the IRSGS operates primarily as a self-generated conditioning system whereby the individual can develop harm avoidance behavioural strategies without experiencing the risks in the real-life dangers. Bickerton (in Abed & de Pauw, 2009, p1) has proposed that there are two fundamental modes of thinking: on and off-line. On-line thinking is common to many complex organisms and involves mental activity designed to solve a problem directly faced by an individual. Off-line thinking involves mental activity aimed at solving problems that the organism may face at some time in the future. The obsessional thinking could be considered as a primitive version of off-line thinking, encoded in the basal ganglia and arising due to dysfunction in these brain centres. Similarly, compulsions and tics in humans have been considered as fragments of once purposeful activities that arise inappropriately due to dysfunction within the cortico-striatal system (Carter as in Abed & de Pauw, 2009, p1). The cognitive theory finds obsessions as dysfunctional beliefs and evaluation of associated threats. Obsessions originate from intrusive cognitions that occur in majority of general population (Rachman & De Silva; Salkovskis as in Neuropsychological, 2003, p3-4). However, persons with OCD not only get more intrusive thoughts, they are more aware of these also. Intrusive cognitions are ideas, feelings, doubts, images or urges and interrupt the person's current stream of consciousness. As a result the discomfort, distress is felt which is unacceptable to the individual. He or she feels personally responsible for intrusive thoughts and takes action to stop feared incident from happening. The action is as neutralizing thoughts seeking reassurance or counterproductive action such as suppression and avoidance. Biological evidences from positron emission tomography suggest more activation in the orbitofrontal cortex, right prefrontal areas and the anterior cingulated cortex of the brain of OCD patients. It is shown by more glucose or blood flow to these areas. As a result the equilibrium between information processing circuits is disrupted and individual is stuck to a thought. Balkom & Dyck (In Swinson, 2001, p349-365) reported that treatment of OCD with combination of antidepressants and cognitive behaviour therapy (CBT) has been as effective as the CBT alone. However treatment with serotonergic antidepressants alone was less effective than the combination treatment. The reasons were relapse or drop out from combination treatment. References Abed, RT & de Pauw, KW. "An Evolutionary Hypothesis for Obsessive Compulsive Disorder: A Psychological Immune System". http://cogprints.org/1147/0/ocd-final.htm[ 30 APR 2009] Abramowitz, JS (2006). Understanding and treating obsessive-compulsive disorder: a cognitive behavioural approach. Routledge. Antony, MM & Stein, MB (2008). Oxford Handbook of Anxiety and Related Disorders. Oxford University Press US. Anxiety care. Causes of OCD. http://www.anxietycare.org.uk/docs/ocdcauses.asp [30APR 2009] Jakes, I (1996). Theoretical approaches to obsessive-compulsive. Cambridge University Press Kaplan, R. "Obsessive-Compulsive Disorder". http://serendip.brynmawr.edu/bb/neuro/neuro98/202s98-paper1/Kaplan.html [30 APR 2009] MacFarlane, MM (2001). Family therapy and mental health: innovations in theory and practice. Haworth Press. Neuropsychological functions implicated in obsessive-compulsive behaviour: A review. From: http://dissertations.ub.rug.nl/FILES/faculties/medicine/2003/m.m.a.nielen/c1.pdf [ 30APR 2009] Science Daily (July 18, 2008). Obsessive Compulsive Disorder Linked To Brain Activity. http://www.sciencedaily.com/releases/2008/07/080717140456.htm[ 30 APR 2009] Swinson, RP (2001). Obsessive-Compulsive Disorder: Theory, Research, and Treatment. Guilford Press Read More