Human Neuropsychology Assignment

Name: Module Code: Student number: Word Count:

Lisa Coyle PSY30050 07403615 2,135 excluding references and table

Note: The neurocognitive studies are displayed in the table as well as numbered in the essay for convenience.

Obsessive Compulsive Disorder Abstract This essay describes the neuro-anatomical basis OCD, etiology and treatment. The debate as to whether neuro-cognitive deficits are present in OCD is explored and the research on the neurocognitive aspects of OCD are investigated critically.

Key words Obsessive Compulsive Disorder Frontal Lobe Neuro-cognitive Cognitive

Behavioural Therapy Orbitofrontal Cortex

Obsessive Compulsive Disorder (OCD) is a condition in which an individual experiences disturbing obsessional thoughts or impulses and carries out behavioural routines or rituals to alleviate the perceived threat associated with this obsession (Carr, 2001). The most common obsessions/thoughts are concerned with dirt, illness, body waste, inappropriate sexual thoughts, need for symmetry and order (Carr, 2001).

Functional neuro-imaging studies have predominantly highlighted the significance of the orbitofrontal subcortical areas in OCD (Saxena & Raugh, 2000). Moritz, Jelinek, Hottenrott, Klinge & Randjbar (2009) found that OCD patients illustrated dysfunctions of the orbital frontal cortex. This study used the Object Alternations Task (OAT) to tap into this region which has been questioned as a reliable instrument in assessing orbital frontal cortex functioning (Kuelz, Riemann, Zahn & Voderholzer, 2004).

Involvement of the orbital frontal cortex has been found in other studies in conjunction with the dorsolateral prefrontal cortex (Rao, Janardhan Reddy, Kumar, Kandovel & Chandrashekar, 2008) and the thalamus (Saxena & Rauch, 2000). Lacerda et al (2003) suggested the involvement of the right superior and inferior frontal cortex and the right and left thalamus, a finding which has received cross cultural agreement.

Some behavioural symptoms of OCD have been suggested to have a neural basis (Mataix Cols et al, 2004). Patients who displayed washing behaviours typically illustrated increased activation in the bilateral ventromedial pre frontal regions while patients with checking behaviours experienced increased activation of the thalamus and dorsal cortical areas (Mataix Cols et al, 2004). Hoarders presented with increased activation of the right orbito frontal cortex and the left pre-central gyrus (Mataix Cols et al, 2004).

OCD is considered to be a common anxiety disorder (Weissman et al, 1994) with a lifetime prevalence rate of approximately 2.5% (APA, 1994; as cited in Carr, 2001). Fontenelle & Hasler (2008) suggest that OCD affects predominantly female adults but male adolescents and children. OCD can also manifest along with other disorders such as Tic disorder, Tourettes syndrome or eating disorders (Carr, 2001). The age of onset of OCD is said to typically occur in adolescence (Fontenelle & Hasler, 2008) or in early to middle adulthood (Weissman et al, 1994).

Although the precise etiology of OCD is not fully understood, cognitive models and neurobiological theories have received great support for their attempts in explaining the development of OCD (Goldman et al, 2008). According to the Basal Ganglia

Hypotheses, strong links exist between the basal ganglia and OCD while the Serotonin Hypotheses recognises reduced levels of serotonin as a principle cause of OCD (Carr, 2001). Cognitive Behavioural Theory argues that OCD arises when environmental stimuli are conditioned to create anxiety and consequently when these stimuli are presented, feelings of anxiety are elicited (Carr, 2001).

OCD is a familial disease and can be inherited genetically (Fontenelle & Hasler, 2008). Non-white individuals are suggested to be at risk candidates for developing OCD as well as substance abusers (Fontenelle & Hasler, 2008) and those who are unemployed (Crum & Anthony, 1993).

In terms of the neurocognitive effects of OCD, studies of this nature have been inconsistent due to extensive methodological flaws (Purcell, Maruff, Kyrios & Pantelis, 1998). There is much speculation and debate as to whether memory systems are effected in OCD (Shin, Kim, Park & Lee, 2004). OCD patients have been reported to have delayed memory (Aycicegi, Dinn, Harris & Erkman, 2003) impairments in non verbal memory (Shin, Kim, Park & Lee, 2004), short term and working memory (Purcell, Maruff, Kyrios & Pantelis, 1998, Martin, Huber, Rief & Exner, 2008), spatial memory (Chamberlain et al, 2007) and episodic memory (Martin, Huber, Rief & Exner, 2008). Martin, Huber, Rief & Exner (2008) and Simpson et al (2006) found working memory and non verbal memory to be unimpaired.

With regards to other executive functions, OCD patients have been found to be impaired on organisation and planning abilities (Shin, Kim, Park & Lee, 2004), although this finding was not observed by Purcell, Maruff, Kyrios & Pantelis (1998)

According to Chamberlain et al (2007), OCD patients displayed planning deficits but only on high intensity levels of the task. Attention deficits were found by Purcell, Maruff, Kyrios & Pantelis (1998) but this deficit was associated with speed based tasks only in the Martin, Huber, Rief & Exner (2008) study. Other research has argued that OCD patients typically display attentional bias (Van de Heuvel, 2005) and have refined attention deficits to impairments in selective and divided attention (Mortiz, Kuelz, Jacobsen, Hoss & Fricke, 2005). Deficits have also been found in visual spatial recognition (Purcell, Maruff, Kyrios & Pantelis, 1998, Mortiz, Kuelz, Jacobsen, Hoss & Fricke, 2005), visual pattern recognition (Chamberlain et al, 2007) as well as in visuo-constructive ability (Aycicegi, Dinn, Harris & Erkman, 2003).

Caution is advised when interpreting the findings from each of these studies for a variety of reasons. Although Chamberlain et al (2007), Aycicegi, Dinn, Harris & Erkman (2003), Martin, Huber, Rief & Exner (2008) and Purcell, Maruff, Kyrios & Pantelis (1998) conducted their research using a battery of objective neuropsychological tests, there were some concerns regarding some of the instruments used. The Rey Osterrieth Complex Figure Task was used by Shin, Kim, Park & Lee (2004) as a measure of planning, organisation, problem solving and memory functions. Gender effects have been identified on this measure with the tendency for males to outperform females (Gallagher & Burke, 2007. As males are over represented in the OCD and control group in this study, this limits the generalisability of findings in this study. The Rey Osterrieth Complex Figure Task (ROCFT) has a variety of different scoring procedures with the result that studies using this measure differ in their findings (Gallagher & Burke, 2007) and the ability to compare findings across studies is limited.

To account for OCD symptoms, self report measures were used in some cases. The Obsessive Compulsive Inventory (OCI) used by Aycicegi, Dinn, Harris & Erkman (2003) as well as the Maudsley Obsessional Compulsive Inventory (MOCI) used by Shin, Kim, Park & Lee (2004) rely on the ability of the patient to accurately determine the presence or absence of a symptom. Aycicegi, Dinn, Harris & Erkman (2003) also used a self report measure of executive function. These measures are subjective and dependent upon the patients acknowledgement of their symptoms which can be prone to bias or selective reporting of symptoms (Moritz, Kuelz, Jacobsen, Kloss & Fricke, 2005).

Failure to control for co-morbidity is a major criticism of neuropsychological studies on OCD (Martin, Huber, Rief & Exner, 2008). Co-morbid diagnosis of depression and other neurological disorders were controlled for by all of the five chosen studies which is a methodological strength with evidence suggesting that task performance is effected by depressive symptoms (Moritz, Kloss, Jahn, Schick & Hand, 2003). Martin, Huber, Rief & Exner (2008) found that all differences between OCD patients and controls were eradicated when depressive symptoms were controlled for. However, in reality, OCD patients typically have co-morbid symptoms so it could be argued that by excluding such patients from research, findings are not representative (Eddy, Dutra, Bradley & Westen, 2004).

There are mixed findings as to whether medication effects task performance in OCD patients and this has been identified as an area for future research (Mataix-Cols, Alonso, Pifarre, Menchon & Vallejo, 2002). In the five studies under examination, a total of 62%* of all OCD patients were on medication, typically SSRIs (Selective

Serotonin Re-uptake Inhibitors). Martin, Huber, Rief & Exner (2008) and Purcell, Maruff, Kyrios & Pantelis (1998) concluded that there were no differences on task performance between medicated and un-medicated patients while Aycicegi, Dinn, Harris & Erkman (2003), Chamberlain et al (2007) and Shin, Kim, Park & Lee (2004) neglected to control for medication effects on the premise that cognition is not effected by SSRI medication (Aycicegi, Dinn, Harris & Erkman, 2003, Mataix Cols, Alonso, Pifarre, Menchon & Vallejo, 2002, Simpson et al, 2006). Neglecting to control for medication effects is a matter of concern as the specific effect of SSRI medication has not yet been determined (Chamberlain et al , 2007, Shin, Kim, Park & Lee, 2004).

*This figure was calculated by getting the average percentage of OCD patients on medication across the five chosen studies.

In relation to cognitive dysfunctions with OCD patients, it is important to realise that there are limitations to which we can generalise on the basis of differences in symptom severity and co- morbidity (Shin, Kim, Park & Lee, 2004). Resolution of these issues should aim to investigate the neural correlates of such deficits and use larger samples (Chamberlain et al 2007, Simpson et al, 2006).

OCD is characterised by the tendency for the individual to conduct certain behaviours to alleviate what the individual views as a threatening or dangerous situation (Carr, 2001). Behaviours are usually repetitive and can include hand washing, checking, recitals or rehearsals such as prayers or rhymes (Bennett, 2003). Although hoarding is commonly perceived as an OCD behavioural symptom, recent research has suggested it

is not specific to OCD (Wu & Watson, 2005). As previously discussed, there has been evidence to suggest that some of these behaviours have neural correlates (Mataix Cols et al, 2004). OCD patients, although were found to have higher levels of anger in comparison to controls, did not express any excessive aggressive behaviour (Radomsky, Ashbaugh & Gelfand, 2007).

Compulsive behaviours undoubtedly restrict the individual in his/her social environment although very few studies have addressed the issue (Koran, 2000). Patients with OCD have been shown to be unable to maintain employment, have difficulty socialising with family and friends (Stein et al, 1996; as cited in Koran, 2000, Hollander et al, 1996; as cited in Koran, 2000) and overall are suggested to have poor social functioning (Bejerot, Nylander & Lindstrom, 2001 as cited in Koran, 2000, Koran et al, 1996; as cited in Koran, 2000). Family relationships tend to suffer if the patient demands assistance from their social network in carrying out rituals or routines (Carr, 2001) which if refused, can lead to the patient displaying aggressive and distressed behaviour (Koran, 2000). Caution is advised when interpreting the findings from studies of this nature because of the sample size and limited construct validity of the instruments (Koran, 2000). Although individuals with OCD show improvements in social and independent living skills with intervention, they still remain impaired in comparison to healthy control groups (Bystritsky et al, 2001).

OCD is most successfully treated with a combination of psychotherapy and pharmacotherapy (Eddy, Dutra, Bradley & Westen, 2004). The cognitive behavioural treatment of OCD involves the presentation of anxiety-provoking cues to the patient in which he/she must refrain from conducting their ritualistic or routine behavioural

responses (Carr, 2001). This operates on the premise that the patient will learn that by not complying with his/her obsessional thoughts, no negative consequences will occur (Bennett, 2003). Indeed, cognitive behavioural group therapy (CBGT) in comparison to a drug treatment of sertraline was shown to be highly effective in reducing compulsive behaviours with the group environment creating a supporting social network (Sousa, Isolan, Oliveria, Manfro & Cardioli, 2006).

In terms of pharmalogical intervention, clomipramine has been shown to be effective as well as other SSRIs [selective serotonin reuptake inhibitors] (Bennett, 2003). Clomipramine is suggested to be the most successful despite having a significant patient drop out rate (Eddy, Dutra, Bradley & Westen, 2004). However, most drug studies fail to conduct a follow up study to test the continual effectiveness of a treatment and tend to present and report participant data poorly (Eddy, Dutra, Bradley & Westen, 2004).

Although OCD does not directly cause mortality and can be treated, increased anxiety or stress can have negative effects to the body (Boardman, 2004). Males are at an increased risk for mortaility than females with this trend remaining constant even with lifestyle factors and other diseases and illnesses controlled for (Van Hout et al, 2004).

In conclusion, OCD presents an opportunity for further research in many domains. It is expected that through accounting for genetics and conducting further neuroanatomic research, many of the unsolved queries with regards to the neuro-biological correlates of OCD can be answered (Saxena & Raugh, 2000). Determining the risk factors for OCD (Fontenelle & Hasler, 2008) as well as the effect of medication on

cognitive tasks (Chamberlain et al, 2007) requires further attention. The current status of neuro-cognitive deficits in OCD is questioning the existence of cognitive impairments in OCD (Simpson et al, 2006). Methodological concerns have limited the extent to which neuropsychological studies can generalise findings and future research should aim to improve this. Future research should also continue examining combined therapy interventions for the treatment of OCD (Eddy, Dutra, Bradley & Westen, 2004).

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Table 1: Summary of studies of neurocognitive functioning in Obsessive Compulsive Disorder

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# Author 1 Shin, . Kim, Park & Lee

Year 2004

Cou ntry JA*

N N=60 30 OCD 30 Healthy controls

Sample Characteristics

Mean age of onset/Gender ration Clinic based sample and DSM-IV criteria for For both, 1: non-professional OCD and Structured 4 males. hospital staff Clinical Interview volunteers. No age of onset given.

Diagnostic Criteria

Deficits Org, planning & nonverbal memory.

2 Aycicegi, . Dinn, Harris & Erkman (2003)

2003

TY*

N=31 16 OCD 15 Healthy controls

Hospital based sample. Both groups matched for education, Socioeconomic status and handedness.

DSM-IV criteria for OCD as well as the Mini International Neuropsychiatric Interview (MINI)

Both OCD and control: 68% female, 32% male. No age of onset given.

Visuo constructi -ve ability & delayed memory.

3 Purcell, Maruff, Kyrios & Pantelis

1998

AU*

N=46 23 OCD 23 Healthy controls N=60 20 OCD 20 Control 20 TC* N=57 19 OCD 19 SC

Clinic based sample. Both groups matched for age, sex, education and I.Q.

The Anxiety Disorders Interview Schedule for DSMIV to confirm OCD.

OCD and control 1:1 M:F Age of onset: Males 14 Females 21 No age of onset given. 1:1 M:F

Spatial & working memory & spatial recog

4 Chamber . -lain et al. 5 Martin, . Huber, Rief & Exner

2007

UK*

Clinic based sample matched for age, I.Q., education and gender. Clinic based sample matched for education and handedness.

MINI

2008

GY*

DSM-IV criteria for OCD, Structured Clinical Interview.

Spatial memory, planning, & pattern recog OCD: 74% Episodic female, 26% memory male. & speed Control: 53% based female, 47% attention male. tasks. Age of onset: 19.4 years.

1.* 2* 3* 4*

Japan Turkey Australia United Kingdom 12

TC 5* SC

Trichotollimania Germany Schizophrenia

References

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Bystritsky, A., Liberman, R.P., Hwang, S., Wallace, C.J., Vapnik, T., Maindment, K. & Saxena, S. (2001). Social functioning and quality of life comparisons between obsessive-compulsive and schizophrenic disorders. Depression & Anxiety, 14, 214-218.

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Fontenelle, L.F. & Hasler, G. (2008). The analytical epidemiology of obsessivecompulsive disorder: Risk Factors and correlates. Progress in Neuro Psychopharmacology & Biological Psychiatry, 32, 1-15.

Gallagher, C. & Burke, T. (2007). Age, Gender & I.Q. effects on the Rey-Osterrieth Complex Figure Task. British Journal of Psychology, 46, 35-45.

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Kuelz, A.K., Riemann, D., Zahn, R. & Voderholzer, U. (2004). Object Alternation Task- is it sensitive enough to detect cognitive dysfunction in obsessive compulsive disorder? European Psychiatry, 19, 441-443.

Lacerda, A.L.T., Dalgalarrondo, P., Caetano, D., Camargo, E.E., Etchebehere, E.C.S.C. & Soares, J.C. (2003). Elevated thalamic and prefrontal regional cerebral blood flow in obsessive compulsive disorder: a SPECT study. Psychiatry Research: Neuroimaging, 123, 125-134.

Martin, V., Huber, M., Rief, W., & Exner, C. (2008). Comparative cognitive profiles of obsessive compulsive disorder and schizophrenia. Archives of Clinical Psychology, 23, 487-500.

Mataix-Cols, D., Alonso, P., Pifarre, J., Menchon, J.M. & Vallejo, J. (2002). Neuropsychological performance in medicated versus unmedicated patients with obsessive compulsive disorder. Psychiatry Research, 109, 255-264.

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Moritz, S., Kuelz,D., Jacobsen, A.K., Kloss, M., & Fricke, S. (2005). Severity of subjective cognitive impairment in patients with obsessive compulsive disorder and depression. Anxiety Disorders, 20, 427-443.

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Rao, N.P., Janardhan Reddy, Y.C., Kumar, K.J., Kandovel, T. & Chandrashekar, C.R. (2008). Are neuropsychological deficits trait markers in OCD? Progress in Neuro psychopharmacology & Biological Psychiatry, 32, 1574-1579.

Saxena, S. & Rauch, S.L (2000). Functional neuroimaging and the neuro-anatomy of obsessive compulsive disorder. Psychiatric Clinics of North America, 23(3), 563-586.

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Shin, M.S., Kim, M.S., Park, S.J. & Lee, Y.M. (2004). Deficits in Organizational strategy of Visual Memory in Obsessive Compulsive Disorder. Neuropsychology, 18(4), 665-672.

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Weissman, M.M., Bland, R.C., Rubino-Stipec, M., Wickramaratne, P.J., Wittchen, H.U. & Yeh, E.K. (1994). The cross national epidemiology of obsessive compulsive disorder. Journal of Clinical Psychiatry, 55(Suppl 3), 5-10.

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