Gyula Demeter

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guided antisaccade task. However, another study found no significant difference between the antisaccade error rates except on the latency of antisaccades which were slower in the OCD group (Maruff, Purcell, Tyler, Pantelis, & Currie, 1999). A more recent work also supports this finding, the OCD group showed higher frequencies of anticipatory saccades with reduced amplitudes only on the predictive saccade task (the timing, amplitude and direction of the targets are predictable) which relies mainly on the circuits between the frontal eye field and basal ganglia and presented a similar performance pattern as the normal subjects on the antisaccade task which predominantly involves the dorsolateral prefrontal cortex (Spengler et al., 2006). From these findings it can be concluded that the results in these paradigms are strongly influenced by the characteristics of the tasks, by the exposition times, by the inter stimulus intervals, by the predictability of the targets and by the proportion of Go and NoGo responses which must be taken into account in futures studies. The low performance on cognitive and motor inhibition neuropsychological tasks supports the theory of frontostriatal dysfunction in OCD (Savage, 1998; Penades et al., 2007). Chamberlain et al. (2005) consider that deficits at the level of inhibition mechanism are responsible for the main symptoms and neuropsychological profiles in OCD. As it can be seen through the overview of the most relevant findings from the executive functions literature the most common approach to investigate neuropsychological profiles in OCD has been to compare the performance levels on different neuropsychological tests to healthy controls. There is a new direction toward the identification of different neuropsychological profiles for OCD subtypes and also toward the establishment of different subgroups based on the neuropsychological performance patterns (Nedeljkovic et al., 2009). Postulating that there is an executive function deficit in OCD is a very broad assumption, and our aim was to focus on the most relevant executive components: inhibition and shifting. 20
Table 1. Summary of OCD patients results in the WCST from previous research Authors Samples Medication Performance Conclusions/Comments Boone et al. (1991) N=20 OCD medication free for at impaired right hemisphere and basal N=16 HC least 4 weeks ganglia dysfunction Hymas et al. (1991) N=16 OCD patients with obsessional slowness N=15 HC Zielinski et al. (1991) N=21 OCD N=21 HC Abbruzzese et al. (1995a) N=35 OCD N=25 HC N=25 SCH Abbruzzese et al. (1995b) N=33 medicated OCD N=14 unmedicated OCD N=33 HC Gross-Isseroff et al. (1996) N=15 OCD women N=15 HC women Abbruzzese et al. (1997) N=60 OCD N=30 HC N=60 SCH Lucey et al. (1997) N=19 OCD N=19 HC Cavedini et al. (1988) N=19 OCD N=19 HC 12 patients were medication free; 4 under medication 12 patients were medication free; 9 under medication OCD patients treated with fluvoxamine OCD patients treated with fluvoxamine medication free for at least 2 weeks OCD patients treated with fluvoxamine; SCH patients with neuroleptica 12 patients were medication free for at least 3 months; 7 patients treated with fluoxetine or sertralin medication free for at least 1 month impaired OCD patients with obsessional slowness might have dysfunctional frontal and basal ganglia system no difference no impaired set shifting ability in OCD no difference dysfunction of the orbitofrontal cortex in OCD and dysfunction of the dorsolateral prefrontal cortex in SCH no difference OCD it is not associated with dysfunction of the dorsolateral prefrontal cortex no difference sample size; the question of gender no difference dysfunction of the orbitofrontal cortex in OCD impaired involvement of the dorsolateral prefrontal cortex in OCD no difference selective impairment of orbitofrontal cortex in OCD 21
Page 1 and 2: Budapest University of Technology a
Page 3 and 4: 6.3. Study 3: Over-monitoring secon
Page 5 and 6: Glossary of abbreviations ACC Anter
Page 7 and 8: WCST-LS Wisconsin Card Sorting Task
Page 9 and 10: Kivonat Az obszesszív-kompulzív z
Page 11 and 12: Introduction In our daily life we r
Page 13 and 14: Chapter 1. Overview of Obsessive co
Page 15 and 16: ilaterally at the ventromedial pref
Page 17 and 18: Chapter 2. The study of executive f
Page 19 and 20: 2.2. Theories and measurement of ex
Page 21 and 22: outcomes etc.) which in many labora
Page 23 and 24: As far as we know no executive task
Page 25 and 26: The tasks that are most commonly us
Page 27 and 28: 2002) and on the Intra-Dimensional/
Page 29: Inhibition In the Miyake et al. (20
Page 33 and 34: Authors Samples Medication Performa
Page 35 and 36: Chapter 3. The study of memory func
Page 37 and 38: 3.2. Prospective memory Prospective
Page 39 and 40: 3.2.1. Theories of prospective memo
Page 41 and 42: According to Guynn (2008) retrieval
Page 43 and 44: intention or the initiation and exe
Page 45 and 46: 3.2.3. Studying PM in OCD While at
Page 47 and 48: 3.2.4. A possible PM model of OCD O
Page 49 and 50: 3.3. The role of inhibition in sele
Page 51 and 52: Further two recent results will be
Page 53 and 54: it, (3) the neuropsychological impa
Page 55 and 56: 4.3. Current neurobiological model
Page 57 and 58: The role of amygdale in the express
Page 59 and 60: 5.1. Main goals 1. To assess the le
Page 61 and 62: Chapter 6. Studies 6.1. Study 1: Im
Page 63 and 64: impairment in this task 15 and othe
Page 65 and 66: Procedure All OCD patients received
Page 67 and 68: series of equal length, and we cons
Page 69 and 70: called error inhibition index (SEII
Page 71 and 72: Reaction Time Colour Naming Conditi
Page 73 and 74: which might be impaired in OCD. 9 I
Page 75 and 76: REFERENCES 1. American Psychiatric
Page 77 and 78: 20. van der Wee NJ., Ramsey NF, Jan
Page 79 and 80: 39. Goodman WK, Price LH, Rasmussen
Page 81:
6.2. Study 2: Impaired prospective
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Table 1 Sample demographics and bas
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Written instructions were read to t
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Table 2 Hit rate in the two experim
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Comparison of patient and healthy a
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can be concluded that OCD patients
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6.5. Study 5: No retrieval induced
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Experimental design and materials T
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Procedure “In the study phase, pa
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RIF effect in the control group, t(
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Chapter 7. Discussion, conclusions
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and retrospective memory processes
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Bjork, & Bjork, 1994), which was of
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of the dACC contributes to the pers
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of patients’ cognitive abilities
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Anderson, M. C., & Spellman, B. A.
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Bajo, M. T., Gómez-Ariza, C. J., F
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Burgess, P. W. (1997). Theory and m
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Duncan, J. (1986). Disorganziation
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Gilbert, S.J. & Shallice, T. (2002)
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Harsányi, A., Csigó, K., Demeter,
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Kearns, N. P., Cruickshank, C. A.,
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Levy, B. J., & Anderson, M. C. (200
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McDaniel, M. A., Guynn, M. J., Eins
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neuropsychological and psychoanalyt
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(Eds.), Prospective memory: Cogniti
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Rogers, R. D., & Monsell, S. (1995)
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Smith, G. V., Della Salla, S., Logi
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Thordarson, D. S., Radomsky, A. S.,
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Wincze, J. (2001). The role of unde
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Gyula Demeter

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