Gyula Demeter

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thalamic loops in OCD (McDougle, Goodman, & Price 1990; Metin, Yazici, Tot, &Yazici, 2003; Bloch, Landeros-Weisenberger, & Kelmendi, 2006). Considering all these findings together, there is some evidence that those brain networks which take part in the realization of PM functions are affected in OCD. 34
3.2.3. Studying PM in OCD While at the beginning of PM research the focus was on the outline, description of main differences between retrospective memory (Einstein & McDaniel, 1990, 1996 ) and PM or on the developmental aspects of prospective remembering (Kliegel, Jäger, & Phillips, 2008) today a move toward the clinical field concentrating mainly on the impairments is experienced. There is a considerable amount of result with different disorders as schizophrenia, Parkinson disease, Alzheimer’s disease, patients with head injuries, with substance abuse and with developmental disorders (see Kliegel et al., 2008, 2011). As far as we know there are just a few studies with OCD patients or with subclinical groups with dominant checking symptoms or obsessive tendencies in the domain of PM literature. Below, the main findings are summarized and the main hypothesis is outlined. In one study using the Rivermead Behavioural Memory Test the authors found no significant difference between OCD patients and healthy controls on the PM score (Jelinek, Moritz, Heeren, & Naber, 2006). In a large heterogeneous clinical OCD sample Moritz, Kuelz, Jacobsen, Kloss, and Fricke (2006) found no evidence about subjective complains related to PM performance compared to a group with depression. In three seminal studies Cuttler and Graf (2007, 2008, 2009) investigated PM functions of subclinical checkers and produced compelling evidence that checking compulsions are associated with lower performance in event and time based PM tasks. Higher checkers reported more everyday PM failures than low and medium checkers. They also found that depression and state and trait anxiety had no influence on PM performance and concluded that checking compulsions are compensatory reactions to experienced PM failures in the past. Their results support the theory that PM deficit contributes to the development and maintenance of checking compulsions. Subclinical checkers are aware of PM failures which induce concerns and an urge to recheck things. Marsh, Jameson, Cook, Amir, & Hicks (2009) in a subclinical population examined the connection of PM retrieval with obsessive-compulsive tendencies (washing compulsions) using threat and neutral information as cues and found that while in case of neutral cues there was a PM impairment, then the threat related stimuli improved PM performance in this subclinical group. The extra attentional bias produced an extended processing of threat-related cues and this improved the subjects PM performance, helping them to overcome their natural deficits. These results are in line with previous findings that people with general anxiety disorder manifest severe attentional biases (Hayes and Hirsh, 2007) and subclinical group of 35
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 and 30: Inhibition In the Miyake et al. (20
Page 31 and 32: Table 1. Summary of OCD patients re
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: intention or the initiation and exe
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
Page 89 and 90: Table 1 Sample demographics and bas
Page 91 and 92: Written instructions were read to t
Page 93 and 94: Table 2 Hit rate in the two experim
Page 95 and 96:
Comparison of patient and healthy a
Page 97 and 98:
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
Page 114 and 115:
and retrospective memory processes
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Gyula Demeter

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