Gyula Demeter

More documents

Recommendations

Info

3.2.2. Main cortical structures and neuronal networks involved in PM – connections with OCD The relationship between monitoring functions of PM cues and OCD symptoms is also interesting from the perspective of neuroimaging studies. A series of studies found evidence that the rostral prefrontal cortex (BA10) is involved in PM (Burgess, Quayle, & Frith, 2001; Burgess, Scott, & Frith, 2003; Simons, Schölvinck, Gilbert, Frith, & Burgess, 2006). In a positron emission tomography (PET) study Burgess et al. (2001) demonstrated that different cortical areas are involved in the maintenance and realization of intentions. They found increased regional cerebral blood flow (rCBF) in the frontal pole bilaterally, in the right lateral prefrontal, inferior parietal cortex and the precuneus, and decreased rCBF in the insula in the left hemisphere when healthy participants maintained and realized an intention. In contrast, they found increased rCBF in the right thalamus and decreased rCBF in the right dorsolateral prefrontal cortex when subjects executed versus maintained an intention. Putting these results together with attention theories Burgess and his colleagues (Burgess et al., 2003, Burgess, Simons, Dumontheil, & Gilbert, 2005; Burgess, Gilbert, & Dumontheil, 2007a, Burgess, Gilbert, & Dumontheil, 2007b) outlined the ‘gateway hypothesis’ which makes a distinction between stimulus-oriented (SO) and stimulus- independent attending (SI) (McGuire, Paulesu, Frackowiak, & Frith, 1996). The former is involved in the processing of the present sensory input, while the latter is required in the realization of self-generated or self-maintained thoughts. According to the hypothesis SO attending is supported by the medial rostral PFC while SI cognition by the lateral rostral PFC which means that the former is mainly involved in suppressing internally generated thoughts while the latter in intention maintenance (Burgess, Gilbert, & Dumontheil, 2007c). We think that OCD patients might have difficulties in SI attending, which has also a negative effect to the SO attending. It is possible that in OCD the maintenance of the intention requires extra SI attentional processes, which impairs the execution of the ongoing activities (SO attending). On the other a hand there is evidence that PM is more sensitive to executive functions deficits than to retrospective storage impairments (Kopp & Thone-Otto, 2003; Kliegel et al., 2004). This pattern of findings supports the idea that PM may more strongly rely on prefrontally mediated (executive control) processes than on temporally mediated (retrospective memory) processes (Brunfaut, Vanoverberghe, & d’Ydewalle, 2000; McDaniel, Glisky, Rubin, Guynn, & Routhieaux, 1999). Specific subprocesses of PM – as planning of an 32
intention or the initiation and execution of an intention which requires executive control mechanism – rely on the prefrontal cortex while others as the retrieval of the intention content, essential for the retrospective component of PM on the medial temporal lobe (Cohen & Reilly, 1996; Guynn, McDaniel & Einstei, 2001). As it has been outlined in the previous chapter of the dissertation, the primary cognitive deficit contributing to the OCD neuropsychological profile is the dysfunction of the executive system (Olley et al., 2007). The neuroimaging research of OCD gave a further hint that PM functions could be relevant in an OCD endophenotype, as it was found that those brain areas that are involved in PM are among the affected brain structures in OCD. Although there is evidence of the altered function of the fronto-striato-pallido-thalamico pathways (Saxena, Brody, Schwartz, & Baxter, 1998; Saxena & Rauch, 2000), the most consistent findings came from structural neuroimaging showing that the volume of the orbitofrontal cortex is significantly reduced (Szeszko et al., 1999; Choi et al., 2004; Kang et al., 2004; Atmaca, Yildirim, Ozdemir, Tezcan, & Poyraz, 2007), while there is a volumetric increase of the thalamus in OCD (Gilbert et al., 2000; Atmaca et al., 2006). The thalamus is involved in the anticipatory attentional processes and in the monitoring of self-generated actions (Portas et al., 1995; Blakemore, Rees, & Frith, 1998). Symptom provocation studies with PET and functional magnetic resonance imaging (fMRI) find increased rCBF and stronger activity bilaterally at the orbitofrontal cortex, at the right nucleus caudatus and at the left anterior cingulate cortex (Rauch et al., 1994; Breiter et al., 1996). It can be argued that over-activated PM intentions in OCD go together with a response inhibition deficit, and these two factors together contribute to the higher rate of false alarms in event based PM task (see Study 3). This interpretation fits well with the neurobiological theories of OCD, where this disorder is perceived as a result of the serotonergic system hypofunction (Stengler-Wenzke, Muller, & Angermeyer, 2004; Hasselbach et al., 2007), which has less effective inhibition on connections to basal ganglions and prefrontal cortex dopaminergic pathways, causing a hyperactivity of the dopaminergic system (Marraziti, Hollander, & Lensi, 1992; Kim, Koo, & Cheon, 2003; van der Wee, Stevens, & Hardeman, 2004; for a review in Hungarian see Harsányi, Csigó, <strong>Demeter</strong> & Németh, 2007). This connection of the two predominant neurotransmitter systems affected in OCD can be one of the reasons that the SSRIs have limited success in the treatment of OCD symptoms. In recent studies, the treatment of SSRI non-responder subgroup of OCD patients was supplemented by antipsychotics with dopaminergic activity. Many studies have confirmed the beneficial effect of these antidopaminergic substances on the hyperactive cortico-striato- 33
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: According to Guynn (2008) retrieval
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
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
Page 104 and 105:
6.5. Study 5: No retrieval induced
Page 106 and 107:
Experimental design and materials T
Page 108 and 109:
Procedure “In the study phase, pa
Page 110 and 111:
RIF effect in the control group, t(
Page 112 and 113:
Chapter 7. Discussion, conclusions
Page 114 and 115:
and retrospective memory processes
Page 116 and 117:
Bjork, & Bjork, 1994), which was of
Page 118 and 119:
of the dACC contributes to the pers
Page 120 and 121:
of patients’ cognitive abilities
Page 122 and 123:
Anderson, M. C., & Spellman, B. A.
Page 124 and 125:
Bajo, M. T., Gómez-Ariza, C. J., F
Page 126 and 127:
Burgess, P. W. (1997). Theory and m
Page 128 and 129:
Cambridge Cognition Limited (2006).
Page 130 and 131:
Cuttler, C., & Graf, P. (2007). Sub
Page 132 and 133:
Duncan, J. (1986). Disorganziation
Page 134 and 135:
Gilbert, S.J. & Shallice, T. (2002)
Page 136 and 137:
Harsányi, A., Csigó, K., Demeter,
Page 138 and 139:
Kearns, N. P., Cruickshank, C. A.,
Page 140 and 141:
Levy, B. J., & Anderson, M. C. (200
Page 142 and 143:
McDaniel, M. A., Guynn, M. J., Eins
Page 144 and 145:
neuropsychological and psychoanalyt
Page 146 and 147:
(Eds.), Prospective memory: Cogniti
Page 148 and 149:
Rogers, R. D., & Monsell, S. (1995)
Page 150 and 151:
Smith, G. V., Della Salla, S., Logi
Page 152 and 153:
Thordarson, D. S., Radomsky, A. S.,
Page 154:
Wincze, J. (2001). The role of unde
show all

Gyula Demeter

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?