“…Indeed, while some fMRI experiments in healthy subjects have reported an activation of only the right caudate nucleus (Huettel et al, 2002;Monchi et al, 2006;Rao et al, 1997), other studies have shown a bilateral caudate activation (Lewis et al, 2004;Monchi et al, 2001). In addition, PET studies in PD have demonstrated only a unilateral striatal involvement with significant correlation between the right caudate nucleus and frontal executive tasks (Bruck et al, 2001;Marie et al, 1999). These discrepancies, however, are not surprising considering the different parameters measured (e.g.…”
Section: Discussionmentioning
confidence: 99%
“…Some neuroimaging studies have proposed that changes in striatal dopamine levels can modulate certain cognitive processes and that level of cognitive impairment may be dependent on the level of dopamine depletion (Cropley et al, 2006). Consistent with this hypothesis, positron emission tomography (PET) studies performed both in healthy subjects (Mehta et al, 2005), following tyrosine and phenylalanine-induced depletion, and patients with Parkinson's disease (PD) (Marie et al, 1999;Lozza et al, 2004) have shown significant correlation between executive task performances and striatal dopamine denervation.…”
To date, while the contribution of the striatum in executive processes is well documented, the role played by striatal dopamine during tasks requiring executive functions is still unknown. We used D2-dopamine receptor ligand [ 11 C] raclopride PET in healthy subjects while performing the Montreal Card Sorting Task (MCST). We observed a striatal reduction in [ 11 C] raclopride binding potential during planning of a set-shift when compared with matching according to an ongoing rule. These findings suggest that striatal dopamine neurotransmission increases significantly during the performance of specific executive processes confirming previous evidence of striatal activation during fMRI studies. The present observation may provide some insights on the origin of cognitive deficits underlying certain neurological disorders associated with dopamine dysfunction, such as Parkinson's disease.
“…Indeed, while some fMRI experiments in healthy subjects have reported an activation of only the right caudate nucleus (Huettel et al, 2002;Monchi et al, 2006;Rao et al, 1997), other studies have shown a bilateral caudate activation (Lewis et al, 2004;Monchi et al, 2001). In addition, PET studies in PD have demonstrated only a unilateral striatal involvement with significant correlation between the right caudate nucleus and frontal executive tasks (Bruck et al, 2001;Marie et al, 1999). These discrepancies, however, are not surprising considering the different parameters measured (e.g.…”
Section: Discussionmentioning
confidence: 99%
“…Some neuroimaging studies have proposed that changes in striatal dopamine levels can modulate certain cognitive processes and that level of cognitive impairment may be dependent on the level of dopamine depletion (Cropley et al, 2006). Consistent with this hypothesis, positron emission tomography (PET) studies performed both in healthy subjects (Mehta et al, 2005), following tyrosine and phenylalanine-induced depletion, and patients with Parkinson's disease (PD) (Marie et al, 1999;Lozza et al, 2004) have shown significant correlation between executive task performances and striatal dopamine denervation.…”
To date, while the contribution of the striatum in executive processes is well documented, the role played by striatal dopamine during tasks requiring executive functions is still unknown. We used D2-dopamine receptor ligand [ 11 C] raclopride PET in healthy subjects while performing the Montreal Card Sorting Task (MCST). We observed a striatal reduction in [ 11 C] raclopride binding potential during planning of a set-shift when compared with matching according to an ongoing rule. These findings suggest that striatal dopamine neurotransmission increases significantly during the performance of specific executive processes confirming previous evidence of striatal activation during fMRI studies. The present observation may provide some insights on the origin of cognitive deficits underlying certain neurological disorders associated with dopamine dysfunction, such as Parkinson's disease.
“…Jokinen et al (2009) found a significant correlation between verbal and visual memory functioning and caudate FDOPA uptake, although they also noted additional associations with hippocampal and prefrontal atrophy. Several other studies have shown relationships between reductions in caudate dopaminergic tracer uptake and impaired performance on tests of memory, executive, and frontal lobe function (Marie et al 1999;Muller et al 2000;Rinne et al 2000;Bruck et al 2001;van Beilen et al 2008). During sequence learning, PD patients showed a correlation between correct acquisition of targets and caudate DAT Learning-related deactivation responses in the ventromedial prefrontal cortex (vmPFC) displayed as an inverted-U function.…”
Section: Imaging Of Specific Neurotransmitters In Pd Cognitionmentioning
“…Reduced ¹⁸F-fl uorodopa uptake in the caudate has been associated with executive dysfunction in patients with PD in some 92,93 but not all studies, 94 thus implicating nigrostriatal dopamine depletion in these cognitive defi cits. The mesocortical dopamine system is also aff ected, 95 although prefrontal overactivity, particularly in the anterior cingulate, has been found at early stages of the disease.…”
Section: Pathophysiology Of Executive Dysfunctionmentioning
A dopaminergic defi ciency in patients with Parkinson's disease (PD) causes abnormalities of movement, behaviour, learning, and emotions. The main motor features (ie, tremor, rigidity, and akinesia) are associated with a defi ciency of dopamine in the posterior putamen and the motor circuit. Hypokinesia and bradykinesia might have a dual anatomo-functional basis: hypokinesia mediated by brainstem mechanisms and bradykinesia by cortical mechanisms. The classic pathophysiological model for PD (ie, hyperactivity in the globus pallidus pars interna and substantia nigra pars reticulata) does not explain rigidity and tremor, which might be caused by changes in primary motor cortex activity. Executive functions (ie, planning and problem solving) are also impaired in early PD, but are usually not clinically noticed. These impairments are associated with dopamine defi ciency in the caudate nucleus and with dysfunction of the associative and other non-motor circuits. Apathy, anxiety, and depression are the main psychiatric manifestations in untreated PD, which might be caused by ventral striatum dopaminergic defi cit and depletion of serotonin and norepinephrine. In this Review we discuss the motor, cognitive, and psychiatric manifestations associated with the dopaminergic defi ciency in the early phase of the parkinsonian state and the diff erent circuits implicated, and we propose distinct mechanisms to explain the wide clinical range of PD symptoms at the time of diagnosis.
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