Serotonin 2A Receptors and Visual Hallucinations in Parkinson Disease - Archive ouverte HAL Accéder directement au contenu
Article Dans Une Revue Archives of Neurology -Chigago- Année : 2010

Serotonin 2A Receptors and Visual Hallucinations in Parkinson Disease

Résumé

Background Complex visual hallucinations (VHs) occur in several pathologic conditions; however, the neural mechanisms underlying these symptoms remain unclear. Although dopamine may have a role, indirect evidence indicates that serotonin may also contribute to the pathogenesis of complex VHs, probably via involvement of the serotonin 2 receptor. Objective To examine for the first time in vivo changes in serotonin 2A receptor neurotransmission among patients having Parkinson disease (PD) with VHs. Design Case-control study. Setting Academic research. Patients Seven patients having PD with VHs and 7 age-matched patients having PD without VHs were recruited. Main Outcome Measures We used the selective serotonin 2A receptor ligand setoperone F 18 during positron emission tomography among nondemented patients having PD with VHs. Results Patients having PD with VHs demonstrate increased serotonin 2A receptor binding in the ventral visual pathway (including the bilateral inferooccipital gyrus, right fusiform gyrus, and inferotemporal cortex) as well as the bilateral dorsolateral prefrontal cortex, medial orbitofrontal cortex, and insula. Conclusions This pilot study provides the first in vivo evidence suggesting a role for serotonin 2A receptors in mediating VHs via the ventral visual pathway in PD. Treatment studies should be performed using selective serotonin 2A receptor antagonists, which have important implications for the clinical management of VHs and psychosis in PD. Visual hallucinations (VHs) are abnormal perceptions in the absence of an adequate visual stimulus. Complex well-formed VHs have been described in several pathologic conditions, including peduncular hallucinosis, schizophrenia, cortical Lewy body dementia, and Parkinson disease (PD). A potential common substrate for complex VHs in all of these conditions is suppression of normal inhibitory cortical inputs over the visual association cortex, leading to complex VHs as a “release phenomenon.”1 However, the neural mechanisms underlying VHs remain unclear. Although dopamine may have a role,2 indirect evidence indicates that serotonin may also contribute to the pathogenesis of complex VHs, probably via involvement of the serotonin 2 receptor. In fact, hallucinogenic lysergic acid diethylamide acts via serotonin 2A receptors,3 and atypical antipsychotics (eg, clozapine and quetiapine fumarate) that effectively reduce VHs, as well as dopamine receptor antagonists, are serotonin 2A and 2C receptor antagonists.4 In PD, this antipsychotic effect on VHs occurs at low dosages (approximately 10-fold less than in schizophrenia); at such dosages, there is high occupancy of serotonin 2A receptors and low occupancy of dopamine receptors.5 Together, these observations suggest that serotonin 2A receptors may be involved in VHs in PD; however, the pathogenesis underlying these phenomena and the potential action site of serotonin 2A ligands in reducing such symptoms is unknown to date. Therefore, the specific objective of this pilot study was to measure for the first time in vivo changes in serotonin 2A receptor binding using the selective serotonin 2A receptor ligand setoperone F 186 during positron emission tomography (PET) among age-matched nondemented patients having PD with well-formed VHs vs patients having PD without VHs.

Domaines

Neurobiologie

Dates et versions

hal-02128300 , version 1 (22-10-2019)

Identifiants

Citer

Benedicte Ballanger, Antonio P. Strafella, Thilo van Eimeren, Mateusz Zurowski, Pablo M Rusjan, et al.. Serotonin 2A Receptors and Visual Hallucinations in Parkinson Disease. Archives of Neurology -Chigago-, 2010, 67 (4), pp.416-421. ⟨10.1001/archneurol.2010.35⟩. ⟨hal-02128300⟩
33 Consultations
0 Téléchargements

Altmetric

Partager

Gmail Facebook X LinkedIn More