Dopamine and social anxiety disorder

Robinson, Hayley; Hood, Sean; Bell, Caroline; Nutt, David

doi:10.1590/s1516-44462006000400003

Cited by 14 publications

(13 citation statements)

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“…However it is also possible that the intrinsic neurobiological mechanism related to PD can predispose to SAD. Different data sources in the literature support the hypothesis that dysfunction in the dopaminergic system might be implicated in the pathogenesis of SAD [10]: 1) the use of dopaminergic antagonist was reported to predispose to social anxiety in Tourette syndrome and schizophrenia [11,12]; 2) abnormal function of the striatum has been demonstrated in neuroimaging studies of SAD patients [13][14][15][16][17]; 3) cerebrospinal fluid levels of homovanilic acid in panic disorder patients with SAD were found to be lower than among panic disorder patients without SAD [18]; 4) functional COMT polymorphism is associated with the development of phobic anxiety [19]; 5) monoamine oxidase inhibitors, known to act by increasing serotonin and noradrenaline levels, as well as dopamine, are more effective than tricyclic antidepressants for the treatment of SAD [20]. Related to this, neurochemical status in these patients may play an important role in the genesis of SAD in PD patients.…”

Section: Introductionmentioning

confidence: 97%

Increased dopamine transporter density in Parkinson's disease patients with social anxiety disorder

Moriyama

Felı́cio

Chagas

et al. 2011

Journal of the Neurological Sciences

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Section: Introductionmentioning

confidence: 97%

Increased dopamine transporter density in Parkinson's disease patients with social anxiety disorder

Moriyama

Felı́cio

Chagas

et al. 2011

Journal of the Neurological Sciences

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“…While the motor symptoms do not cause the pronounced anxiety, the manifestation of anxiety in PD can itself worsen the motor symptoms (Schrag 2006;Siemers et al 1993). The most likely biochemical explanation reflects disturbances in the dopaminergic system, which in theory could be responsible for anxiety by disinhibiting locus ceruleus neuronal activity (Kummer and Teixeira 2009;Robinson al. 2006).…”

Section: Introductionmentioning

confidence: 99%

Epigenome-Wide Association Study for Parkinson’s Disease

et al. 2014

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A methylation-based EWAS on carefully phenotyped individuals with Parkinson's disease (PD) was conducted to reveal prioritised genes and pathways with statistically significant and sizable changes in PD and in the anxiety that often accompanies it. This was followed by subsequent replication of top-ranked CpG sites. Using the Infinium(®) HumanMethylation 450K beadchip (Illumina Inc., USA), twenty unique genes with a sizable difference in methylation (P(adjusted) < 0.05, Δβ ≥ 0.2), after correction for multiple testing, were identified between PD and controls, while seventeen were identified between PD with anxiety and PD without anxiety. Twelve top ranked, significantly associated loci in PD were evaluated in an independent replicate population using Sequenom EpiTYPER for 219 individuals with similar phenotypes to the cross-sectional case-control discovery design. FANCC cg14115740 and TNKS2 cg11963436 show significant differential methylation between PD cases and controls using both techniques and their Δβ values, which have the same direction of effect, are reasonable to warrant further investigation.

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“…The higher frequency of SAD among PD patients may be explained by psychosocial 18 and neurobiological mechanisms 19 . SAD may be a psychosocial reaction to the stigmatizing PD symptoms such as tremor and bradykinesia, but abnormal function of the striatum has been pointed as one of the key pathophysiological mechanism implicated in SAD [20][21][22][23] and it is also plausible that the profound disruption of the main catecholaminergic and serotonergic pathways that occurs in PD 24 predispose patients to SAD.…”

Section: Discussionmentioning

confidence: 99%

Diagnosing social anxiety in Parkinson's disease: characteristics and frequencies according to two diagnostic criteria

Moriyama¹,

Chagas²,

Silveira‐Moriyama³

et al. 2016

Arch. Clin. Psychiatry (São Paulo)

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Background: Studies found inconsistent frequencies of social anxiety disorder (SAD) in Parkinson's disease (PD) (9.7%-50%). Previous reports did not test the impact of applying DSM-IV restrictive criteria that recommends the exclusion of secondary cases when diagnosing SAD in PD. Objective: Our aim is to estimate the frequency of social anxiety according to DSM-IV criteria and according to an inclusive broader approach. Methods: One hundred and ten PD patients were assessed for the presence of SAD using SCID-I, diagnosis of social anxiety were determined according to two different criteria: following and not following DSM-IV recommendation for exclusion of cases though to be secondary to a general medical condition. Results: SAD was present in 34 (31%) of patients, but 17 (15.5%) were secondary to a general medical condition. Patients with SAD were significantly younger, had earlier disease onset, had more severe PD symptoms, and were more frequently depressed. There was no difference in demographic and clinical features between primary and secondary SAD. Discussion: We conclude that the use of different diagnostic criteria may have a massive impact in the estimation of frequency of SAD in PD.

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Dopamine and social anxiety disorder

Cited by 14 publications

References 1 publication

Increased dopamine transporter density in Parkinson's disease patients with social anxiety disorder

Increased dopamine transporter density in Parkinson's disease patients with social anxiety disorder

Epigenome-Wide Association Study for Parkinson’s Disease

Diagnosing social anxiety in Parkinson's disease: characteristics and frequencies according to two diagnostic criteria

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