Frontal dopaminergic abnormality in Tourette syndrome: A postmortem analysis

Yoon, Dustin Y.; Gause, Colin D.; Leckman, James F.; Singer, Harvey S.

doi:10.1016/j.jns.2007.01.069

Cited by 107 publications

(80 citation statements)

References 61 publications

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“…Diffusion-weighted imaging has revealed microstructural alterations in the corpus callosum and other white matter (Jackson et al, 2011). Additional support for frontoparietal network abnormalities are based on alterations of MRI resting-state functional connectivity (Church et al, 2009b), tic generation in association with coactivation of the supplementary motor area (Hampson et al, 2009), appearance of secondary tics after resection of the frontal lobe (Yochelson and David, 2000), and investigations on postmortem tissue showing a greater number of biochemical changes in prefrontal rather than striatal regions (Minzer et al, 2004;Yoon et al, 2007a).…”

Section: Cortex and Subcortical White Mattermentioning

confidence: 99%

“…Dopamine dysfunction is considered a prime abnormality in TS based on tic suppression with the use of dopamine antagonists (antipsychotics), results from various nuclear imaging protocols (Wolf et al, 1996;Wong et al, 1997Wong et al, , 2008Singer et al, 2002;Albin et al, 2003;Serra-Mestres et al, 2004;Liu et al, 2010), CSF analysis (Singer et al, 1982), and postmortem studies (Singer et al, 1991(Singer et al, , 1995Minzer et al, 2004;Yoon et al, 2007a). One hypothesis is that either an overactive dopamine transporter or central abnormality leads to an alteration in phasic dopamine release, which in turn, results in a hyperresponsive spike-dependent dopaminergic system Wong et al, 2008).…”

Section: Neurotransmitter Studiesmentioning

confidence: 99%

“…This dopaminergic tonic-phasic hypothesis could potentially involve either the cortex or striatum. Although most neurotransmitter-related studies have focused on the striatum, support for an extrastriatal dopaminergic dysfunction includes PET findings of decreased cortical receptor binding potentials and increased dopamine release (Steeves et al, 2010) and postmortem identified cortical dopaminergic abnormalities (Minzer et al, 2004;Yoon et al, 2007a). Recognizing the various clinical manifestations seen in TS, it is highly likely that this disorder involves a dysfunction of more than one neurotransmitter system or a second messenger defect (Singer and Minzer, 2003).…”

Section: Neurotransmitter Studiesmentioning

confidence: 99%

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Neurobiology of Tourette Syndrome: Current Status and Need for Further Investigation: Table 1.

Felling¹,

Singer²

2011

J. Neurosci.

196

116

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Tourette syndrome (TS) is a common, chronic neuropsychiatric disorder characterized by the presence of fluctuating motor and phonic tics. The typical age of onset is ϳ5-7 years, and the majority of children improve by their late teens or early adulthood. Affected individuals are at increased risk for the development of various comorbid conditions, such as obsessive-compulsive disorder, attention deficit hyperactivity disorder, school problems, depression, and anxiety. There is no cure for tics, and symptomatic therapy includes behavioral and pharmacological approaches. Evidence supports TS being an inherited disorder; however, the precise genetic abnormality remains unknown. Pathologic involvement of cortico-striatal-thalamo-cortical (CSTC) pathways is supported by neurophysiological, brain imaging, and postmortem studies, but results are often confounded by small numbers, age differences, severity of symptoms, comorbidity, use of pharmacotherapy, and other factors. The primary site of abnormality remains controversial. Although numerous neurotransmitters participate in the transmission of messages through CSTC circuits, a dopaminergic dysfunction is considered a leading candidate. Several animal models have been used to study behaviors similar to tics as well as to pursue potential pathophysiological deficits. TS is a complex disorder with features overlapping a variety of scientific fields. Despite description of this syndrome in the late 19th century, there remain numerous unanswered neurobiological questions.In the 1880's, Georges Gilles de la Tourette published a two-part article in which he emphasized differences between tics and chorea. Although many of the descriptions about the disorder, which now bears his name [Tourette syndrome (TS)], have been revised, his belief that tics are a neurological movement disorder and not a psychiatric condition persists to the present (Goetz and Klawans, 1982). Nevertheless, despite multiple advances and widespread acceptance of TS being a biological disorder, the precise etiology and underlying pathophysiological mechanisms remain unknown. The goals of the present review are to briefly describe the clinical phenomenology of TS and related tic disorders, to review current information on genetic and neurobiological mechanisms, and to identify areas in need of further investigation.

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Section: Cortex and Subcortical White Mattermentioning

confidence: 99%

Section: Neurotransmitter Studiesmentioning

confidence: 99%

Section: Neurotransmitter Studiesmentioning

confidence: 99%

See 1 more Smart Citation

Neurobiology of Tourette Syndrome: Current Status and Need for Further Investigation: Table 1.

Felling¹,

Singer²

2011

J. Neurosci.

196

116

View full text Add to dashboard Cite

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“…Although impairment of color perception with higher vulnerability of the BY axis has also been found in other dopaminergic disorders (e.g., Parkinsonism; Sartucci and Porciatti 2006) and states (cocaine withrawal; Desai et al 1997), its fundamental mechanisms remain unclear . Whereas in CTD hyperdopaminergic neurotransmitter functioning is believed to play a central role in its pathophysiology (Minzer et al 2004;Yoon et al 2007), in ADHD most authors favor a hypodopaminergic model (Sadile and Viggiano 2005). In view of the association between color vision deficits and dopaminergic deviances underlying both disorders, color vision deficits, particularly on the BY axis, in the comorbid condition, ADHD þ CTD, are of special interest.…”

Section: Introductionmentioning

confidence: 99%

Color perception deficits in co-existing attention-deficit/hyperactivity disorder and chronic tic disorders

et al. 2007

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Summary. Preliminary findings suggest that color perception, particularly of blue-yellow stimuli, is impaired in attention-deficit=hyperactivity disorder (ADHD) as well as in chronic tic disorders (CTD). However, these findings have been not replicated and it is unclear what these deficits mean for the comorbidity of ADHD þ CTD.Four groups (ADHD, CTD, ADHD þ CTD, controls) of children with similar age, IQ and gender distribution were investigated with the Farnsworth-Munsell 100 Hue Test (FMT) and the Stroop-Color-Word Task using a factorial design. Color perception deficits, as indexed by the FMT, were found for both main factors (ADHD and CTD), but there were no interaction effects. A preponderance of deficits on the blue-yellow compared to the red-green axis was detected for ADHD. In the Stroop task only the 'pure' ADHD group showed impairments in interference control and other parameters of Stroop performance. No significant correlations between any FMT parameter and color naming in the Stroop task were found. Basic color perception deficits in both ADHD and CTD could be found. Beyond that, it could be shown that these deficits are additive in the case of comorbidity (ADHD þ CTD). Performance deficits on the Stroop task were present only in the 'pure' ADHD group. Hence, the latter may be compensated in the comorbid group by good prefrontal capabilities of CTD. The influence of color perception deficits on Stroop task performance might be negligible.

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“…Disruptions in the PFCCd circuitry may also be pivotal for long-term outcome in TS, since a favorable future outcome in children with TS is associated with increased Cd size (Bloch et al, 2005) and tic suppression is concomitant with activation of the PFC (Peterson et al, 1998). Thus, the cholinergic neuron alterations described here may be a manifestation of hypofunctional frontostriatal circuitry, a characteristic in common between severe TS and schizophrenia (Yoon et al, 2007).…”

Section: Discussionmentioning

confidence: 80%

Decreased Number of Parvalbumin and Cholinergic Interneurons in the Striatum of Individuals with Tourette Syndrome

Kataoka‐Sasaki

Kalanithi

Grantz

et al. 2009

Neuroscience Research

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Frontal dopaminergic abnormality in Tourette syndrome: A postmortem analysis

Cited by 107 publications

References 61 publications

Neurobiology of Tourette Syndrome: Current Status and Need for Further Investigation: Table 1.

Neurobiology of Tourette Syndrome: Current Status and Need for Further Investigation: Table 1.

Color perception deficits in co-existing attention-deficit/hyperactivity disorder and chronic tic disorders

Decreased Number of Parvalbumin and Cholinergic Interneurons in the Striatum of Individuals with Tourette Syndrome

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