Tourette's Syndrome and Attention Deficit Disorder With Hyperactivity

Comings, David E.; Comings, Brenda G.

doi:10.1001/archpsyc.1987.01800230103017

Cited by 59 publications

(48 citation statements)

References 12 publications

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“…The category of ADHD 2" TS included those individuals who had ADHD and a relative with TS but did not have TS themselves [Comings and Comings, 1984. The category of "other patients" included 26 patients with TS-like symptoms who did not fulfill the strict criteria for TS.…”

Section: Methodsmentioning

confidence: 99%

“…In addition to the tics it is associated with a wide range of other behaviors, including attention deficit hyperactivity disorder (ADHD), learning disabilities, dyslexia, obsessive compulsive behaviors, conduct disorder, short temper, anxiety, mood disorders, and many types of impulsive behaviors [Comings, 19901. TS is inherited as an autosomal dominant [Pauls and Leckman, 19861 or semidominant, semirecessive trait [Comings et al, 1984[Comings et al, , 1989aDevor, 19841. Because of the many similarities between the behaviors seen in TS and those reported to be associated with abnormalities in serotonin, blood serotonin, serotonin/ platelets, and blood tryptophan were examined in 1,440 individuals. These included patients with TS, ADHD, or ADHD with a family history of TS (ADHD 2" TS); parents and sibs of TS, ADHD, or ADHD 2" TS patients; other patients with TS-like disorders; and controls.…”

Section: Introductionmentioning

confidence: 99%

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Blood serotonin and tryptophan in Tourette syndrome

Comings

1990

Am. J. Med. Genet.

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Blood serotonin and tryptophan levels were studied in 1,440 individuals. These included patients with Tourette syndrome (TS), attention deficit hyperactivity disorder (ADHA), or ADHD with a family history of TS (ADHD 2 degrees TS); relatives (parents, sibs) of these patients; other patients with TS-like disorders; and controls. There were significant decreases in the serotonin/platelet ratio (P = 0.0001) and in tryptophan (P less than 0.0001) in unmedicated patients with TS. Parents of TS patients showed a comparable, significant decrease in serotonin/platelet ratio (P less than 0.0001) and in tryptophan (P less than 0.0001), and there was no difference between parents with and without symptoms. This suggested that these were trait markers for the Gts gene and agrees with the proposal that TS patients are homozygous for Gts gene and that both parents are Gts gene carriers. Although there was no decrease in the serotonin/platelet ratio in ADHD patients, tryptophan levels were significantly decreased and there was a significant decrease in both the serotonin/platelet ratio and in tryptophan in the parents of patients with ADHD including those without a family history of TS. This is consistent with a close link between TS and ADHD. The basic defect may be a dysregulation of serotonin metabolism. The low blood serotonin and tryptophan levels in TS are consistent with the wide range of behavioral disorders seen in TS and suggest tryptophan oxygenase as a possible candidate gene.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Blood serotonin and tryptophan in Tourette syndrome

Comings

1990

Am. J. Med. Genet.

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“…Die Symptome des hyperkinetischen Syndroms manifestieren sich üblicherweise 2-3 Jahre vor dem Auftreten von Tics und sind häufiger bei Patienten mit schweren TicStörungen [26]. Umgekehrt leiden 50% der Kinder mit hyperkinetischem Syndrom unter Tics oder haben Tics in der Familienanamnese [96].…”

Section: Weitere Assoziierte Störungenunclassified

Das Tourette-SyndromEine Übersicht

et al. 2002

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Tourette's syndrome (TS) is a neuropsychiatric disorder characterised by the occurrence of chronic motor and vocal tics that usually begin in childhood. A prevalence of 4-5/10.000 individuals is estimated. Tourette's syndrome patients frequently show comorbidity with other psychiatric disorders such as obsessive compulsive disorder (OCD), attention deficit hyperactivity disorder (ADHD), anxiety, and affective disorders. Some forms of OCD seem to share a common genetic etiology with TS and to be a facultative part of the TS phenotypic spectrum. Based on MRI, positron emission tomography (PET), and single photon emission computed tomography (SPECT), data alterations in the cortico-striato-pallido-thalamo-cortical functional systems have been discussed. Within these systems, dopaminergic neurotransmission is thought to play an important role in the pathophysiology of TS. Autoimmunological mechanisms seem to be important in some subtypes of TS and OCD that are triggered or exacerbated by infections with hemolytic streptococci. In these cases, immune modulatory therapy proved to be efficient. To date, there is no established treatment regimen for TS. The medications used most frequently are antipsychotics.

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“…Collectively, the results of these 2 studies suggest that stimulant drug therapy may actually have a salutary effect on the natural history of chronic multiple tic disorder, a hypothesis for which there is some, albeit limited, support. [51][52][53][54][55] Third, the generalizability of our findings are limited by the size of the study sample and to children whose tics are primarily of mild to moderate severity.…”

Section: Commentmentioning

confidence: 99%