Cases reported "Tourette Syndrome"

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1/4. A patient with both Gilles de la Tourette's syndrome and chromosome 22q11 deletion syndrome: clue to the genetics of Gilles de la Tourette's syndrome?

    This is the first published case description of the association of Gilles de la Tourette's syndrome (GTS) and chromosome 22q11.2 deletion syndrome (22q11DS; previously referred to as CATCH-22 syndrome). The co-occurrence of GTS, 22q11DS, and their behavioral/neuropsychiatric abnormalities may be due to the common endophenotypic mechanisms shared by these disorders, rather than due to specificity for GTS. research into this genomic region may lead to advancement in neurobehavioral/neuropsychiatric genetics, which will help us in further explicating a broader perspective of gene-brain-behavior interrelationships and of the genetic underpinnings of various developmental psychopathologies and behavioral/neuropsychiatric disorders that are common to both GTS and 22q11DS. Our report should warrant further genetic investigations of the chromosome 22q11.2 deletion site using alternative strategies to the quantitative trait loci endophenotype-based approach, which would be useful for establishing the biological and molecular underpinnings of obsessive-compulsive disorder, attention-deficit/hyperactivity disorder, and GTS.
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2/4. propranolol treatment of akathesia in Tourette's syndrome.

    Akathesia is a common side effect of neuroleptic medication and has been reported to occur in patients with Tourette's Syndrome (TS). In TS, the differentiation between untreated hyperactivity and akathesia can be difficult. A case of neuroleptic treated TS with hyperactivity versus akathesia is presented in which propranolol was successfully used to treat the akathesia. The akathesia reappeared when the propranolol was withdrawn. This case illustrates an alternative to neuroleptic dose reduction in the management of akathesia in TS.
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3/4. A treatment model for motor tics based on a specific tension-reduction technique.

    A model is proposed in which motor tics are considered to be tension reducing responses to a specific sensory stimulus. It is hypothesized that the sensory stimulus is of a proprioceptive nature. The first phase of therapy concerns the identification of the stimulus. The patient is then taught a socially acceptable, alternative response, which also reduces the sensory stimulus. Two case reports illustrate this model. The applicability of the model with respect to other movement disorders is discussed.
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4/4. bupropion exacerbates tics in children with attention-deficit hyperactivity disorder and Tourette's syndrome.

    Concerns have been raised regarding the development of tics in some children with attention-deficit hyperactivity disorder (ADHD) receiving stimulants. Because in many patients with Tourette's syndrome (TS) the ADHD symptoms are the major source of disability, alternative nonstimulant treatments are needed. Initial reports on bupropion have suggested that it may be an effective alternative in children and adults with ADHD. The value of bupropion as an alternative treatment for patients with comorbid TS and ADHD is determined by the question of association with exacerbation of tics. The purpose of this study was to examine an apparent association with exacerbation of tics in patients with comorbid TS and ADHD. A careful retrospective analysis was conducted of clinic cases of patients who all had comorbid TS and ADHD treated with bupropion. We present four cases of children with ADHD and comorbid TS treated with bupropion in whom tics were exacerbated by this medicine. This series suggests that bupropion may not be an appropriate alternative to stimulants in the treatment of ADHD in TS.
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