Tic Symptom Profiles in Subjects with Tourette Syndrome from two Genetically Isolated Populations
Department of Psychiatry, University of California, San Diego, San Diego, California, United States Biological Psychiatry
(Impact Factor: 10.26).
03/2007; 61(3):292-300. DOI: 10.1016/j.biopsych.2006.02.009
Tourette Syndrome (TS) has a complex etiology and wide variability in phenotypic expression. Identifying underlying symptom patterns may be useful for etiological and outcome studies of TS.
Lifetime tic and related symptom data were collected between 1996 and 2001 in 121 TS subjects from the Central Valley of Costa Rica and 133 TS subjects from the Ashkenazi Jewish (AS) population in the US. Subjects were grouped by tic symptoms using an agglomerative hierarchical cluster analysis. Cluster membership was tested for association with available ancillary information (age of onset, tic severity, comorbid disorders, medication treatment and family history).
Cluster analysis identified two distinct groups in each sample, those with predominantly simple tics (cluster 1), and those with multiple complex tics (cluster 2). Membership in cluster 2 was correlated with increased tic severity, global impairment, medication treatment, and presence of comorbid obsessive-compulsive symptoms in both samples, and with family history of tics, lower verbal IQ, earlier age of onset, and comorbid obsessive-compulsive disorder and attention-deficit/hyperactivity disorder in the AS sample.
This study provides evidence for consistent and reproducible symptom profiles in two independent TS study samples. These findings have implications for etiological studies of TS.
Available from: Joseph F McGuire
- "Collectively, these four studies have produced two consistent findings. First, tic symptoms cluster by complexity (simple versus complex) (Mathews et al., 2007; Robertson et al., 2008; Kircanski et al., 2010). Second, compulsive tic behaviors (e.g., touching, repetitive behaviors, echolalia) cluster separately from other tic symptoms (e.g., head movements, leg movements, coprolalia) (Alsobrook and Pauls, 2002; Robertson et al., 2008). "
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ABSTRACT: Cluster analytic methods have examined the symptom presentation of chronic tic disorders (CTDs), with limited agreement across studies. The present study investigated patterns, clinical correlates, and treatment outcome of tic symptoms. 239 youth and adults with CTDs completed a battery of assessments at baseline to determine diagnoses, tic severity, and clinical characteristics. Participants were randomly assigned to receive either a comprehensive behavioral intervention for tics (CBIT) or psychoeducation and supportive therapy (PST). A cluster analysis was conducted on the baseline Yale Global Tic Severity Scale (YGTSS) symptom checklist to identify the constellations of tic symptoms. Four tic clusters were identified: Impulse Control and Complex Phonic Tics; Complex Motor Tics; Simple Head Motor/Vocal Tics; and Primarily Simple Motor Tics. Frequencies of tic symptoms showed few differences across youth and adults. Tic clusters had small associations with clinical characteristics and showed no associations to the presence of coexisting psychiatric conditions. Cluster membership scores did not predict treatment response to CBIT or tic severity reductions. Tic symptoms distinctly cluster with little difference across youth and adults, or coexisting conditions. This study, which is the first to examine tic clusters and response to treatment, suggested that tic symptom profiles respond equally well to CBIT. Clinical trials.gov. identifiers: NCT00218777; NCT00231985.
Available from: Christos Ganos
- "Thus, given the number of comorbidities and the complexity of the phenomenology of tics and tic -related behaviors (Lewis and Kim, 2009; Worbe et al., 2010b) GTS is a prototype of a complex neuropsychiatric spectrum disorder (Cavanna et al., 2009; Robertson, 2011; Roessner et al., 2005, 2007; Wanderer et al., 2012). Using principal component factor and hierarchical cluster analyses different GTS-subtypes have been postulated (Alsobrook and Pauls, 2002; Cavanna et al., 2011; Mathews et al., 2007; Robertson and Cavanna, 2007). Although variations exist between the reported results, depending on the exact factor loadings or the identified clusters, it has become clear that core features of GTS include simple and complex tics, impulsivity , aggressive (self-injurious behavior, coprophenomena) and compulsive (or repetitive) behaviors (Alsobrook and Pauls, 2002; Cavanna et al., 2011; Mathews et al., 2007; Robertson, 2011). "
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ABSTRACT: Gilles de la Tourette syndrome (GTS) holds a prime position as a disorder transgressing the brittle boundaries of neurology and psychiatry with an entangling web of motor and behavioural problems. With tics as the disorder's hallmark and myriads of related signs such as echo-, pali- and coprophenomena, paralleled by a broad neuropsychiatric spectrum of comorbidities encompassing attention deficit hyperactivity disorder, obsessive-compulsive disorder but also self-injurious behaviour and depression, GTS pathophysiology remains enigmatic. In this review, in the light of GTS phenomenology, we will focus on current theories of tic-emergence related to aberrant activity in the basal ganglia and abnormal basal ganglia - cortex interplay through cortico-striato-thalamocortical loops from an anatomical, neurophysiological and functional-neuroimaging perspective. We will attempt a holistic view to the countless major and minor drawbacks of the GTS brain and comment on future directions of neuroscientific research to elucidate this common and complex neuropsychiatric syndrome, which merits scientific understanding and social acceptance.
Available from: Andreas Hartmann
- "Simple and complex tics differed in their phenomenological expression and are thought to represent biologically relevant symptom subclasses (Mathews et al., 2007; Robertson et al., 2008). In contrast to the basic motor patterns of simple tics, complex tics are characterized by complex sequential motor or vocal patterns such as touching behaviour, repetitive word pronunciation or motor action or vocal imitations (Jankovic and Fahn, 1986). "
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ABSTRACT: Gilles de la Tourette syndrome is a childhood-onset neurodevelopmental disorder characterized by tics that are often associated with psychiatric co-morbidities. The clinical heterogeneity of Gilles de la Tourette syndrome has been attributed to the disturbance of functionally distinct cortico-striato-thalamo-cortical circuits, but this remains to be demonstrated. The aim of this study was to determine the structural correlates of the diversity of symptoms observed in Gilles de la Tourette syndrome. We examined 60 adult patients and 30 age- and gender-matched control subjects using cortical thickness measurement and 3 T high-resolution T(1)-weighted images. Patients were divided into three clinical subgroups: (i) simple tics; (ii) simple and complex tics and (iii) tics with associated obsessive-compulsive disorders. Patients with Gilles de la Tourette syndrome had reduced cortical thickness in motor, premotor, prefrontal and lateral orbito-frontal cortical areas. The severity of tics was assessed using the Yale Global Tic Severity Scale and correlated negatively with cortical thinning in these regions, as well as in parietal and temporal cortices. The pattern of cortical thinning differed among the clinical subgroups of patients. In patients with simple tics, cortical thinning was mostly found in primary motor regions. In patients with simple and complex tics, thinning extended into larger premotor, prefrontal and parietal regions. In patients with associated obsessive-compulsive disorders, there was a trend for reduced cortical thickness in the anterior cingulate cortex and hippocampal morphology was altered. In this clinical subgroup, scores on the Yale-Brown Obsessive-Compulsive Scale correlated negatively with cortical thickness in the anterior cingulate cortex and positively in medial premotor regions. These data support the hypothesis that different symptom dimensions in Gilles de la Tourette syndrome are associated with dysfunction of distinct cortical areas and have clear implications for the current neuroanatomical model of this syndrome.
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