title: Antineuronal antibody status and phenotype analysis in Tourette's syndrome.
abstract: The Gilles de la Tourette syndrome (GTS) spectrum includes psychiatric comorbidities, mainly obsessive-compulsive disorder (OCD) and attention-deficit-hyperactivity disorder (ADHD). The role of environmental factors, e.g., antineuronal antibodies (ANeA), remains unclear. We compared the clinical features of ANeA-positive and ANeA-negative patients in 53 children and 75 adults with GTS. All diagnoses were made according to DSM-IV-TR criteria. A positive ANeA Western immunoblot showed bands for at least 1 of 3 reported striatal antigens (40, 45, and 60 kDa). Twelve children (23%) and 18 adults (25%) with GTS were ANeA-positive. Disease duration, tic phenomenology and severity, frequency of echo/pali/coprophenomena, self-injurious and aggressive behavior, or frequency of OCD comorbidity did not significantly differ between ANeA-positive and negative patients. Similar findings were obtained analyzing separately the three different antibody reactivities. A comorbid diagnosis of ADHD was significantly less frequent in GTS patients positive for the anti-60 kDa antibody only. Using a multivariate logistic regression model, adjusting for age, gender, and age at disease onset, a comorbid diagnosis of ADHD remained inversely associated with anti-60 kDa antibodies (odds ratio = 0.14; P = 0.002; 95% confidence interval 0.04-0.49). ANeA status does not differentiate a specific phenotype of GTS.
authors.affiliation: Department of Neuroinflammation, Institute of Neurology, University College London, London, United Kingdom.|Department of Neurological and Psychiatric Sciences, University of Bari, Bari, Italy.
authors.forename: Davide
authors.initials: D
authors.lastname: Martino
authors.affiliation: Department of Neurological and Psychiatric Sciences, University of Bari, Bari, Italy.
authors.forename: Giovanni
authors.initials: G
authors.lastname: Defazio
authors.affiliation: Department of Neuroinflammation, Institute of Neurology, University College London, London, United Kingdom.
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Church
authors.affiliation: Department of Neuroinflammation, Institute of Neurology, University College London, London, United Kingdom.|Neurosciences Unit, Great Ormond Street Hospital NHS Trust and Institute of Child Health, University College London, Queen Square, London, United Kingdom.
authors.forename: Russell C
authors.initials: RC
authors.lastname: Dale
authors.affiliation: Department of Neuroinflammation, Institute of Neurology, University College London, London, United Kingdom.
authors.forename: Gavin
authors.initials: G
authors.lastname: Giovannoni
authors.affiliation: Department of Mental Health Sciences, University College London, Queen Square, London, United Kingdom.
authors.forename: Mary M
authors.initials: MM
authors.lastname: Robertson
authors.affiliation: Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, Queen Square, London, United Kingdom.
authors.forename: Michael
authors.initials: M
authors.lastname: Orth
mesh_terms: D000293:Adolescent; D000328:Adult; D000906:Antibodies / Q000378:metabolism*; D015153:Blotting, Western / Q000379:methods; D002648:Child; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D005260:Female; D006801:Humans; D016015:Logistic Models; D008297:Male; D008970:Molecular Weight; D009419:Nerve Tissue Proteins / Q000276:immunology*; D010641:Phenotype; D012189:Retrospective Studies; D005879:Tourette Syndrome / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology
chemical_list: D000906:Antibodies; D009419:Nerve Tissue Proteins