Author Response: Association of Group A Streptococcus Exposure and Exacerbations of Chronic Tic Disorders: A Multinational Prospective Cohort Study
DavideMartino, Neurologist, Department of Clinical Neurosciences (D.M.), Cumming School of Medicine & Hotchkiss Brain Institute, Univ. of Calgary, Canada
Submitted April 05, 2021
We are grateful to the European Immuno-Neuropsychiatric Association Scientific and Medical Advisory Group for their interest and positive comments on our study. As correctly pointed out, our study exclusively enrolled patients with an established diagnosis of chronic tic disorders, the vast majority of whom had Tourette syndrome.1 Pediatric Acute-onset Neuropsychiatric Syndrome and Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANS/PANDAS) represent a clinical spectrum that is substantially different from the clinical course and phenotype of chronic tic disorders.2 There is growing evidence supporting a direct role of immune-mediated mechanisms in the pathogenesis of chronic, neurodevelopmental disorders like Tourette syndrome, obsessive-compulsive disorder, and ADHD.3 Genetic and early environmental exposures might prompt a very early priming of neural and immune development, which might lead to altered trajectories of maturation and, ultimately, to behavioral abnormalities and hyperactive immune-inflammatory responses.3,4 Our study focused on the role of a specific exogenous trigger (Group A Streptococcus) on the temporal course of core behavioral features of chronic tic disorders during early adolescence. Our results do not refute a mechanistic link between immune and neural mechanisms during early development in chronic tic disorders. At the same time, we agree that our clinical overall message applies to chronic tic disorders but not to acute-onset behavioral presentations which encompass PANS/PANDAS.
Disclosure
The authors report no relevant disclosures. Contact journal@neurology.org for full disclosures.
References
Martino D, Schrag A, Anastasiou Z, et al. Association of Group A Streptococcus Exposure and Exacerbations of Chronic Tic Disorders: A Multinational Prospective Cohort Study. Neurology. 2021;96(12):e1680-e1693. doi:10.1212/WNL.0000000000011610
Chang K, Frankovich J, Cooperstock M, et al. Clinical evaluation of youth with pediatric acute-onset neuropsychiatric syndrome (PANS): recommendations from the 2013 PANS Consensus Conference. J Child Adolesc Psychopharmacol. 2015;25(1):3-13. doi:10.1089/cap.2014.0084
Martino D, Johnson I, Leckman JF. What Does Immunology Have to Do With Normal Brain Development and the Pathophysiology Underlying Tourette Syndrome and Related Neuropsychiatric Disorders?. Front Neurol. 2020;11:567407. Published 2020 Sep 16. doi:10.3389/fneur.2020.567407
Frick L, Pittenger C. Microglial Dysregulation in OCD, Tourette Syndrome, and PANDAS. J Immunol Res. 2016;2016:8606057. doi:10.1155/2016/8606057
We are grateful to the European Immuno-Neuropsychiatric Association Scientific and Medical Advisory Group for their interest and positive comments on our study. As correctly pointed out, our study exclusively enrolled patients with an established diagnosis of chronic tic disorders, the vast majority of whom had Tourette syndrome.1 Pediatric Acute-onset Neuropsychiatric Syndrome and Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANS/PANDAS) represent a clinical spectrum that is substantially different from the clinical course and phenotype of chronic tic disorders.2 There is growing evidence supporting a direct role of immune-mediated mechanisms in the pathogenesis of chronic, neurodevelopmental disorders like Tourette syndrome, obsessive-compulsive disorder, and ADHD.3 Genetic and early environmental exposures might prompt a very early priming of neural and immune development, which might lead to altered trajectories of maturation and, ultimately, to behavioral abnormalities and hyperactive immune-inflammatory responses.3,4 Our study focused on the role of a specific exogenous trigger (Group A Streptococcus) on the temporal course of core behavioral features of chronic tic disorders during early adolescence. Our results do not refute a mechanistic link between immune and neural mechanisms during early development in chronic tic disorders. At the same time, we agree that our clinical overall message applies to chronic tic disorders but not to acute-onset behavioral presentations which encompass PANS/PANDAS.
Disclosure
The authors report no relevant disclosures. Contact journal@neurology.org for full disclosures.
References