The Relationship between Tourette’s Syndrome and Infections
Daniela L Krause*, Norbert Müller
Identifiers and Pagination:Year: 2012
Issue: Suppl 1
First Page: 124
Last Page: 128
Publisher ID: TONEUJ-6-124
Article History:Received Date: 04/8/2011
Revision Received Date: 29/1/2012
Acceptance Date: 02/7/2012
Electronic publication date: 16/11/2012
Collection year: 2012
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
Increasing evidence shows that infections and an activated immune status might be involved in the pathogene-sis of tic disorders. Studies discuss the influence of neurotrophic bacteria and viruses on different psychiatric disorders. In addition, signs of inflammation and immunological abnormalities have been described especially in schizophrenia and Tourette’s syndrome (tic disorder). Neuroimaging studies revealed increased microglial activation in psychiatric diseases; indicating an inflammatory state of the CNS.
However, it still remains unclear what the underlying mechanism is of how infectious agents could contribute to tic symp-toms. One hypothesis is that not only one particular infectious agent causes directly to the disease; instead different (chronic) infections influence the immune balance and are therefore involved in the pathology. In tic disorders, infections with group A streptococci, Borrelia burgdorferi or Mycoplasma pneumoniae seem to be associated with symptoms of the disease. Studies have shown that immunologic treatment improves and prevents the re-occurrence of clinical symptoms in Tourette’s syndrome. Also post-infectious events by cross-reactive antibodies(against M-protein) and an altered dopamine rgic(noradrenergic) neurotransmission as well as inflammatory/immunological dysregulations were considered as possible mechanisms to cause symptoms. Another contributing factor to the pathogenesis of these diseases could be an activation of the tryptophan catabolism through infectious agents. Tryptophan functions as a precursor for neurotransmitters like se-rotonin and becomes degraded to products that can modulate the neurotransmitter balance.
A deeper insight into the precise mechanism of how infectious agents influence immune parameter, tryptophan metabo-lism and the resulting neurotransmitter availability could help finding new therapeutic strategies.