Tourette’s Syndrome: Cause, Onset, Symptoms, and Treatment Options (Part 3)
In addition to disagreement among researchers concerning the biological brain mechanisms responsible for the symptoms of Tourette’s syndrome, a debate has developed pertaining to the origin of this disorder: Is Tourette’s syndrome inherited genetically or through environmental interactions? The Tourette Syndrome Association proposes that Tourette’s may result from an autosomal dominant gene with high sex-specific penetrance, while other researchers feel that a combination of genes working together may be responsible. Genome scans of family history pedigrees of those affected suggest that three regions may be to blame for Tourette’s syndrome on chromosome five, ten, and thirteen (Curtis), although there is no conclusive evidence. Additionally, the dominant gene is expressed differently in each affected family member along a specific history pedigree, and only ten percent of the offspring of an individual affected by Tourette’s syndrome will develop severe enough symptoms to warrant medical attention (Tourette Syndrome Association). In a scientific study conducted by Klug et al, researchers have concluded that in terms of parental, prenatal, and perinatal risk markers, manifestations of interacting environmental and genetic variables, “Tourette’s syndrome is influenced by genetic factors, and is less influenced by environmental factors. ” Approximately seventy percent of Tourette’s syndrome cases are reflections of either an autosomal dominant or polygenetic disorder. In the instances of Tourette’s syndrome that do not have obvious lines of inheritance, environmental roots are suspected in a variation known as sporadic Tourette’s syndrome. Environmental influences on the expression of this condition appear to occur primarily during childhood, and may result from low birth weight (Klug et al. Another discovery recently made in biological research involves the role of immune related disease in the acquisition of Tourette’s syndrome in the form of Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus (PANDAS) (Snider et al. In this theoretic diagnosis, doctors suggest that streptococcal infections, the cause of rheumatic fever, might be behind some cases of Tourette’s because many children first shown signs of the disorder after a strep infection and later infections seem to increase tics in this group of children (Packer). In this conjecture, antibodies generated to combat strep misidentify and damage neurons in the basal ganglia. Further research has shown that the average sizes of the caudate, putamen, and globus pallidus, structures of the basal ganglia, but not the thalamus or total cerebrum are significantly larger in a sample of children with streptococcus-associated OCD and/or tics than in healthy children (Leckman). Although there is no way to determine if streptococcal antibodies are actually “cross-reacting” (Tourette Syndrome Association) with proteins in the basal ganglia, specialized blood tests can be used to indirectly determine ASO and AntiDNA-se-B titers (Leckman). Despite strong evidence from both an environmental and genetic standpoint, an interaction of the two is most likely to blame for the origin of Tourette’s syndrome. This prominent and unresolved question continues to obtain funding to develop a solid understanding. I personally would follow-up the research conducted on PANDAS with the creation of a vaccine that will prevent streptococcal or a development of early diagnosis for this bacterial infection so that it may be treated immediately with the proper antibiotics. Taking a large sample size of vaccinated children or those who had been treated immediately after exposure to the bacteria and comparing these children to a control group, which for ethical reasons would have to voluntarily refuse these early treatments of streptococcal first before joining the study, I would conduct a longitudinal study to determine if there is a high degree of correlation between the illness and the development of Tourette’s. Although I would be unable to infer causation from correlation data, this specific information could provide another avenue for research. In another follow-up experiment, I would also advise a more in-depth study of the human genome now that its initial mapping is completed.
In terms of treatment, various forms of therapy including cognitive behavioral psychotherapy have proven to be helpful in assisting the affected patient and his or her family cope with the implications of diagnosis, and behavioral therapies including behavioral modification, habit reversal, awareness training, competing response, group therapy, hypnosis, exposure-response prevention, relaxation, and a variety of vitamin diets, herbs and trace elements are found to be affective on varying levels of treating symptoms (Tourette Syndrome Association).