Widespread abnormality of the γ-aminobutyric acid-ergic system in Tourette syndrome.

Dysfunction of the γ-aminobutyric acid-ergic system in Tourette syndrome may conceivably underlie the symptoms of motor disinhibition presenting as tics and psychiatric manifestations, such as attention deficit hyperactivity disorder and obsessive-compulsive disorder. The purpose of this study was to identify a possible dysfunction of the γ-aminobutyric acid-ergic system in Tourette patients, especially involving the basal ganglia-thalamo-cortical circuits and the cerebellum. We studied 11 patients with Tourette syndrome and 11 healthy controls. Positron emission tomography procedure: after injection of 20 mCi of [(11)C]flumazenil, dynamic emission images of the brain were acquired. Structural magnetic resonance imaging scans were obtained to provide an anatomical framework for the positron emission tomography data analysis. Images of binding potential were created using the two-step version of the simplified reference tissue model. The binding potential images then were spatially normalized, smoothed and compared between groups using statistical parametric mapping. We found decreased binding of GABA(A) receptors in Tourette patients bilaterally in the ventral striatum, globus pallidus, thalamus, amygdala and right insula. In addition, the GABA(A) receptor binding was increased in the bilateral substantia nigra, left periaqueductal grey, right posterior cingulate cortex and bilateral cerebellum. These results are consistent with the longstanding hypothesis that circuits involving the basal ganglia and thalamus are disinhibited in Tourette syndrome patients. In addition, the abnormalities in GABA(A) receptor binding in the insula and cerebellum appear particularly noteworthy based upon recent evidence implicating these structures in the generation of tics.

Brain.  2012; 135(Pt 6):1926-36

Dr. Reinhardt’s comments:  That low GABA  activity would be involved in Tourettes, or for that matter ADHD, schizophrenia, anxiety disorders, and bipolar does not seem much of a surprise.  GABA release in the synapse is regulated partially by the “conditionally essential” amino acid glycine.  Glycine transport across cell walls is facilitated by lithium.  Veterinary studies have shown that both glycine and very low levels of lithium are useful in controlling hyperactivity and aggression in farm animals;  both are routinely added to animal feed to promote health and growth, particularly with pigs.  MANY human studies have shown both glycine and lithium to be useful in treating all of these conditions. Early 20^th century studies demonstrated that lithium (in very low doses) is an essential nutrient, with deficiency related to aggression and violence.  Low doses are very safe;  this basic element was made into a controlled substance by convincing psychiatrists it should be used in massive, potentially lethal doses, yet no study has ever been published showing a reduced effectiveness for bipolar with a lower starting dose.  Since neither of these nutrients is patentable don’t expect your local primary physician or psychiatrist to know about or recommend them for their patients.  A PubMed search will reveal many hundreds of published studies showing positive results.  Low dose lithium aspartate and lithium orotate in the 5-10 mg range is very safe and available over-the-counter at all health supplement stores, for about $1.20 per month.  Glycine Powder is available online from CHS for about $2.90 per month.  You can order it at http://centerforhealthscience.com/glycine-powder-p-647.html