Prior studies have suggested a common etiology involved in Tourette's syndrome 
and several comorbid conditions and symptomatology. Reportedly, current 
medications used in Tourette's syndrome have intolerable side-effects or are 
ineffective for many patients. After thoroughly researching the literature, I 
hypothesize that magnesium deficiency may be the central precipitating event and 
common pathway for the subsequent biochemical effects on substance P, 
kynurenine, NMDA receptors, and vitamin B6 that may result in the symptomatology 
of Tourette's syndrome and several reported comorbid conditions. These comorbid 
conditions and symptomatology include allergy, asthma, autism, attention deficit 
hyperactivity disorder, obsessive compulsive disorder, coprolalia, copropraxia, 
anxiety, depression, restless leg syndrome, migraine, self-injurious behavior, 
autoimmunity, rage, bruxism, seizure, heart arrhythmia, heightened sensitivity 
to sensory stimuli, and an exaggerated startle response. Common possible 
environmental and genetic factors are discussed, as well as biochemical 
mechanisms. Clinical studies to determine the medical efficacy for a 
comprehensive magnesium treatment option for Tourette's syndrome need to be 
conducted to make this relatively safe, low side-effect treatment option 
available to doctors and their patients.