Abstract |
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.
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Authors | B L Grimaldi |
Journal | Medical hypotheses
(Med Hypotheses)
Vol. 58
Issue 1
Pg. 47-60
(Jan 2002)
ISSN: 0306-9877 [Print] United States |
PMID | 11863398
(Publication Type: Journal Article)
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Copyright | Copyright 2002 Harcourt Publishers Ltd. |
Chemical References |
- Receptors, N-Methyl-D-Aspartate
- Substance P
- Kynurenine
- Vitamin B 6
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Topics |
- Humans
- Kynurenine
(metabolism)
- Magnesium Deficiency
(complications)
- Receptors, N-Methyl-D-Aspartate
(metabolism)
- Substance P
(metabolism)
- Tourette Syndrome
(complications, drug therapy, etiology, metabolism)
- Vitamin B 6
(administration & dosage, metabolism, therapeutic use)
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