It has been suggested that a genetic predisposition for developing TMD (and chronic pain syndromes generally) could exist. This has been postulated to be explained by variations of the gene which codes for the enzyme catechol-O-methyl transferase (COMT) which may produce 3 different phenotypes with regards pain sensitivity. COMT (together with monoamine oxidase) is involved in breaking down catecholamines (e.g. dopamine, epinephrine, and norepinephrine). The variation of the COMT gene which produces less of this enzyme is associated with a high sensitivity to pain. Females with this variation, are at 2–3 times greater risk of developing TMD than females without this variant. However this theory is controversial since there is conflicting evidence. Hormonal factors
Since females are more often affected by TMD than males, the female sex hormone estrogen has been suggested to be involved. The results of one study suggested that the periods of highest pain in TMD can be correlated with rapid periods of change in the circulating estrogen level. Low estrogen was also correlated to higher pain. In the menstrual cycle, estrogen levels fluctuate rapidly during ovulation, and also rapidly increases just before menstruation and rapidly decreases during menstruation. Post-menopausal females who are treated with hormone replacement therapy are more likely to develop TMD, or may experience an exacerbation if they already had TMD. Several possible mechanisms by which estrogen might be involved in TMD symptoms have been proposed. Estrogen may play a role in modulating joint inflammation, nociceptive neurons in the trigeminal nerve, muscle reflexes to pain and μ-opioid receptors.
Diencephalic syndrome, or Russells syndrome, is a rare neurological disorder seen in infants and children and characterised by failure to thrive and severe emaciation despite normal or slightly decreased caloric intake. Classically there is also locomotor hyperactivity and euphoria. Less commonly diencephalic syndrome may involve skin pallor without anaemia, hypoglycaemia, and hypotension. The syndrome is a rare but potentially fatal cause of failure to thrive in children. Failure to thrive presents on average at seven months of age. Of note the syndrome is not associated with developmental delay. There may be associated hydrocephalus.Diencephalic syndrome was first described by Dr. A. Russell in 1951. It is usually caused by a brain tumor such as a low-grade glioma or astrocytoma located in the hypothalamic-optic chiasmatic region. It is not yet understood how diencephalic syndrome causes the effects on appetite and metabolism which are seen, though inappropriately high growth hormone release has been proposed, as has excessive β-lipotropin secretion and overall increased metabolic demand. It is treated with nutritional optimisation while the underlying lesion is treated with chemotherapy, surgery or radiotherapy. == References ==