Mark Morningstar, DC, PhD

Neurotransmitters are the chemicals by which the brain controls nearly every function in the body. These chemicals vary in their locations, amounts, and functions. Many of these neurotransmitters vary their amounts even over the course of one day. For example, melatonin decreases from morning to midday as we wake up, then steadily increases again as it gets closer to nighttime. Melatonin is the neurotransmitter that make us tired and helps us fall asleep. Other neurotransmitters like gamma-amino-butyric acid (GABA) act on the emotional centers of the brain to make us happy. When levels of the neurotransmitters are deficient, excessive, or abnormally fluctuate, neurological or neuropsychological symptoms may result.

Recently, more attention has been paid to the neurological contributions to scoliosis development and progression. Of these contributions, neurotransmitter deficiencies or dysfunctions have been identified as theoretical contributors to the development of scoliosis. For example, one of the most common neurotransmitters, serotonin, is vital for the regulation of normal postural control. However, in the metabolic pathway of serotonin, it eventually converts into melatonin in the pineal gland. Previous researchers have studied the effects of removing the pineal gland in rats and chickens. These animals developed scoliosis more frequently when the pineal gland was removed. This led researchers to conclude that melatonin deficiency could be a cause of scoliosis. However, when we evaluate the metabolic pathways in the brain and spinal cord, many of the postural control pathways require serotonin, not melatonin, for normal postural control. Preliminary testing suggests that adolescents and adults with idiopathic scoliosis are more likely to have serotonin levels below that of non-scoliosis patients. Given that serotonin gets converted into melatonin, it is evident why researchers are observing melatonin deficiencies in patients who are also serotonin deficient.

Identifying these neurotransmitter imbalances is important in scoliosis rehabilitation because scoliosis exercises require repeated neurological stimulation and retraining to work correctly. When a patient is serotonin deficient, it prevents them from receiving the full benefit of scoliosis exercise therapies like those performed at a ScoliSMART clinic. Repeated stimulation of these postural control serotonin-mediated neurological pathways is essential to create long-term muscle memory development and activation. Without this, no scoliosis exercise program will be able to provide as long-term of a benefit as possible.

ScoliSMART clinic

Another important neurotransmitter important in scoliosis treatment is norepinephrine, or noradrenaline. This hormone is produced by the adrenal glands and allows the body to adapt to new or sudden changes in posture. For example, when a scoliosis patient performs a new exercise, the adrenal glands must secrete norepinephrine to allow the body to react appropriately. Otherwise, the patient may develop various autonomic neurological responses, like hypotension, nausea, vertigo, or headache. As most people know, norepinephrine helps to increase muscle strength for a short period of time (such as when people get noradrenaline surges and lift cars off of people trapped underneath). Therefore, when postural muscles are required to perform certain activities they aren’t used to performing, epinephrine helps those muscles accomplish that task until they adapt to that task as a result of repeated performance of that activity over a 2-6 week period.

Since it is becoming quite clear that scoliosis is a whole-body disorder, and not simply a spinal curvature, it is becoming increasingly apparent that steps must be taken to ensure that people with scoliosis are getting the fullest evaluation possible so that their treatment plans can be as comprehensive as possible. An easy step to take is the incorporation of neurotransmitter testing to evaluate for these potential imbalances, which may ultimately prove to be barriers to treatment success if not evaluated or addressed.