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Laurance Johnston, Ph.D.

Part 1 introduced the pineal gland from both a scientific and metaphysical viewpoint. We will now discuss how both cervical spinal cord injury (SCI) and multiple sclerosis (MS) are associated with pineal dysfunction and how the gland’s key hormonal product melatonin may be neuroprotective after injury.

In brief review, the pineal gland is a small, pea-shaped organ located in the middle of the head that secretes melatonin. This hormone is released into the bloodstream and cerebrospinal fluid where it is transported throughout the body. Affecting many bodily functions, melatonin secretion is closely correlated to our sleep-wake cycle and regulates sexual/reproductive function.

Pineal functioning tends to diminish over time, and melatonin-compromising calcification of the gland is not uncommon in adults.


In spite of its mid-brain location, the pineal gland is innervated by nerves that come out of the cervical spinal cord. As demonstrated by several researchers, cervical, but not lower-level, injuries compromise the pineal gland and its melatonin production:

For example, Dr. Y. Li and colleagues (China) compared the daily diurnal rhythm of melatonin secretion in individuals with chronic cervical injuries with subjects with lower level injuries.  In the cervical-injury group, melatonin levels were low, and no diurnal rhythm was observed. In contrast, in subjects with lower-level injuries, melatonin levels and cycles were maintained.

Dr. Jamie Zeitzer et al, Harvard University and the Brockton/West Roxbury VA Medical Center (Massachusetts) compared melatonin production in three subjects with chronic cervical injuries (C6, C6/7, & C4 injuries) with two individuals with thoracic injuries. The investigators concluded that neurologically complete cervical SCI results in a total loss of pineal melatonin production.

Although sleep quality in subjects with thoracic injuries was similar to able-bodied individuals, it was compromised in subjects with cervical injuries who lacked nocturnal melatonin production. For example, the onset of REM sleep averaged 220 minutes in the subjects with cervical injuries compared to only 34 minutes for those with thoracic injuries (REM or rapid-eye-movement sleep is associated with dreaming). The investigators suggested that melatonin supplementation might restore normal sleep in individuals with cervical SCI


Melatonin is also a powerful antioxidant that protects cells from damaging oxidation. Specifically, it is a highly efficient scavenger of free radicals, molecules which seek out electrons to achieve a more stable energetic state. Melatonin’s structural affinity for fat or lipid allows it to diffuse through the lipophilic cell membranes and scavenge free radicals within the cell.



Free radicals mediate damage after acute SCI. Following the initial mechanical injury, a complicated physiological chain reaction generates free-radicals, which, in turn, steal electrons from lipids in nearby neuronal and axonal membranes. Called lipid peroxidation, this process results in further cell death.

Like the commonly administered methylprednisolone, animal studies indicate that melatonin inhibits lipid peroxidation and various injury-aggravating inflammatory processes. Sample studies include:

Dr. Toru Fujimoto and colleagues (Japan) examined melatonin’s neuroprotective effects in rats with SCI produced by placing a weight on the exposed cord. Melatonin was injected into the body cavity before and after injury. Compared to controls, the melatonin-treated rats had less lipid peroxidation, smaller injury-site cavities, and retained more hind-limb function.

Dr. S. F. Erten et al (Turkey) assessed neuroprotection in rabbits with spinal-cord ischemia generated by clamping down on blood vessels serving the area.  Melatonin-treated rabbits had less lipid peroxidation.

Dr. Jin-bo Liu and associates (China) examined melatonin protection in rats with injuries created by dropping a weight on the exposed cord. The investigators concluded that “melatonin can prevent oxidative damage, reduce neurological deficit, and facilitate the recovery from” SCI.

Drs. Tiziana Genovese et al (Italy) evaluated melatonin in rats with injury produced by clipping the cord. The results indicated “that melatonin can exert potent anti-inflammatory effects” and enhanced hind-limb functional recovery.

Dr. Suleyman Cayli et al (Turkey) compared the effectiveness of 1) melatonin, 2) methylprednisolone, and 3) a combination of the two drugs. Improvements were noted in all three treatment groups, including enhanced neuronal conduction, recovery of motor function, decreased lipid peroxidation, and improved injury-site structural integrity. The combination treatment was best at inhibiting lipid peroxidation.

The aforementioned experiments injected high levels of melatonin into the body. However, research by Dr. O. Ates and colleagues (Turkey) suggest that even physiological background levels may be important. Specifically, the investigators assessed the effect of removing the rat’s pineal gland and, hence, the melatonin source before injury. Because pinealectomy increased post-injury lipid peroxidation, the investigators concluded that the reduction in endogenous melatonin made rats more vulnerable to trauma.

These findings have considerable relevance to humans. They suggest that individuals with less pineal function may have more neurological damage after injury. Because pineal functioning and melatonin production tends to diminish with age, the researchers concluded “endogenous melatonin level may make the age of the patient an important parameter for recovery” after SCI.

Because drinking-water fluoridation also impairs pineal melatonin production, it is possible that our efforts to fight cavities have resulted in more paralysis for individuals sustaining injuries.


Unlike cervical SCI which leads to pineal dysfunction, the converse may be true for MS. Because pineal dysfunction and, in turn, low melatonin secretion are correlated with MS symptoms, pineal failure may predispose one to MS. For example, Dr. Reuven Sandyk (New York) has stated “Dysfunction of the pineal gland can explain a far broader range of biological phenomena associated with MS, and therefore the pineal gland should be considered the pivotal mover of the disease.” In his model, various environmental, hormonal, and genetic factors lead to pineal dysfunction. In turn, the resulting low melatonin levels promote MS-associated physiology, such as the disorder’s characteristic neuronal demyelination. He believes therapeutically focusing on demyelination distracts us from dealing with the disorder’s more primary causes.  

Sandyk suggests that MS severity may be related to the degree of pineal failure.

In the case of relapsing-remitting MS, spontaneous remission of MS symptoms may be mediated through the pineal gland’s renewed melatonin production. However, in the case of chronic progressive MS, more extensive pineal dysfunction and calcification prevents the remission.

Clearly, MS is associated with pineal calcification. For example, one study showed 100% of individuals with MS who were consecutively admitted to a hospital had pineal calcification compared to only 43% for similar-aged controls with other neurological disorders.  In addition, groups that have a low MS incidence (e.g., African Americans, Japanese) also have less pineal calcification.


Called the seat of the soul by French philosopher René Descartes, the tiny pineal gland has more mythological mystique than virtually any other body part. Although the mystique is a matter of metaphysical speculation, the gland’s profound role in influencing our physiology is scientifically documented. Unfortunately, on top of paralysis, people with SCI and MS also may have to deal with all the mind-body-spirit ramifications of a dysfunctional pineal gland.

Adapted from article appearing in October 2009 Paraplegia News (For subscriptions, call 602-224-0500) or go to