The central nervous system concentration of magnesium (Mg++) appears to have a critical level below which neurologic dysfunction occurs. Observations presented suggest that the interchange of the Mg++ ion between the cerebrospinal fluid, extracellular fluid, and bone is more rapid and dynamic than is usually believed. This is especially so when the hypertrophied parathyroid gland is associated with significant skeletal depletion of Mg++ as judged by history rather than serum level. Magnesium, much like calcium, has a large presence in bone and has a negative feedback relationship with the parathyroid gland. A decline in central nervous system Mg++ may occur when the skeletal buffer system orchestrated largely by the parathyroid glands is activated by an increase in serum calcium. Observations in veterinary medicine and obstetrics suggest that the transfer of Mg++ from the extracellular fluid into bone during mineralization processes may be extensive. If the inhibition of the hypertrophied parathyroid gland is prolonged and the skeletal depletion of Mg++ extreme, serious neurologic symptoms, including seizures, coma, and death, may occur. Noise, excitement, and bodily contact appear to precipitate neurologic symptoms in Mg+(+)-deficient human subjects as it has been documented to occur in Mg+(+)-deficient experimental animals. The similarity of the acute central nervous system demyelinating syndromes with reactive central nervous system Mg++ deficiency is reviewed.