Disc Degeneration: A Sort of Neuroadaptive Skeletal Dysplasia in the Adult and Aged

Abstract

An attempt is made to extend the undeniable influence of the growing brain upon the shape and size of its neurocranial bony case (an effect called “macroneurotrophic”) to the extracerebral nervous tissue, spinal and peripheral, and to the extracranial bony skeleton. The basic argument is that, in the same way as the shape and size of the neurocranium cannot be understood without taking into account the enclosed growing brain, gross morphology of the vertebral column (the protective bony envelope of its central nervous content), above all its length, cannot be understood without taking into account the co-growing spinal neural content. By extrapolation, vertebroneural developmental interrelation may be extended to the limbs, viz., to “osteoneural” relation between the growing limb skeleton and the peripheral nervous system.

Developing spinal nerve roots and peripheral nerves are generally believed to be “taken in tow and dragged along” by the outgrowing non-nervous tissues, i.e. to follow them passively for the sake of “innervation” with the tacitly accepted implication that the definitive length of nerve roots and/or peripheral nerves is determined by the (phylo)genetically established growth-in-length potential of the vertebral column and/or the limb skeleton. Spinal nerve roots and peripheral nerves should share with the growing brain, however, its high growth activity and vulnerability. It may be deduced from gross osteoneural findings that neural growth lags to a distinct degree behind skeletal growth and, consequently, exerts a “curbing” effect upon the growing spine and limb bones. This physiological vertebroneural and/or osteoneural growth differential is responsible for basic gross features of the skeleton such as physiological curvatures, “waisting” (both of vertebral bodies and of long bones in form of terminal flarings) or angular joint postures. In respect to the growing skeleton (and, after all, to other non-nervous tissues) spinal nerve roots and peripheral nerves play the role of “limiters” rather than that of mere passive “followers” of their outgrowth.

Insufficiency of vulnerable neural growth in the course of development, viz., exaggerated vertebroneural and/or osteoneural growth differential results in accentuation of the abovementioned normal gross features of the skeleton, i.e. in developmental deformities characterized in general by shortening of the involved portions of the skeleton since growing vertebrae and limb bones will have to grow shorter, to find a place, to “cram” — even at the cost of deformity — along the too short, inadequately growing nervous structures. Owing to the craniocaudally proceeding bodily growth, “neuroadaptive” shortening of the skeleton is accomplished as though “from below” since the too short spinal nerve roots and/or peripheral nerves hinder the spine and /or limb bones from growing straight forward in length. The concept is buttressed by experimentation on laboratory animals which suggests a common neuroadaptive pathomechanism of experimental as well as clinical skeletal “dysplasias”.

Vertebroneural and/or osteoneural length disproportion may take place even in the adult and aged as a result of involutional-atrophogenic shortening of spinal nerve roots and/or of peripheral nerves. Also, that disproportion must be compensated by the skeleton since otherwise the shortened nervous elements would be exposed to undue stretching. In the spine this “neuroprotective” measure is accomplished by degenerative narrowing (i.e. shortening) of the disc comparable with “cerebroprotective” dehiscence of cranial sutures under the effect of the expanding brain in obstructive hydrocephalus. Herniation of the disc is just a mechanical complication of the essentially purposeful “degenerative” process. Degenerative “arthrotic” narrowing (shortening) of the joint spaces in the limbs may be ascribed to analogous primary atrophogenic shortening of peripheral nerves.

Degeneration of the disc and joint cartilage would thus represent, as a matter of fact, a special sort of skeletal dysplasia: The latter occurs in classical form during the developmental period of life as a consequence of toxic or endogenous impairment of neural growth (Scheuermann's kyphosis, scoliosis and a number of skeletal “dysplasias”); the former would be due to involutional atrophy and shortening of spinal nerve roots and/or of peripheral nerves in the course of aging.

The advanced concept is based on the existence of two growth types in the vertebrate body, the cellular-divisional and the neural-extensive proceeding side-by-side at a different energetic level and with a different vulnerability. Consideration concerning biological meaning and evolutionary history of the two-growth-types composition of the vertebrate body is put forward.