Human bipedal locomotion is arguably the most defining adaptation in the narrative of human evolution. It has altered the way our bodies dissipate heat, the way we give birth, and even the way we use our hands – to some extent it has influenced the function/morphology of every element of our anatomy. Of course, when such a bauplan altering adaptation evolves there are certain to be a few kinks along the way. Some of these kinks are much more than just minor flaws in function and morphology, and, as I described in detail in an earlier post on plantar fasciitis, have the potential to greatly influence the quality of life of those individuals afflicted. And while there appears to now be a cure for plantar fasciitis, not all conditions are so lucky. Today I will consider one of the unlucky, a condition located a bit further up the bauplan. Being that I have a compulsion towards uniformity I have decided to choose a condition that is, like plantar fasciitis, unique to humans: adolescent idiopathic scoliosis (AIS). Thankfully, an article published recently in the journal Spine has made this task quite easy for me.

First, a little housekeeping: AIS is an extremely complex disorder. It affects all three planes of the spine and has, despite the overwhelming amount of research conducted, no known direct cause. According to Kouwenhoven & Castelein (2008) “practically every structure of the body has been incriminated in” its pathogenesis. There has been a great deal of genetic research done, from which we understand the issue to be unresolved (Is it genetics? Is it environment? Is it both?), and theories of its developmental origin appear to be a dime a dozen. From the endless list of conflicting evidence and theories, compounded with the fact that humans are the only vertebrates afflicted by the condition* leaving us with no model organisms, it appears there exists no light at the end of the tunnel. All hope, however, is not lost; according to these authors, evolution has left a trail.

Using my favorite tool, comparative anatomy, researchers of AIS have uncovered patterns in the structure of the spine that shed light on possible causes. Looking at the figure to the left (Kouwenhoven & Castelein, 2008), you may notice some differences between the chimp and human skeletal morphology. During human evolution, due to the development of an upright posture, we obtained a lordotic curve toward the bottom of our spine known as the lumbar region. Along with the absence of flexion contracture of the hips and knees seen in the chimp, this morphological adaptation allows us a more energetically efficient means of locomotion. It is not without ’side effect’, however: at the lowest portion of the lumbar region vertebra L5 articulates with the first vertebra of the sacrum (S1). Now, this wouldn’t normally be a problem except that this articulation is located at the apex of that lordotic curve I just mentioned, and the angle is so acute the normally ventrally (front) directed shear loads are here dorsally (back) directed. As a result, this location is the most popular for a herniated disk; but, more important to the understanding of AIS, these dorsally directed shear loads reduce the operating efficiency of the anatomical structures controlling rotation.

In contrast, the spine of the quadruped is one long kyphotic curve, which when you are on all fours is quite stable (Not unlike a suspension bridge). From the understanding of these two disparate morphologies, and research done on the topic, it has been demonstrated that bipedalism is a prerequisite for AIS. Where does this leave us, though? What help is it to know our spines are oriented in this fashion because some weirdo 6 million years ago decided to start walking on two feet? Well, its a simple matter of comparison, really.

According to previous research by the same team there is a preexistent pattern of vertebral rotation in the normal spine (Kouwehnoven et. al., 2006a,b). In humans and quadrupeds this rotation is in the middle and lower thoracic region and consists of a rotation predominantly to the right side. Coincidentlly, or not so in this case, in those afflicted with AIS there is an overwhelming majority with this same pattern of rotation. Because this preexistent pattern of rotation exists in quadrupeds, who need I remind you do not develop AIS, the rotation can be considered a physiologically determined process in the normal development of the vertebrate spine.

Let us now gather our puzzle pieces:

1. The morphology of the human spine is unique among vertebrates due to our mode of locomotion
2. This morphology makes us more efficient at bipedal locomotion, but leaves us with a portion of the spine that is constantly exposed to dorsal shear stress
3. Dorsal shear stress affects the anatomical structures controlling rotation of the spine, giving the spine less rotational stability
4. There is a preexistent pattern of right rotation in the spine of quadrupeds and humans, which exists to an extreme in those afflicted with AIS

And fit them together: excessive dorsal shear loads, which we as humans are at risk for, during critical stages of development can lead to rotational instability of the developing spine, thus allowing the basal quadruped rotational pattern to take its course, leading to the initiation and progression of AIS.

See, isn’t evolution cool?

* Some researchers have managed to surgically ‘force’ rats to become bipedal; one group of the bipedal rats were pinealectomized, another group was not – the former developed scoliosis

(References)

Kouwenhoven, J, Vincken, K, Bartels, L & Castelein, R, 2006, 'Analysis of Preexistent Vertebral Rotation in the Normal Spine', Spine, vol. 31, no. 13, pp. 1467-1472. 10.1097/01.brs.0000219938.14686.b3

Kouwenhoven, J, Vincken, K, Bartels, L, Meij, B, ??ner, F & Castelein, R, 2006, 'Analysis of Preexistent Vertebral Rotation in the Normal Quadruped Spine', Spine, vol. 31, no. 20, pp. E754-E758. 10.1097/01.brs.0000240209.85498.01

Kouwenhoven, J & Castelein, R, 2008, 'The Pathogenesis of Adolescent Idiopathic Scoliosis', Spine, vol. 33, no. 26, pp. 2898-2908. 10.1097/BRS.0b013e3181891751