Human balance, the evolution of bipedalism and dysequilibrium syndrome.
A new model of the uniqueness, nature and evolution of human bipedality is presented in the context of the etiology of the balance disorder of dysequilibrium syndrome. Human bipedality is biologically novel in several remarkable respects. Humans are (a) obligate, habitual and diverse in their bipedalism, (b) hold their body carriage spinally erect in a multisegmental "antigravity pole", (c) use their forelimbs exclusively for nonlocomotion, (d) support their body weight exclusively by vertical balance and normally never use prehensile holds. Further, human bipedalism is combined with (e) upper body actions that quickly shift the body's center of mass (e.g. tennis serves, piggy-back carrying of children), (f) use transient unstable erect positions (dance, kicking and fighting), (g) body height that makes falls injurious, (h) stiff gait walking, and (i) endurance running. Underlying these novelties, I conjecture, is a species specific human vertical balance faculty. This faculty synchronizes any action with a skeletomuscular adjustment that corrects its potential destabilizing impact upon the projection of the body's center of mass over its foot support. The balance faculty depends upon internal models of the erect vertical body's geometrical relationship (and its deviations) to its support base. Due to the situation that humans are obligate erect terrestrial animals, two frameworks - the body- and gravity-defined frameworks - are in constant alignment in the vertical z-axis. This alignment allows human balance to adapt egocentric body cognitions to detect body deviations from the gravitational vertical. This link between human balance and the processing of geometrical orientation, I propose, accounts for the close link between balance and spatial cognition found in the cerebral cortex. I argue that cortical areas processing the spatial and other cognitions needed to enable vertical balance was an important reason for brain size expansion of Homo erectus. A novel source of evidence for this conjecture is the rare autosomal recessive condition of dysequilibrium syndrome. In dysequilibrium syndrome, individuals fail to learn to walk bipedally (with this not being due to sensory, vestibular nor motor coordination defects). Dysequilibrium syndrome is associated with severe spatial deficits that I conjecture underlie its balance dysfunction. The associated brain defects and gene mutations of dysequilibrium syndrome provide new opportunities to investigate (i) the neurological processes responsible for the human specific balance faculty, and (ii) through gene dating techniques, its evolution.
Centre for Mathematics and Physics in the Life Sciences and Experimental Biology (CoMPLEX), University College London, UK. j.skoyles@ucl.ac.uk
John R
JR
Skoyles
D000818:Animals; D001259:Ataxia / Q000235:genetics*; D005075:Biological Evolution; D019521:Body Patterning / Q000235:genetics*; D002540:Cerebral Cortex / Q000503:physiopathology*; D006801:Humans; D007866:Leg / Q000502:physiology*; D008957:Models, Genetic; D009929:Organ Size / Q000235:genetics; D004856:Postural Balance; D011187:Posture; D013577:Syndrome