Neuromuscular factors that contribute to spinal stability include trunk stiffness from passive and active tissues as well as active feedback from reflex response in the paraspinal muscles.
These changes in activation can occur via feedforward changes in co-contraction [5], [6] or through changes in the sensitivity of reflex feedback [7] [10].
The cardiovascular system has a complex neural control, which is based on the interaction across different subsystems, central and peripheral oscillators, feedback and feedforward reflex mechanisms, humoral, metabolic and local factors [1].
Following the model of Kapreli and Athanasopoulos [32], mechanoreceptor damage may lead to a disturbance of sensory transmission, contributing to alterations of afferent feedback and stabilizing reflexes that may implicate increased body sway [1, 8, 25, 59].
The simplest form of this feedback system involves a reflex pathway (such as the knee-jerk reflex), in which sensory endings in muscles convey signals to the motor system through direct monosynaptic connections with motor neurons.
But all I did was put one foot in front of the other until I got there with a big pack on my back, reciting poems and getting psycho-bio feedback like Pavlov's reflex.
In this way several interrelated and, through positive feedback loops, ever-increasing reflex arcs become disrupted.
By a reflex negative-feedback mechanism, inhibitory impulses may prevent an organism from working itself to exhaustion.
The primary area sends fibres back to the lateral geniculate nucleus, the superior colliculus, and the pupillary reflex centre for feedback control of input to the visual areas.
A viable route for future studies in this direction is to investigate parallels of the feedback gain matrix L and reflex modulation observed in humans.
