The precise mechanism that causes post-polio syndrome is unknown. It shares many features in common with myalgic encephalomyelitis, a form of chronic fatigue syndrome that is apparently caused by viral infections, but unlike those disorders it tends to be progressive, and can cause tangible loss of muscle strength.Treatment is primarily limited to adequate rest, conservation of available energy, and to supportive measures, such as leg braces and energy-saving devices such as powered wheelchairs, plus pain relievers, sleep aids, etc.
The most widely accepted theory is the "neural fatigue" one. Motor neuron fibers were originally damaged by the polio virus and were subsequently over-stressed because too few surviving neurons activated too many muscles. Eventually these neurons become fatigued and die, leading to the slowly advancing loss of muscle function that is typical of post-polio. This scenario may be accelerated by the fall-off in production of nerve growth factor (NGF) that occurs with menopause/andropause.
This theory assumes that the major symptoms of PPS are a result of some interference with the action of mitochondria in the muscles and possibly the nerves. Failure of the mitochondria to produce sufficient energy would result in the muscle pain typical of PPS, and would, over time, cause muscle death (rhabdomyolysis) due to exerting the muscle beyond its ability to recover. The cause of this interference with mitochondrial action is presumably a change in the body's hormone balance, as mediated by the hypothalamus and other lower brain areas that control hormones (and which were, presumably, damaged by the original polio virus infection). As with the neural fatigue theory, menopause/andropause accelerates the process, though this time by most likely disrupting the NOTCH pathway that controls cell differentiation and damage repair. One significant argument in favor of the mitochondrial disruption theory is that it explains the fatigue and cognitive difficulties ("brain fog") symptoms that usually accompany post-polio better than the neural fatigue theory does.
Reticular activating system damage
Damage to the reticular activating system and related areas such as the thalamus can also produce most of the fatigue, "brain fog", and dysautonomia symptoms of post-polio, and may be able to cause hormonal changes that result in progressive muscle weakness. Post-mortem examinations of polio patients have shown damage to these areas, and some PPS patients show lesions in these areas when examined by MRI. Many authorities believe that these areas are damaged by the initial polio infection, either as a direct result of the polio virus, or due to an autoimmune reaction following the polio infection. One problem with this theory, though, is that it doesn't easily explain the delayed onset of PPS. It may be that this theory needs to be combined with one of the others to explain delayed onset.
The stresses placed on nerves, muscles, and joints in a polio survivor are in many cases several times those experienced by other people. Problems with gait, in particular, can greatly over-stress joints and the surviving muscles, and the polio survivor is also likely to compensate for weakened arms by jerking more when lifting/pulling something. Over time (and again with menopause/andropause), this results in fatigue and damage
Treatment for post-polio is primarily palliative, as very few reliable therapies to reverse symptoms are known.
Very often fatigue is the most disabling symptom of PPS, and many of those with the disease have discovered that by carefully managing energy expenditure they can prevent or reduce the worst fatigue episodes. Further, for many this "energy management" approach appears to reduce pain. Though most authorities agree that rest is an important component of post-polio treatment, there is significant disagreement as to how much rest is necessary. Some hold that the best approach is to expend the absolute minimum amount of energy necessary to enjoy a reasonable lifestyle, while others feel that there is some threshold below which energy conservation is not helpful and may in fact be harmful (due to the general effects caused by lack of exercise).
Leg braces and other orthotics can reduce the stress on joints and, in some cases, muscles, and so may slow the progression of joint and muscle damage related to PPS. However, some authorities feel that many PPS patients rely on such items too much and for too long when they should be graduating to a wheelchair. Wheelchairs (particularly powered wheelchairs) and "scooters" (small battery-powered vehicles) are useful both to conserve energy and to reduce the stress on weakened joints and muscles. Non-powered wheelchairs, however, are not generally recommended since they place too much stress on arm muscles and joints and may take too much energy to operate. In some cases even the scooters are not recommended since operating the "tiller" of the typical scooter can be tiring to arm muscles. A standing frame can be used in conjunction with the wheelchair to provide alternative positioning and prevent secondary complications. http://www.livingwithcerebralpalsy.comMéxico a la vanguardia en el Síndrome de Post Polio