Numerous theories have been proposed to explain<unk> . Despite this, no absolutely defined causes of<unk>  are known. The most widely accepted theory of the mechanism behind the disorder is "neural fatigue". A motor unit is a nerve cell (or neuron) and the muscle fibers it activates.<unk> virus attacks specific neurons in the brainstem and the anterior horn cells of the spinal cord, generally resulting in the death of a substantial fraction of the motor neurons controlling skeletal muscles. In an effort to compensate for the loss of these neurons, surviving motor neurons sprout new nerve terminals to the orphaned muscle fibers. The result is some recovery of movement and the development of enlarged motor units. The neural fatigue theory proposes that the enlargement of the motor neuron fibers places added metabolic stress on the nerve cell body to nourish the additional fibers. After years of use, this stress may be more than the neuron can handle, leading to the gradual deterioration of the sprouted fibers, and eventually, the neuron itself. This causes muscle weakness and paralysis. Restoration of nerve function may occur in some fibers a second time, but eventually, nerve terminals malfunction and permanent weakness occurs. When these neurons no longer carry on sprouting, fatigue occurs due to the increasing metabolic demand of the nervous system. The normal aging process also may play a role. Denervation and reinnervation are going on, but the reinnervation process has an upper limit where the reinnervation cannot compensate for the ongoing denervation, and loss of motor units takes place. What disturbs the denervation-reinnervation equilibrium and causes peripheral denervation, though, is still unclear. With age, most people experience a decrease in the number of spinal motor neurons. Because<unk>  survivors have already lost a considerable number of motor neurons, further age-related loss of neurons may contribute substantially to new muscle weakness. The overuse and underuse of muscles also may contribute to muscle weakness. Another theory is that people who have recovered from<unk>  lose remaining healthy neurons at a faster rate than normal. However, little evidence exists to support this idea. Finally, the initial<unk>  infection is thought to cause an autoimmune reaction, in which the body's immune system attacks normal cells as if they were foreign substances. Again, compared to neural fatigue, the evidence supporting this theory is quite limited.
Post-polio syndrome
Leukomyelitis
Guillain–Barré syndrome
FACES syndrome
Acute disseminated encephalomyelitis
Eastern equine encephalitis
Tension myositis syndrome
Postvaccinal encephalitis