The neurophysiological processes involved in recovery following acute paralytic poliomyelitis are quite effective; muscles are able to retain normal strength even if half the original motor neurons have been lost. Paralysis remaining after one year is likely to be permanent, although some recovery of muscle strength is possible up to 18 months after infection.One mechanism involved in recovery is nerve terminal sprouting, in which remaining brainstem and spinal cord motor neurons develop new branches, or axonal sprouts. These sprouts can reinnervate orphaned muscle fibers that have been denervated by acute polio infection, restoring the fibers capacity to contract and improving strength. Terminal sprouting may generate a few significantly enlarged motor neurons doing work previously performed by as many as four or five units: a single motor neuron that once controlled 200 muscle cells might control 800 to 1000 cells. Other mechanisms that occur during the rehabilitation phase, and contribute to muscle strength restoration, include myofiber hypertrophy – enlargement of muscle fibers through exercise and activity – and transformation of type II muscle fibers to type I muscle fibers.In addition to these physiological processes, the body can compensate for residual paralysis in other ways. Weaker muscles can be used at a higher than usual intensity relative to the muscles maximal capacity, little-used muscles can be developed, and ligaments can enable stability and mobility. Complications
Residual complications of paralytic polio often occur following the initial recovery process. Muscle paresis and paralysis can sometimes result in skeletal deformities, tightening of the joints, and movement disability.
Among young children, boys seem to be more likely to develop minimal change disease than girls (about 2:1). Minimal change disease is seen in about 16 in every 100,000 children, being more common in South Asians and Native Americans, but rarer in African Americans.In adults, it accounts for less than 15% of adults diagnosed with nephrotic syndrome. Etymology
Minimal change disease has been called by many other names in the medical literature, including minimal change nephropathy, minimal change nephrosis, minimal change nephrotic syndrome, minimal change glomerulopathy, foot process disease (referring to the foot processes of the podocytes), nil disease (referring to the lack of pathologic findings on light microscopy), nil lesions, lipid nephrosis, and lipoid nephrosis. References


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