Neuromas may form after any nerve injury. Neuromas result from the abnormal regeneration of sprouting axons. A nerve swelling is formed at the proximal end of the injured nerve. It consists of random proliferating proximal axonal sprouts and scar tissue deposited by fibroblasts.
The most widely held theory behind neuroma formation is that axon fascicles escape out of a damaged perineurium. An intact perineurium is hypothesized to be an impenetrable barrier to axons. However, when the perineurium is damaged, either through sharp laceration or stretch, sprouting axons escape into the extraendoneurial environment.
Macroscopically, the neuroma is a well-circumscribed, firm, and rubbery mass.
The neuroma can be adherent to the surrounding structures bones, muscles, or other tissues.
Microscopically, the neuroma consists of bundles of badly organized nerve fibers and fascicles in various stages of maturation.
The majority of neuromas are asymptomatic. Painful neuroma can develop if the neuroma is chronically irritated or if the axons within the neuroma are constantly stimulated.
Spontaneous activity of neurons within the neuroma or from neurons more proximal to the neuroma, either in the dorsal root ganglion or central nervous system, can cause severe and spontaneous pain.
In addition to regional changes in the peripheral nerve, a cascade of pathologic changes may occur within the dorsal root and spinal cord, which lead to central sensitization.
In the case of neuromas the first approach is pharmacotherapeutic and antineuropathic drugs to reduce the excitability of the peripheral nerve and central connections.
Surgery is also possible by decompression or resection of the neuroma.
Manual mechanical intervention to the involved segment, however not researched, is probably contra-indicated. Also the pain will inhibit such maneuvers.