Cruising about for AMN clinical trials, I found this from the 2012 European Leukodystrophies Association:
ela-asso.com/wp-content/upl...
Some stuff there about AMN, the usual suspects - stem cells and antioxidants, but this study about 4-aminopyridine caught my attention. The final paraagraph says it all.
Improvement of motor function in patients with AMN
Pr. Wolfgang Köhler (Germany)
Leg stiffness and walking disabilities are leading symptoms in patients with Adrenomyeloneuropathy (AMN). The reasons for this spasticity are spinal cord long nerve fiber and myelin damage. The nerve fibers of the spinal cord carry the electrical impulses that transport information from and to the brain
to support the complex control system of the human body. Each microscopically thin nerve fiber is insulated by a regular pattern of myelin sheaths along its length that allow for the efficient conduction of electrical impulses. In AMN some of these myelin sheaths can be damaged leading to an impairment or even disruption of neural conduction of movement information from brain to the muscle. Nerve impulses "short circuit" in demyelinated axons, much like electricity in a wire whose insulation is stripped. Thus, even though a demyelinated axon is alive, it is unable transmit motor or sensory impulses.
Treatment with 4‐Aminopyridine (4‐AP) permits the axon to transmit impulses again, improve nerve conduction thus leading to reduced spasticity and improved walking abilities in patients with multiple sclerosis. Since in AMN similar clinical symptoms are present, we treated 18 AMN patients with 4‐AP
using a standardized study protocol. 13 out of 18 patients improved significantly regarding a timed‐25 foot walking distance. 15 out of 18 patients reported significant reduction of spasticity and pain, 9 out of 18 improved with their bladder function.
In summary treatment with 4‐AP may significantly
improve walking disabilities caused by spastic paraparesis in most patients with AMN.