As a short introduction: We are the manufacturers of the NEURO CARE and also distributors for other electrical stimulators of various types. Established in this business over 14 years ago, we have seen electrical stimulation develop in many different areas.
The NEURO CARE has advanced from use by industry for work related injuries, sports injuries to healing wounds and preventing amputation due to reduced circulation in legs and feet to the most current, treating SCI patients.
Some of the results seen included healing long term, non-healing wounds on heels and buttocks, as well as spasticity and disuse atrophy. All of the treatments were very successful! Even more successful than we expected. When treating the abdomen to strengthen the muscles we found that the patients were also regaining control of their bowels and diaphragm. While working the back for support or to relieve muscle spasms, we found the level of feeling increased. While treating the legs to relieve spasticity or develop the muscles, we found the bladder function was affected.
These were so dramatic that our Medical Department began looking at specific pad placements and protocols for the different symptoms paralyzed patients were having. The more these symptoms were worked, the more feeling returned. They then turned their attention to protocols directed to opening the neurological pathway at the site of injury to the extremities. Success was seen in every case of paralysis which was due to an "incomplete" spinal cord injury.
Simply stated, it is felt that the electrical stimulus "moves" the inflammation, around the injury site, which is restricting the neurological pathway. As studies are being done about the demylenating of the axon, more understanding of "what is happening" is coming to light. Granted, more dedicated studies need to be done to verify the reasons why paralyzed people are regaining feeling and even walking again. In the meantime, these people are enjoying the results!
Because of years working with electrical stimulation we understand there are three primary conductors for the electrical current within the human body. They are, in order of capacitance: 1) water (i.e. interstitial fluids, etc.); 2) muscle fiber, and 3) nerve fibers. Other body tissues have more resistance than capacitance. It is also a known fact that electricity goes to the point of least resistance. The myelin possesses high electrical resistance and low capacitance and thus acts as an insulator around axons. (1)
In a normal, undamaged state, the myelin around the axon protects the electrical signal from outside interference and at the same time keeps a "clean" undisturbed canal or pathway for the signal from the Central Nervous System (CNS) to travel to the extremities. However, when the myelin is permeated by fluids due to lesions, the signal from the CNS dissipates to other regions, causing paralysis beyond that point. (The degree of the paralysis is in relationship to the degree of permeation.)
Studies suggest that axonal damage may be associated with inflammation. And note a relation between axonal injury and inflammation, suggesting that a reduction in the inflammatory response might result in the loss of fewer axons and thus in less clinical deficit. (1) (2) (3)
It has recently been recognized that in some patients with traumatic (nonpenetrating) spinal cord injury there are residual axons that maintain continuity through the lesion but fail to conduct impulses as a result of demyelination. These findings have been reported in some patients with "clinically complete" lesions (i.e., those with no function below the level of the lesion), which are classically considered to due to transection of the spinal cord and its constituent axons within the lesion. The demonstration of these preserved, but demyelinated, axons suggests that in spinal cord injury, at least some degree of functional recovery might be achieved by strategies that restore impulse conduction along demyelinated axons. (1)(4-6)
Recognition that spinal cord injury is, in part, a disorder of myelin should trigger a critical rethinking of these disorders and provides us with new targets for therapy. Ideally, future studies will tell us whether the protection of axons from injury in multiple sclerosis and the repair of demyelinated axons in spinal cord injury are therapeutic strategies that will help preserve neurologic function in patients with these disorders. (1)
Although each patient has an individual recovery schedule, there is a pattern of recovery developing as the pathway reopens/repairs.
After reviewing studies like these of Dr. Waxman, it is thought that either the myelin is re-pairing or the body is producing sufficient Sodium and Potassium levels to compensate for the loss of myelin. It is definite that there is a decrease in the capacitance of the myelin and resistance of the axon.
Perhaps there is a prevention of axonal loss: Axonal function and integrity can be preserved after acute insults by means of neuroprotective interventions that block or modulate injurious ion fluxes at several stages within this molecular death cascade or that interfere with "downstream" degenerative events such as activation of calpains and other destructive enzymes. It is suggested that further studies will be needed to determine whether the reduction in inflammatory responses or the neuroprotection of axons can limit or prevent axonal degeneration in multiple sclerosis or SCI. If so, whether this will reduce or prevent the acquisition of persistent neurologic deficits.(1)
Waxman SG, Demyelinating Diseases-New pathological Insights, New Therapeutic Targets, The New England Journal of Medicine 1998; Vol. 338: 323-25.
Ferguson P., Matyszek MK, Esiri MM, Perry VH. Axonal damage in acute multiple sclerosis lesions. Brain 1997:119;1415.
Trapp BD, Peterson J, Ransohoff RM, Rudick R, Mork S, Ro L. Axonal transection in the lesions of multiple sclerosis. N Engl. J Med. 1998;338:278-85.
Blight AR, Cellular morphology of chronic spinal cord injury in the cat: analysis of myelinated axons by line-sampling. Neuroscience 1983;10: 521-43.
Bunge RP, Puckett WR, Becerra JL, Marcillo A. Quencer RM. Observations on the pathology of human spinal cord injury: a review and classifiction of 22 new cases with details from a case of chronic cord conpression with extensive focal demyelination. Adv Neurol 1993: 59; 75-89.
Waxman SG, Koesis JD. Spinal cord repair: progress towards a daunting goal. Neuroscientist 1997;3:263-9.
