WARNING: This program is not recommended with other electrical stimulation units.
This Publication is to assist physicians, practitioners and other medical personnel in developing a treatment program.
This is not for general distribution. Copyright© 1999 Tom Oliver
STATISTICS: There are an estimated 250,000 spinal cord injured (SCI) individuals living in the United States. On average, 11,000 new injuries are reported every year. Paraplegia (losses of movement and sensation in the lower body) affects 55% of the SCI population, and 44% are affected by quadriplegia (losses of movement and sensation in both the arms and legs). Initial hospitalization (an average of 100 days), adaptive equipment and home modification costs following injury average $140,000. Additional lifetime costs incurred by SCI individuals average $600,000 and can reach as high as $1.35 million depending on the severity of injury and the age at which injury occurred. In 1992, there were 10,000 reported spinal cord injuries nationwide. The lifetime costs associated with these injuries are projected to total $10 billion. HISTORY: …after working with paralyzed patients we noticed some of the results seen included the healing of 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. When working the back for support or to relieve muscle spasms we found that their level of feeling increased. While treating the legs to relieve the spasticity or develop the muscles we found that 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 the paralyzed patients were having. The more the symptoms were worked, the more feeling returned. They then turned their attention to protocols directed at opening the neurological pathway at the site of injury to the extremities. Results were seen in every case of paralysis in which the spinal cord was intact. Although each patient has an individual recovery schedule, there is a pattern of recovery developing as the pathway reopens/repairs.
SUBJECTION: 1) The restricting inflammation is reduced by the movement of electricity as outlined in the NCTP©. 2) There is such a large amount of current that it “fools” the CNS causing it to send the appropriate chemicals to “repair” the damaged area of the axon, which has been demyelinated and “has a leak”.
COMPARE MODALITIES The Neurocare 2000™ has a higher output than any other electrical stimulator on the market today. Where other units invoke the “active” muscle fibers at a maximum of 125 volts the Neurocare 1000 can invoke the “inactive” muscle fibers (due to injury, trauma, disuse, etc.) at a maximum of 440 volts. Amperage is the painful part of electricity. Other EMS units achieve the 125 volts at 90 milliamps of current. Neurocare 2000™ achieves the 440 volts at 4 milliamps of current. Patients can normally tolerate a maximum of about 10 milliamps of current, therefore normal EMS units very seldom reach the potential of 90 milliamps and 125 volts, thus they cannot “saturate” the “active” muscle fibers to reach the “inactive” muscle fibers. Ten milliamps on normal muscle stimulators is 30 volts. Four milliamps on the Neurocare 2000™ is 440 volts.
The reason Neurocare 2000™ has this ability is that it is AC (alternating current) output, whereas the other stimulators are DC (direct current) output. This feature is currently proprietary to Neurocare. The machine is simulating exercise not only to the “active” muscles but also to the “inactive” or injured muscles, thus allowing them to be strengthened and re-educated. The Neurocare 2000™ can do this, even though the patient cannot, because it does not invoke the reflex arch mechanism. Thereby being able to work the inactive muscles without the use or need of medications (narcotics or steroids). By being used at home it allows the patient to have longer treatments for a longer period of time than would be financially possible within a clinical setting. Our company provides clinical technicians via phone for your patients or insurance companies on a 24-hour basis, with no extra charge. All the physician needs to do is fax a prescription to our toll-free fax and we will get a machine to the patient and do all of the instruction on protocol as well as how to begin. Able to achieve deep muscle contractions without discomfort to the patient combined with the NEUROCARE Treatment Program™ patients are able to achieve results in cases from whiplash to diabetic neuropathy.
EASY IN-HOME USE!! SAFE, PORTABLE, NON-INVASIVE, SIMPLE TO USE
EXCERPTS FROM : The New England Journal of Medicine – January 29, 1998 – Volume 338, Number 5 …If axonal injury early in the course of disease contributes to the development of irreversible neurologic deficits, the prevention of axonal loss might be expected to prevent persistent disability. 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 be due to transection of the spinal cord and its constituent axons within the lesion. (16, 17, 18) 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…
FDA Registered August 3, 1993 Study reprints are available upon request. e-mail: firstname.lastname@example.org web: www.neurocare.com Ph: 877-571-3599 or Fax 877-571-0986
MUSCLE SPASMS: Can create great pain and even nerve impingement resulting in “referral pain” to other sites.
DISUSE ATROPHY: Can cause loss of muscle strength and even mass (i.e. an arm that has been in a cast for several months, a paraplegic/quadriplegic, polio victim, even someone who has been without physical activity for a period of time),
MUSCLE RE-EDUCATION: Relates to a muscle being used in a different function than what is its normal function. The muscle responds negatively (i.e. pain, spasm, etc.) until it is re-educated to the activity level placed upon it. (i.e. Occupational Overuse-Carpal Tunnel). The need to re-educate a muscle can be the result of various causes ( a sprain, whiplash, continued keyboard use, etc.).
RANGE OF MOTION: Loss or reduction can be caused by many sources, but almost always results in pain to the patient.
LOCAL BLOOD CIRCULATION: Can be due to a number of causes (i.e. swelling due to an injury/overuse/disease). Increasing local blood circulation reduces this.
WHO IS NEUROCARE?
As a short introduction: We are the manufacturers of the Neurocare™ 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 Neurocare™ 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. There are an estimated 250,000 spinal cord injured (SCI) individuals living in the United States. On average, 11,000 new injuries are reported every year. Paraplegia (losses of movement and sensation in the lower body) affects 55% of the SCI population, and 44% are affected by quadriplegia (losses of movement and sensation in both the arms and legs).
Initial hospitalization (an average of 100 days), adaptive equipment and home modification costs following injury average $140,000. Additional lifetime costs incurred by SCI individuals average $600,000 and can reach as high as $1.35 million depending on the severity of injury and the age at which injury occurred. In 1992, there were 10,000 reported spinal cord injuries nationwide. The lifetime costs associated with these injuries are projected to total $10 billion. By developing therapies for those who are already spinal cord injured, and preventing new injuries, the United States would save as much as $400 billion on future direct and indirect SCI lifetime costs. (Sources: American Paralysis Association, The University of Alabama national Spinal Cord Injury Statistical Center, The Dana Alliance for Brain Initiatives and Paralyzed Veterans of America.) Electrical stimulation has been an effective, yet underestimated method of rehabilitation therapy for SCI patients. In general, the effectiveness has been seen within the maintenance program developed for paralyzed patients dealing with the problems which develop from paralysis (i.e. disuse atrophy, reduced circulation, spasms, and pain caused by all of these). There are even studies which show this as effective maintenance for the paralyzed individual.
Though the Neurocare™ used within a “maintenance program” for paralyzed patients is very effective, it was discovered that more is available! The first SCI patients were treated for symptoms resulting from their paralysis. We found that with the use of the Neurocare™ we were able to get stronger muscle contractions without damaging the skin as some of the other electrical stimulators did when they were turned high enough to get a muscle contraction. Some of the results seen included the healing of 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. When working the back for support or to relieve muscle spasms we found that their level of feeling increased. While treating the legs to relieve the spasticity or develop the muscles we found that 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 the paralyzed patients were having. The more the symptoms were worked, the more feeling returned. They then turned their attention to protocols directed at opening the neurological pathway at the site of injury to the extremities. Success was seen in every case of paralysis that 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. More dedicated studies need to be done to verify the reasons why paralyzed people are regaining feeling and even walking again. We have been using the Neurocare™ SCI Treatment Program© for almost two years and in each, accepted case, there has been a marked change in the patient’s status (quadriplegic to paraplegic, sensation and feeling returning in the lower extremities). The hardest thing we are seeing is not whether feeling will return, but after feeling returns to find a physical therapy program that is able to re-educate the muscles to learn how to walk. As the feeling returns, the patient is like a newborn baby. They have feeling and sensation, but control needs to be learned. Electrical stimulation via the Neurocare™ and the Neurocare™ Treatment Program© are used to defuse the effects of demyelination of the axon in SCI and MS patient.
- The restrictive inflammation is reduced by the movement of electricity as outlined in the NCTP©
- There is such a large amount of current that it “fools” the CNS causing it to send the appropriate chemicals to “repair” the damaged area of the axon which has been demyelinated and “has a leak”.
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:
- Water (i.e. interstitial fluids, etc.)
- Muscle fiber
- 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 through 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.   
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 be 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.  [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. 
This can be related to the results being seen in the SCI patients using the Neurocare™ Treatment Program©. These patients are seeing results! In some cases, the paralyzed patient is walking again. The patients are all individuals who are diagnosed paraplegic or quadriplegic and at least 1-3 years post injury. They have all been told they would be permanently paralyzed. However, during their treatment period they are all seeing changes in their paralyzed state. Feeling and sensation is returning and they are proceeding to strengthen and re-educate the muscular structure to support their weight. Then they are learning to walk again. 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-depositing or the body is producing sufficient Sodium and Potassium levels to compensate for the loss of myelin. 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 Even though the results we are seeing at this time is anecdotal, the effect in multiple sclerosis and SCI patients suggests what Dr. Waxman is seeing is possible. Using the Neuro Care Treatment Program© is an effective medium for achieving it. We are not sure whether the pathway is reopened via a reversal of the demyelination or the depositing of sodium or potassium levels at the axon. In either case we are seeing the reversal of many of the symptoms of SCI over a period of time, from weeks to months. In most cases, less than one year. Due to these anecdotal results we feel further study is warranted.
Each SCI individual has a complete intake and history done. Arrangements are made to give the initial test using the Neurocare™. This test is designed to document information which will allow Ascertain if the individual is a candidate for this program and if so, Design a treatment program schedule. When specific movement is seen or felt at the time of this test it shows there is a pathway for the electrical stimulation to travel on to the extremities. From this it is the goal of the treatments to continue to send the signal, through the injury site, to the extremities. As outlined in the previous paper, this will move fluids and generate a repair to the axon. (It is still speculation on why this is accomplished). At the same time protocols are added to work specific muscle groups to:
- Reduce the disuse atrophy
- Re-educate the muscle
- Relax muscle spasms
- Increase the local circulation
The protocols will vary to individual needs. We really encourage the patient to work directly with the physical therapy department of his medical support group as his progress is seen. In fact, in several cases insurance companies have re-evaluated their policy and extended Physical Therapy for these individuals based on their improvement. Although the treatments are very simplistic and can be done by the patient or caregiver, it takes dedication on behalf of the SCI individual. The treatments must be done as outlined and it is recommended that at least two 45 minute treatment sessions per day be done for the first month, to see rapid, dramatic results.
EXCERPTS FROM PATIENT RECORDS
PATIENT #1 On September 8, 1995 a 78 year old white male paraplegic from an accident on 01/04/95. Diagnosed with transverse myolytis, effecting L3 and L4. He has no sensitivity from the waist down. Twenty-five minutes into the first treatment with the Neurocare™ 1000 4P/XP, a small amount of recruitment was noticed and continued to increase slightly to the finish of the 45 minute treatment. A machine was sent home with him. Treatments twice a day and return in one week.
September 15, 1995: During this treatment in the office good foot movement was documented. Added an electrode placement to the treatment he was doing and sent him home. He was to continue the treatment program and return in one week.
September 20, 1995: He now can feel hot and cold sensation on the buttocks. Can walk backwards in the swimming pool and can get out of the pool into the chair, on his own.
September 22, 1995: An increase in muscle girth is documented in his legs. He can move his feet up and down when sitting in his chair. Continued twice daily, 45-minute treatments.
October 6, 1995: Continues to show improvement and is very encouraged.
October 13, 1995: Feels hot and cold sensation on the top of his left foot. Sensation above and below left and right head of the femur. Still some sensation in buttocks. Small amount of bladder function has returned, without catheter. Muscles in his hips are strengthening. The tibia muscle is palpable now where it was not before starting the treatments. The treatments continue to focus on developing and strengthening the tibia muscles. He discontinued wearing support stockings on 10/7/95 and his legs look much better. His wound is nearly completely gone.
October 20, 1995: He can stand alone in the pool for short periods of time. His hips are getting stronger, but they remain too weak to support him. He has feeling in his feet and legs. The tibia muscle continues to show a marked improvement (can actually see enlargement). Treatment on the left leg is increased to 3 or 4 times per week.
October 27, 1995: Decubitus on his foot is now a small scab. Tibia muscle approximately 1″ in diameter. Sensitivity to sharp and dull with exception of right toes and mid left hamstring.
December 1, 1995: Patient walked into our office using a walker. Right leg and foot (which were the worst) now have good sensitivity and showing signs of nerve return. Left foot not responding as well, so will have patient concentrate on working the left leg and foot for the next week, as well as his standard treatment program.
December 6, 1995: Patient has 50% or more sensitivity return to the left foot and leg and is standing for longer periods of time. Patient continues with his treatment program, calling in at least once per week and stopping by occasionally. He continues to see his Kaiser physician, who originally told him he would never walk again.
September 17, 1996: Patient rides his three wheel bicycle, taps his foot to music, and swings foot back and forth. He continues his treatments, sometimes just once per day.
January 24, 1997: Patient is continuing to improve. The treatments are now concentrating on strengthening the hip and outer thigh muscles to stabilize his gait.
PATIENT #2 Patient is a 24 year old white male. Diagnosed as a quadriplegic since January 20, 1995. On a ventilator due to the paralysis. He had been very athletic. While working with weights in a weight room he heard a “snap”. Took a shower and drove himself home. It began to bother him so he went to the doctor. They gave him a MRI and before he left the office, he was paralyzed.
January 29, 1997: Initial visit and treatment. He is having physical therapy treatments on a regular basis. His muscle toneness is better than expected. We are working through his physical therapist and family members. This young man communicates to us on a weekly average, by telephone and E-mail. On May 28, 1997 we received an E-mail:
” . . .Since I started using the Neurocare™ system in February, I feel I’ve made great progress. In the two years prior to starting the treatment, I had some limited use of my left wrist and a little trunk strength. Now I feel I have gained some use of my diaphragm that will eventually and hopefully soon get my breathing on my own without the ventilator. I have also gained substantial range of motion in my neck. I can also bend my waist and pull myself back into a sitting position with a little help. I used to have a badly separated right shoulder, that is now stronger and in perfect shape. This development has started to give me some trace movement in my right arm, hand and fingers. I have increased sensation in my back and stomach, in addition to the sensation I already had. Now it is even better. My left arm is getting stronger also. Now by bicep is getting stronger and I can contract it better. Also, my tricep is beginning to come along. I can also make a fist with my left hand.
More updates to come, Thank You”
PATIENT #3 Patient lives in Austria and began his treatments while in a physical treatment facility in Austria. He is a 39 year old male who is diagnosed paraplegic due to an injury at T-11 in June of 1996. He began treatment with the Neurocare™ in February 1997. He suffered from burning pain sensations so severe he contemplated committing suicide. He found that the pain cycle was interrupted and came less often after beginning treatment.
February report: “Pain-free – no burning, heavy feeling.” Noticed a burning, heavy feeling in legs and parasthesia in feet.
March report: “More pain-free days … Increased tingling, sometimes feeling in legs like rubber.” In the May report, patient is having a “rubbery” feeling in gluteal muscles.
Between Feb. and middle of May the pain was alternating; one day pain(mainly strong, burning sensation in the entire paralyzed area) followed by one day pain free (except for parasthesia in feet). In the middle of May, the pattern started to reverse: the burning pain experienced during “pain” days, decreased to a degree of discomfort. On the other hand, the burning of the feet started to increase during (former) pain free days. The overall level of pain has gone down further during the month of June. Spasticity increased in the left leg from almost none, mainly in the evening. A rubbery feeling in gluteal muscles continues to increase.
BLADDER FUNCTION: A few days ago, bladder spontaneously started to release liquid when it reached the filled state. I was able then to further release about 200 ml to a minimum level of 200-250 ml residual urine.
July report: was no change other than Rubbery feeling in gluteal and thigh muscles continues to increase.
August Report: Still increasing “rubbery” sensation obviously has been caused by the Neuro Care™. Experienced muscle tension in the hip and thigh area starting in May. As a consequence in July I was able to go from the wheel chair or bed in a squatting position, from there onto my knees and crawl. I can crawl to a chair or a couch and pull myself up to sit. At the same time the pain pattern changed and the overall pain level was reduced to an endurable level. Over the last two weeks the pain pattern seems to be changing again.
PATIENT #4 Started treatment on 11/05/97. A 51 year old male, paraplegic. 3/18/98 Patient reports an increase of sensitivity and feeling into his feet. He is now working on developing his quadriceps so he can lock his knees. He will be standing in 2-3 weeks.
- 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.” New England Journal of Medicine 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 compression 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.