Dooley D.M., Sharkey J., Keller W., and Kasprak M. (1978)
Treatment of demyelinating and degenerative diseases by electro stimulation of
the spinal cord. Med. Prog. Technol. 6, 1-14.
Abstract: Electrical stimulation was applied to the spinal cord of 75 patients
who had demyelinating and degenerative diseases of the central nervous system,
and 3 patients who had sustained spinal cord injuries. The electrical energy
was delivered to the central nervous system by the percutaneous technique. The
amount of electrical energy required to produce the perception of paresthesias
was measured in 11 patients. The minimum power necessary was 76.89 muW, the
maximum was 868 muW, and the average was 448.8 muW. The patients were evaluated
by 4 examiners by means of routine neurologic examination, videotape movies,
and measurement of urinary bladder function. Continued improvement in
neurological status, which allowed the patient to live a better lifestyle,
occurred in 30 of the 61 patients with multiple sclerosis, and 6 of the 10
patients with ataxia. The patient with transverse Myelitis, the patient with
primary lateral sclerosis, and 1 patient with olivopontocerebellar atrophy; also
noted similar enhancement of neurological function. The patients with
amyotrophic lateral sclerosis and spinal cord injuries had no changes of
significance. Thirty-two out of 44 patients who were ambulatory had significant
improvement, whereas 10 of the 19 patients who were not ambulatory had
improvement. There was no evidence that electrical stimulation of the spinal
cord, when applied via dorsally placed percutaneous electrodes and when carried
only to the perception of a paresthesias, has any adverse effect on
neurological function. It is hypothecated that the electrical current alters
neurotransmitters to enhance the transmission along nervous and neurochemical
pathways. The exact mechanisms are unknown at the present time
Dooley D.M. and
Abstract: Patients with dystonia, spinocerebellar and cerebellar ataxia and
spasmodic torticollis have a reasonable chance of being significantly aided in
their control of motor function and neurogenic bladder by electrical
stimulation of the cervical or thoracic spinal cord. This mode of therapy has
the advantages that it is not destructive of neurological tissue, effects can
be varied by altering the intensity and rate of the stimulus and preliminary
testing with externalization of the electrodes is predictive of the effects of
chronic stimulation
Erb D.E., Mora R.J., and Bunge R.P. (1993) Reinnervation of
adult rat gastrocnemius muscle by embryonic motoneurons transplanted into the
axotomized tibial nerve. Exp. Neurol. 124, 372-376.
Abstract: In some cases of spinal cord injury and in certain motoneuron
diseases, such as amyotrophic lateral sclerosis and spinal muscular atrophies,
lower motoneurons are destroyed and muscle function cannot be restored except
by reinnervation from alternate motoneuron sources. We have tested the
feasibility of employing local transplantation of embryonic motoneurons to
restore innervation to denervated somatic muscle as a first step in salvaging
muscle function and enabling use of functional electric stimulation.
Dissociated ventral spinal cord cells from Embryonic Days 14 and 15 rats were
transplanted into the distal stump of axotomized tibial nerves of adult rats.
Animals were killed 3-18 weeks after transplantation. After 3 weeks large
multipolar cells, resembling alpha motoneurons, were observed within the
transplant site surrounded by myelinated and unmyelinated axons and dendrites.
Axons emanating from these transplanted motoneurons were identified within the
nerve stump and within the previously denervated gastrocnemius muscle, forming
neuromuscular junctions. Transplanted motoneurons survived up to 18 weeks and
were labeled after intramuscular injection of fast blue. This study
demonstrates that embryonic spinal motoneurons, transplanted into the distal
adult peripheral nerve stump, are able to survive and reinnervate the
denervated target muscle. We are now exploring the possibility of using this
experimental approach to retard the atrophy of denervated skeletal muscle, thus
providing a muscle capable of useful response to functional electrical
stimulation
Handa I., Matsushita N., Ihashi K., Yagi R., Mochizuki R.,
Mochizuki H., Abe Y., Shiga Y., Hoshimiya N., Itoyama Y., and . (1995) A
clinical trial of therapeutic electrical stimulation for amyotrophic lateral
sclerosis. Tohoku J. Exp. Med. 175, 123-134.
Abstract: This paper describes the effects of therapeutic electrical
stimulation (TES) on the wasting muscles in a patient with amyotrophic lateral
sclerosis. The patient is a 47-year-old male, and he has a history of
progressive muscle weakness and atrophy, affected more in the right side. Percutaneously
indwelling intramuscular electrodes were implanted to the affected muscles in
the right upper and lower extremities but no electrode in the corresponding
left region. Within a month of TES therapy, a rapid improvement of extremity
motion appeared in the TES treated side. Long-term application of TES more than
3 months increased the strength of the muscle which had been evidently weaker
than the non- treated side. CT findings of both the upper and lower extremities
with TES therapy showed an increase in the density and a reduction in the
moth-eaten image. An increase in the thickness of the muscles was also observed
in the TES treated side while deterioration was observed in the muscles on the
non-treated side
Schriefer T.N., Hess C.W., Mills K.R., and
Abstract: Central motor conduction (CMC) to abductor digiti minimi (ADM) was
evaluated in 22 patients with motor neurone disease (MND) using magnetic
stimulation of the motor cortex and electrical stimulation at the C7/T1
interspace. CMC was abnormal in 14 patients; prolonged CMC time and absence of
response to brain stimulation were more frequent abnormalities than low
amplitude responses without prolonged CMC time. The technique can reveal
subclinical upper motor neurone involvement and document central motor pathway
dysfunction in MND. The patterns of abnormality are not specific to MND; all
may occur in other neurological disorders including multiple sclerosis