The
stimulus frequency was either 20, 50, or 100Hz. The abscissa
of Figure 4.3 is the percentage of myelinated axons undergoing
early axonal degeneration at 7 days after the stimulation
[25]. It should be interpreted as a relative, rather than
an absolute, scale of axonal injury since, during EAD, a
particular myelinated fiber may appear quite normal at one
point along the nerve (i.e. in a particular histological
cross-section) but will appear markedly degenerated at another
level [20]. When the stimulus frequency was 20Hz, there was
virtually no axonal injury that could be attributed to the
stimulation, even when the stimulus amplitude was eight times
greater than that necessary to recruit fully the a component
of the compound action potential; when the stimulus frequency
was 50Hz, axonal damage occurred when the stimulus amplitude
exceeded approximately one a unit; when the stimulus frequency
was 100Hz, the threshold for the neural injury was nearly
unchanged, but the slope of the regression line increased
markedly.
TISSUE REACTION: SUMMARY
The mechanism of stimulation induced tissue damage is still
unknown. Excessive neural activity and the toxic products
of electrochemical reactions are two strong candidates.
Heating and poreation are generally not considered viable
candidates for inducing tissue injury under conditions
that most neural prostheses operate.
Self-sizing cuffs such at the CWRU spiral cuff and the Huntington
helical cuff are recommended.
Safe charge densities have not been worked out for peripheral
nerve. However, one could use a number like 50 µC/cm2
as a maximum safe value, drawn from brain work.
Most of the work on peripheral nerve has been done in the
framework of mass action causing the damage. These results
indicate that intermittent stimulation (50 Hz with a 50%
duty cycle) and continuous stimulation at 20 Hz can be tolerated
at a stimulus amplitude that yields full activation of the
large nerve fibers. In addition, continuous stimulation for
less than four hours can be tolerated at 50 Hz. There has
been no functional manifestation observed for animals exhibiting
signs of EAD.
The dissection process, associated with mobilizing a peripheral
in preparation for an electrode implant, has a 25% to 30%
risk of inducing some trauma to axons. The myelin seems to
be the most vulnerable and the source is believed to be ischemia
induced during the dissection process. This suggests that
care should be given to avoid manipulations that could compromise
blood flow. Nerve fibers sustaining this type of damage appear
to almost always recover normal function. Often there is
no functional manifestation of the myelin insult.
Agnew, W.F., and D.B. McCreery. "Principles of safe
and effective nerve stimulation", In: New perspectives
in sacral nerve stimulation, edited by U. Jonas, and V. Grunewald.
London: Martin Dunitz, 2002, pp. 29-42