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296 Neuropathy – overview
However, there is little evidence supporting first-line use of nerve blocks
for the ED treatment of NP. Similar reservations preclude recommendation
for ED providers to apply transcutaneous electrical nerve stimulation (TENS).
CORTICOSTEROIDS
Since inflammatory mediators sensitize nociception, the anti-inflammatory
corticosteroids have been used for NP. Corticosteroids also decrease local
edema, thus reducing pressure on peripheral nerves. As dexamethasone has
relative few mineralocorticoid effects, it is preferred by many who use corticosteroids
in NP.
Despite widespread use and theoretical benefits, controlled trials of corticosteroids
in NP are lacking. There is a trial that demonstrated effectiveness
of oral prednisone for one type of NP (chronic regional pain syndrome). 32
With this possible exception, there is insufficient evidence to support any
recommendation for ED initiation of corticosteroids for NP.
MISCELLANEOUS AGENTS
The alpha-2-adrenergic agents (e.g. clonidine) decrease nocioceptive input
into the CNS by activating a2-adrenoceptors in the spinal cord and brainstem.
They also decrease sympathetic tone, which makes them potentially
valuable in patients with complex regional pain syndrome. Animal models
and preliminary work suggest clonidine may have a therapeutic role in NP
(e.g. as an opioid-sparing agent), but there is insufficient evidence to support
a recommendation for ED prescription of alpha-2-adrenergic agents
for NP. 33,34
Other approaches to NP that may have current or future utility include
agents with agonism at NMDA or gamma-aminobutyric acid (GABA) receptors.
Despite occasional clinical utility for some of these drugs (e.g. baclofen
for spasticity), there is no evidence supporting ED prescription of these
agents for NP.
Cannabinoids include agents such as delta-trans-tetrahydrocannabinol
(THC). These drugs may have analgesic effects (including synergism with