Difficulty of treating central pain has become a challenging battle. Historically as first line therapy, we often chose oral medications that are easily available, relatively safe, and do not require much resources.
Obstacles to treating pain include: difficulty in complete understanding of central pain pathophysiology, failure of opioid therapy, difficulty of treating central pain, limited success, between 30 to 50% max effectiveness for different disease processes.
From historical evidence, we have learned that previous attempts at primarily and solely using long-term narcotics have led us to challenges in healthcare and the community. One of the challenges to treating long-term pain is our limited understanding of the pathophysiology of central pain processing.
Current regimens include lidocaine, magnesium, ketamine and opioids. Lidocaine acts on sodium channel receptors which function as the basic unit of action potential generation. Neuropathic pain generates from ectopic, abnormal discharges of injured nerves in many neuropathic pain conditions (Nordin 1984). Lidocaine has a differential action; suppresses the ectopic discharges but does not interfere in the normal neural discharges.
First clinical use of lidocaine infusion in pain treatments was by 2 anesthesiologists (Bartlett and Hutaserani, 1961) for post-operative pain relief. Since then it has been used for various chronic pain syndromes, mostly of the neuropathic nature, such as diabetic neuropathy, post herpetic neuralgia, and deafferentation pain.
Limitations: authors noted that (1) lidocaine’s short serum half-life (120 minutes) precludes the use of this drug for chronic use, and (2) all of the trials measured pain relief within 24 hours because in most patients, the effect disappears a few hours after treatment. Given the high frequency of AEs and the short duration of action, thehealth benefits of IV lidocaine remain unclear.
NMDA receptors are known to be involved in the development of wind up phenomenon and generation of central sensitization and hence chronic pain. Increasing evidence that NMDA receptors are also involved in peripheral sensitization and visceral pain. Evidence shows that Ketamine primarily acts at NMDA receptors but also has actions at other sites.
Ketamine is also active at opioid, norepinephrine, serotonin, and muscarinic cholinergic receptors; it acts by inhibiting serotonin and dopamine reuptake and inhibits voltage-gated Na+ and K+ channels (Okon, 2007). Some studies suggest that analgesic effects of Ketamine are actually due to its activation of monoaminergic descending inhibitory pathways, rather than NMDA receptor
A comprehensive systematic review of the treatment of chronic neuropathic pain with ketamine, published in 2003, assessed the quality of evidence for ketamine’s effectiveness in central pain, CRPS, fibromyalgia, ischemic pain, nonspecific pain of neuropathic origin, acute pain in patients with chronic neuropathic pain, orofacial pain, phantom/stump pain, and post- herpetic neuralgia. Some small RCTs were available for review, and meta-analysis was considered not appropriate. Report concluded that despite the use of ketamine for more than 30 years, there was insufficient evidence to advocate the routine use of this treatment for patients with chronic pain. Of particular concern were the significant.
What are some challenges, side effects and limitations of the medications involved? •Ketamine:
Use is off label
Most frequently observed were effects on the central nervous system, such as
sedation, somnolence, dizziness, sensory illusions, hallucinations, nightmares,
dissociative feeling and blurred vision
Long term effects are not studied well
Possibility of addiction
As with all the therapies requires resources, monitoring and investment from
Even in patients in whom it works, the duration of analgesia has only been shown to be short lasting thus far
This also needs resources to administer, monitor treatment.
Most orally available substitutes do not have the same results when used on
patients responsive to lidocaine
Pain on infiltration
Long term cognitive defects
Any new research or advancements upcoming in the field?
At our institution we are currently using a mixture of lidocaine, ketamine, propofol with or without toradol based on renal function for a multitude of different chronic pain pathologies, predominantly fibromyalgia, long standing CPRS, peripheral neuropathy.
In addition to the previous medications discussed we are combing our regimens with an IV NSAID (Toradol) to target inflammatory processes and Propofol which is commonly thought to not have analgesic effects. It is predominantly added to our regimen because it is common knowledge that ketamine’s PCP like properties cause hallucinations, although some preliminary studies are showing that along with propofol's actions on the GABA receptors it has some minor effect on opioid receptors, we acknowledge evidence is still lacking on this theory.
To standardize our results with the previous studies referred we are using a Visual analog scale along with pre, post and followup surveys
We would have liked to present our data at this conference but currently it is insufficient in participants. We can comment that our preliminary data h