Dr. Ken Casey is a world-renowned neurosurgeon and a Professor at both Michigan State and Wayne State Universities. He trained under Dr. Peter Jannetta- the pioneer of the Microvascular Decompression surgery- and is also the co-author of “Striking Back,” what many consider the “Bible of TN.”  

It’s constantly a subject of debate “why we continue to do research” and “where should research be focused in medicine” A corollary is “When will it work?.  In the case of the arena of pain, it’s a very simple answer:  We have an enormous number of patients in need.  Chronic pain is estimated to affect some 100 million Americans each yearThis is the estimate from the Institute of Medicine.  One need only to look at the national headlines to understand the concern about our current approaches to chronic pain, especially the use of opioids.

Current oral therapies of a non-opioid nature are equally disappointing. In a recent consensus statement from the International Association for the Study of Pain as well as a subgroup of the International Headache Society, the drug that was deemed most effective from the evidence, was gabapentin (Neurontin) for chronic pain.  Although the industry and literature suggests that the effectiveness is that one in three patients using the drug will get relief, in fact a closer review by the neuroscientists in these groups show that seven out of eight patients who take the drug experience no relief.  Unfortunately that is the top rated drug and the others that are currently used including duloxetine (Cymbalta) have a much wider gap between the number of patients taking the drug until one patient experiences relief, a term in medicine known as number needed to treat for effectiveness.   In the case of certain types of trigeminal neuropathic pain a much touted agent (carbamazepine/oxycarbamazepine) is suggested to have a high success rate but in fact the number needed to treat there is estimated to be one in four from a meta-analysis of studies.

When we turn to current surgical options for patients with neuropathic pain, especially neuropathic facial pain, we find that the data is equally sparse and suggests that there is still a wide gap between an effective durable treatment and our patients. Current surgical procedures of a non-destructive nature can be applied to a small group of patients with a success rate up to 80-85%, but with a  consistent recurrence rate; so that by 10 years some 15-18% of patients are in pain again.  With the ablative procedures the numbers are even more bleak with some 60% of the patients experiencing control but on average only four years.

So, we neuroscientists caring for patients with chronic pain have not yet clearly identified a consistent successful and safe form of treatment. The answer to that dilemma lies in more research. As more and more is understood about the different sites of pain in the brain and the different cell systems that contribute to the pain experience, we uncover a larger body of knowledge which does not at the current time take us from the laboratory directly to the bedside. It can be safely said that while we know where pain centers are in the brain and what cells are responsible, we have very little understanding of how they function together and how, in different circumstances and different times, the responses can be so varied.  Again the answer is in more research into the mechanisms of pain, a very difficult prospect in the human being.  Laboratory experiments on animal models of pain have certainly contributed to this quest, but will only take us so far because the element of suffering, the element of the grading of pain, the element of why the same injury is pain in certain settings and not as painful in others, all need to be addressed before we have effective medications. How do we help the patients?

Functional MRI has allowed us to look at some of the differences in brain activity in chronic pain versus acute pain, and it looks like a promising tool to help us take it one step further by possibly allowing us to identify drug therapies that are effective in changing the patterns of the functional MRI. This would be an important goal, insofar as patients who are suffering are in themselves changed by the pain experience.  Clinical trials in which the simple question of pain relief in addressed oftentimes come to conclusions that a certain drug or class of drugs are largely ineffective.  If we could see changes in the brain and follow these on a regular basis, we may discover more about the compounds that are effective, and some of the duration and dose issues that are often so elusive in the care of the chronic pain patient.

Recent work in the field of gene classification has suggested that there are patients who suffer from changes in the voltage-gated sodium channel receptors as a component of their chronic pain, but from those same research labs comes a clear understanding that this is only a small portion of the overall experience.

We need more research into the basic understanding of the dichotomy between pain as a protective experience and pain which inflicts suffering. Once we begin to find some of the keys to this dichotomy, we will be successful in opening a number of doors to additional activities whether they be medicines, external therapies, neuromodulation, or even surgical procedures.