What was the pain pattern prior to the index operation? Was it primarily back pain or leg pain?

Lumbar decompressions are not effective or indicated for primarily axial pain. There may be a short placebo decrease in LBP, but it is generally not sustained. Patients can usually clearly answer this question. If the leg pain is more severe but of short duration, this is not primarily a radicular problem. Even with a history of neurogenic claudication, it is often the back, not leg pain that causes people stop ambulating and sit down for relief.

How long was it presenting before the surgery? Is this a chronic pain situation that had not changed much during the few months prior to the surgery?

Chronic formerly was defined as pain that persists after the expected healing time. Neuroscience research has demonstrated chronic pain is “that which is memorized and becomes enmeshed with ongoing life experiences. The memory can’t be erased” [11]. The classic example is that of phantom limb pain, which can occur in any area of the body. It has been demonstrated that acute pain shifts from the nociceptive areas of the brain to the emotional ones. The nociceptive area becomes dormant. Even if the original source of pain was clearly identifiable, brain can and will memorize the pain. It has been documented to occur within 12 months [12].

What was the pattern of the pain? Did it follow a specific dermatome or was it diffuse?

Pain from an isolated soft disc rupture should follow a specific matching dermatome or myotome. If the original pain was diffuse or not a close match, then the original surgery may not have been a good idea. Surgery is only indicated for a specific identifiable structural problem with matching symptoms.

Spinal stenosis can present with diffuse symptoms and doesn’t have to have an exact match for surgery to be effective. Central stenosis can present with bilateral or unilateral symptoms and often looks like the lesion should be at a lower level of spine. If the pain is in a specific dermatome, then the compression should specifically correlate with the pattern of pain whether proximal to the exiting nerve root level or at the nerve root level.

Was it consistently positional?

Generally soft disc ruptures are worse with sitting and stenosis is worse with standing and walking. This is not an absolute pattern but if a stenosis patient is worse with sitting, that is a warning sign that the scenario is not straightforward. With severe stenosis and a large disc rupture, the pain can be constant regardless of the position. This is frequently the case with disc herniations in the setting of spinal stenosis at the same level, and the disc herniation has been present for longer than a year. Frequently, the initial presentation of a disc herniation in the presence of preexisting spinal stenosis causes dermatomal pain with sitting. However, as the inflammation from the herniated disc resolves, the pain may become more like neurogenic claudication and be more symptomatic with walking or standing.

How severe was it? Was it bad enough to require surgical intervention?

Probably the most consistent complaint a spine surgeon will hear is that, “If I just knew how bad my pain could be after surgery, I would never have undergone surgery.” If the original pain was relatively mild, then surgery wasn’t likely to help and often the persistent or recurrent symptoms are much worse. The current pathology may be similar to the original pathology and more of the same type of surgery won’t be helpful. You are also now dealing with a frustrated and often overtly angry patient. Animal studies show that under stress that nerve conduction increases, and the pain will worsen [5].

Were there any neurological deficits?

This is critical in that many patients suffer neurological deficits, usually associated with a dural tear. If the deficit was there pre-op, it may or may not improve with the index surgery. If the deficit occurred after the surgery and is persistent, then there is a high likelihood that further surgery won’t help improve function. If the neurological deficit is a new presenting complaint, then the whole situation is different, in that improvement might be more of a possibility, although the data is scant. Patients will present with “recurrent radiculopathy” when they really are asking for help in regaining neurological function.

Of note, bowel and bladder symptoms are rarely caused by chronic lumber spinal canal compression. It is remarkable how tight a lumbar stenosis can be without GI or GU compromise. It is easier to sort out the situation if the onset of true cauda equina symptoms are acute and there is a new compression from any cause. However, without subjective paresthesias or objective sensory changes, bowel and bladders symptoms are unlikely to be from the spine. The classic symptoms include saddle paresthesias/anesthesia, loss of bladder control, bilateral leg weakness, and numbness. This is a true emergency.

However, patients more often complain of urgency that gets construed by the surgeon as a cauda equina syndrome. Even in the presence of severe, even extreme stenosis, this is not a cauda equine syndrome nor an emergency. It is more likely to be an irritable bladder syndrome, which is associated with chronic pain. By treating the chronic pain, these symptoms will subside [13].

Were the risk factors that have been documented to be associated with poor outcomes addressed prior to the index operation?

It has been shown in several different ways that surgeons are not addressing the risk factors for a poor outcome prior to surgery. A 2014 paper showed that only about 10% of surgeons are addressing them prior to recommending surgery [14]. If they weren’t addressed, then it shouldn’t be surprising when the pain persists after surgery. The risk factors are well-known to all fields of medicine and include: depression, anxiety, catastrophizing, fear avoidance, insomnia, obesity, younger age, female, duration of the pain, level of opioid dependence, disability status, family member on disability, job satisfaction, smoking, illicit substance abuse, excessive ETOH intake, other chronic pain, situational stress, and a history of childhood abuse [15–17].

Additionally, it has been demonstrated that physicians cannot identify the “at-risk” patients in the clinical setting. The ability to pick up a high-risk patient is between 25% and 40%, in spite of the physicians being confident of their general assessment. It doesn’t matter whether the physician is a first-year resident or a senior attending. There is too much to assess in a busy clinic [18].

The high-risk patient with recurrent or persistent symptoms will still be at risk and unless these issues are systematically addressed and treated. Otherwise, additional surgery is unlikely to be helpful.