This is the highest quality of research design: double-blinded, randomized, and placebo-controlled – you can ask for nothing more – and it showed NO hyperalgesia.
Although often successful in acute settings, long-term use of opioid pain medications may be accompanied by waning levels of analgesic response not readily attributable to advancing underlying disease, necessitating dose escalation to attain pain relief.
How would a doctor or even a patient be able to tell the difference between increasing tolerance and “advancing underlying disease”?
Aging alone will worsen many chronic pain conditions.
If we walk upright, back pain will worsen over the years. If we have a connective tissue disorder, the damage will accumulate over the years.
As the huge group of “baby boomers” age, their existing pain will worsen and new pains will appear in this massive cohort of citizens.
Analgesic tolerance, and more recently opioid-induced hyperalgesia, have been invoked to explain such declines in opioid effectiveness over time. Because both phenomena result in inadequate analgesia, they are difficult to distinguish in a clinical setting.
Nowadays, when your pain increases from further wear and tear on the body, and when currently prescribed pain-relievers cannot keep up, doctors choose to believe it’s hyperalgesia because that gives them an excuse to take opioids away,
Patients with otherwise uncomplicated low-back pain were titrated to comfort or dose-limiting side effects in a prospective, randomized, double-blind, placebo-controlled clinical trial using sustained-release morphine or weight-matched placebo capsules for 1 month.
A total of 103 patients completed the study, with an average end titration dose of 78 mg morphine/d.
After 1 month, the morphine-treated patients developed tolerance to the analgesic effects of remifentanil, but did not develop opioid-induced hyperalgesia.
On average, these patients experienced a 42% reduction in analgesic potency.
The morphine-treated patients experienced clinically relevant improvements in pain relief, as shown by
- a 44% reduction in average visual analogue scale pain levels and
- a 31% improvement in functional ability.
The differences in visual analogue scale pain levels (P = .003) and self-reported disability (P = .03) between both treatment groups were statistically significant.
After 1 month of oral morphine therapy, patients with chronic low-back pain developed tolerance but not opioid-induced hyperalgesia.
Improvements in pain and functional ability were observed.
This abstract didn’t indicate what method they used to determine the difference between tolerance and hyperalgesia.
In clinical practice, the two are only distinguishable if a doctor is willing to try raising the opioid dose. A patient’s response to the change will show whether the problem is tolerance or hyperalgesia:
- If the pain worsens, it’s hyperalgesia: more opioid actually causes more pain sensitivity.
- If the pain eases, even a little bit, it’s a case of tolerance and more opioid is required to meet pain control needs.
Unfortunately, most doctors these days are unwilling to raise opioid doses to try this out.
Patients using opioids long-term usually reach a plateau of tolerance after which that same dose is sufficient for many years.
However, as we age, our bodies
- wear down with age,
- become less resilient, and
- develop various malfunctions like arthritis.
Therefore, when patients complain of increasing pain even as their doses remain steady, the simplest and most common explanation is that their pain has increased.
Another reason could be the development of tolerance.
However, opioid alarmists want to insist it’s hyperalgesia, because this gives them an excuse to deny dose increases and even remove opioids entirely from the patient’s care.
Hyperalgesia causes a freakish increase in pain sensitivity: the more you take, the more you hurt.
Therefore, the need for more pain relief cannot be blamed on hyperalgesia if the doctor isn’t willing to raise the dosage to make this determination.