Tag Archives: medication

COVID worsens shortage of hospital opioids

Special Report: COVID deepens the other opioid crisis – a shortage of hospital painkillers – Reuters – Lisa Girion, Dan Levine, Robin Respaut – June 2020 

The DEA, an agency of law enforcement without a medical purpose, controls the amount of opioid medication manufactured by giving several companies strict quotas to produce each year. Because the DEA has no ties to or knowledge of medicine, they react purely to police agency reports of illicit opioids.

They still don’t understand that overdoses are from street opioids, not medication, so they want to keep reducing the opioid medication supply in a misdirected effort to reduce overdoses from street drugs.

As opioid pills and patches fueled a two-decade epidemic of overdoses in the United States, hospitals faced chronic shortages of the same painkillers in injectable form – narcotics vital to patients on breathing machines.   Continue reading

EDS: Analysis of Current Treatment Options

Ehlers-Danlos Syndrome: An Analysis of the Current Treatment Options – Pain Physician – 2020

Background: Ehlers-Danlos syndrome (EDS) is a multifaceted disease that can present with a variety of types of pain.

Unfortunately, both the mechanisms and treatments for pain are poorly understood. The proposed treatments for the various musculoskeletal pain syndromes in EDS have had variable success, and it becomes much more imperative to better define and evaluate the current treatment modalities in treating this debilitating disease.

Objectives: The purpose of this study was to investigate the currently available treatment modalities for patients with EDS and their efficacies in pain and symptom relief.  Continue reading

Self-administration of Hydrocortisone for Pain

General theory of inflammation: patient self-administration of hydrocortisone safely achieves superior control of hydrocortisone-responding disorders by matching dosage with symptom intensity – free full-text /PMC6581742/ – J Inflamm Res. 2019;

Objective: To determine if patient self-administration of hydrocortisone will safely achieve superior symptom control for all hydrocortisone-responding disorders as it does for Addison’s disease and rheumatoid arthritis.

Methods: 2,480 participants with hydrocortisone-responding disorders were brought to a minimum symptom state using daily administered hydrocortisone tablets in a 24-week, open study.

Thereafter, participants used 5-day, low-dose hydrocortisone regimens to quench subsequent disorder exacerbations (flares) to maintain the minimum symptom state. Stressors such as emotional traumas, infections, allergies, and injuries were minimized to reduce disorder intensity, hydrocortisone consumption, and participant discomfort.   Continue reading

Tapentadol (Nucynta) Prolonged Release: A Review

Tapentadol Prolonged Release: A Review in Pain Management – free full-text /PMC6422986/ – 2018 Nov

Tapentadol prolonged release (tapentadol PR) [Palexia® SR in EU] is a long-acting tablet formulation of the strong central analgesic tapentadol, which acts as both a μ-opioid receptor (MOR) agonist and a noradrenaline reuptake inhibitor.

Tapentadol PR is approved for chronic pain in various countries, with its EU indication (severe chronic pain manageable only with opioid analgesics) being the focus here.

Well-designed trials and clinical practice data support tapentadol PR use in this setting.    Continue reading

Tax-payers Fund Research, Pharma Profits

Will Big Pharma Fleece Us On A COVID Treatment That We Helped Fund? – Too Much Informationby David Sirota – June 2020

Usually, it’s people with chronic illnesses that suffer the most from high drug prices, but now even the healthy are forced to look at the corrupted state of our pharmaceutical industry (and the whole healthcare system.)

The pharmaceutical industry and its political allies are trying to use the COVID crisis to portray drug companies as modern-day Jonas Salks — the hero from history who refused to patent and profit off the polio vaccine.

It’s a nice tale, but it can obscure the other story of pharmaceutical price gouging and the laws that may help corporations unduly profit off public health crises.   Continue reading

Pharmacological rationale for tapentadol/Nucynta

Pharmacological rationale for tapentadol therapy: a review of new evidence – free full-text /PMC6526917/ – 2019 May

Chronic pain could be considered as a neurological disorder.

Tapentadol is an analgesic drug which acts both as a μ-opioid receptor (MOR) agonistand as a noradrenaline reuptake inhibitor (NRI), thereby generating a synergistic action in terms of analgesic efficacy, but not for the burden of adverse effects.

Therefore, tapentadol can be defined as the first “MOR-NRI” drug. This molecule holds the potential to address at least some of the current limitations of analgesic therapy due to its unique mechanism of action and has shown to be safe and effective in the treatment of chronic pain of cancer and noncancer etiologies including nociceptive, neuropathic and mixed pain.   Continue reading

The best treatment(s) for chronic primary musculoskeletal pain

The best treatment option(s) for adult and elderly patients with chronic primary musculoskeletal pain: a protocol for a systematic review and network meta-analysis –  free full-text /PMC6842192/ – Nov 2019

When researchers try to design studies about pain without differentiating between different kinds of pain, which I think invalidates those studies right away.

For myself, I’ve noticed several types of pain and each requires a different treatment:

  • For the pain from subluxations in joints, opioids work.
  • For my cervicogenic headaches, neck exercises work (and opioids initially).
  • For muscle spasms along the spine, muscle-relaxants are effective.
  • For the burn in muscles being used, nothing has worked.

Different pain requires different treatment, and I haven’t seen any studies about “pain” that rigorously control what kind of pain subjects have.  Continue reading

Noradrenergic System in Chronic Pain: Microglia Activation

Rescue of Noradrenergic System as a Novel Pharmacological Strategy in the Treatment of Chronic Pain: Focus on Microglia Activation – free full-text /PMC6751320/ – Sep 2019

Different types of pain can evolve toward a chronic condition characterized by hyperalgesia and allodynia, with an abnormal response to normal or even innocuous stimuli, respectively.

A key role in endogenous analgesia is recognized to descending noradrenergic pathways that originate from the locus coeruleus and project to the dorsal horn of the spinal cord. Impairment of this system is associated with pain chronicization.

More recently, activation of glial cells, in particular microglia, toward a pro-inflammatory state has also been implicated in the transition from acute to chronic pain. Both α2- and β2-adrenergic receptors are expressed in microglia, and their activation leads to acquisition of an anti-inflammatory phenotype.

This review analyses in more detail the interconnection between descending noradrenergic system and neuroinflammation, focusing on drugs that, by rescuing the noradrenergic control, exert also an anti-inflammatory effect, ultimately leading to analgesia.

More specifically, the potential efficacy in the treatment of neuropathic pain of different drugs will be analyzed.

On one side, drugs acting as inhibitors of the reuptake of serotonin and noradrenaline, such as duloxetine and venlafaxine, and on the other, tapentadol, inhibitor of the reuptake of noradrenaline, and agonist of the µ-opioid receptor.


Chronic pain, a disease entity with a major impact on healthcare costs, is characterized by hyperalgesia, an increased response to noxious thermal and mechanical stimuli, and allodynia, in which nociceptive responses occur to normally innocuous stimuli such as light touch (known as mechanical allodynia).

Pain of different origins including:

(i) inflammatory pain following tissue injury,

(ii) cancer pain, and

(iii) neuropathic pain following nerve, spinal cord or brain (e.g., stroke) injuries can become chronic.

Chronic “pathologic” pain results from a maladaptive functional and structural transformation process, sustained by mechanisms of peripheral and central sensitizations involving an altered neuronal activity.

In the present review, we will briefly examine two key elements in the pathophysiology of chronic pain, recently proven to be correlated, i.e., the noradrenergic system and neuroinflammation.

The Impairment of Noradrenergic System in the Transition From Acute to Chronic Pain

Descending monoaminergic inhibitory pathways project from the brain stem to the spinal cord and finely regulate pain threshold.

Activation of descending serotonergic pathways has been shown to play a central role in the analgesic effects of tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), and serotonin–noradrenaline reuptake inhibitors (SNRIs e.g., duloxetine and venlafaxine) in acute models of pain.

Activation of different serotonin receptors can in fact produce either pro-nociceptive effects (5-HT2A, 5-HT3 receptors) or anti-nociceptive effects (5-HT1A, 5-HT7 receptors).

Impairment of endogenous adrenergic analgesia is thought to be responsible for the transition from acute to chronic pain (Table 1).

Table 1

Impairment of descending noradrenergic system in neuropathic pain: evidence from animal models.

Animal model Preclinical phenotype Reference
Spinal nerve ligation Enhanced stimulus-evoked and spontaneous firing reduced by clonidine Patel et al., 2018
L5-L6 spinal nerve ligation Increased extracellular glutamate in the LC and impaired pain-evoked endogenous analgesia after nerve injury Kimura et al., 2015
L5-L6 spinal nerve ligation Mechanical hypersensitivity reduced by α2-agonists Hayashida et al., 2008
Streptozotocin-induced diabetic rats Mechanical allodynia and thermal hyperalgesia reduced by duloxetine Kinoshita et al., 2013
Rats with tibial nerve transection Mechanical and cold allodynia and heat hypersensitivity, all increased by α2-antagonists Hughes et al., 2013
Incisional pain model combined with DβH-saporin Selective degeneration of NA neurons with delayed recovery of mechanical hypersensitivity and increased spinal glial activation reduced by α2-agonists Arora et al., 2016
LC, locus coeruleus; DβH-saporin, dopamine β-hydroxylase conjugated to saporin; NA, noradrenaline.

Neuroinflammation and Microglial Activation in the Pathophysiology of Chronic Pain: A Protective Role for Noradrenaline

Neuroinflammation is characterized by infiltration of immune cells, glial activation, and production of inflammatory mediators in the peripheral and central nervous system (CNS), and it plays a central role in the pathophysiology of chronic pain.

Glial activation, involving both astrocytes and microglia, represents a common pathophysiological event in chronic pain, Alzheimer’s disease (AD), and also depression, although neurodegenerative disorders are characterized by significant neuronal loss

Microglia are the resident immune cells of the CNS, with a primary role in maintaining CNS homeostasis, but are rapidly activated in response to any subtle change in the surrounding microenvironment

Although microglia appear to drive neuroinflammatory mechanisms in pain chronicization, an important role in central sensitization and chronic pain is also played by spinal astrocytes

Noradrenaline is known to exert strong anti-inflammatory activity in the CNS  and its endogenous neuroprotective role in chronic pain is likely linked to this action

Overall, the preclinical data here reported suggest that the selective deficiency of noradrenergic system impacts both at neuronal and glial levels.

According to this scenario, the rescue of the noradrenergic system might represent a novel pharmacological approach to prevent the transition from acute to chronic pain ( Figure 1 ).

Rescue of Noradrenergic System as a Novel Pharmacological Approach to Reduce Microglia Activation and Neuroinflammation in Chronic Pain

Preliminary evidence obtained with the SNRIs duloxetine and ammoxetine opens the path for future studies with analgesic drugs, such as tapentadol, which combines MOR activation and potentiation of noradrenergic system.

Inhibition of microglial activation has been recently identified as a new mechanism which strongly contributes to the analgesic effects of duloxetine

Different molecular mechanisms seem to contribute to the effect of duloxetine on microglia.

The novel SNRI ammoxetine inhibits microglia activation.

it can be hypothesized that drugs that are able to rescue the noradrenergic system, such as SNRIs and tapentadol, can exert their analgesic efficacy by inhibiting microglia activation, thereby preventing the transition from acute to chronic pain.

Tapentadol is the only approved centrally acting analgesic that was developed from the beginning to enhance analgesic efficacy by combining two specific synergistic mechanisms of analgesic action.

Recent studies demonstrate the clinical efficacy of tapentadol in a broad spectrum of acute and chronic pain conditions including post-surgical, musculoskeletal, and neuropathic pains.

How to find doctors still prescribing opioids

I received what I believe to be excellent advice from Richard A “Red” Lawhern for anyone looking for doctors still prescribing opioids:

I very often receive inquiries from patients who have been deserted by their doctors due to concerns for malicious persecution by DEA, DoJ, State Medical Boards or State drug enforcement authorities.

It is hard these days to find any doctor who is taking on new patients for the treatment of chronic pain. But a medical professional associated with the Alliance offered this insight: talk to your local independent pharmacist and ask which doctors they know who may be treating patients for pain.   Continue reading

A Key Truth About Avoiding Addiction

How a Famous IQ Study Revealed a Key Truth About Avoiding Addiction – Filterby Stanton Peele – Feb 2019

What makes you live longer? What makes life more satisfying? What enables people to resist addiction?

These three questions have an answer in common—a remarkably good piece of news about which we should continually remind ourselves.

The answer is certainly not simply to stop taking opioids for chronic pain, when no other treatments have been able to relieve your pain.  Continue reading