Pain responsiveness to opioids: Central versus peripheral neuropathic pain

2011 ◽  
Vol 7 (5) ◽  
pp. 391-400 ◽  
Author(s):  
Howard S. Smith, MD ◽  
Patrick D. Meek, PharmD, MSPH

Neuropathic pain is initiated or caused by a primary lesion or dysfunction in the nervous system. Neuropathic pain is composed of peripheral neuropathic pain (with a primary lesion or dysfunction in the peripheral nervous system) and central neuropathic pain (CNP; with a primary lesion or dysfunction in the central nervous system). CNP may be further subdivided into supraspinal central neuropathic pain and spinal central neuropathic pain. Opioids have a role in the pharmacologic management of neuropathic pain; however, there is a scarcity of literature on the treatment of CNP with opioids. One of the few statements in the literature regarding the analgesic efficacy of opioids for CNP suggests that despite limited data, the opioid responsiveness for neuropathic pain of central and peripheral etiologies is similar. After reviewing the extremely limited data, it is proposed that although there may be a subpopulation of patients with CNP who have a reasonable analgesic response to opioids, overall, when sensory pain rating is used as the yardstick, CNP appears to respond less well to opioids than peripheral neuropathic pain. Thus, opioids should be considered a second- or third-line agent in any algorithm of the pharmacologic treatment of CNP. Also within CNP, it appears that supraspinal central neuropathic pain may respond less well to a trial of opioids than spinal central neuropathic pain. Moreover, under close monitoring for side effects (eg, constipation), it is suggested that clinicians may want to consider titrating to higher doses of potent opioids before the trial is judged to be unsuccessful for refractory supraspinal central neuropathic pain.

2007 ◽  
Vol 12 (1) ◽  
pp. 13-21 ◽  
Author(s):  
DE Moulin ◽  
AJ Clark ◽  
I Gilron ◽  
MA Ware ◽  
CPN Watson ◽  
...  

Neuropathic pain (NeP), generated by disorders of the peripheral and central nervous system, can be particularly severe and disabling. Prevalence estimates indicate that 2% to 3% of the population in the developed world suffer from NeP, which suggests that up to one million Canadians have this disabling condition. Evidence-based guidelines for the pharmacological management of NeP are therefore urgently needed. Randomized, controlled trials, systematic reviews and existing guidelines focusing on the pharmacological management of NeP were evaluated at a consensus meeting. Medications are recommended in the guidelines if their analgesic efficacy was supported by at least one methodologically sound, randomized, controlled trial showing significant benefit relative to placebo or another relevant control group. Recommendations for treatment are based on degree of evidence of analgesic efficacy, safety, ease of use and cost-effectiveness. Analgesic agents recommended for first-line treatments are certain antidepressants (tricyclics) and anticonvulsants (gabapentin and pregabalin). Second-line treatments recommended are serotonin noradrenaline reuptake inhibitors and topical lidocaine. Tramadol and controlled-release opioid analgesics are recommended as third-line treatments for moderate to severe pain. Recommended fourth-line treatments include cannabinoids, methadone and anticonvulsants with lesser evidence of efficacy, such as lamotrigine, topiramate and valproic acid. Treatment must be individualized for each patient based on efficacy, side-effect profile and drug accessibility, including cost. Further studies are required to examine head-to-head comparisons among analgesics, combinations of analgesics, long-term outcomes, and treatment of pediatric and central NeP.


2020 ◽  
Vol 21 (15) ◽  
pp. 5330 ◽  
Author(s):  
Ramona D’Amico ◽  
Daniela Impellizzeri ◽  
Salvatore Cuzzocrea ◽  
Rosanna Di Paola

Neuropathic pain results from lesions or diseases of the somatosensory nervous system and it remains largely difficult to treat. Peripheral neuropathic pain originates from injury to the peripheral nervous system (PNS) and manifests as a series of symptoms and complications, including allodynia and hyperalgesia. The aim of this review is to discuss a novel approach on neuropathic pain management, which is based on the knowledge of processes that underlie the development of peripheral neuropathic pain; in particular highlights the role of glia and mast cells in pain and neuroinflammation. ALIAmides (autacoid local injury antagonist amides) represent a group of endogenous bioactive lipids, including palmitoylethanolamide (PEA), which play a central role in numerous biological processes, including pain, inflammation, and lipid metabolism. These compounds are emerging thanks to their anti-inflammatory and anti-hyperalgesic effects, due to the down-regulation of activation of mast cells. Collectively, preclinical and clinical studies support the idea that ALIAmides merit further consideration as therapeutic approach for controlling inflammatory responses, pain, and related peripheral neuropathic pain.


2020 ◽  
Vol 47 (3) ◽  
pp. 265-283
Author(s):  
Douglas Murphy ◽  
Denise Lester ◽  
F. Clay Smither ◽  
Ellie Balakhanlou

Neuropathic pain (NP) can have either central nervous system causes or ones from the peripheral nervous system. This article will focus on the epidemiology, classifications, pathology, non-invasive treatments and invasive treatments as a general review of NP involving the peripheral nervous system. NP has characteristic symptomatology such as burning and electrical sensations. It occurs in up to 10% of the general population. Its frequency can be attributed to its occurrence in neck and back pain, diabetes and patients receiving chemotherapy. There are a wide range of pharmacologic options to control this type of pain and when such measures fail, numerous interventional methods can be employed such as nerve blocks and implanted stimulators. NP has a cost to the patient and society in terms of emotional consequences, quality of life, lost wages and the cost of assistance from the medical system and thus deserves serious consideration for prevention, treatment and control.


2015 ◽  
Vol 20 (1) ◽  
pp. 116-129 ◽  
Author(s):  
T. Mainka ◽  
N.M. Malewicz ◽  
R. Baron ◽  
E.K. Enax-Krumova ◽  
R.-D. Treede ◽  
...  

Pain medicine ◽  
2019 ◽  
Vol 4 (2) ◽  
pp. 4-32
Author(s):  
Dmytro Dmytriiev ◽  
Pylyp Prudius ◽  
Olesia Zaletskaya ◽  
Yevhen Lisak ◽  
Yurii Rudnitsky ◽  
...  

Neuropathic pain is a pain caused by a disease or focal damage to the somatosensory nervous system. The prevalence of chronic pain with neuropathic features in different countries is estimated at 7–10 %. Damages to the nervous system can occur at the level of peripheral nerves, plexus and dorsal roots (peripheral neuropathic pain) or spinal cord and brain (central neuropathic pain). Neuropathic pain is based on pathological activation of pain pathways. Neuropathic pain occurs with diabetic polyneuropathy more often than with all polyneuropathies of another etiology. Hyperglycemia is the major cause of chronic diabetes mellitus and its progression. Since the cause of pain can rarely be cured, treatment is usually symptomatic. Neuropathic pain is generally poorly controlled by analgesics. NB management is started with conservative pharmacotherapy before applying invasive analgesia. Although there are many drugs that can be used in patients with DPN, monotherapy can not always stop pain syndrome. In addition, the patient may not tolerate the full therapeutic dose of the drug. All this dictates the need for combination therapy.


2022 ◽  
Vol 12 ◽  
Author(s):  
Michael K. Racke ◽  
Elliot M. Frohman ◽  
Teresa Frohman

Neuropathic pain and other pain syndromes occur in the vast majority of patients with multiple sclerosis at some time during their disease course. Pain can become chronic and paroxysmal. In this review, we will utilize clinical vignettes to describe various pain syndromes associated with multiple sclerosis and their pathophysiology. These syndromes vary from central neuropathic pain or Lhermitte's phenomenon associated with central nervous system lesions to trigeminal neuralgia and optic neuritis pain associated with nerve lesions. Muscular pain can also arise due to spasticity. In addition, we will discuss strategies utilized to help patients manage these symptoms.


2019 ◽  
Vol 21 (2) ◽  
pp. 76-80 ◽  
Author(s):  
Maureen A. Mealy ◽  
Scott D. Newsome ◽  
Sharon L. Kozachik ◽  
Michael Levy ◽  
Thomas J. Smith

Abstract Central neuropathic pain is a severely disabling consequence of conditions that cause tissue damage in the central nervous system. It is often refractory to treatments commonly used for peripheral neuropathy. Scrambler therapy is an emerging noninvasive pain-modifying technique that uses transcutaneous electrical stimulation of nociceptive fibers with the intent of reorganizing maladaptive signaling pathways. It has been examined for the treatment of peripheral neuropathy with favorable safety and efficacy outcomes, but its application to central neuropathic pain has not been reported in transverse myelitis. We describe the use of Scrambler therapy in a patient with persistent central neuropathic pain due to transverse myelitis. The patient had tried multiple drugs for treatment of the pain, but they were not effective or caused adverse effects. After a course of Scrambler therapy, pain scores improved considerably more than what was reported with previous pharmacologic and nonpharmacologic interventions. This case supports further investigation of Scrambler therapy in multiple sclerosis, neuromyelitis optica spectrum disorder, and other immune-mediated disorders that damage the central nervous system.


Author(s):  
MD Staudt ◽  
AJ Clark ◽  
AS Gordon ◽  
ME Lynch ◽  
PK Morley-Forster ◽  
...  

Background: Central neuropathic pain syndromes are a result of central nervous system injury, most commonly related to stroke, spinal cord injury, or multiple sclerosis. These syndromes are much less common than peripheral etiologies, with less known regarding optimal treatment. The objective of this study was to determine the long-term clinical effectiveness of the management of central relative to peripheral neuropathic pain at tertiary pain centers. Methods: Patients diagnosed with central (n=79) and peripheral (n=710) neuropathic pain were identified from a prospective observational cohort from seven Canadian tertiary centers. Data regarding patient -characteristics, analgesic use, and patient-reported outcomes were collected at baseline and 12-month follow-up. The primary outcome was the composite of reduced average pain intensity and pain interference. Secondary outcomes included assessments of function, mood, and quality-of-life. Results: At 12-month follow-up, 13.5% (95%CI,5.6-25.8) of patients achieved ≥30% reduction in pain, whereas 38.5% (95%CI,25.3-53.0) achieved a ≥1 point reduction in pain interference; 9.6% (95%CI,3.2-21.0) of patients achieving both these measures. Patients with peripheral neuropathic pain were more likely to achieve this primary outcome at 12-months (25.3% of patients; 95%CI,21.4-29.5) (p=.012). Conclusions: Patients with central neuropathic pain were less likely to achieve a meaningful improvement in pain and function compared to patients with peripheral neuropathic pain at 12-month follow-up.


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