Improved Opioid Analgesic Effect Following Opioid Dose Reduction
Department of Anesthesiology, Pain Medicine Division, Penn State Milton S Hershey Medical Center, Penn State College of Medicine, Hershey, Pennsylvania 17033-0850, USA. Pain Medicine
(Impact Factor: 2.3).
10/2008; 9(6):724-7. DOI: 10.1111/j.1526-4637.2008.00501.x
Traditionally, opioids have been the cornerstone of therapy for patients suffering from cancer pain, regardless of the potential to develop opioid tolerance. In chronic pain patients who experience worsening pain despite increasing doses of opioids, the clinical role of opioid-induced hyperalgesia is gaining more recognition.
Presented here is the case of a 56-year-old man with recurrent squamous cell lung carcinoma and spinal metastases, suffering with intractable 8/10 pain on the visual analog scale in his chest, lower thoracic spine, and upper lumbar spine. He was admitted five times for pain control. In spite of escalating doses of oxycodone, morphine, and hydromorphone, the patient continued to experience severe pain. Also, he endured undesirable sedation, fatigue, and generalized weakness. The clinical picture suggested the possibility of opioid-induced hyperalgesia. We decreased the hydromorphone dose by 40-50% and started methadone. The patient's pain level dropped to a more acceptable 3/10. He was more alert, and his pain was tolerable until his death.
Opioid-induced hyperalgesia might be considered in a patient who has no evidence of disease progression, who is on clinically reasonable doses of opioids, and whose pain escalates as opioid doses are increased. A reduction of opioids and the addition of a low-dose N-methyl-D-aspartate receptor antagonist may provide a favorable clinical outcome in those patients who have failed to benefit from opioid rotation and other adjunctive pain treatments.
Available from: Sergio D Bergese
- "This NMDAR increase leads in turn to an upregulation of the NO synthase cascade and negative functional regulation of morphine algesia, as well as to protein kinase C-mediated phosphorylation of opioid receptors (Koppert and Schmelz, 2007; da Cunha Leal et al., 2010; Rodríguez-Muñoz et al., 2012). Increased NMDAR activation may also downregulate glutamate reuptake mechanisms, leading to central sensitization (Vorobeychik et al., 2008; da Cunha Leal et al., 2010; Lenz et al., 2011; Tompkins and Campbell, 2011; Wilson et al., 2011; Holtman and Jellish, 2012; Juba et al., 2013). Patients receiving NMDA receptor antagonists including ketamine (da Cunha Leal et al., 2010) and MgSO 4 alongside opioids have exhibited recovery of opioid analgesic effect, further substantiating these proposed mechanisms (Figure 1) (Daeninck and Bruera, 1999; Gupta et al., 2011; Colvin and Fallon, 2010; Pasero and McCaffery, 2012; Lee et al., 2013a). "
[Show abstract] [Hide abstract]
ABSTRACT: Chronic pain patients receiving opioid drugs are at risk for opioid-induced hyperalgesia (OIH), wherein opioid pain medication leads to a paradoxical pain state. OIH involves central sensitization of primary and secondary afferent neurons in the dorsal horn and dorsal root ganglion, similar to neuropathic pain. Gabapentin, a gamma-aminobutyric acid (GABA) analogue anticonvulsant used to treat neuropathic pain, has been shown in animal models to reduce fentanyl hyperalgesia without compromising analgesic effect. Chronic pain patients have also exhibited lower opioid consumption and improved pain response when given gabapentin. However, few human studies investigating gabapentin use in OIH have been performed in recent years. In this review, we discuss the potential mechanisms that underlie OIH and provide a critical overview of interventional therapeutic strategies, especially the clinically-successful drug gabapentin, which may reduce OIH.
Frontiers in Pharmacology 05/2015; 6. DOI:10.3389/fphar.2015.00104 · 3.80 Impact Factor
Available from: Sanford Silverman
[Show abstract] [Hide abstract]
ABSTRACT: Opioids have been and continue to be used for the treatment of chronic pain. Evidence supports the notion that opioids can be safely administered in patients with chronic pain without the development of addiction or chemical dependency. However, over the past several years, concerns have arisen with respect to administration of opioids for the treatment of chronic pain, particularly non-cancer pain. Many of these involve legal issues with respect to diversion and prescription opioid abuse. Amongst these, opioid induced hyperalgesia (OIH) is becoming more prevalent as the population receiving opioids for chronic pain increases. OIH is a recognized complication of opioid therapy. It is a pro-nocioceptive process which is related to, but different from, tolerance. This focused review will elaborate on the neurobiological mechanisms of OIH as well as summarize the pre-clinical and clinical studies supporting the existence of OIH. In particular, the role of the excitatory neurotransmitter, N-methyl-D-aspartate appears to play a central, but not the only, role in OIH. Other mechanisms of OIH include the role of spinal dynorphins and descending facilitation from the rostral ventromedial medulla. The links between pain, tolerance, and OIH will be discussed with respect to their common neurobiology. Practical considerations for diagnosis and treatment for OIH will be discussed. It is crucial for the pain specialist to differentiate amongst clinically worsening pain, tolerance, and OIH since the treatment of these conditions differ. Tolerance is a necessary condition for OIH but the converse is not necessarily true. Office-based detoxification, reduction of opioid dose, opioid rotation, and the use of specific NMDA receptor antagonists are all viable treatment options for OIH. The role of sublingual buprenorphine appears to be an attractive, simple option for the treatment of OIH and is particularly advantageous for a busy interventional pain practice.
Pain physician 01/2009; 12(3):679-84. · 3.54 Impact Factor
Available from: ecu.edu.au
[Show abstract] [Hide abstract]
ABSTRACT: Advances in liquid crystal (LC) materials and VLSI technology have enabled the development of multi-phase spatial light modulators (SLM) that can perform high-resolution, dynamic optical beam positioning as well as temporal and spatial beam shaping in the 1550 nm optical communication window. These attractive features can effectively be used to achieve optical switching, optical spectral equalization, tunable optical filtering and many other functions that are important for future reconfigurable optical telecommunication networks. We review potential optical telecommunication applications based on LC-SLMs.
High Speed Networks and Multimedia Communications 5th IEEE International Conference on; 02/2002
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.