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Abstract
Lumbar foraminal pathology causing entrapment of neurovascular contents and radicular
symptoms are commonly associated with foraminal stenosis. Foraminal neuropathy can
also be derived from inflammation of the neighboring lateral recess or extraforaminal
spaces. Conservative and interventional therapies have been used for the treatment
of foraminal inflammation, fibrotic adhesion, and pain. This update reviews the anatomy,
pathophysiology, clinical presentation, diagnosis, and current treatment options of
foraminal neuropathy.
Opioids are the cornerstone therapy for the treatment of moderate to severe pain. Although common concerns regarding the use of opioids include the potential for detrimental side effects, physical dependence, and addiction, accumulating evidence suggests that opioids may yet cause another problem, often referred to as opioid-induced hyperalgesia. Somewhat paradoxically, opioid therapy aiming at alleviating pain may render patients more sensitive to pain and potentially may aggravate their preexisting pain. This review provides a comprehensive summary of basic and clinical research concerning opioid-induced hyperalgesia, suggests a framework for organizing pertinent information, delineates the status quo of our knowledge, identifies potential clinical implications, and discusses future research directions.
The anaesthetic ketamine is used to treat various chronic pain syndromes, especially those that have a neuropathic component. Low dose ketamine produces strong analgesia in neuropathic pain states, presumably by inhibition of the N-methyl-D-aspartate receptor although other mechanisms are possibly involved, including enhancement of descending inhibition and anti-inflammatory effects at central sites. Current data on short term infusions indicate that ketamine produces potent analgesia during administration only, while three studies on the effect of prolonged infusion (4-14 days) show long-term analgesic effects up to 3 months following infusion. The side effects of ketamine noted in clinical studies include psychedelic symptoms (hallucinations, memory defects, panic attacks), nausea/vomiting, somnolence, cardiovascular stimulation and, in a minority of patients, hepatoxicity. The recreational use of ketamine is increasing and comes with a variety of additional risks ranging from bladder and renal complications to persistent psychotypical behaviour and memory defects. Blind extrapolation of these risks to clinical patients is difficult because of the variable, high and recurrent exposure to the drug in ketamine abusers and the high frequency of abuse of other illicit substances in this population. In clinical settings, ketamine is well tolerated, especially when benzodiazepines are used to tame the psychotropic side effects. Irrespective, close monitoring of patients receiving ketamine is mandatory, particularly aimed at CNS, haemodynamic, renal and hepatic symptoms as well as abuse. Further research is required to assess whether the benefits outweigh the risks and costs. Until definite proof is obtained ketamine administration should be restricted to patients with therapy-resistant severe neuropathic pain.
New Jersey Pain Medicine for the Difficult and Failed Pain, Robert Wood Johnson University
Hospital Rahway, Rahway, NJ,
USA
Author notes
Correspondence to: Young Kook Choi, New Jersey Pain Medicine for the Difficult and
Failed Pain, Robert Wood Johnson University Hospital Rahway, 865 Stone Street, Rahway,
NJ 07065, USA, Tel: +1-732-754-0369, Fax: +1-855-492-5768, E-mail:
choiyomd@
123456hotmail.com
, ORCID:
https://orcid.org/0000-0002-9572-011X
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