What is a Pinched Nerve?

A pinched nerve typically refers to nerve compression due to a variety of factors. Local degenerative changes in or near the spinal column involving intervertebral discs, facet joints and ligaments can cause nerve root compression. These can be due to disc bulges or herniations, facet hypertrophy, ligament hypertrophy, osteochondral spurs or spondylolisthesis or slippage of a one vertebral body over another.

Pinched nerves can occur anywhere in the body where nerves travel through bony and ligamentous structures. Some of the most common sites of nerve compression are the neck and the lower back.

“Pinched Nerve” or nerve compression is typically diagnosed by a physician or chiropractor after careful history taking from the patient. This is followed by a physical exam where the pain may be reproduced after certain motions. A physician may order additional studies such as an MRI to look for pathologic changes in or near the spine that may be causing the nerve compression.

Nerve root compression symptoms typically include pain, inflammation and often shooting pain down the arm or leg. Treatment includes conservative measures such as over-the-counter pain relievers, rest and physical therapy. Most cases have symptomatic resolution over time and only conservative treatment measures are needed.

If pinched nerve symptoms persist after conservative therapy, interventional pain management injections may be warranted. These are typically performed under fluoroscopy which is a “live” x-ray. It allows the physician to see bone and some other anatomical structures in different “frames” while performing a procedures or surgery.

The most common interventional pain management procedures for nerve root compression near the spine is called a selective nerve root block. During this procedure, the physician guides a fine needle under fluoroscopy near the pinched nerve. The fluoroscopy helps the physician guide the needle close to the nerve compression while avoiding anatomical structures that might be damaged if penetrated by the tip of the needle. Once the tip of the needle is close to the nerve root compression, steroid is injected next to the pinched nerve but not into the nerve. The purpose of the steroid is to decrease inflammation and improve symptoms. If symptoms do not resolve, the procedure can be repeated. Typically, it is repeated up to two times with each procedure separated by a time interval of two weeks.

If symptoms are severe to the point where the nerve root compression causes unbearable, unremitting pain, neurological symptoms such as arm or leg weakness or in the case of a pinched nerve in the lower back, loss of bowel or bladder control, surgery is the preferred intervention.

The most common spinal decompressive surgery has traditionally been microdiscectomy. It is considered a minimally invasive surgery in which the herniated intervertebral disc fragments that are causing the nerve root compression are removed. A newer, even less invasive technique involves using a narrow, hollow tube through which instruments are passed to remove the disc fragments. Visualization during this “endoscopic” surgical procedure is aided by a digital camera positioned on the end of the instrument along with a light source. This technique is meant to minimize the surgical trauma to the patient, reduce the incidence of complications and to shorten the recovery time.

Interventional pain management procedures such as selective nerve root block and surgical procedures such as microdiscectomy for pinched nerves are typically followed by a course of physical therapy in order to assist in the patient’s recovery and allow her/him to get back to their daily routine.

Ketamine for Chronic Pain Management

Ketamine is a phencyclidine derivative which acts primarily as an N-methyl-D-aspartate (NMDA) antagonist. Its unique anesthetic profile includes relative hemodynamic stability due to its sympathomimetic properties (though in some patients who are catecholamine deplete, it can cause myocardial depression), preservation of respiratory drive, bronchodilatory properties, and significant non-opiate mediated analgesic properties. It is an attractive adjuvant in patients with chronic pain, who are often opiate-tolerant. At sub-anesthetic doses, ketamine has been shown to be opiate-sparing in the perioperative setting, as well as reducing post-operative nausea and vomiting. Sub-anesthetic, or “low-dose” ketamine, is defined as <2mg/kg intramuscularly or 1mg/kg intravenously. For continuous infusions, <1.2mg/kg/hr has been suggested

In sub-group analyses, ketamine’s opiate sparing effects were greatest in upper abdominal and thoracic procedures. It was still effective, though less so, in orthopedic and lower abdominal surgery. It did not significantly reduce opiate consumption in ear, nose and throat and oral surgery. Furthermore, the more painful the surgery (i.e. high VAS scores), the greater ketamine’s opiate sparing effect.

In addition to sparing opiates in chronic pain patients, ketamine may help prevent chronic postsurgical pain by diminishing central sensitization via its NMDA blocking effects. Anywhere from 10-50% of patients have persistent pain after surgery, much of which may be attributed to iatrogenic nerve injury. Blocking central sensitization could help prevent these injuries from persisting in the form of chronic pain. In one systemic review, the relative risk of developing chronic pain after surgery was reduced by 25% (NNT 12) at 3 months and 30% at 6 months.

Short term use of ketamine has been described in the treatment of neuropathic pain, migraine, fibromyalgia, ischemic pain, whiplash injury, and TMJ disease. The mechanism of action is likely NMDA antagonism and potentially enhancement of descending inhibition, though ketamine also acts on other central receptors, including opioid, with their contributing roles still uncertain. Ketamine has also showed promise in reducing opioid-induced hyperalgesia.

Long term benefit of ketamine has been best studied in complex regional pain syndrome (CPRS). Several studies have showed reduction of pain scores for up to 3 months with a several-day course of intravenous ketamine.

The safety of long-term ketamine use is ill-defined, and the logistics of delivery are a barrier. Ketamine has poor oral bioavailability, and while intramuscular, sublingual, nasal and rectal formulations exist, they have yet to be widely used or studied. Caveats for long-term ketamine use include urologic complications such as cystitis and bladder contractions, hepatic dysfunction, and psychologic side effects including addiction.

While further studies are warranted in long-term use of ketamine for chronic pain, there is ample evidence in its efficacy as a perioperative adjuvant. It behooves anesthesiologists to be familiar with its use, particularly in the chronic pain population.

References:

Gorlin AW, Rosenfeld DM, Ramakrishna H. Intravenous sub-anesthetic ketamine for perioperative analgesia. J Anaesthesiol Clin Pharmacol [serial online] 2016 [cited 2017 Jun 6];32:160-7

 

Peltoniemi, M.A., Hagelberg, N.M., Olkkola, K.T. et al. Ketamine: A Review of Clinical Pharmacokinetics and Pharmacodynamics in Anesthesia and Pain Therapy. Clin Pharmacokinet (2016) 55: 1059.