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January/February 2007
Volume 3, Issue 1
In this Issue:
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Arachnoiditis: Without a Cure
An Original Contribution by Michael S. Slobasky, D.O.
Arachnoiditis is a broad term meaning inflammation of the arachnoid (one of the membranous coverings of the spinal cord). Causes include infections, inflammation, and cancer. Infectious episodes can be caused by bacterial, viral, fungal and parasitic organisms. Noninfectious inflammatory etiologies include surgery, intrathecal hemorrhage, and patients who receive intrathecal injections of contrast, anesthetics, and steroids. Neoplasia (cancer) can lead to arachnoiditis through hematogenous spread of systemic tumors (breast and lung cancer), melanoma, and non-Hodgkin’s lymphoma. Patients who have multiple lumbar punctures, with bloody taps, may also be susceptible.
The differential diagnosis for arachnoiditis includes arachnoid cyst, ependymoma, Hodgkin’s disease of thoracic spine, leptomeningeal carcinomatosis, meningioma of the spine, bacterial meningitis, sarcoidosis, spinal stenosis, spondylodiskitis, and tuberculosis.
Arachnoiditis is primarily a disease of adults, as it may take years for an individual to exhibit symptoms. No race or gender predilection exists. A patient will present with symptoms of low back pain, radicular pain, leg weakness, gait abnormalities, and incontinence. Bizarre sensations, such as insects crawling on the skin or water trickling down the leg, can occur. Muscle cramps, spasms and uncontrolled twitching may also be noted with arachnoiditis.
MRI is the radiologic test of choice to diagnose the disease. CT myelography can be performed for patients in which MRI cannot be done. The images reveal unclear or absent spinal cord outline due to increased signal intensity of the Cerebral Spinal Fluid (CSF). This can be due to an increased protein count in the CSF, inflammatory mediators, or adhesion formation along the spinal cord itself. Myelogram may reveal clumped nerve roots as seen below.
There is no cure for arachnoiditis. Treatment is symptomatic and is designed similar to other chronic pain syndromes. Treatment options include NSAIDS, steroids, antispasmodics, and oftentimes narcotics are necessary. Physical therapy with modalities, such as hydrotherapy, massage and hot/cold treatments can be beneficial. Transcutaneous Electrical Nerve Stimulation (TENS) and spinal cord stimulator implantation has been noted to have a positive effect. Surgery is not recommended as it may cause increased trauma to the already inflamed spinal cord. More research needs to be done for other options regarding treating arachnoiditis.
Preemptive Analgesia
An Original Contribution by James P. Murphy, M.D.
Preemptive analgesia involves giving pain medications prior to an incision or other surgical procedure. It is thought that by preventing pain transmission via peripheral nerves it may prevent sensitization of pain pathways. The theory is that by preventing this sensitization a patient will require less pain medication after the procedure. The concept of administering analgesic medications prior to surgical procedures or “preemptive analgesia” has found limited success in clinical trials. It does, however, continue to hold promise of reducing post-operative pain.
Sensitization of pain pathways involves both peripheral and central mechanisms. Peripheral sensitization involves pain pathways from the site of the incision or pain source to the dorsal root ganglion. Central sensitization involves pain pathways in the spinal cord and brain. Hypersensitivity in the central nervous system may cause pain which persists after the painful stimulus is removed. Peripheral nerves (C fibers), bringing the pain signal to the DRG, can become sensitized to send an increased pain signal to the spinal cord. Other neurons, representing areas surrounding the pain sources, may also begin sending pain signals.
Primary hyperalgesia is pain and increased sensitivity in the region of an injury and secondary hyperalgesia is pain and increased sensitivity in the uninjured area surrounding the site of injury. NMDA (Glutamate) receptors are involved in sending pain signals. Normally, the receptor is blocked by magnesium, however, intense painful stimuli can unblock this receptor allowing an increased pain signal transmission. C fiber stimulation may also lead to changes in the fiber itself, including increased channels and receptors facilitating signal transmission. These changes can persist for months and cause non-painful stimuli to become painful.
Studies have not shown clear evidence for the utility of this type of analgesia, however, it does show promise. Proposed medications for Preemptive analgesia include NSAIDs, Neurontin, intravenous opioids, ketamine and local anesthetics, and epidural analgesia. One of the factors confounding the study of the effectiveness of Preemptive analgesia is the duration of its use. The Preemptive analgesia may wear off while the site of injury is still generating pain, thus allowing it to send the pain signal and cause sensitization. Inflammation following the injury or surgery may also contribute to the sensitization process.
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