Letters to the Editor
Nonsurgical Treatment of Pain in Lumbar Spine Stenosis
TO THE EDITOR: I am board-certified in family medicine but have been working exclusively in pain management for 10 years. The article by Drs. Hardy and Alvarez on spinal stenosis1 seems to recommend surgery for virtually all cases. I believe this recommendation is inappropriate and misleading.
Spinal stenosis is a chronic condition that is less prone to spontaneous improvement than disc disease. However, a Swedish study documented the remarkable stability of the condition, with only 15 percent of cases progressing in severity, although not seriously, over 49 months.2
The majority of patients with spinal stenosis are elderly at the onset of symptoms, and most will not progress to a severe neurologic deficit within their lifetime. If neurologic deficits develop, the progression is gradual. Therefore, most patients must deal with pain as the primary symptom. In elderly patients, justification of extensive surgery to treat a pain problem demands that other treatments must first be tried. Rarely do patients receive many nonsurgical treatments.
Many patients with symptomatic spinal stenosis are obese with pendulous abdomens, causing hyperlordosis that accentuates the stenosis. Many of these patients improve with weight loss.
As pointed out in the article, the degree of stenosis is poorly correlated with the degree of pain. One reason is that physicians are basing the diagnosis on magnetic resonance imaging rather than taking an adequate history and giving a physical examination. Many elderly patients have weakness of the sacroiliac ligament that generates pain similar to that of spinal stenosis--that is, pain on ambulation and standing. This diagnosis is easily confirmed by injection of local anesthetic. Such patients will respond to ligament prolotherapy.
Epidural administration of corticosteroids is, of course, not curative; however, many patients who receive them experience a prolonged period of relief. If the interval of relief is good--for instance, six months or more--then this treatment is a practical alternative to surgery with its inherent risks.
Patients with a difference in the length of their legs and pain on the side with the longer leg may respond to a lift to correct the shorter leg.
Patients with clearly unilateral symptoms often respond to ligament prolotherapy on the painful side of the body.
Patients with listhesis and/or disc disease that contributes to the stenosis often respond to prolotherapy at that level in the spine.
Physical therapy and chiropractic treatments sometimes provide adequate relief.
Every physician's practice has an inherent selection bias. In a pain management practice, it would appear that surgery rarely helps. Of course, we often see the patients in whom surgery has failed. However, I do believe that the figures presented by Drs. Hardy and Alvarez in their article are overly optimistic. As they point out in the article, decompressive surgery can worsen instability of the spine. As a consequence, the sciatic pain often improves, but the lower back pain often worsens.
In summary, in the absence of any serious neurologic signs, many forms of treatment should be explored before surgery is recommended.
JAMES H. MATTHEWS, M.D.
Pain Management
4725 Transit Rd., Ste. 16
Depew, NY 14043REFERENCES
- Alvarez JA, Hardy RH Jr. Lumbar spine stenosis: a common cause of back and leg pain. Am Fam Physician 1998;57:1825-34.
- Johnsson KE, Rosen I, Uden A. The natural course of lumbar spinal stenosis. Acta Orthop Scand Suppl 1993;251:67-8.
IN REPLY: We appreciate Dr. Matthew's comments in regard to our article on the treatment of lumbar spine stenosis.
Controversy exists among subgroups of clinicians about whether symptomatic lumbar canal stenosis should be managed solely with nonsurgical "conservative methods," or whether all patients should undergo a nonsurgical treatment regimen and be given the option of surgery if the initial therapy fails.
Dr. Matthews stated that so-called weakness of the sacroiliac ligament can mimic the symptoms of neurologic claudication. He suggested that treatments such as "ligament prolotherapy," chiropractic manipulation and corticosteroid injections be offered to patients in lieu of surgical decompression. He did not, however, address the risks or benefits of these treatment modalities or their long-term efficacy (if any) in relieving the symptoms of claudication, nor did he substantiate his claims with data from the existing literature.
We agree that lumbar stenosis and its clinical syndrome may be underdiagnosed, misdiagnosed and, at times, overdiagnosed. Entities such as weakness of the sacroiliac ligament should not be confused with neurologic claudication, since the latter condition presents with classic, almost unmistakable signs and symptoms. It is unfortunate that patients who are misdiagnosed often undergo multiple noninvasive therapies that may provide short-term relief (as stated by Dr. Matthews), yet provide little or no long-term benefit to the patient.
Dr. Matthews commented that he sees many patients in whom surgery has failed; however, he did not specify which types of surgical procedures these patients underwent and for what indications. In a prospective study, Javid and colleagues1 found that 70.8 percent of patients who underwent decompressive laminectomies for stenosis improved postoperatively. The follow-up period was from one to 11 years. Silvers and colleagues2 noted a success rate of 93 percent after surgery for lumbar spine stenosis. Of course, the literature is replete with studies on decompressive surgery with wide-ranging improvement rates. However, most of the recent literature confirms that more than two thirds of symptomatic patients benefit from surgery.
Meticulous adherence to strict surgical criteria is imperative to ensure a good outcome. Back pain should not be the sole criterion used when deciding to operate on a patient with lumbar stenosis. Discogenic or degenerative back pain in patients with or without stenosis is a completely different entity, and the management algorithm, which may include surgical fusion, is different than that for neurogenic claudication.
Failure to differentiate among patients on the basis of their clinical presentation, pathology (e.g., lumbar canal stenosis, discogenic back pain, traumatic instability, spondylolisthesis) and radiologic findings, and thus to make treatment recommendations accordingly, may be why some groups have had such low success rates with surgery. Furthermore, the psychologic and medical profiles of a patient can also significantly influence the surgical outcome. This was demonstrated by Thomas and colleagues,3 who found a statistically significant relationship between the presence of comorbid medical and emotional problems and surgical outcome following decompressive lumbar laminotomies for stenosis. Therefore, the overall medical and biopsychosocial status of the patient should be taken into serious consideration in the presurgical evaluation and, in selected cases, this may influence which patients are optimal candidates for surgery and which patients are not.
As clearly stated in our article, patients with mild leg pain or symptoms of short duration may be offered physical therapy, analgesics or other nonsurgical therapies initially. Morbidly obese patients may indeed improve by following a weight loss program. We feel that while it is reasonable to recommend a nonsurgical treatment regimen initially, patients who present to the primary care provider with unremitting, disabling leg and back pain caused by lumbar canal stenosis with appropriate radiologic correlation should be offered the option of surgical decompression. Surgical management is by far the most effective treatment for this disabling disease and delaying surgery with unproven "therapies" may result in the progression of symptoms and unnecessary prolonged suffering. This is clearly a disservice to our patients.
JAIME ALVAREZ, M.D.
RUSSELL HARDY, JR., M.D.
Department of Neurological Surgery
University Hospitals of Cleveland
11100 Euclid Ave.
Cleveland, OH 44106REFERENCES
- Javid MJ, Hadar EJ. Long-term follow-up review of patients who underwent laminectomy for lumbar stenosis: a prospective study. J Neurosurg 1998;89:1-7.
- Silvers HR, Lewis PJ, Asch HL. Decompressive lumbar laminectomy for spinal stenosis. J Neurosurg 1993;78:695-701.
- Thomas NW, Rea GL, Pikul BK, Mervis LJ, Irsik R, McGregor JM. Quantitative outcomes and radiographic comparisons between laminectomy and laminotomy in the treatment of acquired lumbar stenosis. Neurosurgery 1997;41:567-74.
Over-the-Counter Melatonin Products and Contamination
TO THE EDITOR: The use and efficacy of melatonin have been discussed in American Family Physician in an article by Dr. Cupp.1 This over-the-counter medication is widely used to treat a number of ailments.1,2 Numerous studies have been and continue to be conducted on the value of melatonin in such treatments.2 However, in a reply to a letter to the editor, Dr. Cupp commented that the compound has not been "objectively evaluated in clinical trials involving large numbers of patients."3 This observation is also noteworthy and requires more consideration.
The use of "naturally occurring" alternative medications continues to strike a chord with the American public. The value and efficacy of alternative medications in the treatment of ailments and disease as compared with pharmaceutically derived therapeutics need to be carefully evaluated and tested. Hence, a healthy debate on the use of melatonin clearly must continue.
A separate and more immediate concern is the quality control exercised in the production of compounds such as melatonin. This was obliquely referred to by Dr. Cupp3 but not discussed or developed in any detail. With the advent of the Dietary Supplement Health and Education Act passed by Congress in 1994, the production and purity of such compounds are not directly regulated by the U.S. Food and Drug Administration.
The impact and effect of contaminants that are present in dietary supplements were dramatically highlighted by the outbreak of eosinophilia-myalgia syndrome that occurred in 1989. The outbreak was triggered by the consumption of contaminated L-tryptophan manufactured by Showa Denko K.K. of Japan. Subsequently, researchers at the Centers for Disease Control and Prevention demonstrated that at least six contaminants, namely peaks E, C, FF, UV-5 (also known as PAA), 200 and AAA, were case-implicated compounds.4
More recently, we have characterized the structure of a number of contaminants present in over-the-counter melatonin products.5 We used online high-performance liquid chromatography mass spectrometry to analyze three different samples of melatonin that were commercially available and purchased in the Rochester, Minn., area. Seven different contaminants were detected at the 0.1 to 0.5 percent level of parent melatonin and were presumably formed during the manufacturing process. The most significant finding was that five of the contaminants were melatonin structural analogs of case-implicated contaminants obtained from L-tryptophan made by Showa Denko K.K. In particular, four compounds were melatonin analogs of peak E and another was a melatonin analog of the indoline contaminants peaks C and FF.
It is disturbing that the contaminants found in melatonin are structurally very similar to case-implicated contaminants that were present in L-tryptophan manufactured by Showa Denko K.K. The fact that no cases of disease similar to eosinophilia-myalgia syndrome have been reported, to our knowledge, from patients ingesting melatonin may be due to differences in consumption. A typical daily intake of melatonin for jet lag is approximately 5 mg per day for an average of seven days. In contrast, the daily intake of L-tryptophan in patients who contracted eosinophilia-myalgia syndrome was approximately 500 mg--15 g per day over several months (3 g per day for patients using it as a health food supplement and 3 to 15 g per day for patients under medical supervision).
It is important to note that the efficacy of melatonin is still open to question, but to date there is no indication that the parent compound is, in itself, toxic. However, the presence of such impurities in commercially available melatonin raises serious questions about the possible consequences after long-term consumption, especially when used at doses higher than recommended.
STEPHEN NAYLOR, PH.D.
Director, Biomedical Mass Spectrometry Facility
Department of Biochemistry and Molecular Biology
Mayo Clinic
Rochester, MN 55905GERALD J. GLEICH, M.D.
Department of Immunology and Medicine
Mayo Clinic
Rochester, MNREFERENCES
- Cupp MJ. Melatonin. Am Fam Physician 1997;56: 1421-8.
- Sahelian R. Melatonin: nature's sleeping pill. Marina Del Rey, Calif.: Be Happier Press, 1995:143.
- Sahelian R. Use of melatonin for insomnia [Letter]. Am Fam Physician 1998;57:1783-7.
- Hill RH Jr, Caudill SP, Philen RM, Bailey SL, Flanders WD, Driskell WJ, et al. Contaminants in L-tryptophan associated with eosinophilia myalgia syndrome. Arch Environ Contam Toxicol 1993;25:134-42.
- Williamson BL, Tomlinson AJ, Mishra PK, Gleich GJ, Naylor S. Structural characterization of contaminants found in commercial preparations of melatonin: similarities to case-related compounds from L-tryptophan associated with eosinophilia-myalgia syndrome. Chem Res Toxicol 1998;11:234-40.
IN REPLY: I wish to thank Drs. Naylor and Gleich for their letter concerning the important new information on the purity of melatonin products.
In the article, I mentioned that " . . . contamination of melatonin products by harmful substances is a possibility."1 I also mentioned in the abstract and the patient information handout that the potency and purity of melatonin products cannot be assured. I did not elaborate on these points because at the time, there was no published information available. The potency and purity of melatonin products are certainly important considerations in the evaluation of data on safety and efficacy. Studies of melatonin products that contain either contaminants or more or less than their labeled content cannot be accurately evaluated.
I am unaware of studies that specifically address the potency of melatonin products, but such information from an objective, independent source would be welcomed by many clinicians.
MELANIE CUPP, PHARM.D., BCPS
Department of Clinical Pharmacy
West Virginia University School of Pharmacy
1124 HSN
P.O. Box 9550
Morgantown, WV 26506-9550REFERENCE
- Cupp MJ. Melatonin. Am Fam Physician 1997;56: 1421-8.
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