Although several attempts have been made to discover the relationship between nerve root pathology and pain in DH, many questions still remained unsolved. Traction, while an accepted method of treatment, has poor results. Stabholz concluded the poor results applied to the techniques, and not to the principles of the traction itself. He introduced some cardinal changes and constructed a new traction device, Vertetrac.”
“The finding of disc herniation (DH)” by Mixter and Barr1 appeared to revolutionize the treatment of low back disorders. Nevertheless, according to the National Center for Health Statistics (USA), the number of disabled people as a result of low back pain (LBP) for the decade 1971 – 1981 was 14-fold greater than the population growth. This is an indication of the extent of unsatisfactory results of treatment and prevention problems related to LBP. The primary requisite for applying suitable treatment and prevention of recurrence is an accurate knowledge of the illness and the cause of pain resulting therefrom. However, despite the recent introduction of sophisticated diagnostic methods such as magnetic resonance imaging (MRI), computerized tomography (CT), CT-discography, infrared-tomography and others that provide us with the ability to evaluate correctly many aspects concerning disorders of disc origin, we are still unaware of the real cause of back pain. One of the most important etiological factors in low back disorders is a degenerative process in the intervertebral discs (ID) that may be very slow and may also cause no pain. However, when this process is constantly aggravated by increase in intradiscal pressure due to mechanical acute or chronic factors, disc lesion is accelerated and subsequently leads to disk herniation (DH). Workers who repeatedly lift 20 kg or more (construction workers, porters, stevedores, hospital workers and farmers), operate machinery causing vibrational insults, drive heavy motor vehicles (bus, truck, tractor), sit incorrectly for prolonged periods, as well as participate in some professional sports, and those with spinal deformities and other problems are at high risk for increase in intradiscal pressure and subsequent DH. An increase in intradiscal pressure is commonly recognized as a cause of initial LBP. This increase proved to be an important factor in the pathogenesis of disc lesions. Lindblom2 and later Hirsch3 proved that lumbar pain could be reproduced by an increase in intradiscal pressure. Nachemson4 explained that an increase in intradiscal pressure leads to gradual loss of normal hydrostatic mechanical behavior of the disc. Subsequently this leads to posterior displacement of the nucleus pulposus (NP), to its impingement on posterior structures of the annulus fibrosus (AF) richly innervated with sensory and sympathetic fibers of the sinuvertebral nerve, and causes pain which is initially concentrated only in the lower back. Further increase of intradiscal pressure causes disc bulging. The degeneration of the disc is already greater and increased hydraulic pressure causes more posterior displacement of the NP and strong pressure on the AF, which begins to bulge and according to Hirsch,3 gives rise to more severe clinical symptoms. Elliot and Schutta5 found that already at this stage there was referred pain similar to that of sciatic pain, but it never radiated below the knee and was never accompanied by neurological deficit, sciatic scoliosis and parestesiae. McCarron et al.6 observed severe LBP that occasionally accompanied leg pain, but was without nerve impingement or neurological deficit as a result of a sharp increase in intradiscal pressure after sudden lifting strain, or other trauma. He coined this disorder internal disc disruption and presumed that it may result from a tear in AF, leakage of NP material and subsequent chemical or immunologic inflammation of the neural sac. The most advanced stage of increased intradiscal pressure causes annular rupture and subsequent extrusion of disc cavity contents and of the AF. The most important, and also most common symptom for this stage is sciatic pain, that is referred in character and beyond this has specific features: mechanical origin and variability. The mechanical character expresses itself by immediate increase in pain with every movement or change in weight-bearing, which proves to be of great importance for treatment. The variability of discomfort is an important consideration in the diagnosis of disc lesions. The severe initial pain may suddenly disappear. This variability can be explained by the possibility that the protruding mass may alter its direct contact with pain-producing tissues: AF, posterior longitudinal ligament, dura mater and nerve roots. Rydevik et al7 have investigated biochemical aspects of nerve root deformation induced by compression. They hypothesized that mechanical nerve fibre deformation may cause functional changes, which may also result in disturbed nerve root microcirculation leading to ischemia, formation of intraneural oedema and axonal transport block–all critical factors for the production of pain, sensory deficit, state of hyperexcitability and motor weakness. In recent years, excellent progress has been made in the chemistry of pain. We know that pain starts as an initial electrical transmission message along peripheral nerves, and later the perception is filled by different neurotransmitters. Also, nociception as a chemical event has been clearly defined. Different investigations identified the dorsal root ganglions as being more important than the nerve roots in the production of sciatica. From endogenous chemical mediators such as serotonin, bradikinin, histamine, acetylcholine, prostaglandins E1, and E2 and leukotrien peripheral receptors in dorsal root ganglions can produce pain. These mediators increase nerve hyperexcitability and this explains why only lumbar nerve roots compressed by lumbar disc herniations are susceptible to mechanical stimuli. However, neural tissues also produce neurogenic inflammatory mediators identified as substance P, somatostatin, cholecystokin, neurotensin, calcitonin gene-related peptide and angiotensin-2. These belong to neurotransmitters and are located in the dorsal root ganglion and produce increased blood flow and vascular permeability, followed by oedema. Body vibration increases their release and thus appears to be an epidemiologic risk factor for LBP and lumbar DH. In addition to the progress achieved in clarification of the peripheral mechanism of pain, central pain modulation has also been better elucidated.
Saal et al8 found the activity of an enzymatic marker for inflammation, i.e., phospholipase A2. In human disc samples removed at surgery it is 100,000-fold greater than normal and authors have speculated whether within the NP this could serve as inflammogenic material. Although several attempts have been made to discover the relationship between nerve root pathology and pain in DH, many questions still remained unresolved. We know that the compression of the nerve root produces numbness, not pain. What then, is the real factor producing pain? What is the cause of chronic pain of the causalgic type after severe pains in longstanding cases? What is the mechanism of relieving pain in major disc protrusions with nerve compression and nerve dysfunction? Why is the CT unchanged in many cases of disc protrusion after successful traction treatment with complete disappearance of all symptoms and signs? Why is the CT scan normal in some clinically-diagnosed DH? Despite the progress achieved in biochemistry, biomechanics and diagnosis, the answers to these questions seem to be more elusive than ever. Traction has been an accepted method of treatment for disc lesions, but the results have been poor. Stabholz9 concluded that the poor results applied to the techniques, and not to the principles of the traction itself. On the basis of daily observations it can be affirmed that an increase in weight loading causes clear aggravation of the existing LBP. Stabholz assumed that the application of opposing force to the weight loading should be exploited in the treatment. He introduced some cardinal changes and constructed a new traction device, labeled, Vertetrac (Figure One). Approximately 10,000 patients with low back disorders of disc origin (56% men and 44% women, aged 17 – 79) were treated by this new traction in different medical centers in the world: in our clinic, at the Wooridul Hospital Spine Loser Clinic in Seoul (South Korea); at the Basildon, Preston Hall and Crawley Hospitals in England; Chicago College and Rehabilitation Sports Clinic of Christensen in Oregon and Washington, USA, and at the University of Orthopaedic studies in Munster, Germany. The success rate of 85% – 90% achieved in these institutions has never been achieved by any other method of DH treatment. The treatment with traction is based on the results from experiments of Mathews and Yates10 and Gupta and Ramarao,11 who found that with epidurography traction exerts negative intradiscal pressure and counter suction. The changes introduced to the traction device by Stabholz9 enabled maximal decrease in intradiscal pressure and maximal increase in suction, and thus enabled successful repositioning of prolapsed parts of the disc to return to its normal position. This was confirmed by CT scanning and the patient’s condition. The great number of recurrences of DH, (65% according to Frymoyer et al12) makes the problem of prevention no less important than the treatment of the illness itself. They felt that we were constantly in the midst of an epidemic of LBP which is still the nemesis of medicine and the albatross of industry. After obtaining very good results in treatment of DH with Vertetrac, we tried to resolve the problem of recurrences. In our study, all patients suffered from DH affirmed by CT or MRI, and were at high risk for increase in intradiscal pressure and subsequent DH. Despite the fact that they were already completely asymptomatic after Vertetrac treatment, all received additional Vertetrac treatment once a week during the first three months and thereafter twice a month during the following three months. By using our method of periodic decrease in intradiscal pressure (deloading) by powerful Vertetrac traction, we succeeded in decreasing recurrence of DH to 8% in patients < 35 years of age, and to almost 0 in patients > 35 years of age. Although these results are based on only one year of follow-up, one can hypothesize that they are the best whenever achieved. The particularly low number of recurrences in people > 35 years of age suggests the possibility of disc lesion healing in these patients. Armstrong13 affirmed the possibility of healing disc lesions by fibrosis. The findings of Hirsch and Schajowitz14 seem to confirm our results. They maintain that fibrosis in ID is only possible after the age of 35 when degenerative changes reach the outer layers of the AF, thus enabling a capillary network to ingrow into an avascular disc substance. It is possible that our method of periodical lumbar spine deloading that frees damaged discs from pressure enables faster and larger growth of blood vessels, mainly into AF, thereby enhancing the development of a solid block of fibrotic scar and healing. We feel that this method should also be recommended for prevention of primary disc lesions, particularly in large industrial centers, work unions, sports associations and other bodies where people are at greatest risk of suffering from ID problems. It would be very important to confirm whether using the method of periodical ID deloading would also decrease the number of primary DH in especially high risk patients. The clinical entity of DH probably is one of the most annoying afflictions of our generation. There is probably no other pathological condition so self-limiting, with the tendency to spontaneous recovery in 80% of cases. The cause is undoubtedly the great variability of the illness. An enormous medical problem is created by 20% of cases who do not have a tendency to spontaneous recovery. All methods for treatment of these cases have proved, until now, to be generally unsatisfactory, and sometimes even worsens the condition. The high rate of recurrence aggravates the problem even further. Although the process of spontaneous recovery, or progress of illness is not well understood, the main reason for failure seems to be that the treatment of cases without a self-healing tendency disregards the pathogenesis of illness, and is directed rather against its symptoms, and not against its cause. It appears that the unique structure of the ID and of spinal nerves are not sufficiently acknowledged as one of the main causes of failure. The ID has always been considered a normal joint, although it is unrelated to joints except for the fact that it permits motion. This is probably the reason why immobilisation provides excellent results in joint lesions, but provides poor results in ID lesions (bed rest, supports). Why does the mechanical overload cause so many problems in the lumbar region, but almost never in ankle joints where it is substantially greater? This example clearly illustrates that the ID operates under different rules of damage and recovery, and therefore treatment and prevention should be adequately adjusted.
Another reason for failure may be the unique structure of the spinal nerves. They have no epineurium which, as we know, resists mechanical pressure. The lack of epineurium enables every mechanical stimulation to immediately contract the vessels and subsequently results in grave complications such as ischemia, defecting nutrition of roots, oedema, compression of venous plexuses and others. Hyper-sensitivity, chemical radiculitis, axonal transport block, obstruction of neurotransmitters, inflammation and fibrosis are complications generally not connected with compression of vessels. Most of these changes are difficult to treat, and our efforts should initially be directed at their prevention. The mechanism of pain, caused by DH, changes with the progress of illness. In the beginning, the pain, sometimes severe and mainly appearing only in the lower back, is caused by the backward displacement of the NP and its compression on the AF. This indicates that pain is clearly of mechanical origin. This is also confirmed by the dramatic relief of pain when freeing the AF from compression with our traction device.
Rupture of AF and compression of herniated parts of the disc on the nerve root does not cause pain. This compression, however, quickly leads to ischemia– a grave and very painful complication. The origin of this pain is also mechanical. The freeing of the roots from compression by way of our traction rapidly restores the normal blood supply and nutrition of roots and thus stops irritation of nociceptors and relieves the pain. However, in prolonged cases with protracted sciatic pain, grave painful complications develop, such as chemical radiculitis, inflammation, oedema, hypersensitivity and others. These complications are already not mechanical in character and therefore the pain cannot be quickly mechanically relieved by traction. Although freeing the disc with these nonmechanical complications from compression by traction may finally help to restore the normal condition, this process is generally extremely slow. On the basis of our experience, early Vertetrac treatment proved to be most important to attain good results (time advantage). Despite the fact that 80% of patients have a tendency to spontaneous recovery independent of the nature of treatment, it is impossible at the outset to differentiate among even mild cases whether they have or do not have this tendency. Thus, we initiate the traction no later than after two days in cases who have been treated during this period by highly recommended bed rest, or other treatment, but have shown no improvement. We do not consider longer bed rest or other applied treatment to be of benefit. Loss of the time factor advantage may lead to unnecessary, grave complications and chronic suffering. The early application of Vertetrac treatment almost always prevented all complications. Prevention proved to be the best cure. As an additional preventive measure we recommend exercises (flexion or extension) according to the physical requirements of each patient. However, only continued traction applied to already asymptomatic patients after DH proved to be the best solution. The present study demonstrates that Vertetrac, the new traction system, provides the best results for treatment of DH and other related low back disorders. This has been affirmed by many medical centers that compared the results achieved by using this method with results achieved by all other methods commonly used. After many investigations concerning pathogenesis of LBP we concluded that the best method for treatment of pain, especially of disc origin, is traction. However, the traction device had to be adapted in order to provide the quickest relief of LBP and sciatica while they are still of mechanical origin. To achieve this, it was necessary to introduce a vertical, upward, thrusting distraction force, greater than that of a weight-bearing force (approximately 40 kg on each side), which frees the ID from compression and enables the extruded parts to slide back into place. This resulted in the immediate complete, or almost complete, disappearance of pain by loss of contact of extruded parts with pain-producing tissue. Without doubt, such a course indicates that the initial origin of pain is clearly mechanical. The best results are attained when the treatment with Vertetrac is initiated as early as possible (time advantage). This also confirms that initially the origin of pain is mechanical. This proved to be the only way to prevent different complications, which are not mechanical in character and their treatment is far more complicated and of long duration. Bed rest, especially prolonged, seemed to have an adverse effect that causes different complications through loss of time. Possibility of movements during treatment with Vertetrac makes development of spinal root adhesions almost impossible and thus eliminating one of the main causes of chronic pain. The possibility of movement greatly increases the flow of nutrients into the disc, that according to Holm and Nachemson15 is very important for normal function of the disc. In our extensive study for prevention of DH recurrences we succeeded in achieving unexpectedly excellent results. The decrease of recurrences to almost 0 in people > 35 years of age by applying intermittent deloading, seems to be possible only by rapid increase of the ingrowth of fibrous tissues into damaged AF, formation of a solid fibrous scar and probable complete healing.
References
1Mixter W. Barr J. Rupture of ID with involvement of the spinal canal. N Eng J Med 1934; 211:210-215.
2Lindblom K. Technic and results of diagnostic disc puncture and injection (discography) in the lumbar region. Acta Orthop Scand 1951; 20:315.
3Hirsch C. Etiology and pathogenesis of low back pain. Isr J Med Sci 1966; 3:362-70.
4Nachemson A. Lumbar intradiscal pressure. Experimental studies on post-mortem material. Acta Orthop Scand 1960; (Suppl) 43:62-72.
5Elliot F. Schutta S. The differential diagnosis of sciatica. Orthop Clin North Am 1971; 2:2.
6McCarron R. Wimpee M, Hudkins P. Larros G. The inflammatory effect of NP. A possible effect in the pathogenesis of LBP. Spine 1987; 12:760-64.
7Rydevik B. Brown M, Lundborg H. Pathoanatomy and pathophysiology of nerve root compression. Spine 1984; 9:7-15.
8Saal JS, Franson R. Dobrow R. Saal JA, White A, Goldthwaite N. High levels of inflammatory phospholipase A2 activity in lumber DH. Spine 1990; 15:674-78.
9Stabholz L. Low back disorders. New York: Vantage Press Inc., 1992 :356.
10Mathews J. Yates D. Preliminary communication. Br Med J 1969; 3:696-97.
11Gupta R. Ramarao S. Epidurography in reduction of lumbar disc prolapse by traction. Arch Phys Med Rehabilit 1978; 59:322.
12Frymoyer J. Pope M, Rosen J. et al. Epidemiologic studies of LBP. Spine 1980; 5:419-23.
13Armstrong J. The clinical picture in lumbar disc lesions. Br J Clin Pract 1966; 20:227-31.
14Hirsch C, Schajowitz F. Studies on structural changes in the lumbar AF. Acta Orthop Scand 1952; 22:184-231.
15Holm S. Nachemson A. Variations in the nutrition of canine ID induced by motion. Spine 1983; 8:866.
[NOTE: Article refers to one figure.]” “Ludwig M. Stabholz, MD, PhD is a 1939 graduate from the faculty of Medicine in Poland. During World War II he worked in the Department of Surgery in the Jewish Hospital and was then appointed as a department head of surgery in the Polish Army Hospital. In 1950 Dr. Stabholz immigrated to Israel and worked as a back disease specialist in both public and private medical institutions. It was during this period he invented the Vertetrac ambulatory traction devise. He is also the author of Low Back Disorders – Innovative Ambulatory Treatment and Self Treatment published by Vantage Press, NY in 1992.
Arieh Grober, MD is a native of Israel who served in the Israeli Army and is a 1977 graduate of Haifa University-Technion Medical School with a specialization in Orthopedic Surgery. Dr. Grober attended Tel-Aviv University from 1982-1986 for post graduate studies and worked as an Orthopedic surgeon in Belinson Hospital. He participates every year in the American Back Society Seminar, A.B.S., and has been a member of Israel Pediatric Orthopedic Society since 1988. Dr. Grober currently operates two private clinics which specialize in spine disorders and low back pain.
