Journal of Manipulative and Physiological Therapeutics Volume 23 Number 3 MarcldApdl 2000 76/81105110- Letters to the Editor

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LETTERSTO THE EDITOR

A REVIEWOF BIOMECHANICS OFTHE CENTRALNERVOUI SYSTEM.PARTI: SPINALCANALDEFORMATIONS CAUSED BY CHANGESIN POSTURE To the Editor:
Tile article by. Harrison et al ~ is incomplete and in need of reply. It states that flexion causes an increase in canal diameter and volume as the vertebral lamina are separated and extension causes a small decrease in cana diameter and volume as the vertebral lamina approximated. These changes are cited by H a t ~ u , , et al as a reduction of less than 1.5 mm in extension and a small increase in flexion of approximately 1 mm. These changes are actually much greater than those quoted by Harrison et al. Harrison et al I state they did a literature search of hzdex Medicus to find references for their statements of canal diameter changes during flexion and extension. Many references on this subject that do not agree with their statements by such authors as Schonstrom, Bolander, Finneson, Clark, Yoo, Farmer, Zamani, Wetzel, Onel, Epstein, Liyang, Penning, Wilmink, Schmid, Revel, and Goupille are not cited. I will cite these authors in this letter. Harrison et al ~ state that ligamentum flavum hypertrophy and buckling, along with posterior disk bulging in extension, are not enough to cause compression of the spinal cord or nerve roots in healthy spines. This is true. However, the spines seen for care are rarely normal spines, and factors like disk herniation, ligamentum flavum hypertrophy, endplate hypertrophy, facet imbrication subluxation, degenerative disk disease, and spinal stenosis can be accentuated in extension. Harrison et al I stated that the change from neutral to extension can only narrow the spinal canal sagittal diameter by 1.1 to 1.5 mm but do state that the small difference of 1.5 mm of stenotic reduction in extension would compress the spinal cord and nerve roots in the presence of canal stenosis. Breig is cited as the author validating extension as a method of shortening spinal cord length, with the resultant relief of neural longitudinal stress. This is valid reasoning, but stenotic factors must alter the application of extension motion. Also, I concur that marked flexion is not good to use in stenotic canals with posterior endplate hypertrophy because the anterior cord will be compressed and indented by such pathology. However, most stenotic patients will seek the degree of flexion that affords the greatest sagittal diameter of the spinal

al and thus the greatest relief of neural comression. The dorsal and ventral subarachnoid spaces vary in diameter depending on the degree of flexion and extension. Patients seek the posture that relieves their pain. The dura mater also shows its greatest tissue resistance in longitudinal orientation. 2 Intervertebral foraminal dimensions are admitted by ~arrison et al I to decrease during extension 1 increase during flexion. This is true. Exten~ u . uccreases foraminal size from 20% to 33%. I will present literature citations on the effects of flexion and extension that I feel were very noticeably missing from the article by Harrison et al.

Flexionand ExtensionEffectsin DistractionAdjusting

Flexion-distraction effects are as follows (Fig 1): 1. The posterior disk space increases in height. 3"6 2. Flexion decreases disk protrusion and reduces stenosis. 3-5"7-9 Note that disks protrude and degenerate into the concavity of a curve into the side of extension, io 3. Flexion stretches (tautens) the ligamentum flavum to reduce stenosis. 3,5 4. Flexion opens the vertebral canal by 2 mm (16%) or 3.5 to 6 mm. 8"9 5. Flexion increases metabolite transport into the disk. I i 6. Flexion opens the apophyseal joints and reduces posterior disk stress, it.t2 7. Intradiscal pressure drops under distraction 4 to below-100 mm H g ) 3 On extension, the nucleus or anulus is seen to protrude posteriorly into the vertebral canal. 3,7,14,15 The nucleus pulposus does not move on flexion.~6 8. Intervertebral foraminal openings enlarge, giving patency to the nerve or dorsal root ganglion.12 Extension-distraction effects are as follows (Fig 2): 1. The posterior disk space decreases in height. 3 2. Extension causes disks to protrude, producing stenosis.3.7.9,1o

doi: I 0,1067/mmt.2000.1051 I 0

3. Extension causes the ligamentum flavum to buckle into the vertebral canal, causing stenosis or cauda equina compression. 3 4. Extension causes the vertebral canal to close 2 m m (16%) or 3.5 to 6 mm from flexion, causing stenosis, s.9 5. Extension closes the apophyseal joints and increases posterior disk s t r e s s . 3'12 6. The intradiscal pressure is higher on extension. Nucleus pulposus and anulus fibrosus move posteriorly on extension.3,5,7.12,14,17

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Fig I.

Flexion-distraction effects.

Fig 2. Extension-distraction effects.

Revel et a119confirmed these findings and noted decreased foraminal size in extension caused by posterior bulging of the disks, anterior movements of the ligamentum flava, and decrease of the neural foraminal heights. Compression produced by ordinary weight bearing in an upright neutral position diminishes the diameter and cross-sectional area of the spinal and neural canals. 2 Foraminal stenosis is found to be most pronounced in extension. 2]-23 Zamani et a124 performed magnetic resonance imaging of the lumbar spine in 30 subjects who were imaged in a sitting position while performing flexion and extension. The alterations in the posterior disk margin, the size of the neural foramina, and the size of the central canal were measured. Supine imaging was also done in 15 of the subjects. With extension, there was an increased disk bulge in 27% of the disks (40% of those with desiccation) and decreased central canal size (50%) and foraminal size (27%). Harrison et al] miscited reference 67 as being from Dvorak in the journal S p i n e as stating, "Volume decreases during extension while increasing during flexion, results which are not surprising, do not explain the clinical observation of having more symptoms and signs during flexion (Lhermitte sign) as the authors correctly point out." That reference from S p i n e is an article about neck muscle parameters and is not authored by Dvorak. I can cite Dvorak, 25 however, from another article that is of interest. He states that in acute lumbar disk hemiation, axial manual traction along the body axis may be beneficial by temporarily or permanently relieving the pain and other symptoms. He is against using the high-velocity thrust technique for these cases.

7. Extension causes the intervertebral foraminal openings to close, causing stenosis to the nerve. 12.17 Research articles vividly illustrate the cross-sectional spinal canal and intervertebral foraminal measurement changes in body positions of extension and flexion. 18.19 Twelve asymptomatic volunteers had magnetic resonance imaging examinations of their lumbar spines performed in neutral, flexion, and extension upright studies and supine extended positions. The changes in the spinal and neural canals were as follows: 18 1. The spinal canal cross-sectional diameter was 268 mm 2 in upright flexion and reduced to 224 mm 2 in upright extension, which was a significant change. This was a 16.4% decrease in area. 2. The neural canal cross-sectional area significantly decreased by 23.2% from upright neutral to upright extension and increased by 19.2% from upright neutral to flexion positions. None of these asymptomatic volunteers had nerve root compression in any position. Seven of the 12 volunteers described low-to-moderate discomfort in the upright positions, especially the upright extended position. 3. The ligamentum flavum thickness in upright extension was 4.3 mm, and that in upright flexion was 1.8 mm, which was an increase of over 2.5 mm. The ligamentum flavum buckles during extension because of decreased interlaminar space. 18 4. Significant cross-sectional decrease of the spinal canal occurred in extension. 5. The intervertebral disk bulging narrows the spinal canal during extension. The data suggests that even minor disk bulging extension could cause significant spinal canal narrowing because of the large proportion of the spinal canal border formed by the disk. 6. The factors causing significant decrease of the neural foramen in extension and increase in flexion are that in extension the intervertebral disk bulges posteriorly, the height of the foramen decreases because of compression of the posterior part of the disk and decreasing distance between the pedicles, and the ligamentum flavum may narrow the opening of the neural canal. 7. The combination of ligamentum flava, facet joints, and the intervertebral disk can cause spinal canal stenosis, and all of these factors are accentuated in extension posture. 18

Vertebral Canal Diameter Increasesby 2 to 6 mm With Flexion

Schonstrom et al s report the hypothesis that flexion increases the sagittal diameter of the vertebral canal 16% (2 mm) over extension; the cross-sectional area of the vertebral canal increased 40 mm 2 when moving from extension to flexion. Liyang et al 9 report that the lumbar spinal capacity in flexion-extension lateral myelogram motion studies of 10 cadavers showed a larger capacity of the dural sac in flexion over extension by 3.5 to 6 mm. This increased spinal capacity is highly significant and suggests maintaining the flexed lumbar spine to enlarge the spinal canal capacity and mitigate symptoms.

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Penning and Wilmink t2 show widening of the spinal canal with relief of pain seen in flexion, whereas narrowing of the spinal canal is seen in extension, creating a "pincer effect" of the canal. Ram Gudavalli, PhD, in preliminary unembahned cadaver studies, showed that intervertebral foramen dimensions increased under distraction adjusting as much as 21% in area, 12% in height, and 5% in width during flexion-distraction adjustment at L4-L5. 26 Extension narrows foraminal size. Farmer and Wisneski 27 reported that cervical spine extension significantly increases nerve root pressure to increase radicular symptoms, whereas results with neck flexion were variable. There is a decrease in foraminal size in extension. Yoo et a128reported on the neurotbramen size ofarthritic and herniated nucleus pulposus cervical spines when placed through flexion, extension, and rotation positions; in flexion the foraminal size increased 8% and 10% at 20 to 30 , respectfully. Extension reduced the foramen diameter by 10% and 13 % at 20 and 30 of extension. Two.millimeter change of canal diameter relieves pain. The size of the vertebral canal is also very important because Clark et a129 point out that a 2-mm difference in canal size separates persons with and without back pain. Such narrowing of the vertebral canal can be due to stenosis introduced by discal protrusion, facet hypertrophy, ligamentum flavum hypertrophy, or a combination of such forces. When a nerve root is compressed by these stenotic changes within the neural or vertebral canal, it is important to release the pressure. Extension can increase stenosis and nerve root or dorsal root ganglion compression, and therefore I use axial distraction with adjusting and mobilizing spinal segments. To me, if the nerve is compressed by disk bulge, ligamentum flavum hypertrophy, facet hypertrophy, endplate hypertrophy, subluxatiot~, instability, or a combination of these factors, extension will not release the nerve compression. To relax the spinal cord or nerve roots will only relax them adjacent to the compressions, while the stenosed compressed nerve remains compromised. Imagine a tube in a vice. To relax the part of the tube adjacent to the compressed area will not release pressure on the compressed area. The greater the pathologic changes (disk narrowing, bulging, sequestration, osteophytes, disruption of anular enthesis, fibrosis of the nucleus, longitudinal splits in the nucleus, extension of splits into the anulus, endplate damage, and vascularization), the more likely that pain develops. 3

2. The widened disk space drops intradiscal pressure and probably creates a negative intradiscal pressure that sucks the herniated disk back into place. 3. The anterior and posterior ligaments are stretched under distraction. The posterior longitudinal ligament is stretched and may "push back" the herniated disk toward the disk space. Therefore the herniated nucleus pulposus is reduced by the combination of the lowered intradiscal pressure, sucking the nucleus pulposus back into the disk space, as well as pushing back of the disk by retraction of the posterior longitudinal ligament. 4. The interspinous spaces are seen to increase during distraction, with the ligamentum flavum becoming thinner. It is believed that there is separation of the facet joints and stretching of the posterior longitudinal ligament. Intervertebral disk height increase with distraction adjusting. Our distraction study of a 57-year-old white male unembalmed cadaver showed L5-S 1 disk space to increase by 3 mm and L4-L5 to increase by 1.87 mm. The flexion angle attained during distraction was 6 at L5-S 1 and 3.5 at 14-L5. 49

tigamentum flavum protrudes 2.96 mm to 3.5 mm on extension.

Flexion allows the ligamentum flavum to stretch and decrease its bulging into the vertebral canal, whereas extension causes bulging of the ligamentum flavum into the canal to create stenosis and further nerve root compression (Figs 1 and 2). 3.5 Ten fresh cadavers studied in hyperflexion and hyperextension showed that the ligament was elongated and became thinner in hyperflexion and shortened, thickened, and protruded into the cervical canal in hyperextension (3.5 mm at C5-C6, 3.25 mm at C4-C5, and 2.96 mm at C6-C7). Segmental stenosis was noted at the level of the disk in hyperextension. 5 Flexion improves disk metabolism. Being avascular, the disk receives nutrients from two sources: from the blood vessels in the vertebral bodies and tissue fluid surrounding the anulus fibrosus. Fluid flow into the disk depends on changing pressures within the disk structure. High pressure occurs in compression and weight bearing and forces fluid out of the disk, whereas low pressure, as in lying down, allows fluid to be sucked up by the disk, primarily the nucleus pulposus. Flexion improves the transport of metabolites in the-intervertebral disk, reduces the stresses on the apophyseal joints and on the posterior half of the anulus fibrosus, and gives the spine a high compressive strength. ~! The erect upright posture allows diffusion more readily into the anterior anulus than the posterior anulus. The inner posterior anulus is the most critical area of the disk to be deprived of nutrients; flexion improves transport of metabolites into the inner posterior anulus. 5~ Improving the metabolic transport of the disk is of real value because the supply of glucose tothe disk is barely adequate. 52 Deficient metabolite transport has been linked with degenerative changes in the disk. 53,54 Tilaro 55 states that reducing intradiscal pressure creates a diffusion gradient into the disk, allowing improved nourishment of the nucleus pulposus and reduced lactate levels, l_ntradiscal pressure higher than capillary pressure impedes diffusion and healing.

Flexion Distraction Reduces Disk Protrusion

Many research articles show the reduction of disk protrusion on flexion and distraction.3.5,7.1.l 2,29,31-48 Onel et al 5 reported that 78.5% of medial, 66.6% of posterolateral, and 57% of lateral herniated disks retracted under 45 kg of distraction in 28 of 30 patients studied. Onel et al state the following about distraction of the lumbar disks: I. Static lumbar traction opens the discal spaces and apophyseal joint spaces, reduces the herniated nucleus pulposus, and opens the anatomic structures of the lumbar spine.

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Intradiscal Pressure and Table Motion Versus Duration of Treatment

Table I. Mean intradiscal pressures during the flexion-distraction

~rocedure (disks not pressurized)

Cadaver No. 3 4 5 Pressure in initial prone position (ram Hg) 27 (22) 24 (7) 13(13) -87(37) Pressure in distracted position (mnl Hg) -165 (37) -15 (2) -48(2) -150(11) Decrease in pressure (mm Hg) 192 (37) 39 (3) 61 (12) 63(10)

Joint L3-L4 L2-L3 L3-L4 L4-L5

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Table 2. Mean intradiscal plessures dutqng the low back treatment

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Pressure in initial prone position (mm Hg) 228 228 226 226 240 240 Pressure in distracted position (ram Hg) - 19.5 1250 747 - 151 530 -120

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Duration of Treatment (Secs.)

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Table motion Flexion Extension Right lateral flexion Left lateral flexion Right lateral circumduction Left lateral circumduction

Decrease in pressure (mm Hg) 247.5 1022 521 377 290 360

Fig 3. Intradiscal pressure and table motion versus duration o f

treatment.

What Are the Intradiscal PressureChangeson Distraction? As part of a Chiropractic Demonstrations Projects Grant Program (Health Resources and Services Administration Grant #1 R 18 AH 10001-01A 1) entitled "Biomechanics of Low Back Flexion-Distraction Therapy,''26 which was funded from 1994 to 1997, 5 whole unembalmed cadavers were studied for intradiscal pressure changes during distraction adjusting. The study was a collaborative study between the National College of Chiropractic and the Department of Orthopedic Surgery at the Loyola University Stritch School of Medicine. The results have been presented at the 1997 meeting of the International Society for the Study of the Lumbar Spine 56 and The American Society of Mechanical Engineers in November 199757 by M.R. Gudavalli, PhD, principle investigator. These articles are presently under revision or being written for publication. The intradiscal pressure studies were not a part of the funded study, but they were performed with it. Measurements of intradiscal pressures during distraction adjusting coupled with flexion, extension, lateral flexion, and circumduction motions of the lumbar spine were performed on 5 unembalmed cadavers by placing two miniature pressure transducers into the nucleus pulposus of the L2-L3, L3-L4, and L4-L5 disks. We connected the pressure transducers to a computer through a signal amplifier and analogto-digital converter. We placed the cadavers in a prone position on the flexion-distraction table, which was similar to the positioning for a living patient. The drop in intradiscal pressure with table flexion distraction motion (performed with five 4-second distraction motions of the intervertebral segment) is shown in Fig 3, which also shows the table motion. The drop in intradiscal pressure was 39 mm Hg to 192 mm Hg of negative pressure (Table 1), which was a significant decrease in intradiscal pressure during the flexion-distraction procedure for low back pain. The pressure increased during extension motion of the table. 58

Table 2 and Fig 4 are the intradiscal pressures measured during the movements of flexion, extension, lateral flexion, and circumduction of the facet joints. The pressures have increased during right lateral motion, whereas the pressures have decreased during the left lateral motion. During circumduction, the pressure has decreased during the left lateral and flexion motions, whereas it has increased during the right lateral and flexion combined motions. In all of the motions, the pressures returned to their original values when the spine was brought back t the initial prone position. One of the reasons for the increase and decrease during lateral motions is due to the fact that the transducer was inserted into the right side of the disk, and as pointed out earlier in this article, disks bulge into the concavity of a curve. The results clearly show that the pressures are affected during different motions of the spine associated with the motions of the table. From Table 2 and Fig 4, note that the intradiscal pressure in extension reached 1250 mm Hg, the highest pressure that could be measured on the transducer, meaning an increase of 1022 mm Hg from the neutral position into extension. This is my reason to avoid extension movement in contained disk herniations and the reason that persons with sciatica stand in a flexed, sciatic-type scoliosis position--they seek to lower the intradiscal pressure by means of posture adapation. Ramos and Martin 59 reported on the intradiscal pressure during a vertebral axial decompression procedure performed on 3 patients measured intraoperatively. The results showed that the disk pressures reduced during the vertebral axial decompression therapy. They demonstrated that the disk pressures can go as low as -160 mm Hg. The results of the present study are in general agreement with the study reported by Ramos and Martin. Andersson et al 6 reported the intradiscal pressures at the L3-L4 disk on 4 volunteers dur-

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Letters to the Editor

Intervertebral Disc Pressure Changes During Low Back Trealment Procedures 1400
Extension/Flexion 1200 lOOO

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4. Intela,ertebral disk pressure changes during low back treatment procedures.

ing standing, lying, active traction, and passive traction. The findings showed an increase in the disk pressure during both active and passive traction. The results from the present study do not agree with the results reported by Andersson et al. A possible reason could be that the muscles of the in vivo subjects could have been contracting while under active and passive traction. Work is in progress to monitor the muscle activity during in vivo situations of treating the patients by using flexion-distraction procedures. Ligament loads with distraction adjusting. Gudavalli 61 reported that the ligament loads applied to the lumbar spine during distraction adjusting show less than 50% of their ultimate strength for failure.

REFERENCES
1. Harrison DE, Cailliet R, Harrison DD, Troyanovich SJ, Hardson SO. A review of biomechanics of the central nervous system. Part 1: Spinal canal deformations resulting from changes in posture. J Manipulative Physiol Ther 1999;22:227-34. 2. Runza M, Pietrabissa R, Mantero S, Albani A, Qualglini V, Contro R. Lumbar dura mater biomechanics: experienced characterization and scanning electron microscopy observations. In: Anesthesia and analgesia. Baltimore: Lippincott Williams & Wilkins; 1999. p. 1317-21. 3. Finneson BE Low back pain. Philadelphia: JB Lippincott; 1973. p. 258-9. 4. Burton CV. Gravity lumbar reduction. In: Kirkaldy-Willis WH, editor. Managing low back pain. New York: Churchill Livingstone; 1983. p. 191-8. 5. Oriel D, Tuzlaci M, Sari H, Demir K. Computed tomographic investigation of the effect of traction on lumbar disc herniations. Spine 1989; 14:82-90. 6. Cox JM. Low back pain: mechanism, diagnosis, treatment. Fifth ed. Baltimore: Williams & Wilkins; 1990. p. 437-66. 7. Epstein NE, Hyman RA, Epstein JA, Rosenthal AD. Technical note: "dynamic" MRI scanning of the cervical spine. Spine 1988;13:937-8. 8. Schonstrom N, Linciahl S, Wilen J, Hansson T. Dynamic changes in dimensions of the lumbar spinal canal: an experimental study in vitro. J Orthop Res 1989;7:115-21. 9. Liyang Dai, Yinkan X, Wenming Z, Zhihua Z. The effect of flexion-extension motion of the lumbar spine on the capacity of the spinal cord. Spine 1989; 14:523-5. 10. Lindbolm K. Intervertebral disc degeneration considered as a pressure atrophy. J Bone Joint Surg Am 1957;39A:933-4. 11. Adams MA, HuttonWC. The effect of posture on the lumbar spine. J Bone Joint Surg Br 1985;67B:625-9. 12. Penning L, Wilmink JT. Posture dependent bilateral compression of L4 on L5 nerve roots in facet hypertrophy: a dynamic CT-myelographic study [abstract]. Spine 1987;12:488. 13. Ramos G, Martin W. Effects of vertebral axial decompression on intradiscal pressure. J Neurosurg 1994;81:350-3. 14. Gill K, Videman T, Shimizu T, Mooney V. The effect of repeated extensions on the discographic dye patterns in cadaverie lumbar motion segments. Clin Biomech 1987;2:205,10. 15. Seroussi RE, Krag MH, Muller DL, Pope MH. Internal deformations of intact and denulceated human lumbar discs Subjected to compression, flexion, a n d e x t e n s i o n loads. J O~rthopRes 1989;7:122-31.

Summation
Finally, extension is questioned in treating low back pain. A study showed that spinal manipulation and an ongoing flexion and extension exercise program resulted in more rapid resolution of symptoms and improvement in functional limitations than an established extension program alone. 62 Other well-done articles 6366 question the extension principles cited by Harrison et al.I This does not mean extension posturing is not helpful but rather that it is part of therapy. The same is true of flexion posturing--it is not the total answer for back pain but offers a significant benefit to be used by the practicing chiropractor in the daily care of patients. Rather than only being a 1- to 1.5-mm change in the sagittal diameter of the spinal canal and intervertebral foramen in extension motion, as stated by Harrison et al, ! the articles cited in this reply show that the combined narrowing in extension by the disk herniation, ligamentum flaval hypertrophy, and buckling can approach 10 mm. These true changes in canal diameter on motion demand therapeutic consideration and demand patient tolerance testing before flexion or extension adjusting is undertaken. James M. Cox, DC, DACBR 3125 Hobson Road Fort Wayne, IN 46805

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16. Vanharanta H, Ohnmeiss D. Stith W, Rashbaum R, Hochschuler S, Guyer R. et al. Effect of repeated trunk extension and flexion movements as seen by CT/Discography [abstract]. Ortho Tran 1989;13:28. 17. Adams M, Dolan P, Hutton W. The lumbar spine in backward bending [abstract]. Spine 1988; 13:1019. 18. Schmid MR, Stucki G, Duewell S. Wildermuth S, Romanowski B, Hodler J. Changes in cross-sectional measurements of the spinal canal and intervertebral foramina as a function of a body position: in vivo studies on an open-configuration MR system. AJRAm J Roentgenol 1999;172:1095-102. 19. Revel M, Mayoux-Benhamou MA. Aaranon C, Amor B. Morphological variations of the lumbar foramina during flexion-extension and disc collapse. Rev Rhum Mal Osteoartic 1988;55:361-6. 20. Nowicki BH, Yu S, Reinartz J, Pintar F, Yoganandan N, Haughton VM. Effect of axial loading on neural foramina and nerve roots in the lumbar spine. Radiology 1990;176:433-7. 21. Nowicki BH, Haugbton VM, Schmidt TA, Lim TH, An HS, Riley LH 3rd, et al. Occult lumbar lateral spinal stenosis in neural foramina subjected to physiologic loading. AJNR Am J Neuroradiol 1996;17:1605-14. 22. Sortland O, Mangnaes B, Hauge T. Functional myelography with metrizamide in the diagnosis of lumbar spinal stenosis. Acta Radiol 1977;355(Suppl):42-54. 23. Amundsen T, Weber H, Lilleas F, Nordal HJ, Aabdelnoor M, Magnaes B. Lumbar spinal stenosis: clinical and radiologic features. Spine 1995;20:1178-6. 24. Zamani AA, Moriarty T, Hsu L, Winalski CS, Schaffer JL, Isbister H, et al. Functional MRI of the lumbar spine in erect position in a superconducting open-configuration MR system: preliminary results. J Magn Reson Imaging 1998;8:1329-33. 25. Dvorak J. Inappropriate indications and contraindications for manual therapy. J Manual Med 1991 ;6:85-8. 26. Gudavalli MR. Biomechanics of low back flexion-distraction therapy, Chiropractic Demonstrations Projects Grant ProgramFiscal year 1997 Grants. Health Resources and Services Administration; 1997. Grant No. 1 R18 AH10001-01A1. In press. 27. Farmer JC, Wisneski RJ. Cervical spine nerve root compression. Spine 1994;19:1850-5. 28. Yoo JR, Zou D, Edwards WT, Bayley J, Yuan HA. Effect of cervical spine motion on the neuroforaminal dimensions of human cervical spines. Spine 1992; 17:1131-6. 29. Clark GA, Panjabi MM, Wetzel FT. Can infant malnutrition cause adult vertebral stenosis? Spine 1985; I 0:165-70. 30. Goupille P, Jayson MIV, Hoyland JA, Valat MP, Freemont AJ. Association between increased extend and multilevel lesions with low back pain: a cadavaric study [abstract]. Arthritis Rheum 1998;41:343. 31. White AA, Panjabi MM. Clinical biomechanics of the spine. Philadelphia: JB Lippincott; 1978. p. 7. 32. Brown T, Hansen R, Yorra A. Some mechanical tests on the lumbosacral spine with particular reference to the intervertebral discs. J Bone Joint Surg Am 1957;39A: 1135-62. 33. Schlegel JD, Champine J, Taylor MS, Watson JT, Champine M, Schleusener RL, et al. The role of distraction in improving the space available in the lumbar stenotic canal and foramen. Spine 1994;19:2041-7. 34. Quellette JP. Low back pain: an orthopedic medicine approach. Can Fam Physician 1987;33:639-4. 35. Stephens MM, O'Brien JP. The morphological changes in the lumbar intervertebral foramina in normal and abnormal motion segments after distraction [abstract]. Ann R Coil Surg Engl 1986;68:4. 36. Awad EA. Effects of pelvic traction on the intervertebral disc [abstract]. Arch Phys Med Rehabil 1988;69:785.

37. Gillstrom P, Ericson K, Hindmarsh T. Cornputed tomography examination of the influence of autotraction on herniation of the lumbar disc. Arch Orthop Trauma Surg 1985; 104:289-93. 38. Cox JM, Aspegren DD. A hypothesis introducing a new calculation for discal reduction: emphasis on stenotic factors aJld manipulative treatment. J Manipulative Physiol Ther 1987; 10:287-94. 39. Kessler RM. Acute symptomatic disk prolapse. Phys Ther 1979;59:978-87. 40. Cyriax J. Textbook of orthopedic medicine. 8th ed. London: Bailliere Tindall: 1982. p. 315-16. 41. Calliette R. Low back syndrome. 3rd ed. Philadelphia: Davis; 1981. 42. Wyke BD. Neurological aspects of low back pain. In: Jayson M, ed. The lumbar spine and back pain. London: Sector Publishing; 1976. p. 189-256. 43. DeSeze S, Levernieux J. Les tractions vertebrales. Premiers etude experimentales et resultats therapeutiques d'apres un experience de quatre annees [abstract]. Semaine ole hospitales Paris 1951 ;27:2085. 44. Mathews JA, Yates DAH. Treatment of sciatica [abstract]. Lancet 1974;1:352. 45. Neugebauer J. Re-establishing of the intervertebral disc by decompression [abstract]. Med Welt 1976;27:19. 46. Tien-You F. Lumbar intervertebral disc protrusion, new method of management and its theoretical basis. Chin Med J (Engl) 1976; I : 183-94. 47. Kramer J. Intervertebral disc diseases: causes, diagnosis, treatment, and prophylaxis. Chicago: Year Book Publishers: 1981. p. 164-6. 48. Yefu L, Jixiang E Zuliang L, Zhenqian L. Traction and manipulative reduction for the treatment of protrusion of lumbar intervertebral disc--an analysis of 1,455 cases. J Tradit Chin Med 1986;6:31-3. 49. Pilot project reported in biomechanics of low back flexion-distraction therapy. Chiropractic Demonstrations Projects Grant Program--Fiscal year 1997 Grants. Health Resources and Services Administration. Grant No. 1 R18 AH10001-01AI. In press. 50. Lian-shun J, Quiang S, De-yu C, Wen-ming Z. Dynamic changes of cervical ligamental flavum in hyperextensionhyperflexion movement and their measurements. Chin Med J 1990; 103:66-70. 51. Nachemson AL. The lumbar spine: an orthopedic challenge. Spine 1976; 1:59-71. 52. Maroudas A, Stockwell RA, Nachamson A, Urban J. Factors involved in the nutrition of the human lumbar intervertebral disc; cellularity and diffusion of glucose in vitro. J Anat 1975;120:113-30. 53. Nachemson AL, Lewin T, Maroudas A, Freeman MAR. In vitro diffusion of dye through the end plates and the anulus fibrosus of human intervertebral discs. Acta Orthop Scand 1970;41:589-607. 54. Holm S, Nachemson A. Nutritional changes in the canine intervertebral disc after spinal fusion. Clin Orthop 1982; 169:234-58. 55. Tilaro F. An overview of vertebral axial decompression. Can J Clin Med 1998. 56. Gudavalli MR, Cox JM, Baker JA, Cramer GD, Patwardhan AG. Intervertebral disc pressure changes during the flexiondistraction procedure for low back pain. International Society for the Study of the Lumbar Spine; 1997. 57. Gudavalli MR, Cox JM, Baker GD, Cramer GD, Patwardhan AG. Intervertebral disc pressure changes during a chiropractic procedure. Dallas [TX]: American Society of Mechanical Engineers; 1997. 58. Gudavalli MR, Cox JM, Baker JM, Cramer GC, Patwardhan AG. Intervertebral disc pressure changes during a chiropractic procedure. Adv Bioengineering 1997;36:215-6.

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Letters to the Editor

59. Ramos G, Martin W. Effects of vertebral axial decompression on intradiscal pressure. J Neurosurg 1994:81:350-3. 60. Andersson GBJ, Schultz AB, Nachemson AL. Intervertebral disc pressures during traction. Scand J Rehabil 1983;9(Suppl):88-91. 61. Gudavalli MR. Biomechanics research on flexion-distraction procedure. In: Gudavalli MR, editor.Low back pain: mechanism, diagnosis, and treatment. 6th ed. Philadelphia: Williams & Wilkins: 1999. p. 269-71. 62. Erhard RE. Delitto A, Cibulka MT. Relative effectiveness of an extension program and a combined program of manipulation and flexion and extension exercises in patients with acute low back syndrome. Phys Ther 1994;74:1093- 100. 63. Riddle D. McKenzie system: popular but how reliable? Backletter 1992;7:1-2. 64. Fernando CK. Letter to the editor, Spine 1991 ; 16:1008. 65. Riddle DL. Rothstein JM. Intertester reliability of McKenzie's classification-of the syndrome types present in patients with low back pain. Spine 1993;18:1333-44. 66. Beattie PF. Brooks WM, Rothstein JM. Sibbitt WL Jr. Robergs R.A, MacLean T, et al. Effect of lordosis on the position of the nucleus pulposus in supine subjects: a study using MRI. Spine 1994; 19:2096-102.

In Response:
Thank you for allowing us to respond to Dr Cox's letter to the editor concerning our recent review article concerning spinal canal deformations published in J M P T . J After going into a long review of disk herniations, which had nothing to do with our original paper, Dr Cox wants to validate flexion as a treatment for low back pain. Dr Cox's whole letter concerns canal stenosis. We specifically stated that we reviewed canal deformations in the absence of stenosis, as the following quote indicates: "We do not deny the clinical significance of this issue, nor do we intend to minimize it. However, we believe that an equally important issue, and more prevalent, has typically been under appreciated by many clinicians and researchers. This issue being neural tissue stress and strain in the absence of stenotic conditions. Since stenotic canals are present in only a minority of individuals, we feel that the latter condition may encompass a larger volume of patients and neurologic conditions. This is because altered alignment of upright posture, viewed as rotations and translations in three dimensions, and poor ergonomics are relatively common place among todays patient populations. This review is presented with emphasis on this position. 'q First, Dr Cox would have us believe that the vast majority of our patients have nerve root compression and canal stenosis, when in fact these patients represent less than 5% of patients coming to health care providers w.ith low back pain (notwithstanding neck pain, thoracic pain, headache, and other diseases). 2'3 "Pure osteoligamentous lateral stenosis is a fairly uncommon condition. ''4 Thus 95% of the patients that we clinicians take care of have neither IVF encroachment nor canal stenosis as a cause of their complaints. Second, we presented a review of canal deformation in the whole spine, whereas D r Cox would like to restrict us to the lumbar spine only. He cited articles on lumbar disk bulging, disk rupture, and ligamenta flava ossification (OLF). Before addressing some of his lumbar studies, we note that it is good that he restricts himself to the lumbar area because cervical

and thoracic disk rupture, disk bulging, and OLF are rare. The cervical disk anatomy is completely different from the lumbar disk anatomy, 5 and cervical disk herniation occurs only in traumatic rupture. ~' Ossification of the thoracic ligamenta flava is very rare. 7 Thoracic disk ruptures are rare s and account for only 1% of all intervertebral disks treated surgically. 9 In flexion-extension the thoracic cage moves as if it is one rigid body. In Cervical OLF is also rare, and even when present on computed tomography scans, it only compresses the cord in a small percentage of cases in hyperextension. Houser et al II evaluated 93 patients with cervical spondylotic stenosis and associated myelopathy by using computed tomographic myelography. Hypertrophy of the ligamentum flavum was present in 25% of the subjects. However, they reported displacement of the posterior spinal cord in hyperextension in only two cases. This study suggests that approximately 2% of individuals with canal stenosis or 8% of individuals with hypertrophy of the ligamentum flavum might have an abnormal cord compression during cervical hyperextension. In a study of 997 Japanese subjects (age range, 15-79 years), cervical ossification of the posterior longitudinal ligament only occurred in 2.1% of the subjects.12 Concerning stenosis in the lumbar spine, compression of the cauda eqina can be caused by thickened posterior vertebral elements, facet joints, marginal osteophytes, or soft tissue structures. J3 The spinal cord ends at approximately L1, and the cauda equina occupies the lumbar canal below that level. Stenosis of the lumbar spine most commonly affects the middle-aged and elderly populations.13 "In typical forms of degenerative stenosis, the disk is not involved in neural compression. ''4 Because preferred medical treatment for the symptomatic lumbar stenosis is usually surgical decompression, Dr Cox's technique might offer an important alternative in such cases but not if any anterospondylolisthesis is present. However, another important conservative alternative when the stenosis is caused by disk bulge or rupture is a lumbar torsion manipulation. Lumbar torsion manipulations have been shown to immediately reduce painful disk lesions in 50% to 80% of patients with ruptured disks.~4"la The required equipment for lumbar torsion manipulation (low back bench) is very cost effective compared with a flexion-distraction table. Flexion, specifically prolonged flexion, is bad for the spine, especially in pathologic conditions. Indeed, Dr Cox has ignored 40 years of texts by Alf Breig, 19"2~Breig's Index M e d i c u s articles, 22"3 and literature that supports Breig's findings. 3j-47 Also, we note that extension movements have been shown to centralize pain in the McKenzie methods protocols. 4s'61 The fundamental flaw in avoiding extension because of the minute changes in spinal canal diameter in extension (usually 1-2 mm) was recently discussed by Dvorak. 62 He noted that flexion increases and extension reduces pain in most subjects. Dr Cox cites hyperextension articles for bad effects, when "slight" extension means lordosis and is the preferred position of the lumbar spine. Most studies on canal diameter changes during flexion, extension neglect the fact that only extension relaxes the