Disc Herniation Size vs. Symptoms

Introduction | Other Sciatica Pain Mechanisms | The Study | Results | MRI Results | Points of Interest | Downfalls | Good Quotes | Acknowledgments |

Karppinen J. et al. “Severity of Symptoms and Signs in Relation to Magnetic Resonance Imaging Findings Among Sciatic Patients.” Spine 2001 ;26(7):E149-E154

INTRODUCTION:

Traditionally it had been thought that the size of the disc herniation and amount of nerve root compression are directly related to the magnitude of patient pain and disability (26-28); however, there is now conclusive evidence that this may not be the case (1,18).

In 2001, Karppinen et al. published an investigation that demonstrated neither the size of a patient's disc herniation nor the degree of nerve root compression correlated with the magnitude of the patients subjective pain or level of functional disability. Or in plain english, bigger and more compressive disc herniations do not create proportionally stronger pain and disability when compared to smaller non-compressive disc bulges--there is no correlation between size, compression, and patient pain.

In that same investigation, was discovered that 20% of the sciatica-suffering patients had no compressive disc disc herniation of any kind on MRI, despite the fact that they were suffering moderate to severe sciatic pain and disability. Amazingly, more than one-half of those non-herniation patients suffered classic radicular pain (62%), in the absents of nerve root compression!

That information begs the question, "if nothing was compressing the nerve roots, then how could these patients be suffering real nerve-root related radicular pain? In response the author stated, "pain mechanisms other than the extent of disc herniation ... generate the subjective symptoms among sciatic patients."

Other Possible Pain Mechanisms which may Generate Sciatica:

One possible explanation for this bizarre finding was put forth by both Ohnmeiss et al. (19,20) and Milette et al. (21) These investigators experimentally demonstrated that disruptions within the substance of the disc (annular tears) not only caused low back pain, but it also caused ‘referred pain’ into the lower limb; we may call this referred lower limb pain ‘discogenic sciatica’.   [Ohnmeiss Paper & Milette Paper]

Another explanation is based upon the investigations of Olmarker et al.   This group has repeatedly demonstrated that the application of nucleus pulposus upon the spinal nerve root can create marked morphological change (axon damage) and functional change (decreased conduction speed) to the micro-anatomy of that nerve root, as well as cause ‘pain-related behaviors’ to occur within the test animals (90-95).  

Therefore, if this nucleus pulposus get ‘loose’ in the epidural space (most likely from a grade 5 posterior annular disc tear), it may well cause the pathological spinal nerve root changes described by Olmarker (90-95) and result in a painful sciatica syndrome without nerve root compression.   Researchers have termed this phenomenon “Chemical Radiculopathy” (257,285).

The final theory on non-compression induced sciatica implicates the activation of the patient's own immune system against the nucleus pulposus-soaked nerve root (30, 31). This ‘auto-immune’ type reaction may help perpetuate the syndrome of chronic sciatic pain.

Whatever the cause, it is clear that non-compressive disc defects (bulges and contained herniations) are just as painful and disabling as the classic large compressive disc herniation.   Therefore the symptoms of sciatic pain without disc herniation on MRI should not be simply dismissed by the doctor.  

The Study:

In year two-thousand, 160 consecutive acute sciatica patients were gathered for an investigation.   The objective of this study was to determine whether or not the patient’s perceived-pain and level of disability were related to the degree of disc displacement on MRI, i.e., the size of their disc herniation.

All of the patients suffered a major complaint of unilateral sciatica that traveled downward from the low back, past the knee, and into the leg. The average patient age was 43.7 years, and the average duration of the sciatica was 2 months.   There were no outcomes reported as part of the study.

All patients underwent a contrast-enhanced MRI, EMG testing, and a thorough Physical examination.   The physical examination included range-of-motion testing, the straight leg raise test, dermatome testing, and “root-specific testing,” which was defined as follows: L4 = diminished Patellar Reflex, L5 = diminished great toe dorsiflexion power and S1 = diminished Achilles’ Reflex.

The patients were next put through some standard self-assessment testing.   These tests included the Visual Analogue Scale (VAS), the Oswestry Low Back Disability Questionnaire (6), and patient-completed pain drawings.  

MRI interpretations were done by two radiologists who were blinded to the study.   Any disagreements on the classification of disc displacement were settled between then.   Over-all, their agreement were excellent and the only disagreements concerned the difference between contained versus noncontained herniations (this did not affect the results of the study).

The following classification system was used to differentiate the degree of disc displacement:

The radiologists also categorized the amount of ‘nerve root compression’.   The categories were none (no compression of the root at all), minor (dislocation of the nerve root by disc herniation), or major (compression of the nerve root by the disc herniation against the bony structures of the vertebrae).

Exclusions:

The following patients-conditions were excluded from this investigation:

1) Stenosis.

2) Non-degenerative spondylolisthesis.

3) Pending applications for early-retirement. (I like this one!)

4) Clinical depression.

5) Prior back surgery.

6) Complaints of Low Back Pain being greater than Leg Pain.

7) Rare causes of sciatica. (Synovial cysts, tumors, etc.)

RESULTS:

DISC DISPLACEMENT versus PATIENT EXAM FINDINGS & SYMPTOMS:

MAIN POINTS OF INTEREST:

GOOD QUOTES FROM THE AUTHORS:

DOWNFALLS:

Print error: I was horrified to learn that Spine had published this paper despite it containing a rather large error. I spotted it immediately and contacted the author: Thankfully I receive an e-mail from the author who stated that not all patients had positive EMGs for radiculopathy, as was stated on page E151 under the heading “Characteristics of the Study Population”. More explicitly, in the sentence, “Five patients had L4, 89 had L5, and 66 had S1 radiculopathy.” the word “radiculopathy” should have been “radicular pain”.   Which cleared up that issue but creates another, for now it appears all of the patients had “radicular pain”, but the results-table states that only 140/160 had radicular pain?  Is anyone proofing these investigations for content over at Spine???

Acknowledgements:

I would like to thank Dr. Karppinen MD for taking the time out of his busy schedule to answer my barrage of e-mail questions about his investigation. He graciously answered everything that was asked which certainly added to the quality of my review.

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References:

1) Karppinen J. et al. “Severity of Symptoms and Signs in Relation to Magnetic Resonance Imaging Findings Among Sciatic Patients.” Spine 2001 ;26(7):E149-E154

2) Errico TJ, et al. “Open discectomy as treatment for herniated nucleus pulposus of the lumbar spine” Spine 1995 ;20:1829-33.

[3] Lurie, JK.   ‘Point of View’:E154 IN: Karppinen J. et al. “Severity of Symptoms and Signs in Relation to Magnetic Resonance Imaging Findings Among Sciatic Patients.” Spine 2001 ;26(7):E149-E154

6) Fairbanks JC, et al. "The Oswestry low back pain disability questionnaire". Physiotherapy 1980;66:271-273

12) Hasue M. “Pain and the nerve root: An interdisciplinary approach.” Spine 1993 ;18:2053-2058

15) Jonsson B, Stromqvist B. “The straight leg raising test and the severity of symptoms in lumbar disc herniation. A preoperative evaluation.” Spine 1995 ;20:27-30

18) Modic MT, et al. “Contrast-enhanced MR imaging in acute lumbar radiculopathy: a pilot study of the natural history.” Radiology 1995 ;195:429-35

19) Ohnmeiss DD, et al. "Degree of disc disruption and lower extremity pain" Spine 1997; 22(14):1600-1605

20) Ohnmeiss DD, et al. "Relation between pain location and disc pathology: a study of pain drawings and CT/discography." Clin J Pain 1999 ;15:210-7.

21) Milette PC, et al. “Radiating Pain to the Lower Extremities Caused by Lumbar Disk Rupture without Spinal Nerve Root Involvement.” AJNR Am J Neuroradiol 1995; 16:1605-1613

22) Olmarker K, Rydevik B, Nordborg C. “Autologous nucleus pulposus induces neurophysiologic and histologic changes in porcine cauda equina nerve roots.” Spine 1993 ;18:1425-32.

25) Thelander U, et al. “Straight leg raising test versus radiologic size, shape, and position of lumbar disc hernias.” Spine 1992 ;17:395-9

26) Thelander U, et al. “Describing the size of lumbar disc herniations using computed tomography. A comparison of different size index calculations and their relation to sciatica.” Spine 1994 ;19:1979-84.

27) Monteiro A et al. “lateral decompression of a pathological disc in the treatment of lumbar pain & sciatica.” Clin Orthop 1989; 56-63

28) Schreiber A, et al. “Does percutaneous nucleotomy with discoscopy replace conventional discectomy? Eight years of experience and results in treatment of herniated lumbar disc.” Clin Orthop 1989; 35-42

29) van Akkerveeken PF.   “Pain patterns and diagnostic blocks.” In: Wiesel SW, Weinstein JN, Herkowitz H, eds.   The Lumbar Spine. Philadelphia: W.B. Saunders Company, 1996:105-22.

30) Brisby H, Rydevik B, et al. " Glycosphingolipid antibodies in serum in patients with sciatica." Spine 2002 ;27(4):380-6.

31) Chacur M, et al. "A new model of sciatic inflammatory neuritis (SIN): induction of unilateral and bilateral mechanical allodynia following acute unilateral peri-sciatic immune activation in rats." Pain 2001 ;94(3):231-44.

90) Olmarker K, Rydevik B, et al. “Autologous nucleus pulposus induced neurophysiologic and histologic changes in porcine cauda equina nerve roots.” Spine 1993; 18:1425-32

91) Olmarker K, Rydevik B, et al. “ Ultrastructural changes in spinal nerve roots induced by autologous nucleus pulposus.” Spine 1996; 21:411-4

92) Olmarker K, et al. “Inflammatory properties of nucleus pulposus.” Spine 1995; 20:665-9

93) kayama S, Olmarker K, et al. “Incision of the annulus fibrosus induces nerve root morphological, vascular and functional changes: an experimental study.” Spine 1996; 21:2539-43

94) Olmarker K, Brisby H, et al. “The effects of normal, frozen and hyaluronidase-digested nucleus pulposus on nerve root structure and function.” Spine 1997; 22:471-5

95) Olmarker K, Larsson K. “Tumor necrosis factor alpha, and nucleus-pulposus-induced nerve root injury.” Spine 1998; 23:2538-2544

257) Marshall LL, et al. “Chemical irritation of nerve root in disc prolapse.” Lancet 1973; 2:320

258) Marshall LL, et al. “Chemical Radiculitis: A clinical, physiological and immunological study. Clin Orthop 129:61-67, 1977