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THE LUMBAR SPINAL NERVE ROOT CANALS

THE necessity for exact knowledge of muscle attachmentand lines of action to determine loads on joints, and of thegeometry of joints to design prostheses, has helped to dispelthe notion that gross anatomy is a thing of the past. Not onlydo biomechanical studies of peripheral joints require detailedanatomical knowledge, but so too does understanding of thecauses of back pain. The nerve root syndrome associated withspinal stenosis is an example.2 Papers on this subject,however, tend to use vague terminology such as "hiddenzone", "lateral recess", "lateral canal stenosis", and "laterallumbar nerve root entrapment". Crock3 has lately describedthe relations of the lumbar nerve roots as they passdownwards from the spinal cord through the nerve root canalinto the extravertebral tissue. He has clarified the precisenature of the lumbar spinal nerve root canal-a term whichshould now replace those mentioned above-and argues thatthis will lead to a better understanding of factors which canproduce pressure on the nerve root, such as isolated discresorption, spondylolysis, congenital hypertrophy of thesacroiliac facet, and osteoarthrosis of the lumbar facets.This is particularly true of the effect of isolated disc

resorption, usually at L5/S1,4-9—a condition which has again. been described under various names including chronic disc

degeneration and lumbar spondylosis. There is a correlationepidemiologically between disc space narrowing and backsymptoms, although it is by no means absolute.’° Anarrowing of more than 2 mm in intervertebral disc heightseems to be associated with low back pain in the 5th decade. 11 iObstruction of the nerve root as a major cause of this type ofpain is in keeping with the direct experiments which showedthat impingement of tissue on a spinal nerve is a major causeof low back pain with sciatic radiation.12 Confusion resultswhen writers do not differentiate between low back pain andsciatica.13 Kirkcaldy-Willis and Hills mentioned isolated discresorption only in relation to sciatic pain.An appreciation of the factors contributing to troubles in

the back may help in planning of surgical decompression atthis level. Venner and Crock13 describe a procedure forfenestration and foraminectomy that can be extended toinclude unilateral laminectomy. Their paper might perhapshave emphasised that the nerve root should be followed, andthose tissues compressing it should be removed so long as theposterior joint is left intact. They claimed complete succcessin 62% and partial success in 24%. Other workers prefer discexcision (complete relief of both sciatic and low back pain in

1. Dowson D, Wright V. Introduction to the biomechanics of joints and jointreplacement. London: Mechanical Engineering Publications, 1981.

2. Verbiest H. A radicular syndrome from developmental narrowing of the lumbarvertebral canal. J Bone Joint Surg 1954; 36B: 230-37.

3. Crock HV. Normal and pathological anatomy of lumbar spinal nerve root canals. JBone Joint Surg 1981; 63B: 487-90.

4. Williams PC. Reduced lumbo-sacral joint space: its relation to sciatic irritation. JAMA1932; 99: 1677-82.

5. Crock HV. A reappraisal of intervertebral disc lesions. Med J Aust 1970; i: 983-89.6. Crock HV. Observations on the management of failed spinal operations. J Bone Joint

Surg 1976; 58B: 193-99.7. Macnab I. Backache. Baltimore: Williams and Williams, 1977.8. Burton CV, Heithoff KB, Kirkaldy-Willis W, Ray CD. Computed tomographic

scanning and the lumbar spine. Part II Clinical considerations. Spine 1979; 4:356-68.

9. Lancourt JE, Glenn WV, Wiltse LL. Multiplanar computerised tomography in thenormal spine and in the diagnosis of spinal stenosis: a gross anatomic-computerisedtomographic correlation. Spine 1979; 4: 379-90.

10. Lawrence JS. Rheumatism in populations. London: Heinemann, 1977: 68-97.11. Torgerson WR, Dotter WE. Comparative roentgenographic study of the

assymptomatic and symptomatic lumbar spine. J Bone Joint Surg 1976; 58A:850-53.

12. Smyth MJ, Wright V. Sciatica and the intervertebral disc: an experimental study. JBone Joint Surg 1958; 40A: 1401-18.

13. Venner RM, Crock HV. Clinical studies of isolated disc resorption in the lumbar spine.J Bone Joint Surg 1981; 63B: 491-94.

60%14), posterolateral fusion (72% success rateI5), and

chemonucleolysis (70% favourable response). The results aredifficult to compare because of selection factors and the

imprecise definition of success.

CORTICOSTEROIDS FOR CEREBRAL MALARIA

CEREBRAL malaria-a life-threatening complication ofinfection with Plasmodium falciparum in those with lowimmunity-is caused by the endothelial damage whichaccompanies schizogony (asexual multiplication) of the

parasites in the capillaries of the brain. Its salient featuresinclude fits, disturbances of consciousness, and sometimesfocal neurological signs in a patient with fever andP. falciparum parasites in the blood. Without treatment it isnearly always fatal, and even with effective antimalarial

chemotherapy the case fatality rate may be as high as 20%.Clearly any measure which reduces this mortality should bewelcomed.

Many workers have claimed that corticosteroids, added tothe usual antimalarial regimen, can improve the survivalprospects of patients with cerebral malaria. 1-5 Criticalexamination of these claims soon reveals the weakness of thecase: all the studies were uncontrolled, all involved smallnumbers, and some were complicated by the profusion ofregimens used. The case was unconvincing. It was high time,then, that a good double-blind trial was conducted. But sopervasive was the view that corticosteroids were helpful incerebral malaria that it was difficult to set up an ethicallyacceptable trial. David Warrell and his colleagues inThailand have now reported such atrial, 6 which

incorporated a safety device to detect the supposedly obviousadvantage of corticosteroid, and in that event, a mechanism toterminate the trial promptly.They established the comparability of the dexamethasone

and control groups with great attention to detail. The dose ofdexamethasone was also chosen with care, being on the highside of the acceptable dosage, so anticipating the criticismthat not enough was given to reveal the hoped-for benefit.The antimalarial treatment (with quinine) was the same for allpatients, and reflects the necessity to use this drug in

Thailand, where chloroquine resistance is so common. Theresults of the trial are clear-cut: there is no advantage in givingdexamethasone. The deaths numbered 8 out of 50 in thedexamethasone group and 9 out of 50 in the placebo group.The outcome might well have been less favourable to

dexamethasone had the standard of medical care been lessthan excellent, for serious complications were far morenumerous in the dexamethasone-treated patients. Pneumonia(7 versus 1) and gastrointestinal bleeding (4 versus 0) weresignificantly more frequent with dexamethasone. Anddexamethasone significantly prolonged coma. How

satisfying to see the corpus of ex-cathedra statements on thevalue of corticosteroids laid finally to rest.

14. Spangfort EV. The lumbar disc herniation. Acta Orthopaed Scand; 1972; suppl. 142.15. Stauffer RN, Coventry MB. Postero-lateral lumbar spine fusion: analysis of Mayo

Clinic series. J Bone Joint Surg 1972; 54A: 1195-1204.16. McCullough JA. Chemonucleolysis. J Bone Joint Surg 1977; 59B: 45-52.1. Daroff RB, Deller JJ, Jr, Kastl AJ Jr, Blocker WW Jr. Cerebral malaria. JAMA 1967,

202: 679-82.2. Woodruff AW, Dickinson CT. Use of dexamethasone in cerebral malaria. Br Med J

1968; iii: 31-32.3. Oriscello RG. Cerebral malaria. Br Med J 1968; iii: 617-18.4. Blount RE Jr. Acute falciparum malaria: Field experience with quinine/pyrimethamine

combined therapy. Ann Intern Med 1969; 70: 142-47.5. Smitskamp H, Wolthuis FH. New concepts in treatment of malignant tertian malaria

with cerebral involvement. Br Med J 1971; i: 714-16.6 Warrell DA, Looareesuran S, Warrell MJ, et al. Dexamethasone proves deleterious in

cerebral malaria. N Engl J Med 1982; 306: 313-19.