To the Editor:—

In their case report, Avidan et al. , 1suggested that transient nerve root irritation may be evident in magnetic resonance imaging as an enhancement of the affected nerve roots. Fortunately, their case was apparently transient, although it was not followed with a second magnetic resonance imaging weeks or months later. In figure 1 of Avidan et al. , 1enhancement of nerve roots implies inflammation and edema 2as the contrast media gadolinium is extruded into the extraneural vascular space (endoneurium), probably in the early phase of arachnoradiculitis. 3From this point on, some cases may evolve into the proliferative phase of arachnoiditis with infiltration of fibroblasts and progressively denser collagen forming adhesions, fibrosis, and scarring. 4Why some cases advance and others do not is not yet clear, but Myers and Sommer 3noted that neurotoxic injury to the cauda equina may be patchy because the neurotoxic agent distribution may be uneven, which is also a characteristic distribution of pain and dysesthesia in arachnoiditis. 5 

Enhanced but not abnormally distributed nerve roots, noted in figure 1 of Avidan et al. , 1are seen in the inflammatory stage of arachnoiditis. In contrast, clumped nerve roots, usually abnormally distributed in the thecal sac, shown in figure 2, seen 3 to 7 months after the injurious event, 6may indicate that fibrinous bands and thicker collagen are beginning to develop, forming adhesive and sometimes constrictive arachnoiditis. Matsui et al.  7showed in serial magnetic resonance imaging studies performed every 7 days after laminectomy up to the 49th day that only 20% of the cases with evidence of nerve root enhancement progressed to arachnoiditis.

Obviously, we need to learn more about this phenomenon. Nevertheless, it is important to identify these cases at this point because the duration of the inflammatory period has not yet been defined precisely and because early treatment with nonsteroidal antiinflammatory drugs and corticosteroids may prevent its evolution into the proliferative phase.

Avidan A, Gomori M, Davidson E: Nerve root inflammation demonstrated by magnetic resonance imaging in a patient with transient neurologic symptoms after intrathecal injection of lidocaine. A nesthesiology 2002; 97: 257–8
Johnson CE, Sze G: Benign lumbar arachnoiditis: MR imaging with gadopentetate dimeglumine. AJR Am J Roentgenol 1990; 155: 873–80
Myers RR, Sommer C: Methodology for spinal neurotoxity studies. Reg Anesth 1993; 18: 439–47
Myers RR, Olmaker K: Anatomy of DRG, intrathecal nerve roots and epidural nerves with emphasis on mechanisms of neurotoxicity injury, Spinal Drug Delivery. Edited by Yaksh TL. Amsterdam, Elsevier Science BV, 1999, pp 115–31
Aldrete JA: Clinical diagnosis, Arachnoiditis: The Silent Epidemic, Edited by Aldrete JA. Denver, Future Med, 2000, pp 201–20
Ross JS, Masaryk TJ, Modic MT, Delamater R, Bohlman H, Wilbur G, Kaufman B: MR imaging of lumbar arachnoiditis. AJNR 1987; 8: 885–92
Matsui H, Tsuji H, Kanamori M, Kawaguchi Y, Yudoh K, Futatsuya R: Laminectomy-induced arachnoradiculitis: A postoperative serial MRI study. Neuroradiology 1995; 37: 660–6