September 01, 2006
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Oral nimodipine improves lumbar IVD diffusion up to 11%

The drug might prove to be a degenerative disc treatment once proper dosages are identified.

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BERGEN, Norway — Researchers exploring the potential of oral nimodipine to increase lumbar endplate hypervascularity and disc diffusion found that the calcium channel blocker improves diffusion and is safe.

Clinicians can use diffusion studies to noninvasively assess the condition of intervertebral discs and endplates, said lead investigator S. Rajasekaran, MD, from Coimbatore, India.

"Other [researchers] determined calcium channel blockers had a positive effect on endplate vascularity in rats through histological analysis," he said. But Rajasekaran's prospective study was the first to demonstrate that a calcium channel blocker significantly increased the sequential-type of diffusion in human intervertebral discs (IVD).

He presented results at the International Society for the Study of the Lumbar Spine 33rd Annual Meeting, here.

Rajasekaran and colleagues based their findings on serial postcontrast MRI analyses and proved human IVD diffusion starts in the subchondral bone, extends to the peripheral nucleus pulposus (NP) and then to the central NP.

They studied 40 lumbar endplates, 10 each from four men who did not smoke or have a history of low back pain. Researchers first determined each endplate's normal diffusion level via baseline and sequential midline T1-weighted sagittal MRIs, with and without contrast (0.3 mmol/kg of gadodimide), at intervals of 10 minutes and 2, 4, 6, 12 and 24 hours.

After waiting 10 days for the gadodimide to wash out, volunteers took oral nimodipine on 5 consecutive days (30 mg QID). Investigators repeated that same imaging sequences at the same intervals previously used.

They analyzed the MRIs to determine differences in signal intensity for each endplate, looking closely at such areas of interest as the subchondral bone, endplate region, and peripheral, inferior and central portions of the NP.

"In the subchondral bone, it is obvious that signal intensity at maximum was obtained at 10 minutes, which is actually in the vascular phase," Rajasekaran said. Intensity increased by 15 units (8%), which was statistically significant.

Signal intensity increased in the endplate zone by 6.8 units.

"In the peripheral NP, we found that the increase maximum was obtained at 12 hours (8.9%). ... Most important, in the center of the NP, the maximum was obtained at 12 hours and an 11% increase in diffusion was obtained."

The sequential diffusion seen ranging from 8% in the subchondral bone leading to 11% in the central NP showed that if "there is a problem with increased vascularity and diffusion, this would account for it."

Rajasekaran reported no side effects or changes in blood pressure from oral nimodipine, but two volunteers experienced headaches for 2 weeks after the study. Future areas to focus on related to this drug's potential as degenerative disc treatment include dosage and identifying its therapeutic window, he said.

For more information:

  • Rajasekaran S, Naresh Babu J, Murugan KS, Prasad Shetty A. Diffusion of human lumbar intravertebral discs can be enhanced pharmacologically with oral nimodipine. #22. Presented at the International Society for the Study of the Lumbar Spine 33rd Annual Meeting. June 14-17, 2006. Bergen, Norway.