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NeuroLogic - MS: More than Counting Lesions

Spring 2010

MS: More than Counting Lesions

Date: March 1, 2010

Peter Calabresi
OCT is poised to turn the eye into a reliable window into MS, says Peter Calabresi.

It’s one of the great frustrations in treating patients with MS,” says neurologist Peter Calabresi. “You get a high-quality scan. You see the white spots that signify lesions in the brain,” he says. “But that doesn’t always correlate with what you see happening to your patient.”

A patient could, for example, have neuralgia’s electric shocks running down both arms and suffer the numbing fatigue of a flare-up, yet clinicians might see no change from the last imaging.

This clinicoradiological paradox isn’t unusual, says Calabresi, head of Hopkins’ Multiple Sclerosis Center. And not only can it keep the severity of MS out of sync with how aggressively to treat it, but more cosmic effects can follow. Pharma companies, for example, are less likely to invest the millions needed to test new drugs because it’s so hard to verify their effects in a reasonable time.

The problem is that lesions don’t always define the underlying pathology in MS. Calabresi and his colleagues, however, are finding ways around that. One method, optical coherence tomography (OCT), is newly pulled from ophthalmic clinics where it’s used to assess retinal damage from glaucoma or macular degeneration. Now OCT is poised to turn the eye into an easy, reliable window into MS. “It’s ready for prime time,” says Calabresi.

In an OCT scan, a beam of infrared light plays across the retina and the resulting data on the “bounce-back” gets crunched by a microprocessor into a meaningful readout. It’s like ultrasound, only with light. Within 10 minutes, in the comfort of a neurologist’s office, Calabresi says, you can measure the thickness of the retinal nerve fiber layer. And that’s becoming a valuable metric.

“Originally,” he explains, “we used OCT just to assess the optic neuritis that’s common with MS.” But there’s been a sea change in the way medicine views MS, with the realization that the lasting damage comes from neurodegeneration as well as autoimmune attacks on myelin. So Calabresi and colleagues track a patient’s thinning retina as a finger on degeneration’s pulse. It goes beyond counting brain lesions. “The inflammatory attacks are just the tip of the iceberg,” he says.

But it’s one thing to say Now we can measure the loss of naked axons in the eye and another to prove that reflects a whole demyelinating disease. So Calabresi and colleagues on a select multicenter team have, for five years, followed MS patients with OCT. They’ve shown, for example, that the retinal layer thickness is in sync with how patients do on clinical tests of vision loss—a true structure-function link. They’ve also found that the more progressive the MS, the more rapid the thinning.

Most important is that Calabresi’s team showed a significant tie between retinal changes and increased brain atrophy, the MS hallmark. “These matches,” he says, “are better than we could have hoped for.

“At Hopkins, we’re at a point where we’re using OCT cautiously in clinical practice. We have the newest generation machine. Its resolution is spectacular.”

This isn’t, however, to dismiss the usefulness of MRI, Calabresi emphasizes. Great strides have been made recently with that method, particularly with diffusion tensor imaging. “It’s important,” he adds, “to be able to check the integrity of entire nerve fibers.” What we hope,” he says, “is that both techniques will help predict who’s going to have brainatrophy. Then we might intervene before the brain is greatly affected.”

The Johns Hopkins Multiple Sclerosis Center at 410-614-1522

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