By Symeon Missios, MD — Long Island Brain & Spine

A man in his early seventies comes to see me because of his hands. That is how he puts it. Not his neck. His hands.

He has started dropping things. A coffee mug six weeks ago. His keys, more often than he wants to admit. Buttons have become a small daily project, and his handwriting, he tells me, looks like it belongs to somebody else. When I ask whether anything else has changed, he pauses, and his wife answers for him. He holds the railing going down the stairs now. He never used to.

His neck barely hurts. That is exactly why he had not mentioned any of this to his primary care doctor for the better part of a year. He assumed it was age. Hands get clumsy. Balance gets worse. Everyone says so.

He was not simply getting older. He had cervical myelopathy, and by the time he sat down across from me he had been quietly losing spinal cord function for months.

Most of what I write about the spine argues for patience. I have made the case at length that a great many people are offered spine surgery they do not need, and that waiting is frequently the wisest thing a patient can do. I stand by all of it.

This condition is the exception. Cervical myelopathy is the one spine problem where waiting carries a real and often permanent cost, and it is the one I most often see missed.

Radiculopathy Is a Nerve Problem. Myelopathy Is a Cord Problem.

These two words sound similar and get confused constantly, including by clinicians. The difference is the whole article.

Cervical radiculopathy is compression of a single nerve root as it exits the spine on its way to the arm. It is loud. It produces sharp, burning pain that travels a specific route down the shoulder, arm, and into particular fingers. Patients know something is wrong because it hurts, often badly. It is the neck’s version of sciatica, and like sciatica, it usually improves on its own.

Cervical myelopathy is compression of the spinal cord itself, inside the spinal canal. The spinal cord is not a nerve. It is the cable carrying every signal between your brain and everything below your neck: hand function, leg strength, balance, bladder control, sensation. And unlike a pinched nerve root, a compressed spinal cord does not reliably generate pain.

It generates dysfunction.

That single fact is why this condition goes unrecognized for so long. Radiculopathy hurts. Myelopathy takes.

Why It Hides

Cervical myelopathy in adults is usually degenerative. Over decades, discs flatten, bone spurs form, ligaments thicken, and the canal that comfortably housed your spinal cord at twenty gradually narrows. In some people the canal was congenitally narrow to begin with, and less degeneration is required to cause trouble. It is among the most common causes of spinal cord dysfunction in adults over fifty [1].

It hides for four reasons, and I see all four regularly:

• It is gradual. There is no day it started. Patients cannot give me a date, only a vague sense that this year is worse than last year.
• It gets blamed on aging. Clumsy hands and an unsteady gait are exactly what people expect from getting older, so they do not report them.
• The neck often does not hurt. Patients reasonably conclude that a painless neck cannot be the source of the problem.
• The symptoms are far from the neck. Numb, clumsy hands send people to a hand specialist for suspected carpal tunnel syndrome. Unsteadiness sends them to a neurologist, or to nobody at all. This is a different situation from the one I describe in when to see a surgeon for back pain, where the symptom at least points at the spine.

What the Symptoms Actually Look Like

This is the cluster that should prompt an evaluation, particularly when several appear together and have been slowly worsening:

• Loss of hand dexterity. Buttons, zippers, coins, jewelry clasps, keys in a lock. Handwriting that has deteriorated.
• Dropping objects without an obvious reason.
• Numbness or tingling in both hands, often in a pattern that does not match any one nerve.
• A change in walking. Unsteadiness, a wider stance, reaching for railings and furniture, a sense of walking on an uneven surface. Some patients describe feeling mildly drunk.
• Falls or near-falls, especially in the dark or on uneven ground.
• Heaviness or stiffness in the legs, as though they are not receiving instructions cleanly.
• An electric sensation down the spine when bending the neck forward. This is called Lhermitte’s sign and is worth reporting.
• Urinary urgency or frequency, typically a later development and easily attributed to other causes.

Notice what is absent from that list. Severe neck pain is not required, and its absence never rules this out.

What I Look For on Examination

Myelopathy is one of the conditions where a careful physical examination still outperforms a patient’s own account, because the findings are objective and the patient cannot feel most of them.

When the spinal cord is compressed, the reflex pathways below the level of compression lose their normal braking signal from the brain and become overactive. So I check for brisk reflexes in the arms and legs, for a Hoffmann’s sign in the hand, for clonus at the ankle, for an upgoing toe on plantar stimulation, and for increased muscle tone. I watch the patient walk, including heel-to-toe, which is often the first thing to fail. I use a simple grip-and-release test: most healthy adults can open and close a fist twenty times in ten seconds, and many myelopathic patients cannot.

One honest caveat. These signs can be blunted or absent, especially in patients who also have diabetic neuropathy or significant lumbar stenosis, which can suppress the very reflexes I am looking for. A normal-looking reflex examination in the right clinical story does not close the case.

Why Waiting Is Different Here

This is the heart of it, and it is worth being precise rather than alarming.

Degenerative cervical myelopathy does not follow one predictable course. Some patients remain stable for long stretches. Many, however, follow a stepwise pattern: a period of stability, then a decline to a new and lower baseline, then stability again at that lower level [2]. The declines tend not to reverse on their own.

That is the asymmetry that changes the calculation. With radiculopathy or a herniated lumbar disc, waiting risks continued pain, and pain in those conditions usually resolves on its own. With myelopathy, waiting risks function, and lost cord function does not reliably come back.

Which is why I describe the operation to patients this way: surgery for cervical myelopathy is not primarily a pain operation. It is a preservation operation. The main thing I am buying is the function you still have.

The best predictor of how much function a patient recovers after surgery is how much function they still had going in, and how long they had been losing it. That is an argument for evaluation sooner rather than later.

What Imaging Shows, and What It Doesn’t Settle

MRI is the test. It shows the degree of canal narrowing, whether the cerebrospinal fluid cushion around the cord has been effaced, and whether there is signal change within the cord itself, which suggests the cord has actually been injured rather than merely crowded.

But I want to apply the same caution here that I apply everywhere else in spine care. Impressive-looking compression on an MRI, in a patient with no symptoms and a normal examination, is not automatically an operation. Treating the picture instead of the patient is how people end up with surgery that does not help them, a point I have made about back pain and imaging before. The MRI confirms and localizes what the history and examination already suspect. It does not replace them.

The Operation, and What It Achieves

The goal of surgery is simple to state: create room for the spinal cord. How that is best accomplished depends on where the compression is, how many levels are involved, and the alignment of the neck.

Compression coming mainly from the front, at one or two levels, is usually addressed from the front, by removing the offending disc or a portion of the vertebral body and reconstructing that segment. Compression across multiple levels, particularly when the neck’s natural curve is preserved, is often better addressed from the back, either by reshaping the bony arch to enlarge the canal or by removing it and stabilizing the segment. Each approach has real advantages and real trade-offs, and the right answer genuinely varies between patients.

What the evidence supports is the value of decompression itself. In a large prospective multicenter study, surgical decompression produced significant improvement in neurological function, disability, and quality of life across the range of severity, with an acceptable complication profile [3]. Current clinical practice guidelines recommend surgery for patients with moderate or severe myelopathy [4].

What Surgery Does Not Do

I want to be as clear about the limits as about the benefits.

• It stops the injury more reliably than it reverses it. The primary aim is to halt progression. Recovery of lost function is a hoped-for bonus, not a promise.
• Recovery is slow. Improvement unfolds over months, not weeks, and it plateaus.
• Longer and more severe means less recovery. Patients who present after years of decline, with significant weakness and cord signal change, generally recover less than those who present early [3].
• Numbness is stubborn. Strength and balance often improve more than sensation does.
• Fusion changes mechanics. When the operation involves fusing levels, motion is permanently redistributed to the neighboring segments, which carries its own long-term consequences. That trade-off deserves its own discussion, and I take it up in a companion article on when spinal fusion is and is not necessary.

The Honest Gray Zone: Mild Myelopathy

Not every patient with myelopathy needs an operation tomorrow, and I would be overstating the case if I implied otherwise.

For patients with clearly moderate or severe myelopathy, the guidelines recommend surgery, and I agree with that without much hesitation. For patients with genuinely mild myelopathy, the guidelines permit either surgery or a supervised trial of structured rehabilitation with close, scheduled follow-up [4]. Some of those patients remain stable for years.

What pushes me toward operating in that mild group is a combination of factors: cord signal change on MRI, severe canal narrowing, a congenitally narrow canal, documented worsening between visits, or a patient whose work or independence leaves no margin for a stepwise decline. What pushes me toward watching is a stable examination, mild findings, and a patient who will genuinely return for reassessment. This is an area of active research, and better tools for predicting which mild patients will deteriorate are among the field’s main open questions [5].

The one option I do not support is drifting. Choosing to watch cervical myelopathy is a legitimate plan only when it is an actual plan, with a scheduled examination to detect change. Watching without follow-up is not conservative management. It is just delay.

The Bottom Line

Cervical myelopathy is compression of the spinal cord in the neck. It usually announces itself not with pain but with clumsy hands, deteriorating handwriting, dropped objects, and an unsteady walk, and it is very commonly mistaken for ordinary aging or for a hand problem. Because the cord recovers poorly once injured, this is the spine condition where a prompt evaluation matters most, and where the value of surgery lies chiefly in protecting the function a patient still has.

If you have read the symptom list above and recognized yourself or a parent in it, the useful next step is not more waiting. It is an examination.

If your hands have become clumsy, your handwriting has changed, or your balance has slipped over the last year, and you have been telling yourself it is just age, that is worth an evaluation rather than another six months of watching. Our offices in West Islip and Smithtown are available for consultation and second opinions. Please bring any imaging you have had, including the disc itself and not only the written report. For comprehensive brain and spine care across the practice, you can also reach Long Island Brain & Spine at longislandbrainandspine.com. If your symptoms began suddenly, or include new weakness, difficulty walking, or loss of bladder control, treat that as an emergency and go to the nearest emergency department.

Dr. Symeon Missios is a board-certified neurosurgeon practicing on Long Island, with expertise in brain and spine surgery, cerebrovascular disease, and stereotactic radiosurgery. To schedule a consultation or second opinion, request an appointment or call (631) 422-5371 or toll-free (888) 737-5427.

References

1. Nouri A, Tetreault L, Singh A, Karadimas SK, Fehlings MG. Degenerative Cervical Myelopathy: Epidemiology, Genetics, and Pathogenesis. Spine (Phila Pa 1976). 2015;40(12):E675–E693. PubMed: 25839387
2. Karadimas SK, Erwin WM, Ely CG, Dettori JR, Fehlings MG. Pathophysiology and natural history of cervical spondylotic myelopathy. Spine (Phila Pa 1976). 2013;38(22 Suppl 1):S21–S36. PubMed: 23963004
3. Fehlings MG, Wilson JR, Kopjar B, et al. Efficacy and safety of surgical decompression in patients with cervical spondylotic myelopathy: results of the AOSpine North America prospective multi-center study. J Bone Joint Surg Am. 2013;95(18):1651–1658. PubMed: 24048552
4. Fehlings MG, Tetreault LA, Riew KD, et al. A Clinical Practice Guideline for the Management of Patients With Degenerative Cervical Myelopathy. Global Spine J. 2017;7(3 Suppl):70S–83S. PubMed: 29164035
5. Badhiwala JH, Ahuja CS, Akbar MA, et al. Degenerative cervical myelopathy — update and future directions. Nat Rev Neurol. 2020;16(2):108–124. PubMed: 31974455