Latest / Deep Dive Ortho — Orthopaedic Surgery, AI & Digital Health Podcast. / Cervical Mylopathy

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Cervical Mylopathy · Deep Dive Ortho — Orthopaedic Surgery, AI & Digital Health Podcast.

0:00
Imagine this, the single most common cause of
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spinal cord problems in adults, not from accidents,
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but developing silently, often missed, progressing
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almost unnoticed until, well, until function
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is significantly lost. We're talking about potential
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paralysis, a huge change in life quality. It's
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cervical myelopathy, or DCM, and the clock is
0:20
always ticking, early diagnosis, early intervention.
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They're absolutely vital. It really is a race
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against irreversible neurological decline. Welcome
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to the Deep Dive. We unpack complex medical topics
0:32
to give you the essential knowledge you need
0:33
quickly and thoroughly. Today, we're diving deep
0:37
into cervical myelopathy. It's a condition that's
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becoming, well, a really significant public health
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issue, especially with our aging population worldwide.
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Understanding DCM isn't just about clinical knowledge,
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it's fundamentally about improving lives. And
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we're incredibly fortunate today. We have a truly
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distinguished expert with us to guide us through
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this. He's a highly respected figure in orthopedic
0:55
surgery, director of laser spine, and also chief
0:58
spine surgeon at Dr. Babasaheb Ambedkar Central
1:00
Railway Hospital in Mumbai. His background includes
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extensive fellowships globally, UK, USA Top Hospitals,
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and he's an executive member of the Association
1:08
of Spine Surgeons of India. His expertise, particularly
1:11
in minimally invasive spine surgery and, of course,
1:15
cervical myelopathy, is profound. We're really
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keen to get his insights on this vital and sometimes
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quite elusive area. So to kick us off, let's
1:23
get right to the heart of it. Cervical myelopathy
1:25
can be tricky to spot, presentations often vague.
1:28
In your view, what's the single most defining
1:30
characteristic that really sets it apart from
1:32
other neck conditions, the thing that helps clinicians
1:34
make that crucial distinction? That's a great
1:36
question. The defining thing, the one thing that
1:39
really makes it stand out, is direct spinal cord
1:42
compression. and that compression leads to very
1:45
specific upper motor neuron signs plus these
1:48
widespread often symmetrical neurological deficits.
1:52
It's quite different from say a simple radiculopathy.
1:55
That's just irritation of a single nerve root
1:57
giving you focal pain or maybe sensory changes
1:59
in one specific dermatome. Myelopathy involves
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the central nervous system itself so the symptoms
2:05
are more diffuse. I think hand clumsiness, maybe
2:09
difficulty with buttons or handwriting. And crucially,
2:12
that distinct gait instability, not just localized
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pain. These are systemic indicators that the
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spinal cord itself is involved. A much broader
2:19
neurological impact. Right. That makes sense.
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The sort of widespread non -focal nature points
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towards something more central, doesn't it? You
2:27
mentioned it can creep up slowly, insidiously,
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sometimes over months or even years. What's one
2:32
symptom that's perhaps surprising or maybe commonly
2:34
overlooked that health care professionals really
2:36
need to be sharp on, especially in those earlier
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stages when it could easily be mistaken for something
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else? Oh, yes. Without a doubt, it's a gait disturbance,
2:44
that feeling of unsteadyness on the feet. It's
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often the most important clinical predictor,
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but frequently overlooked. Patients might not
2:51
actually report severe neck pain initially, which
2:53
can be very misleading. Instead, they might describe
2:56
subtle changes, feeling a bit off balance, perhaps
2:58
struggling on stairs up or down. Or maybe they
3:01
can't do a tandem gait properly, you know, walking
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heel to toe in a line. These seemingly minor
3:06
changes in balance and coordination, they're
3:09
crucial red flags. They demand a closer look
3:11
at the cervical spine, even if the patient isn't
3:13
complaining about their neck. Spotting these
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early gait changes can really shift the timeline
3:17
for intervention, and that directly impacts the
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long -term prognosis. We do see patients, unfortunately,
3:23
who've been misdiagnosed. Maybe with peripheral
3:25
neuropathy, we're just told it's old age for
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far too long. That's incredibly insightful. Shifting
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the focus away from just the neck to these more
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distal but very telling signs, you've really
3:36
emphasized how crucial early intervention is.
3:38
Could you just briefly explain why timing is
3:40
so critical? It feels like a race against the
3:43
clock with DCM. I mean, lots of conditions benefit
3:45
from early diagnosis, but what makes the window
3:48
for DCM particularly unforgiving, maybe more
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so than other spinal conditions? That's a key
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point. The urgency really stems from the spinal
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cord's very, very limited ability to regenerate.
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Once that spinal cord tissue is damaged, either
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from the chronic compression, the direct mechanical
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stress, or from the resulting lack of blood flow,
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which we call ischemic injury, well, it's incredibly
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difficult for it to recover. Think of it like
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this. Peripheral nerves, they have a better capacity
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to heal, to regenerate. But the spinal cord,
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that's central nervous system tissue. It just
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doesn't have that same ability. So, recognizing
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it early and getting treatment before that irreversible
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damage kicks in, that is absolutely critical.
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It's key for achieving good clinical outcomes
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and, frankly, for preventing permanent disability.
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Delaying treatment, unfortunately, often leads
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to this sort of step -wise irreversible decline
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in function. We're talking about a gradual, sometimes
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relentless, worsening of neurological deficits
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that, even after successful surgery, to decompress
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the cord often can't be fully regained. That
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window for maximum recovery, it's directly tied
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to how quickly you relieve that compression.
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Every month a delay can genuinely mean lost neurological
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function that's just gone. OK, let's unpack this
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a bit more then delve deeper into where it comes
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from. It's fascinating, isn't it? How often cervical
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myelopathy seems to arise from what we might
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just consider. Well, normal age -related changes.
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Everyday wear and tear. Could you elaborate on
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the main causes and exactly how they lead to
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that critical spinal cord compression and maybe
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touch on that dual attack mechanism you mentioned?
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Absolutely. The primary cause, overwhelmingly,
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is degenerative cervical spondylosis, or DCSM.
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Essentially, yes, it's the cumulative effect
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of wear and tear on the neck over decades. The
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body's natural aging process affecting the discs.
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the facet joints, the ligaments. For the professionals
5:32
listening, this isn't just arthritis. It's a
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really complex interplay of biomechanical stresses
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and biological responses over time. Now, how
5:40
does that degeneration actually compress the
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cord? Several key things happen. First, you get
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osteophytes forming. Those are bone spurs growing
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around the degenerating discs and facet joints.
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Now osteophytes are common, but in DCM, it's
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their specific shape and location that matter.
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They often grow backwards and sideways from the
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uncomfortable joints, or forwards from the vertebral
6:00
bodies, projecting right into the spinal canal.
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Then you have the discosteophyte complex. That's
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a combination of a degenerated, often bulging
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disc and the bone spurs around it. Together,
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they form a bigger mass pushing on the cord,
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especially when the neck extends. We also see
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degenerative spondylolisthesis. That's where
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one vertebra can slip slightly forward on the
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one below, narrowing the canal front to back.
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Instability can make this worse, causing dynamic
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compression with movement. And finally, a really
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significant contributor is hypertrophy of the
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ligamentum flavum. That's the ligament at the
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back of the spinal canal. It can thicken and
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sort of buckle inwards, particularly during neck
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extension, eating into that precious space for
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the spinal cord. And it's not just plosive thickening.
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It can become quite fibrous, quite rigid. So
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it's like multiple factors converging to narrow
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that space. Precisely. And beyond those degenerative
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changes, you can have a predisposition if you're
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born with a naturally narrow spinal canal. That's
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congenital stenosis. These patients might have
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a canal diameter that's already quite small,
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say less than 13 millimeters. It might be fine
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for years, but then later degenerative changes
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come along, and that already limited space becomes
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critically compromised. It's like the final straw.
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It's the straw that breaks the camel's back.
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Exactly. And there are other significant causes
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too, though less common. Ossification of the
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posterior longitudinal ligament, OPLL. That's
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where a ligament behind the vertebrae turns into
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bone. It's particularly common in some Asian
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populations and can form a continuous sheet of
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bone, making surgery tricky. Then you have rarer
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things. Tumors, epidural abscesses, trauma causing
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fractures or dislocations, or even severe cervical
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kyphosis, that abnormal forward curve of the
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neck. That can stretch and compress the cord
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like a bowstring over time. And the dual attack.
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Ah yes, the mechanism of injury. It really is
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a dual attack. It's not just the direct mechanical
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squeeze on the cord causing axon damage. There's
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also a really significant ischemic component.
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The compression affects blood flow, especially
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to the anterior spinal artery which feeds the
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cord. This lack of blood flow leads to hypoxia,
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energy depletion within the cord cells. So it's
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this double whammy mechanical pressure and vascular
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compromise that drives progressive damage, often
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leading to glial scarring and demyelination.
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And you mentioned tandem stenosis earlier. Yes,
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that's important too. About 20 % of patients
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have compression in both the cervical and the
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lumbar spine. Tandem stenosis. That poses a real
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diagnostic and management challenge. You might
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have someone with gait instability from myopathy,
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but also neurogenic claudication from lumbar
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stenosis. Figuring out what's causing which symptom
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is crucial for planning effective surgery. Sometimes
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you even need staged operations. Right. So it
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sounds like the body's attempt to stabilize itself
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with age can ironically cause major problems
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for the court. It's not just one thing, but often
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this perfect storm of factors. OK, so connecting
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that pathophysiology to how patients actually
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walk into your clinic. What are the really characteristic
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symptoms that should set alarm bells ringing
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for cervical myelopathy? And what are those subtle
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signs that might get missed if you're not specifically
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looking? Perhaps you could walk us through a
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typical sort of patient presentation. Certainly.
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Let's think about a hypothetical patient. Let's
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call our Mrs. Davies, perhaps a 68 -year -old
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retired librarian. She might come in complaining
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less about neck pain and more that her hands
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just aren't working properly. And this is where
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clinical sharpness is so important, because the
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symptoms are often widespread, sometimes a bit
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vague, easily dismissed if you're not thinking
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myelopathy. So firstly, Mrs. Davies might describe
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extremity parasthesias, not just tingling, but
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often diffuse bilateral both sides and non -dermatomal
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numbness and tingling. It doesn't follow a neat
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nerve root pattern, which helps distinguish it
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from radiculopathy. It's more of a general pins
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and needles in her hands, maybe her feet too.
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Secondly, you'll often see weakness and clumsiness,
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especially in the hands. Bilateral weakness,
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decreased manual dexterity. Mrs. Davies might
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say she's dropping things more often, maybe struggling
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with buttons on her cardigan or her handwriting,
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which used to be neat, has become messy. Maybe
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she can't till coins apart in her purse just
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by feel anymore. These are often the first things
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that really bother patients functionally and
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make them seek help. We actually use scoring
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systems, like the Modified Japanese Orthopedic
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Association score, the MJOA, to quantify this.
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Scores below 17 often point towards functional
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myelopathy. And the gait issue you mentioned
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earlier. Yes, absolutely crucial. Gait instability.
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As we said, perhaps the most important predictor.
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Mrs. Davies might feel unsteady on her feet,
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struggle with balance, find stairs difficult.
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It can manifest as a wide -based, slightly stiff,
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or spastic gait. Patients might describe their
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legs feeling clumsy or heavy. And the really
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key thing here is that significant neck pain
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and stiffness, they can actually be absent in
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many myelopathy patients. That's a huge differentiator
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from simpler neck problems where pain is central.
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This lack of pain often leads to delays, as investigations
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might focus elsewhere, Parkinson's perhaps, or
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peripheral neuropathy. What about later stage
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symptoms? In later stages, you might see urinary
10:58
retention or other bowel issues, maybe more generalized
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weakness. But urinary symptoms, honestly, they're
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rarely helpful for early diagnosis because they're
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so common in older people due to other causes,
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prostate issues in men, bladder problems. Late
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stage symptoms usually mean more advanced disease,
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more significant cord compromise, and generally
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point to a poor prognosis, unfortunately. So
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what about on physical examination? What specific
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signs are you looking for? Right, the examination
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is critical. For motor signs, overall weakness
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can be subtle, but look closely at the lower
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extremities. Weakness there is often more concerning
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initially. Two specific hand tests are very revealing.
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The finger escape sign asks the patient to hold
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their fingers straight and together, and the
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little finger might drift away into abduction
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due to intrinsic muscle weakness. And the grip
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and release test can make and release a fifth
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rapidly, say 20 times in 10 seconds. Myelopathic
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patients often struggle with this speed and coordination.
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It quantifies that fine motor difficulty. And
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sensory. Sensory signs can include proprioception
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problems, difficulty knowing where their limbs
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are in space, that points to dorsal column involvement
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and isn't a great sign in advanced disease, assessed
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joint position sense, you might find decreased
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pinprick sensation, maybe changes in vibration
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sense, though vibration usually only changes
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in severe long -standing cases. But the classic
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signs are the upper motor neuron signs, right?
12:20
Exactly. Those are the hallmarks indicating spasticity
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and hyperreflexia from the spinal cord involvement.
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So you're looking for hyperreflexia exaggerated
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reflexes, often graded 3 plus or 4 plus date
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OP. The inverted radial reflex or brachioradialis
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reflex, tapping the brachioradialis tendon causes
12:38
finger flexion instead of just elbow flexion.
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Hoffman's sign flicking the patient's middle
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finger causes the thumb and index finger to flex.
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This is incredibly common, often the most reliable
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physical sign. Sustained clonus more than three
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beats of rhythmic muscle contraction after a
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rapid stretch that's highly specific for myelopathy,
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but not very sensitive, meaning its absence doesn't
12:57
rule it out. And the Babinski test, stroking
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the sole of the foot causes the big toe to extend
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upwards, indicates pyramidal tract issues. Are
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there any pitfalls with those signs? Yes, a really
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crucial nuance. These upper motor neuron signs
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can actually be absent or masked if the patient
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also has a peripheral nerve problem. Things like
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nerve root compression, lower down, diabetic
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neuropathy, or other peripheral neuropathies
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can interfere. This can really muddy the waters.
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That's why a full neurological exam and knowing
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the patient's complete medical history is absolutely
13:27
essential. And gait and balance tests. Definitely
13:30
assess gait directly. Look for that spastic wide
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-based shuffling pattern. Difficulty with tandem
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walking heel to toe is common. A positive Romberg
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test, where they lose balance standing with feet
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together and eyes closed, suggests post to your
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column dysfunction. Any provocative tests? Lermit's
13:47
sign is the key one. Asking the patient to flex
13:49
their neck sharply might produce an electric
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shock -like sensation down the spine or into
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the limbs. Put all these together, the history,
13:56
the symptoms, these specific exam findings, and
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you start to build a very strong clinical picture
14:00
of spinal cord compression. That's incredibly
14:03
thorough, a really systematic way to approach
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it, moving beyond just neck pain. So once you
14:08
have that strong clinical suspicion, based on
14:10
the history in the exam, how do you actually
14:12
confirm the diagnosis? What imaging is really
14:15
essential? And what are the specific, maybe subtle
14:17
findings you're looking for that seal the deal
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and perhaps even give you clues about prognosis?
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And how do these help rule out other conditions?
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Right, once suspicion is high, imaging becomes
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absolutely central to confirming the diagnosis
14:29
and planning treatment. We usually start with
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plane radiographs x -rays, though they have limitations.
14:34
We typically get AP, lateral, oblique views,
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and importantly, flexion and extension views.
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On these, you look for general degenerative changes
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those osteophytes we talked about, disc space
14:44
narrowing. Critically, on the lateral view, we
14:47
measure the sagittal diameter of the spinal canal.
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Less than 13 millimeters strongly suggest cord
14:52
compression risk or relative stenosis. Another
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useful measure is the Pavlov ratio comparing
14:58
the canal diameter to the vertebral body width.
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A ratio under 0 .8 points toward the congenitally
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narrow canal, a predisposing factor. We also
15:06
assess alignment, the overall C2 -C7 curve, any
15:09
local kyphosis. And those flexion extension views
15:12
are vital for spotting instability, any abnormal
15:15
slipping or angulation between vertebrae or maybe
15:17
compensatory movement above or below stiff segments.
15:20
Static images can miss dynamic compression. But
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x -rays aren't the whole story. No, definitely
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not. The big caveat is that degenerative changes
15:27
on x -ray are incredibly common, especially as
15:30
we age, maybe 70 % of 70 -year -olds show them.
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But they don't always correlate with symptoms.
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So x -rays give you bony architecture, alignment,
15:37
stability, but they don't show the cord itself.
15:40
They're a starting point. So MRI is key, then.
15:43
MRI, magnetic resonance imaging, is unequivocally
15:46
the study of choice. It's the best way to directly
15:49
visualize the spinal cord and the degree of compression.
15:51
On MRI, we look for effacement of the CSF, the
15:55
cerebrospinal fluid, around the cord. If that
15:57
space is squeezed out, it indicates functional
15:59
stenosis. The most significant findings relate
16:02
to signal changes within the cord itself. A bright
16:05
signal on the T2 -weighted images, we call this
16:07
myelomalacia, suggest edema, swelling, or gliosis,
16:11
which is scarring, within the cord due to the
16:13
compression. The T2 hyperintensity indicates
16:15
acute or subacute injury. Even more important
16:17
for prognosis, though, are signal changes on
16:19
T1 -weighted images. A low signal, or T1 hypotensity,
16:24
generally correlates with a poorer prognosis
16:25
after surgery. Why is that? Because that T1 hypotensity
16:29
usually represents more chronic, irreversible
16:31
damage established myelomalacia, maybe even cavitation
16:34
or cystic change within the cord, it suggests
16:37
actual tissue loss, less potential for recovery.
16:40
We also look at the compression ratio. the cord's
16:43
smallest front -to -back diameter, divided by
16:45
its widest side -to -side diameter. A ratio less
16:48
than 0 .4 also carries a poorer prognosis. But
16:51
MRIs aren't perfect either. No, and that's crucial
16:54
to remember. MRI has a high rate of false positives.
16:58
Studies show up to maybe 19 % of completely asymptomatic
17:01
people can have significant -looking cervical
17:03
abnormalities on their MRI. This really hammers
17:06
on the point. You must interpret imaging findings
17:08
in the context of the clinical picture. Never
17:10
treat this scan in isolation. This clinical correlation
17:13
is also key for differentiating true DCM from
17:16
mimics like multiple sclerosis, where you might
17:18
see T2 lesions but they have a different pattern,
17:20
disseminated in space and time, or other rare
17:22
things like vascular malformations. What about
17:24
CT scans? CT, without contrast, is very useful
17:28
for complementary bony detail. It's excellent
17:31
for visualizing things like OPLL, that ossified
17:34
ligament and really clearly defining osteophytes
17:36
may be better than MRI sometimes. It helps where
17:39
bone detail is critical, especially for surgical
17:42
planning involving calcified structures. And
17:44
CT myelography. CT myelography is more invasive.
17:47
It involves injecting contrast dye into the spinal
17:50
fluid space, usually via a lumbar puncture or
17:52
sometimes a C1, C2 puncture. But it gives excellent
17:56
detail on the exact degree of spinal cord compression,
17:59
especially dynamic compression. We tend to use
18:01
it when MRI is contraindicated. Maybe the patient
18:03
has a pacemaker or certain metallic implants,
18:06
or if there's a lot of artifact on the MRI, perhaps
18:08
from previous spinal hardware obscuring the view,
18:11
it can sometimes show the compression dynamics
18:13
more clearly. And nerve conduction studies, electrophysiology.
18:16
Yes, nerve conduction studies, NCS, and electromyography,
18:20
EMG, they actually have a high false negative
18:23
rate for myelopathy itself, so they might miss
18:25
it if used alone. However, they are incredibly
18:28
useful for differentiating. They help distinguish
18:30
a central process like myelopathy from peripheral
18:33
nerve problems that might cause similar symptoms.
18:36
Think ALS, amyotrophic lateral sclerosis, severe
18:39
diabetic neuropathy, or other peripheral neuropathies.
18:42
For example, ALS might show both upper and lower
18:45
motor neuron signs clinically, but EMG can reveal
18:48
widespread denervation signals like fibrillations.
18:52
Myelopathy, on the other hand, usually shows
18:53
normal peripheral nerve studies but might show
18:56
abnormalities on evoked potentials, SSFPs or
18:58
MEPs indicating slowed conduction through the
19:00
spinal cord itself. They help confirm if weakness
19:03
is coming from the cord, a nerve root. peripheral
19:05
nerve. So it really is about putting all the
19:07
pieces together. Exactly. The key message is
19:10
the need for a comprehensive evaluation. You
19:13
integrate the clinical story, the detailed exam
19:15
findings, and the information from the various
19:17
imaging modalities. Relying solely on one piece
19:20
or dismissing findings because symptoms seem
19:23
subtle can lead to misdiagnosis. It needs that
19:25
holistic integrated approach. Okay that gives
19:27
us a really solid grasp on diagnosis navigating
19:30
those potential pitfalls. Let's shift gears now
19:34
to Treatment. This often involves some pretty
19:36
significant decisions, doesn't it, especially
19:38
given the progressive nature you've described.
19:40
What are the current strategies for managing
19:43
cervical myelopathy? How do you distinguish between
19:46
non -operative and operative routes, and what
19:48
really guides your choice for an individual patient,
19:50
especially when facing those complex cases? Right,
19:53
treatment. The general philosophy now strongly
19:56
leans towards early intervention for most patients
19:58
with confirmed myelopathy. The overarching goal,
20:01
whatever technique we use, is simple. increase
20:03
the space in the spinal canal, and relieve that
20:05
pressure, that compression, on the spinal cord.
20:08
Now, when we talk about non -operative management,
20:11
it's really important to understand its very
20:12
limited role. It's primarily reserved for patients
20:15
with very mild disease, where there's essentially
20:18
no functional impairment, their daily activities
20:20
aren't significantly affected, and importantly,
20:22
no clear signs of progression. Or, of course,
20:25
for patients who are genuinely too medically
20:26
unwell for surgery. In these mild cases, the
20:29
patient's functional status, perhaps measured
20:31
by that MGAOA score, is actually a more critical
20:34
factor in deciding about surgery than just the
20:36
physical exam findings alone. Non -operative
20:38
measures might include medications, NSAIDs for
20:41
pain, maybe gabapentinoids for neuropathic symptoms.
20:45
Sometimes temporary immobilization with a hard
20:47
collar, often in slight flexion, can give some
20:49
symptomatic relief by reducing movement. Physical
20:52
therapy can also play a role focusing on neck
20:54
strengthening, balance exercises, gait training,
20:57
trying to maintain existing function, and proprioception.
21:00
But critically, therapy won't actually decompress
21:03
the cord. What about things like traction or
21:05
chiropractic? Good question. Generally, traction
21:09
spinal manipulation chiropractic approaches are
21:12
not recommended as primary treatments for myelopathy.
21:15
There's no proven benefit for actually decompressing
21:18
the cord, and they carry potential risks that
21:20
could even worsen symptoms or cause neurological
21:23
decline. While some studies show temporary symptom
21:26
improvement with immobilization in very mild
21:28
cases, particularly if the cord still has a decent
21:32
cross -sectional area, you absolutely have to
21:35
monitor these patients incredibly closely for
21:37
any sign of progression. Non -operative management
21:40
is rarely a definitive solution for progressive
21:42
myelopathy. The evidence strongly suggests conservative
21:45
treatment doesn't change the natural history,
21:47
which is typically progressive decline. So choosing
21:50
this route involves very careful discussion with
21:52
the patient about the risks of delaying potential
21:54
surgery. So surgery is often the main route then?
21:57
For progressive or significant myelopathy, yes.
22:00
Operative management is generally the definitive
22:02
treatment. The indications are fairly clear.
22:04
significant functional impairment, often reflected
22:08
in that MJOA score, or clear evidence that symptoms
22:11
are progressing over time. It's also generally
22:14
indicated for disease affecting one or two levels,
22:17
regardless of whether the neck alignment is lordotic,
22:19
neutral, or even mildly kyphotic. The main goal
22:22
of surgery isn't always about making symptoms
22:24
dramatically better, although that's obviously
22:26
the hope. Primarily it's about preventing continued
22:29
neurological decline. As we keep saying, Early
22:32
recognition and treatment before irreversible
22:34
cord damage occurs are critical for the best
22:37
possible clinical outcomes and maximizing any
22:39
potential recovery. How do you choose which surgery?
22:41
There seem to be quite a few options. Yes. The
22:44
selection of the specific procedure is highly
22:46
individualized. It really depends on several
22:48
key factors. We look at the overall cervical
22:51
-sagittal alignment. Is the neck curved normally?
22:54
Lordotic. Straight or abnormally bent forward?
22:58
How many levels are affected by stenosis? Where
23:00
is the compression coming from mostly the front
23:02
interior, like discs, osteophytes, or PLL? Or
23:05
mostly the back posterior, like the ligamentum,
23:08
flavum, or facet joints? And of course, the patient's
23:11
overall medical condition and any comorbidities
23:13
play a big role. Can you walk us through the
23:15
main techniques, maybe starting with the anterior
23:17
approaches? Certainly. Anterior cervical dissectomy
23:21
and fusion, or ACDF, is a real mainstay, especially
23:24
for disease affecting one or two levels. We approach
23:27
from the front of the neck the Smith -Robinson
23:29
approach. This gives direct access to the discs
23:32
and vertebral bodies. It's excellent for correcting
23:35
kyphosis because you can restore disc height
23:37
and alignment, and you directly remove the anterior
23:40
pathology, herniated discs, osteophytes, even
23:43
segments of OPLL. You remove the problem disc
23:46
of discs and then fuse the vertebrae together
23:48
usually with a cage and an anterior plate for
23:50
stability. Advantages, generally lower infection
23:53
risk than posterior approaches, often less blood
23:56
loss and maybe less post -operative pain. The
23:59
main dilemma often revolves around one versus
24:01
two levels. Fusion rates can drop slightly with
24:04
two levels, and there's always the long -term
24:06
concern about adjacent segment disease. Also,
24:08
you'd avoid it in patients with significant pre
24:10
-existing swallowing problems, as transient dysphagia
24:13
is a common light effect. What if the problem
24:15
is more extensive, or behind the vertebral body?
24:18
Then we might consider an anterior carpectomy
24:20
infusion, or ACF. This involves removing not
24:24
just the disc, but one or more of the vertebral
24:27
bodies themselves. This gives really wide decompression,
24:30
especially for disease situated right behind
24:32
the vertebral body, or if there's significant
24:35
kyphosis that you need to correct from the front.
24:37
However, corpectomies, especially multilevel
24:40
ones, come with stability issues. Two -level
24:43
corpectomies have a significant risk, maybe seven
24:45
to 20%, of the bone graft dislodging, which can
24:48
have severe consequences. Often, we try to combine
24:51
a single corpectomy with an adjacent disectomy
24:53
to minimize this. And critically, for three -level
24:56
corpectomies or more, combined anterior and posterior
24:59
fixation is generally considered mandatory. The
25:02
failure rate with anterior -only fixation at
25:04
three levels is just too high, potentially over
25:06
70%. So the dilemma is balancing adequate decompression
25:10
with maintaining spinal stability, sometimes
25:12
needing a second posterior surgery. Okay, what
25:14
about approaching from the back? Posterior approaches?
25:17
Right. Laminectomy with posterior fusion is a
25:19
common one. This is suitable for an ultilevel
25:21
compression, but generally only if the cervical
25:24
spine isn't significantly kyphotic. Yearly less
25:27
than 10 degrees of fixed kyphosis. Why that limitation
25:30
on kyphosis? Because if the spine is bent too
25:33
far forward, the spinal cord is stretched taut
25:35
over the front of the canal like a bowstring.
25:38
Just removing the bone at the back, the lamina,
25:41
won't allow the cord to drift backwards sufficiently
25:43
to decompress it effectively. It might even tether
25:46
the cord. In a laminectomy with fusion, we remove
25:50
the lamina and then stabilize the spine with
25:52
screws, usually lateral mass screws and rods.
25:55
The fusion helps prevent post -laminectomy kyphosis
25:58
developing later and can also help with neck
26:00
pain from arthritic facet joints. I've heard
26:03
a lot about laminoplasty recently. How does that
26:05
fit in? Yes. Laminoplasty is gaining significant
26:08
popularity. The main appeal is that it aims to
26:11
preserve motion in the cervical spine, unlike
26:14
fusion. It's particularly useful when you want
26:16
to avoid the potential complications of fusion,
26:19
like pseudoarthrosis or adjacent segment disease,
26:22
maybe in younger patients, or those at high risk
26:24
of fusion failing. It's also good for congenital
26:26
stenosis, or sometimes for a multi -level OPLL
26:29
where a big anterior operation seems too risky.
26:32
The technique essentially creates a hinged door
26:35
with the lamina. You cut one side and hinge it
26:36
open on the other. Open door technique, or hinge
26:39
both sides open. French door. This expands the
26:42
volume of the spinal canal, typically from C3
26:44
down to C7, decompressing the cord posteriorly
26:47
while keeping the basic bony structure intact.
26:49
What are the pros and cons? Advantages. Avoids
26:52
post -laminectomy kyphosis. Generally has a lower
26:55
complication rate than extensive multi -level
26:57
ACDF, especially with OPLO, and it preserves
27:00
some motion. Disadvantages. Can have higher blood
27:03
loss than ACDF. There's a higher incidence of
27:06
post -operative axial neck pain or stiffness.
27:09
And while it preserves motion, some range is
27:11
still usually lost compared to pre -op. Outcomes,
27:14
though, are generally considered equivalent to
27:16
multilevel ACDF or laminectomy with fusion for
27:18
the right indications. The choice between laminoplasty
27:21
and fusion for multilevel disease is often a
27:24
key clinical debate, balancing motion preservation
27:26
against the type and location of compression.
27:29
There are times you need to do both front and
27:31
back surgery. Yes. Combined anterior and posterior
27:34
surgery is reserved for the most complex cases.
27:37
Things like multi -level stenosis in a spine
27:39
that's rigidly kyphotic. Or after multi -level
27:42
anterior carpectomies needing extra stability.
27:45
Or if someone already has kyphosis after a previous
27:47
laminectomy, it offers the most robust decompression
27:50
and stability. But logically, it also carries
27:53
the highest overall morbidity and risk. And just
27:55
laminectomy on its own. without fusion. Laminectomy
27:58
alone is rarely done these days for myelopathy.
28:00
There's just too high a risk anywhere from 11
28:02
to 47 percent in various studies of progressive
28:05
kyphosis developing afterwards, post -laminectomy
28:08
kyphosis. And that can lead to the myelopathy
28:10
coming back due to cord tethering. So if you
28:13
do a laminectomy, you almost always add a fusion
28:15
for stability. Krash, it's clear the surgical
28:17
decision -making is incredibly complex, really
28:20
tailored to each individual's specific anatomy
28:22
and pathology. Now, with any surgery, especially
28:25
complex spine surgery, complications are always
28:28
a concern for the patient and the clinician.
28:31
What are the key complications people should
28:32
be aware of with these cervical procedures? And
28:35
importantly, how are these risks minimized to
28:37
keep patients as safe as possible? Maybe highlight
28:39
some of the more challenging ones. Absolutely.
28:42
Understanding and mitigating complications is
28:44
paramount. Firstly, there are the general surgical
28:47
risks that apply to almost any operation. Things
28:50
like infection, interestingly, often slightly
28:52
higher risk with posterior approaches due to
28:55
more muscle dissection compared to anterior.
28:58
Bleeding, the risk of direct nerve or spinal
29:00
cord injury during the procedure itself, reactions
29:03
to anesthesia, the possibility of needing more
29:06
surgery down the line. failure to actually relieve
29:08
the symptoms the patient came in with, dural
29:10
tear, a leak of spinal fluid, and in rare cases,
29:14
serious systemic complications like heart attack
29:16
or stroke. These general risks tend to be higher
29:19
in elderly patients, those carrying excess weight,
29:21
smokers, diabetics, people with multiple other
29:23
health problems. This really underscores why
29:26
thorough preoperative assessment and optimizing
29:28
these conditions beforehand is so important.
29:30
Standard mitigation includes prophylactic antibiotics,
29:34
meticulous surgical technique to control bleeding,
29:36
and careful patient selection. Okay, what about
29:38
risks specific to the approach, anterior first?
29:41
For anterior approaches, like ACDF or carpectomy,
29:44
some degree of soreness, dysphagia, difficulty
29:47
swallowing, and maybe transient voice changes
29:49
or hoarseness are quite common. Affecting maybe
29:51
9 to 27 percent of patients initially, they usually
29:54
resolve within, say, 12 weeks and are often related
29:57
to the retractors used during surgery, putting
29:59
pressure on the esophagus and larynx. Sometimes
30:02
using local steroids near the retractors before
30:04
closing can help reduce dysphagia. Recurrent
30:07
laryngeal nerve injury is less common, around
30:10
3 % maybe, causing more persistent hoarseness.
30:13
It used to be thought right -sided approaches
30:15
were riskier due to the nerves anatomy, but large
30:17
studies haven't really borne that out. If it
30:20
happens, we usually observe for about six weeks.
30:22
If no improvement, an ENT consultation is needed
30:25
for assessment, maybe vocal cord medialization
30:27
procedures, and a key point for revision surgery.
30:30
If there's a known or suspected presious RLN
30:33
injury, you absolutely perform the revision on
30:36
the same side to avoid the catastrophe of bilateral
30:39
nerve injury. which would compromise the airway.
30:41
What about the hardware? Hardware failure or
30:43
migration is a concern, especially, as I mentioned,
30:46
with two -level anterior crepectomies that 720
30:49
% risk often necessitates adding posterior backup.
30:52
Non -union or pseudorathrosis, where the bones
30:54
don't fuse properly, is another issue. Maybe
30:57
12 % risk for a single -level fusion, rising
30:59
to 30 % or more for multi -level fusions. This
31:02
might need repeat surgery. Smoking, NSAAD, use
31:05
post -op. Poor bone quality are risk factors.
31:08
And finally, a rare but serious risk is airway
31:11
compromise. This risk increases with very long
31:13
surgery, say over five hours, significant blood
31:16
loss, or when operating high up at C2, C3, C4
31:19
levels, which can cause a lot of prevertebral
31:21
swelling. Careful post -op monitoring, sometimes
31:24
even keeping the patient intubated for a period,
31:26
is crucial in high -risk cases. Okay, and the
31:28
posterior approach risks. With posterior approaches
31:30
like laminectomy or laminoplasty, a notable and
31:33
often quite challenging complication is postoperative
31:35
C5 palsy. This affects roughly 4 .6 % of patients
31:39
undergoing surgery for cervical myelopathy. It
31:43
seems more common in men, and particularly after
31:45
posterior laminectomy infusion. The exact cause
31:48
is still debated, but a leading theory involves
31:50
tethering or ischemia of the C5 nerve root as
31:53
the spinal cord shifts backwards after the posterior
31:56
elements are removed or opened. It causes a sort
31:58
of bow -stringing effect on the nerve root as
32:01
it exits. Clinically, it presents its weakness,
32:04
often quite profound, in the deltoid and biceps
32:06
muscles. While the prognosis for recovery is
32:09
generally good, it can take 6 to 12 months, sometimes
32:12
longer, which is obviously very distressing for
32:14
the patient. Some surgeons perform prophylactic
32:16
keyhole form monotomies at C45, widening the
32:19
nerve exit hole to try and reduce the risk. Other
32:22
posterior risks. The big one is post -laminectomy
32:24
kyphosis. if fusion isn't performed alongside
32:27
the laminectomy. That high incidence, 1147 %
32:32
of the neck gradually drifting into a forward
32:34
bend, potentially causing recurrent myelopathy.
32:38
Axial neck pain is also more common after posterior
32:41
approaches, likely due to the extensive muscle
32:43
dissection and altered biomechanics. How do you
32:46
mitigate all these? Mitigation is multifaceted.
32:48
It starts with meticulous preoperative planning,
32:50
choosing the right operation for the right patient.
32:53
Then, meticulous surgical technique during the
32:55
procedure itself is vital to minimize tissue
32:58
damage and protect neural structures. Intraoperative
33:01
neural monitoring, using SFPs and MEPs, is now
33:04
standard practice in most centers to provide
33:06
real -time feedback on spinal cord and nerve
33:08
root function during surgery. prophylactic antibiotics
33:10
or routine, early mobilization after surgery,
33:13
plus measures like compression stockings help
33:15
prevent blood clots, and critically, it's about
33:18
vigilant post -operative monitoring and prompt
33:21
management of any issue that arises. A post -operative
33:24
hematoma causing airway issues, for instance,
33:26
is a surgical emergency needing immediate return
33:28
to theater. With such complex operations and
33:30
these potential complications, it's vital to
33:32
look at the bigger picture. What does a prognosis
33:35
actually look like for patients after treatment?
33:37
And what's exciting on the research horizon?
33:40
What new developments are really shaping how
33:42
we approach recovery and try to improve those
33:44
long -term outcomes? This is where it gets really
33:46
interesting, doesn't it? Yes. Prognosis and future
33:49
directions. It's a really dynamic area. Historically,
33:53
as we know, the natural history of untreated
33:56
cervical myopathy is generally that slow stepwise
33:59
deterioration. It rarely gets better on its own.
34:02
Without treatment, patients can progress toward
34:04
significant disability, even becoming wheelchair
34:07
dependent in some cases if diagnosis is delayed.
34:10
But with surgery, the outlook changes significantly.
34:13
The typical outcomes, we quote, are roughly one
34:16
-third of patients see a definite improvement
34:18
in their symptoms compared to before surgery.
34:20
Another third remain stable, meaning the surgery
34:22
halts the progression, and unfortunately about
34:24
one -third may continue to worsen somewhat over
34:26
time, despite technically successful decompression.
34:30
This variability is why understanding the prognostic
34:32
factors is so critical when counseling patients.
34:36
Several things significantly influence how well
34:39
patients do. Early recognition and treatment
34:41
are paramount. Patients with symptoms for less
34:44
than six months generally have better outcomes.
34:47
Conversely, symptom duration longer than, say,
34:49
18 months is a strong poor prognostic factor.
34:53
It really reflects that window before irreversible
34:55
damage occurs. Age plays a role too. Younger
34:58
patients tend to have better recovery potential,
35:00
though it's crucial to stress that older patients
35:02
can still benefit significantly and shouldn't
35:04
be denied surgery based on age alone, assuming
35:07
they're medically fit enough. MRI findings give
35:10
us important clues. High signal on T2 images
35:13
combined with low signal on T1 images within
35:15
the cord, a high T2 signal intensity ratio, or
35:18
that cord compression ratio being less than 0
35:20
.4. These all predict poor neurological recovery
35:23
after surgery. That T1 change, indicating irreversible
35:26
damage, is particularly significant. Interestingly,
35:29
female gender has been linked with poor prognosis
35:31
in some large studies, though the exact reasons
35:33
aren't fully clear yet. And finally, the severity
35:35
of symptoms before surgery matters. Patients
35:38
going into surgery with very significant motor
35:40
weakness or profound loss of proprioception generally
35:44
have less favorable outcomes in terms of recovery.
35:47
Okay, so that leads us to the future. What's
35:49
emerging? This is where things get really exciting.
35:52
We're moving beyond just mechanical decompression
35:54
towards trying to influence the biology of recovery.
35:57
Medical and regenerative therapies are still
35:58
relatively early days, but they represent a potential
36:01
paradigm shift. The focus is on trying to halt
36:04
the chemical cascade of damage within the cord
36:06
and actively promote neural repair. One area
36:09
generating quite a bit of interest is cerebral
36:11
lysine. It's a neuroprotective drug, a mixture
36:14
of amino acids and peptides, including neurotrophic
36:17
factors. A pilot study published in Spine looked
36:20
at patients having surgery for DCM. They found
36:23
that those who received cerebral lysine showed
36:25
significantly better improvement in hand function
36:27
and overall neurological recovery compared to
36:30
placebo at one year follow -up. The recovery
36:32
rate, measured by MJOA, was about 67 % in the
36:36
treatment group versus 57 % in the placebo group.
36:39
And importantly, it seemed safe, with no major
36:41
adverse effects reported. This suggests a real
36:43
potential for agents like cerebral lysine to
36:45
maybe maximize recovery after surgery. It could
36:48
potentially protect neurons, enhance the cord's
36:50
own repair mechanisms, reduce secondary injury
36:52
after decompression. Imagine not just decompressing
36:56
the cord, but actively helping it heal. That
36:58
could be a game changer. That sounds incredibly
37:00
promising. What else? Another fascinating and
37:03
very practical area is intraoperative mean arterial
37:07
pressure MAP optimization. There's growing evidence
37:10
that maintaining a higher blood pressure during
37:12
surgery can improve blood flow or perfusion to
37:16
the compromised spinal cord. A recent pilot study
37:19
found that individualizing the MAP target, specifically
37:22
aiming for 20 mmHg above the patient's own preoperative
37:25
average blood pressure, led to better neurological
37:28
outcomes compared to a standard MAP target. This
37:31
highlights how crucial, precise hemodynamic management
37:34
by the anesthetic team is during surgery. Ensuring
37:37
adequate oxygen delivery to the vulnerable cord
37:39
might significantly reduce ischemic injury and
37:41
improve recovery potential. It's a relatively
37:43
simple intervention with potentially big impact.
37:46
So we're finding the perioperative care. Exactly.
37:48
And beyond specific drugs or techniques, there's
37:51
a much broader recognition of the need for a
37:53
personalized, multidisciplinary approach. Clinicians
37:57
need to be really attuned to those early, subtle
37:59
signs for timely diagnosis. Looking ahead, we
38:02
might see advancements in chemical biomarkers,
38:05
perhaps found in spinal fluid or even blood in
38:07
more sophisticated ancillary tests. These could
38:10
help diagnose DCM earlier, track its progression
38:13
more accurately, and monitor response to treatment.
38:15
Imagine a blood test indicating the degree of
38:18
cord injury or inflammation. And involving patients
38:20
more. Yes, that's hugely important too. The emphasis
38:24
on patient -centered care is growing. Initiatives
38:27
like the RICO -DCM project are fantastic examples.
38:29
They bring together patients, clinicians, researchers,
38:32
all stakeholders to define research priorities
38:35
based on patients' lived experiences. The goal
38:37
is to create a research toolkit to accelerate
38:40
knowledge and improve outcomes by making sure
38:42
research actually addresses what matters most
38:44
to patients. This really underscores how vital
38:46
it is to understand individual patient factors,
38:49
their preferences, their goals, especially in
38:52
those tricky cases of mild DCM where the decision
38:54
between surgery and non -operative management
38:57
isn't clear -cut. It's about tailoring care to
38:59
the whole person, not just their MRI scan. A
39:02
patient's job, hobbies, life goals, these all
39:05
weigh into the decision. That's incredibly forward
39:07
-looking, moving beyond just the mechanics to
39:09
actual neurological recovery and patient priorities.
39:13
Professor, before we go to the final quick round,
39:14
what's one common misconception about DCM that
39:17
you often encounter, even among experienced colleagues,
39:19
and how do you usually clarify it? A very common
39:22
one is the belief that significant neck pain
39:24
must be present for a diagnosis of cervical myelopathy.
39:28
I often see clinicians potentially dismissing
39:30
myelopathy if the patient isn't complaining of
39:32
severe neck pain. But as we've discussed, things
39:35
like gait disturbance or hand clumsiness can
39:38
absolutely be the main or even the only presenting
39:40
symptoms. I clarify it by really stressing the
39:43
difference between radiculopathy, which is often
39:46
painful nerve root irritation, and myelopathy,
39:49
which is about spinal cord dysfunction itself.
39:51
The symptoms reflect where the problem is. Excellent
39:53
point. Okay, let's move into our lightning round
39:56
for some quick, sharp answers. What single physical
39:59
exam finding, if positive, should immediately
40:01
raise a massive red flag for myelopathy during
40:04
your assessment? Hoffman's sign. It's easy to
40:06
elicit and a strong indicator of upper motor
40:09
neuron involvement. Perfect. Is non -operative
40:12
treatment ever really a definitive, long -term
40:15
fix for a progressive cervical myelopathy? Rarely,
40:18
if ever. It might provide temporary symptom relief
40:20
in very mild stable cases, but it doesn't fundamentally
40:24
alter the natural history of progression in established
40:26
symptomatic myelopathy. You mentioned a specific
40:29
ratio on MRI that suggests a poorer prognosis.
40:33
What was that again? A spinal cord compression
40:35
ratio of less than 0 .4. Got it. Beyond the standard
40:39
surgical techniques, what's one cutting -edge
40:41
research area you're personally most excited
40:44
about for potentially improving DCM outcomes
40:47
in the next few years? I think the potential
40:49
role of pharmacological neuroprotective agents,
40:52
things like cerebellicin, used in conjunction
40:54
with surgery. That's where boosting actual neurological
40:57
recovery might come from. And finally, post -operatively,
41:00
beyond just the wound healing, what's the most
41:02
crucial aspect of care for a patient recovering
41:05
from cervical myelopathy surgery? comprehensive
41:07
structured physical rehabilitation. It needs
41:10
to be tailored to the individual patient to really
41:12
maximize their functional recovery potential.
41:15
Fantastic. So wrapping all this up, what does
41:18
it mean for you, the clinician, dealing with
41:21
the complexities of cervical myelopathy day to
41:23
day? Here are our key takeaways. First, be vigilant
41:27
for cervical myelopathy. Remember, it's often
41:29
vague, sometimes neck pain absent symptoms like
41:32
hand clumsiness, gait instability. Though subtle
41:35
balance changes are critical red flags, don't
41:37
just put them down to aging. Early diagnosis
41:39
is absolutely paramount for outcomes. Second,
41:42
physical exam and imaging are your essential
41:44
tools. Actively look for those upper motor neuron
41:47
signs like Hoffman's hyperreflexia. Understand
41:49
their nuances. Know the prognostic value of MRI
41:52
findings, T1, T2 signal changes, chord compression
41:55
ratios, but always interpret imaging in clinical
41:57
context to differentiate from mimics. Third,
42:00
treatment is usually surgical. and early intervention
42:02
is key. While non -op has a very limited role
42:05
for mild stable cases, definitive management
42:07
for progressive symptoms generally means surgical
42:09
decompression. Choosing the right approach anterior
42:11
-posterior combined is a highly nuanced individualized
42:14
decision. Fourth, stay updated on emerging insights.
42:18
This field is moving fast. Things like optimizing
42:20
intraoperative blood pressure, the potential
42:22
of neuroprotective drugs like cerebellicin. These
42:26
are actively shaping better outcomes and offer
42:28
hope for enhancing neurological recovery. And
42:31
finally, perhaps most importantly, embrace the
42:34
multidisciplinary approach in patient -centered
42:36
care. Effective management needs team surgeons,
42:40
neurologists, physios, allied health. And increasingly,
42:43
it demands understanding and integrating patient
42:46
-specific factors, preferences, and goals into
42:48
decision -making, especially for those borderline
42:51
mild cases. That brings us to the end of another
42:54
really insightful deep dive. We truly hope this
42:57
exploration into cervical myelopathy has given
43:00
you valuable perspectives and actionable knowledge
43:02
for your practice, helping you identify, understand,
43:05
and manage this complex condition more effectively.
43:08
If you found this deep dive valuable, please
43:10
do take a moment to rate and share the show with
43:12
your colleagues. It genuinely helps us reach
43:14
more dedicated professionals like you. Thank
43:16
you so much for joining us on the deep dive.
43:18
Until next time, keep learning, keep questioning,
43:20
and stay well informed. Remember that in medicine,
43:23
pursuing knowledge is a lifelong journey with
43:26
profound impact.