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