Neuro: Anterior Spinal Artery Syndrome: Free MSRA Podcast

⚕️ FREE MSRA PODCAST – Anterior Spinal Artery Syndrome
🎧 In this episode, we break down a rare but high-yield neurology topic: anterior spinal artery syndrome (ASAS) – a condition marked by sudden motor weakness, loss of pain and temperature sensation, but preserved proprioception. Designed for fast, focused MSRA revision.

🧠 Key Learning Points

📌 Definition
• Anterior spinal artery syndrome (ASAS) is caused by ischaemia or infarction of the anterior two-thirds of the spinal cord.
• Results in motor deficits and loss of pain & temperature sensation, but preservation of vibration and proprioception.
• Classic example of a “sensory dissociation” pattern.

📌 Causes & Risk Factors
• Common causes include:

• Atherosclerosis (most common)

• Aortic dissection or aneurysm

• Spinal trauma or surgery

• External compression (e.g. tumour, herniated disc)

• Vasculitis

• Hypotension or embolism
  • Risk factors:

• Advanced age

• Cardiovascular disease (e.g. hypertension, diabetes, AF)

• Smoking, hyperlipidaemia

• Previous spinal or vascular trauma

📌 Pathophysiology
• The anterior spinal artery supplies the spinothalamic tracts (pain/temp), corticospinal tracts (motor), and autonomic fibres.
• Occlusion → ischaemia → infarction → sudden loss of function in these areas.
• Posterior columns spared, explaining preserved vibration and position sense.

📌 Symptoms
• Sudden onset of symptoms (within minutes to hours)
• Bilateral weakness/paralysis below lesion
• Loss of pain and temperature sensation
• Bladder/bowel dysfunction
• Autonomic instability: hypotension, sweating issues
• ⚠️ Proprioception and vibration preserved – crucial diagnostic clue
• May be preceded by sudden back pain at level of infarction

📌 Differential Diagnosis
• Spinal cord compression (e.g. tumour, epidural abscess)
• Transverse myelitis
• Guillain-Barré syndrome (though it’s peripheral)
• Spinal cord infarcts from other arterial sources
• Use MRI to rule out compression or inflammatory conditions
• Mnemonic: "STG" – Spinal compression, Transverse myelitis, Guillain-Barré

📌 Diagnosis
• Clinical exam + MRI spine = gold standard
• Look for “Owl’s Eye” sign on T2 MRI – symmetrical hyperintensity in anterior cord
• Additional tests:

• FBC, U&Es, clotting, autoimmune screen

• Lumbar puncture (rule out infection/inflammation)

• Spinal angiography (rarely used)

📌 Management
• No way to reverse cord infarction directly – supportive care is key
• Time-sensitive thrombolysis may be considered in select cases (<4.5 hours)
• Medical options:

• Antiplatelets (e.g. aspirin)

• Anticoagulants (if embolic cause suspected)

• Fluids & vasopressors for hypotension

• Consider steroids in inflammatory causes
  • Non-prescribing management

Episode Transcript

(00:00):
All right, let's jump right in. We've got some really detailed
revision notes here from a listener, all focused on
anterior spinal artery syndrome,which is, well, quite a
condition. Imagine, you know, sudden
paralysis, losing that ability to feel pain or temperature, but
you can still feel touch. It's that strange pattern we're
diving into. So our mission today is to take

(00:20):
these notes you shared and really unpack them.
We would have sift through, pullout the absolute high yield
stuff, the key facts you need maybe for revision or just to
get a good handle on the specific and thankfully quite
rare neurological issue. Think of it as your focus guide
to anterior spinal artery syndrome.
Yeah. And it's definitely worth
understanding because at its core, like these notes say, it's

(00:43):
all about the spinal cord. It happens when the blood supply
specifically from that anterior spinal artery gets blocked,
basically disrupted. It's not common, no, but the
notes are right to stress how severe it can be.
The impact, the long term stuff,OK.
Let's unpack this then, startingright at the basics based on
these notes. Yeah.
What exactly is anterior spinal artery syndrome?
What's the definition we're working with?

(01:04):
So the notes define it as a, well, a rare neurological
condition, and the cause is occlusion, a blockage of the
anterior spinal artery. Simple as that.
And this blockage leads to ischemia which is just lack of
blood flow, which then causes damage or infarction.
You know, tissue death in the spinal cord itself.

(01:26):
Right. And the location supplied by
that artery is key as. Exactly.
It mainly feeds the front 2/3 ofthe spinal cord and the notes
are specific here. This includes really important
pathways, the spinothalamic tracts they carry, pain and
temperature signals, and the corticospinal tracts, vital for
voluntary movement, plus some autonomic fibres too.
OK. So because those specific

(01:47):
pathways get hit, the symptoms, the deficits are quite distinct.
Precisely. The damage there translates
directly into that clinical picture the notes describe.
You get loss of pain and temperature sensation always
below the level of the damage, loss of voluntary motor
function, so weakness or even paralysis and autonomic
dysfunction. Things like problems regulating
blood pressure, pressure, often hypotension.

(02:09):
OK. And the notes mentioned a common
trigger for this blockage, something about the aorta.
Yeah. They highlight that often the
root issue is a disruption somewhere in the aortic blood
supply because that's sort of where the anterior spinal artery
branches off from indirectly. And the notes, well, they don't
really sugarcoat the severity. Do they even read at the start?
No they don't. They state it clearly.
It's linked with high mortality,often a poor long term prognosis

(02:33):
and yeah, frequently leads to permanent disability.
Which is why getting the detailsright is so crucial.
You know if you're revising or needing to spot this.
OK, so that's the what? Serious stuff, but why does it
happen? What causes this blockage?
What's the the aetiology according to the notes?
Why does this artery get blocked?
Well, the most common cause mentioned is atherosclerosis.

(02:56):
You know, the hardening and narrowing of arteries.
That whole process can lead to blood clots forming or bits
breaking off emboli, which then travel and block smaller
arteries like this one. But it's not just
atherosclerosis, right? The notes listed other things.
Correct, atherosclerosis is the big one, but not the only one.
The notes also mention trauma, direct injury to the spine or

(03:17):
maybe the aorta, artery dissection or rupture the artery
wall itself, tearing, vasculitis, which is
inflammation of blood vessels. Also compression from the
outside, like a big herniated disc or a tumour pressing on the
cord or its blood supply and systemic vascular diseases,
things affecting blood vessels all over the body.
Wow. OK, quite a range of potential

(03:38):
causes. So who's most likely to run into
this? What about risk factors?
What are the notes say there? The notes give a pretty standard
list, but it's important things that make someone more
vulnerable like advanced age, having a history of
atherosclerosis already conditions that damage vessel.
So hypertension, smoking, high cholesterol, hyperlipidemia,
diabetes, those usual suspects having existing cardiovascular

(04:00):
disease. Generally.
The notes also flag conditions that make clots more likely,
like atrial fibrillation and as we mentioned, a history of
traumatic injury to the spine orneck.
They all basically increase the risk of those underlying causes
we just talked about. OK, now this is where it gets
really interesting for me. Connecting the dots, how does
blocking this specific artery lead to that specific set of

(04:20):
symptoms? Let's dig into the
pathophysiology. Right.
So the notes really emphasise the anatomy here.
The anterior spinal artery supplies the front 2/3 of the
spinal cord. That's the key take away and why
that matters as the motes detailis because that anterior part
houses those critical tracks, the corticospinal tracts for
movement, the spinal thalamic for pain and temperature and

(04:42):
those autonomic fibres. So cut off the blood supply
there and. Boom, pretty much.
Occlusion means ischemia, no oxygen, no nutrients, and that
quickly leads to infarction, irreversible tissue death in
those parts of the cord. The result of that tissue dying
in those specific areas is exactly what you see clinically.
Loss of motor function, those specific sensory losses, pain

(05:03):
and temp below the lesion, and the impaired autonomic
functions. The notes are clear, though the
severity really depends on wherethe blockage is along the cord
and how much tissue is affected.Higher up means more deficits.
Makes perfect sense when you mapthe arteries territory to the
symptoms. OK, but sudden weakness?
Sensory changes? It could be other things too.
What else needs to be considered?

(05:24):
What are the main differential diagnosis the notes mention?
Yeah, good point. The notes list conditions that
also cause acute myelopathy, that sudden spinal cord problem.
So the main things to rule out are spinal cord compression,
something pushing on the cord like a tumour or a bad disc
herniation. Transverse myelitis is on the
list, that's inflammation of thecord.

(05:45):
Guillain Barre syndrome gets a mention too, though the notes
rightly point out it's usually more of a peripheral nerve issue
and acute inflammatory demyelinating polyradiculo
neuropathy, quite a mouthful, but it causes acute weakness.
So it's on the differential list, right?
And then spinal cord infraction from maybe a different artery or
other sort of vascular or skebicspinal cord problems.

(06:06):
In that point, you mentioned about using MRI later to
distinguish from things like cauda, iguina or compression.
That seems crucial here for sorting these out.
Oh, absolutely. MRI is key, not just to look for
the signs of ASAS, but critically to rule out that
compression or see if it looks more like inflammation, like in
transverse myelitis. It helps separate these

(06:28):
possibilities. Gotcha.
And just quickly how common is this?
The notes mentioned epidemiologyin the UK.
Yeah, the main point there is just that the actual prevalence
isn't well known. It's considered relatively
uncommon, so important to know about, but not something you'll
see constantly. OK.
Let's paint a picture. What does this actually look
like in a patient? What are the typical clinical

(06:48):
features the notes outline? The number one thing emphasised
in the notes is the sudden onset.
It's rapid, not gradual. We're talking minutes to hours.
That's critical for recognition.OK, sudden and the deficits.
We've touched on them but to list them out from the notes.
Weakness or paralysis. Limbs below the level of the
lesion. Sensory loss, but again, it's

(07:08):
specific. Impaired pain and temperature
perception is the key. Often loss of bladder and bowel
control too because of those autonomic pathways and other
autonomic signs like orthostatichypotension that dizziness or
blood pressure drop when standing up.
Sometimes issues with sweating too.
And here it is, the really high yield bit for exams or just

(07:28):
remembering this condition right, that sensory split.
Absolutely. The notes are very clear.
A critical feature is the preservation of light touch,
vibration sense and proprioception.
Knowing where your limbs are in space.
So lose pain and temp, keep light touch and vibration.
That's the classic pattern. A must know.
The notes also add that sometimes the very first symptom
might just be sudden severe backpain right at the level of the

(07:51):
cord damage. OK, so someone presents like
that sudden onset, that specificsensory loss, how do doctors
confirm it's a SAS and not one of those other possibilities?
What investigations are key? Well, it always starts with the
clinical picture, right? A thorough evaluation,
neurological exam, testing reflexes, strength, all the
sensations carefully. But then imaging is absolutely

(08:12):
vital. MRI or CT scans to actually look
at the spinal cord and the noteshighlight MRI of the spine as
the gold standard investigation here.
And there's a specific sign theymentioned.
Yes, another high yield detail from the notes on specific MRI
sequences, T2 weighted images, you might see this
characteristic pattern in the anterior cord called the owl eye
sign. It looks like, well, owl eyes.

(08:34):
It strongly suggests ischemia inthat anterior spinal artery
distribution. And like we said, the MRI is
also crucial for ruling out compression or distinguishing
ischemia from inflammation like transverse myelitis.
Makes sense? Any other tests?
Yeah, the notes mention others that might be done.
Blood tests looking for risk factors, lipids, clotting
factors, maybe autoimmune markers, electrophysiological

(08:56):
studies like nerve conduction studies might sometimes be used,
and a lumbar puncture. A Spinal Tap could be done
mainly to rule out infection or inflammation, though it might
show some general signs of cord damage too.
But the notes really stress thatclinical suspicion.
Recognising that pattern early is key for getting things moving
quickly. Time can be a factor depending

(09:18):
on the 'cause. Right.
So if the diagnosis is made or strongly suspected, what's the
plan? What's the management approach?
The notes split this into prescribing and non prescribing.
The main focus, according to thenotes, is supportive care and
trying to address whatever underlying cause led to the
blockage, if possible. But here's the really critical
point the notes make. There's no specific treatment

(09:40):
that can actually restore blood flow directly to those damaged
bits of the spinal cord once theinfarction the damage has
happened. Wow, so the damage is largely
done? Pretty much, which really
highlights why prevention and spotting risk factors are so
important. OK, so let's look at the
prescribing treatment options mentioned.
It really depends heavily on the'cause if it's thought to be
from an acute clot, say from atherosclerosis.

(10:02):
The notes do mention thrombolysis clot busting drugs.
But, and this is a big but, that's only potentially helpful
in a very narrow time window, often stated as 4.5 hours from
when symptoms started. And it's not suitable for
everyone or every cause. So a very specific scenario.
What else? Other medical treatments include
things like antiplatelet drugs like aspirin to help prevent

(10:25):
more clots, 5E fluids and maybe vasopressors, drugs to support
blood pressure. Especially with that autonomic
dysfunction and anticoagulation.Blood thinners are usually
needed both short and long term.The notes mentioned.
Steroids have limited evidence but might be considered right at
the start, though it's not standard therapy.
OK. And given there's no direct fix
for the court itself, that nonprescribing management sounds

(10:48):
incredibly important. Oh it's absolutely central to
long term care. It's all about preventing
secondary complications and trying to maximise whatever
functional recovery is possible.So the notes list things like
mechanical measures to prevent blood clots like DVT.
Especially when someone can't move much.
Extensive rehabilitation is crucial.
Physio for movement, occupational therapy for

(11:10):
adapting daily tasks, maybe speech therapy if the lesion is
high up affecting breathing or swallowing.
Managing complications is key. Bladder issues might need
catheterization, respiratory support, even mechanical
ventilation might be needed for high cervical lesions.
And the notes emphasise needing a whole multidisciplinary team,
neurologists, rehabilitation doctors, physiatrists,

(11:31):
therapists, nurses. Given everything we've said
about severity, what's the outlook?
Typically what the Prognotes is like.
The notes describe it as guarded, which basically means,
you know, approach with caution.Outcomes are uncertain and often
lean towards being less favourable.
Unfortunately, complete neurological recovery is rare.
That said, the notes are clear that significant functional

(11:52):
improvement is possible with really good supportive care and
intensive rehab. But residual problems, long term
impairments, they are very common.
And what sort of long term issues or complications might
people face down the line? It's a long list, sadly,
reflecting how much the spinal cord controls.
The notes mentioned things like chronic pain, persistent muscle
weakness, ongoing sensory issues, problems with bladder,

(12:16):
bowel and sexual function that orthostatic hypotension can
persist, respiratory issues, bigrisks from being immobile
include pressure sores and deep vein thrombosis, possibly
leading to pulmonary embolism, must contractures where joints
get stiff, and importantly, the psychological impact,
depression, anxiety are common. And as you'd expect, the notes

(12:36):
say the risk and severity of allthese complications really
depends on how bad the initial cord damage was.
So ongoing monitoring and prevention are vital.
OK, we have covered a lot of ground from these notes.
If someone listening is trying to nail this down for revision,
what are the absolute key high yield takeaways they should lock
in? Right, based on how the notes
emphasise things, definitely that sensory pattern, loss of

(12:58):
pain and temperature, but crucially, preservation of
light, touch, vibration, and proprioception.
That dissociation is classic Acus.
Got it. Sensory split.
What else? The sudden, rapid onset.
That's key for spotting it diagnostically.
Remember that owl eye sign on the spinal MRI?
That's the characteristic finding to look for.

(13:18):
OK, owl eyes on the MRI. Management wise, the big thing
is no direct cure for the damaged core tissue itself, so
it's all about supportive care and intense rehab.
And remember that very limited window that 4.5 hours for
thrombolysis if it's the right kind of cause.
And finally, I'd say connect thesymptoms back to the anatomy.
Knowing the anterior spinal artery feeds the motor tracks

(13:39):
and the spinothalamic tracks, itjust makes sense of why you get
weakness plus that specific pain, temp loss.
Understanding the why helps it stick.
So pulling it all together, we've really dug into anterior
spinal artery syndrome using these detailed revision notes.
It's definitely rare, but it hasits very specific way of
presenting itself, all stemming from that blocked artery.

(14:00):
It poses real challenges for diagnosis and management and
often leaves a lasting impact. Absolutely.
And whether you are revising forsomething like the MSRA or just
want to broaden your medical knowledge, getting a handle on
that sudden onset, the unique sensory findings, the role of
MRI and the fact that managementis primarily supportive, that's
all really valuable stuff from these notes.

(14:22):
It is complex for sure, and digging into it like this really
shows how interconnected everything is, doesn't it?
How vulnerable the nervous system can be to just a plumbing
problem, essentially. If you found this deep dive
approach helpful for getting your head around tricky medical
topics, you might find more resources over a past the mass
sra.com. And also free massra.com both

(14:42):
have great stuff for study support definitely.
Check them out. You know, understanding
conditions like this, even the rare ones, it really underlines
the critical importance of vascular health for, well,
everything, especially the central nervous system.
Makes you think, doesn't it? It really does well.
Thanks for joining us on this deep dive.
Keep exploring. See you on the next one.