May 30, 2025 • 19 mins
⚡ FREE MSRA PODCAST – Amaurosis Fugax: Sudden Vision Loss & Stroke Warning Signs
🎧 Get a concise, exam-focused breakdown of amaurosis fugax—what it is, how to recognise it, and why it’s a clinical red flag. Perfect for MSRA revision and real-world GP practice.
🧠 Key Learning Points
📌 Definition
• Amaurosis fugax = transient, painless loss of vision (usually one eye) due to temporary loss of retinal blood supply.
• Classic “curtain descending” or “shade over vision” description—typically lasts a few seconds to 15 minutes.
📌 Causes & Mechanism
• Most common: Emboli from carotid artery atherosclerosis (fatty plaques breaking off).
• Can also result from cardiac sources, giant cell arteritis (GCA), ocular migraine, vasospasm, or hypercoagulable states.
• Mechanism: Temporary blockage of retinal/optic nerve blood flow → brief ischaemia → vision returns as flow restores.
📌 Risk Factors
• Age >60, hypertension, diabetes, smoking, high cholesterol, obesity, cardiovascular/cerebrovascular disease, family history of stroke/TIA, clotting disorders.
📌 Symptoms
• Sudden, monocular (one eye) or occasionally binocular, painless loss of vision—“blackout” or “curtain” effect.
• Vision returns fully after minutes.
• May have associated flashes, blurring, or pressure sensation.
📌 Differential Diagnosis
• Retinal migraine, retinal detachment, vitreous haemorrhage, angle closure glaucoma, optic neuritis, ocular ischaemic syndrome.
📌 Investigations
• Clinical history (focus on vascular risk factors).
• Carotid Doppler ultrasound (look for plaques), cardiac evaluation (ECG, echo), bloods (lipids, clotting, inflammation), MRI/CT angiography if needed.
• Ophthalmic assessment—visual acuity, fields, fundoscopy.
📌 Management
• Address underlying cause and reduce stroke risk.
• Lifestyle: Stop smoking, healthy diet, exercise.
• Medications: Antiplatelets (aspirin/clopidogrel), statins, antihypertensives, diabetes control.
• High-dose steroids if GCA.
• Carotid endarterectomy if severe carotid stenosis.
• Advise: No driving for 1 month unless vision is fully and permanently recovered.
📌 Prognosis & Complications
• Prompt management reduces risk of TIA/stroke and permanent vision loss.
• Untreated = high risk of future stroke, visual impairment, disability.
📎 More MSRA Resources for Amaurosis Fugax:
📝 Revision Notes: https://www.passthemsra.com/topic/amaurosis-fugax-revision-notes/
🧠 Flashcards: https://www.passthemsra.com/topic/amaurosis-fugax-flashcards/
💬 Accordion Q&A: https://www.passthemsra.com/topic/amaurosis-fugax-accordion-qa-notes/
🚀 Rapid Quiz: https://www.passthemsra.com/topic/amaurosis-fugax-rapid-quiz/
🎓 Full Course: https://www.passthemsra.com/courses/neurology-for-the-msra/
#MSRA #MSRARevision #MSRATextbook #MSRAQuiz #MSRAFlashcards #MSRAAccordions #AmaurosisFugax #StrokeWarning #VisionLoss #Neurology #GPExam #TIA #MSRAOnlineRevision
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:00):
Imagine this. Suddenly it feels like a dark
curtain is being pulled down over your vision.
It might cover everything, or maybe just part of it, and it's
totally painless. It only lasts a few minutes,
maybe, but it's, well, it's incredibly alarming.
That really vivid description comes straight from the source
material for today's Deep Dive. It's a very striking image,
isn't it? It really is.
(00:21):
So today we're taking a deep dive into Amorosis Fugacs.
It sounds maybe a bit complicated, medically speaking,
but the revision notes you've provided give us a fantastic
map. Yeah, absolutely.
And our mission today is really to unpack these notes, pull out
the the highest yield information, the really key
stuff and help you understand this condition thoroughly, but
(00:42):
you know, efficiently. We're basically guiding you
through the essentials from these notes.
And this really matters because,as the source highlights pretty
clearly, this temporary visual loss is often a critical warning
sign, something you absolutely shouldn't ignore.
Exactly a major red flag O Let'sstart right at the beginning
with the definition. The notes define amyrosis fugacs
(01:04):
as a temporary, painless loss orreduction of vision in one or
sometimes both eyes. And the source puts a real
emphasis on that description. You mentioned that really
distinct curtain like or shade like effect.
It feels like a key way to remember what patients actually
report. It is.
It's very memorable. And the underlying cause is a
temporary disruption of blood flow specifically to the retina
(01:27):
or perhaps the optic nerve. OK.
And this interruption of supply is precisely why it's such an
important warning sign. It strongly suggests an
underlying issue with blood vessels, maybe further upstream,
and it needs prompt medical evaluation.
So it's not usually a problem inthe eye itself causing the
vision loss, it's more about theblood getting to the eye.
Exactly right. Think of it like a supply line
(01:47):
issue, the notes state. These episodes typically last
somewhere between, say, 5 and 15minutes.
OK. And crucially, amorosis fugex
often presents as a type of transient ischemic attack or
Tia. Right atia like a mini stroke
people sometimes call it. That's the term, yes, a mini
stroke. And these episodes, this
amorosis fugacs can sometimes even come before a more serious
(02:11):
full blown stroke or even permanent visual loss.
It's a warning. OK, let's unpack this further
then. What actually causes this
temporary disruption? Where does the problem in that
supply line originate? Well, the notes are very clear
on this. Often the cause is a transient
ischemic. A Tia means temporary poor blood
(02:32):
flow, usually thought of in relation to the brain, but in
this context it's affecting the blood supply to the eyes, retina
or optic nerve. And what's the most common
reason for that Tia affecting the eye?
What's behind it? The source points overwhelmingly
towards atherosclerosis. That's the buildup of fatty
plaques inside the arteries. These plaques can narrow the
arteries, obviously, or bits of them can break off, forming
(02:53):
blood clots or what we call emboli.
Little fragments travelling in the blood.
Precisely. These fragments travel through
the bloodstream, and if they happen to lodge in and block the
small blood vessels supplying the eye, well, that's when you
get the temporary vision loss. So it's like debris clogging a
pipe basically. That's a good analogy, yes.
Like debris in the body's plumbing system.
And that plaque breaking off from, say, the carotid artery in
(03:16):
the neck, is that a common scenario described in the notes?
Absolutely. That's mentioned as a frequent
source of these emboli, but the notes also list other potential
pauses such as well, emboli can come from the heart itself.
Perhaps due to certain heart conditions, there can be
vasospasm where the blood vesseltemporarily clamps down really
tightly, right? Increased blood viscosity,
(03:39):
thicker blood that doesn't flow as easily, or just generally
reduced overall blood flow for various other reasons.
And are there specific medical conditions the notes flag up as
potential triggers? Yes, they specifically mentioned
conditions like giant cell arteritis or GCA.
That's an inflammatory conditionaffecting blood vessels, OK, And
also ocular migraine. But again, the notes really
(04:00):
highlight that vascular blockage, usually from
atherosclerosis causing MLI, is the most frequent mechanism they
detail. So given all these potential
causes linked to blood flow and vessels, who is more likely to
experience this? What are the key risk factors
listed in the source? The list includes many familiar
cardiovascular risk factors, things you might expect.
(04:23):
Yeah, so straight from the source.
Older ages 1A history of cardiovascular disease, things
like hypertension, coronary artery disease, smoking,
definitely diabetes, hyperlipidemia which is high
cholesterol and obesity. Makes sense.
Family history of stroke or Tia is also listed which fits the
(04:44):
pattern. It does, and also certain
genetic or acquired conditions that might make blood more prone
to clotting or cause other vascular abnormalities.
What's interesting here, and it ties back to what you're saying
earlier, is how many of these connect directly to just broader
cardiovascular health? Exactly.
It really underscores that this isn't just some isolated eye
thing, is it? It's often a symptom reflecting
systemic problems, usually with the blood vessels.
(05:06):
Precisely. It's a sign from the system
which leads us nicely into how it actually happens
physiologically, the path of Physiology.
How does that blood flow disruption translate into that
temporary vision loss? Yeah, what's in the mechanism?
Well, at its core, as we've said, the blood flow to the
retina or the optic nerve gets compromised temporarily.
(05:28):
And the typical reason for that compromise like we discussed
with the causes? Most often, according to the
notes, it's these blood clots orbits of plaque obstructing those
vital small vessels that supply the eye.
And this blockage, or reduced flow then leads to what the
notes call an ischemic episode. Correct, Ischemia just means a
period where there's reduced blood flow and therefore reduce
(05:50):
oxygen supply to the tissue, in this case the retina or the
optic nerve tissue. And the immediate result of that
temporary lack of oxygen is? Temporary loss of vision.
Simple as that. Pretty much.
And it's temporary because usually the obstruction itself
is transient. The clot might break up and move
on, or maybe a spasm resolves, blood flow gets spontaneously
restored. And vision comes back relatively
(06:11):
quickly. Exactly.
Vision returns to normal. The notes do mention that the
duration can vary quite a bit, sometimes just a few seconds,
other times several minutes. OK.
So moving on to what you actually see or feel, the
clinical features, the main one we've kept coming back to is
that sudden temporary vision loss, usually just in one eye,
(06:32):
though the notes say it can affect both.
Right. And to really lock it in your
memory, that distinct curtain like or shade like effect is the
classic description you'll oftenhear or read about.
It's a very helpful detail, definitely.
And the vision loss itself, can it vary in intensity?
Yes, it can be complete, like a total blackout in that eye.
Or it might be partial, maybe just affecting the top half or
(06:55):
the bottom half of the visual. Field And just to reiterate,
these episodes last seconds to minutes before fully resolving
on their own that spontaneity iskey.
It is. Associated symptoms, according
to the notes, can sometimes include things like flashes of
light, maybe some blurry vision during the episode, or even a
feeling of pressure behind the affected eye.
But the crucial detail, and thishelps differentiate it perhaps,
(07:18):
is that Vision usually returns completely to normal after the
episode passes, no lasting deficit from the event itself.
That's the typical pattern, yes.OK, so if someone experiences
sudden temporary vision loss, how do doctors know for sure
it's amorosis, fugacs and not one of the many other things
that can cause sudden visual disturbances?
(07:40):
This must be where the differential diagnosis comes in.
Precisely. It's a critical step.
The source notes list several conditions that can look similar
and absolutely need to be ruled out.
What sort of things are on that list?
Things like ocular migraine or retinal migraine, which are
related but distinct. Retinal detachment, that's an
emergency vitreous haemorrhage, which is bleeding inside the
eye. Angle closure.
(08:01):
Glaucoma, another urgent condition, optic neuritis, which
is inflammation of the optic nerve and something called
ocular ischemic syndrome, which is more chronic.
Poor blood flow. Wow, that's quite a list.
So how do doctors sort through that?
How do they differentiate? Well, a really comprehensive
evaluation is essential, the notes describe.
This involves taking a thorough medical history, paying close
(08:23):
attention to those cardiovascular risk factors we
talked about earlier makes sense.
Then a detailed ophthalmic examination to actually look at
the eye structure itself, visualfield testing to map out any
vision loss, and various imagingtechniques.
Right, like the Doppler scans orMRI.
Exactly. Things like carotid Doppler,
ultrasound, maybe an MRI or CT angiography.
(08:45):
And the aim of all this investigation?
What are they trying to achieve?It's really twofold.
First, assess the patient's overall vascular status.
Hunt for blockages, sources of emboli, that sort of thing.
Find the upstream. Problem.
Find the upstream problem, yes, and 2nd, definitively exclude
those other potential causes on the differentialist.
The eye exam, for instance, helps rule out things happening
(09:07):
inside the eye itself, like a detachment or a haemorrhage.
Got it. And just briefly on the
epidemiology, who gets this and how often?
The notes mention UK figures. Yes, they do mention that
specific prevalence just for amorosis fugax itself isn't
perfectly defined in the source notes we have OK, but they give
an estimate for TI as in general, which as we know
(09:29):
amorosis fugax often falls under.
And they estimate around 46,000 annual cases of TI as in England
alone so. It's not uncommon.
Not at all, and while it can occur at various ages, it
mirrors the risk factors become significantly more common in
people over the age of 60. Right.
So digging into those investigations a bit more than
(09:49):
How exactly do doctors figure out the underlying cause?
The investigation section in thenotes lays out the steps quite
clearly. It does.
It usually starts with, as we mentioned, a detailed medical
history and a physical examination.
They're actively looking for signs of underlying vascular
disease or those risk factors welisted.
Then come blood tests. What are they specifically
checking for in the bloods in this context?
(10:10):
They'll check things like cholesterol levels, blood
clotting factors to see if the blood is too prone to clotting
and maybe markers that could indicate systemic inflammation
or other vascular issues. It helps build that overall
picture of cardiovascular health.
And imaging studies, you mentioned carotid ultrasound,
MRI, CT angiography. What's the main focus there?
(10:31):
Imaging is absolutely crucial because they're trying to
pinpoint the source of that temporary blockage if possible.
A carotid ultrasound is very common.
It looks directly for plaque buildup in those big arteries in
the neck, a really frequent source of emboli going to the
eye. OK, MRI and CT angiography give
even more detailed pictures of blood vessels, helping to
(10:53):
identify abnormalities or blockages elsewhere, maybe
higher up or in the brain circulation.
What about checking the heart? Is that usually part of the work
up? Often, yes, a cardiac
evaluation, maybe with an ECG oran echocardiogram and ultrasound
of the heart is needed because the heart itself can be a source
of emboli. They're looking for things like
irregular heartbeats, valve problems, things that could
(11:14):
generate clots. And of course the eye itself
gets a proper look too. Oh definitely.
A detailed ophthalmic examination is standard.
That includes checking visual acuity, how well you see the
chart, visual fields, and doing a fundoscopy, which means
looking right inside the eye at the retina and the optic nerve
head. And that helps confirm it looks
(11:34):
like amorosis Fugacs and rule out primary eye problems.
Exactly, and depending on what all these initial tests find,
the notes mention additional tests might be needed as well.
Right, tailored to the individual.
Precisely. And this whole investigation
process, it really connects backto that central idea, Amorosis
Fugacs is usually a sign of a deeper systemic issue.
(11:55):
The tests are looking upstream at the blood vessels, the heart,
the whole system, not just focusing narrowly on the eye.
It's about finding the root cause of the disruption.
So once they've hopefully figured out the likely cause,
what's the plan? What's the management?
What do doctors actually do for someone who's had an episode of
Amorosis Fugacs? Well, the goals are very clear
(12:15):
from the source material. Number one, prevent future
vascular events, especially stroke and #2 preserve vision as
much as possible. And the focus isn't just on
treating the eye symptoms themselves then?
No, not primarily. The focus is squarely on
treating the underlying cause, whatever that may be, and
aggressively managing those cardiovascular risk factors we
(12:36):
identified earlier. That's absolutely key to
preventing future, potentially much more serious events.
So what does that treatment actually involve?
What kind of approaches do the notes describe?
It's really multi pronged based on the source.
First off, crucial lifestyle modifications.
Things like smoking cessation. Stopping smoking is huge,
(12:56):
Adopting a healthy diet, gettingregular exercise, the
foundations. Medications, I assume they play
a big role. Yes, medications are key, both
for controlling the risk factorsand preventing clots.
The notes list controlling bloodpressure, cholesterol levels and
diabetes effectively. Then there's often
anticoagulation therapy to reduce the overall risk of clot
formation and long term antiplatelet therapy.
(13:18):
Medications like aspirin or clopidogrel is very commonly
prescribed, particularly if an embolic cause like from
atherosclerosis is suspected or found.
And what if the cause is inflammatory, like that giant
cell arteritis he mentioned? Good point.
The notes specify that for inflammatory causes like GCA,
high dose steroids are really the cornerstone of treatment and
(13:39):
often these are needed long term.
Is surgery ever an option? Sometimes, yes.
In cases where there's severe narrowing or stenosis of the
carotid artery in the neck, thatcommon source of emboli we
talked about, then surgical intervention might be necessary,
like. Clearing out the plaque.
Exactly, a procedure called carotid endarterectomy to
physically remove the blockage. The notes also wisely mention
(14:02):
the importance of considering the status of the other carotid
artery as well, as atherosclerosis is often
bilateral. And follow up is essential.
I imagine this isn't A1 off treatment.
Absolutely critical regular monitoring is needed.
Treatment might need adjusting overtime and often it involves
collaboration between different specialists, maybe vascular
medicine, neurology, ophthalmology, to ensure all
(14:23):
aspects of the underlying issue are being addressed properly.
The notes give a few specific treatment details too, don't
they? For different causes they do.
For presumed carotid artery emboli, for instance, the
initial treatment often involvesa short course of high dose
aspirin, maybe for two weeks, followed by that long term
antiplatelet therapy. And if there are other reasons
(14:44):
for clots, perhaps coming from the heart, then long term
anticoagulation medications likewarfarin or newer agents might
also be appropriate. And going back to those steroids
for GCA, any other considerations there?
Yes, the source reminds us that when a patient is on high dose
steroids, especially long term, Co prescribing certain other
medications is important for protection.
(15:05):
Things like proton pump inhibitors or PPI's to protect
the stomach lining from ulcers which can be a side effect of
steroids, and also bisphosphonates which help
protect bone density because long term steroids can
unfortunately weaken bones. Right.
Managing the side effects of thetreatment itself.
Yeah. And reinforcing those lifestyle
factors, healthy diet, exercise,quitting smoking, reducing
(15:29):
alcohol. That sounds foundational
regardless of the specific medical treatment pathway.
They really are. They address the underlying
systemic vascular health that isso often the root issue here.
The notes also include the specific point about driving.
Oh yes, it mentions you should avoid driving for one month
after experiencing symptoms, andyou can only return to driving
if the visual symptoms have fully and permanently resolved.
(15:51):
That's an important practical point.
Definitely. And if unfortunately, despite
everything, someone is left withsome permanent visual deficits,
is there support mentioned? Yes, the notes mentioned the
availability of support through occupational therapy
interventions to help adapt to any vision loss and also
considering registration as visually impaired, which can
(16:12):
provide access to various resources and support services.
OK, so looking at the long term picture, then the prognosis,
Yeah. What happens after an episode of
Amyrosis Fugacs? What do the notes say about the
outlook? Well, it heavily depends on the
underlying 'cause that's identified and crucially how
effectively the individual's cardiovascular risk factors are
(16:32):
managed going forward. But a key point, the notes
emphasise, is that prompt evaluation and getting the right
management significantly reduce the risk of having subsequent
vascular events right. Yes, absolutely.
Getting it checked out and treated makes a big difference,
but on the flip side the warningis that there is a potential
increased risk of future TI As or even full strokes if those
(16:54):
underlying issues aren't investigated and treated
aggressively. So regular follow up, sticking
with those lifestyle changes, taking the prescribed
medications, all that is absolutely crucial for the long
term outlook and trying to prevent something worse down the
line. Couldn't agree more.
And finally, let's just touch onthe potential complications.
What are the bad outcomes if amorosis Fugacs isn't properly
(17:16):
addressed? The major complication, as we've
really been highlighting throughout this, is that
increased risk of subsequent TI as or most seriously a full
blown stroke. That's the big danger.
It is, and if the underlying vascular disease isn't treated
and is allowed to progress, it can unfortunately lead to severe
visual impairment or even permanent blindness in some
(17:37):
cases. So the message from the notes is
pretty stark. Immediate medical attention is
crucial when you experience these symptoms.
It's all about preventing these serious complications.
Exactly, and getting appropriate, timely treatment is
absolutely essential to reduce that risk of future vascular
events and protect both brain health and vision long term.
So there you have it. Amorosis Fugacs That temporary
(17:58):
visual warning sign, often described so vividly as a
curtain falling, is frequently linked to some pretty serious
underlying systemic vascular issues like atherosclerosis.
Yeah, and probably the single most important thing to take
away from these notes, the key message is that this symptom is
a significant red flag. It absolutely needs prompt
medical investigation to preventsomething potentially far more
(18:20):
serious like a stroke or permanent visual loss.
It's your body sending a clear warning signal.
It really makes you think, what does this tell us about
seemingly isolated symptoms? You know, how can paying close
attention to these transient events, like a temporary loss of
vision, be such a crucial early step in potentially preventing
(18:42):
major health crises down the line?
It really highlights how incredibly interconnected the
body systems are, doesn't it? Especially that vital vascular
network trouble in one small part can indicate a much wider
problem. Absolutely.
Well, these notes provided an excellent basis for this deep
dive, offering a really high yield look at such a crucial
topic. They were very well structured.
(19:02):
For those of you listening who might be preparing for exams or
maybe just want more high yield medical knowledge drawn directly
from relevant sources like these, do check out pass
themezrae.com. And for free resources as well
to help you keep learning and exploring these kinds of
topicsfreemestrae.com is also available for you.
Keep exploring, stay curious. We'll see you on the next deep
(19:22):
dive.
Imagine this. Suddenly it feels like a dark
curtain is being pulled down over your vision.
It might cover everything, or maybe just part of it, and it's
totally painless. It only lasts a few minutes,
maybe, but it's, well, it's incredibly alarming.
That really vivid description comes straight from the source
material for today's Deep Dive. It's a very striking image,
isn't it? It really is.
(00:21):
So today we're taking a deep dive into Amorosis Fugacs.
It sounds maybe a bit complicated, medically speaking,
but the revision notes you've provided give us a fantastic
map. Yeah, absolutely.
And our mission today is really to unpack these notes, pull out
the the highest yield information, the really key
stuff and help you understand this condition thoroughly, but
(00:42):
you know, efficiently. We're basically guiding you
through the essentials from these notes.
And this really matters because,as the source highlights pretty
clearly, this temporary visual loss is often a critical warning
sign, something you absolutely shouldn't ignore.
Exactly a major red flag O Let'sstart right at the beginning
with the definition. The notes define amyrosis fugacs
(01:04):
as a temporary, painless loss orreduction of vision in one or
sometimes both eyes. And the source puts a real
emphasis on that description. You mentioned that really
distinct curtain like or shade like effect.
It feels like a key way to remember what patients actually
report. It is.
It's very memorable. And the underlying cause is a
temporary disruption of blood flow specifically to the retina
(01:27):
or perhaps the optic nerve. OK.
And this interruption of supply is precisely why it's such an
important warning sign. It strongly suggests an
underlying issue with blood vessels, maybe further upstream,
and it needs prompt medical evaluation.
So it's not usually a problem inthe eye itself causing the
vision loss, it's more about theblood getting to the eye.
Exactly right. Think of it like a supply line
(01:47):
issue, the notes state. These episodes typically last
somewhere between, say, 5 and 15minutes.
OK. And crucially, amorosis fugex
often presents as a type of transient ischemic attack or
Tia. Right atia like a mini stroke
people sometimes call it. That's the term, yes, a mini
stroke. And these episodes, this
amorosis fugacs can sometimes even come before a more serious
(02:11):
full blown stroke or even permanent visual loss.
It's a warning. OK, let's unpack this further
then. What actually causes this
temporary disruption? Where does the problem in that
supply line originate? Well, the notes are very clear
on this. Often the cause is a transient
ischemic. A Tia means temporary poor blood
(02:32):
flow, usually thought of in relation to the brain, but in
this context it's affecting the blood supply to the eyes, retina
or optic nerve. And what's the most common
reason for that Tia affecting the eye?
What's behind it? The source points overwhelmingly
towards atherosclerosis. That's the buildup of fatty
plaques inside the arteries. These plaques can narrow the
arteries, obviously, or bits of them can break off, forming
(02:53):
blood clots or what we call emboli.
Little fragments travelling in the blood.
Precisely. These fragments travel through
the bloodstream, and if they happen to lodge in and block the
small blood vessels supplying the eye, well, that's when you
get the temporary vision loss. So it's like debris clogging a
pipe basically. That's a good analogy, yes.
Like debris in the body's plumbing system.
And that plaque breaking off from, say, the carotid artery in
(03:16):
the neck, is that a common scenario described in the notes?
Absolutely. That's mentioned as a frequent
source of these emboli, but the notes also list other potential
pauses such as well, emboli can come from the heart itself.
Perhaps due to certain heart conditions, there can be
vasospasm where the blood vesseltemporarily clamps down really
tightly, right? Increased blood viscosity,
(03:39):
thicker blood that doesn't flow as easily, or just generally
reduced overall blood flow for various other reasons.
And are there specific medical conditions the notes flag up as
potential triggers? Yes, they specifically mentioned
conditions like giant cell arteritis or GCA.
That's an inflammatory conditionaffecting blood vessels, OK, And
also ocular migraine. But again, the notes really
(04:00):
highlight that vascular blockage, usually from
atherosclerosis causing MLI, is the most frequent mechanism they
detail. So given all these potential
causes linked to blood flow and vessels, who is more likely to
experience this? What are the key risk factors
listed in the source? The list includes many familiar
cardiovascular risk factors, things you might expect.
(04:23):
Yeah, so straight from the source.
Older ages 1A history of cardiovascular disease, things
like hypertension, coronary artery disease, smoking,
definitely diabetes, hyperlipidemia which is high
cholesterol and obesity. Makes sense.
Family history of stroke or Tia is also listed which fits the
(04:44):
pattern. It does, and also certain
genetic or acquired conditions that might make blood more prone
to clotting or cause other vascular abnormalities.
What's interesting here, and it ties back to what you're saying
earlier, is how many of these connect directly to just broader
cardiovascular health? Exactly.
It really underscores that this isn't just some isolated eye
thing, is it? It's often a symptom reflecting
systemic problems, usually with the blood vessels.
(05:06):
Precisely. It's a sign from the system
which leads us nicely into how it actually happens
physiologically, the path of Physiology.
How does that blood flow disruption translate into that
temporary vision loss? Yeah, what's in the mechanism?
Well, at its core, as we've said, the blood flow to the
retina or the optic nerve gets compromised temporarily.
(05:28):
And the typical reason for that compromise like we discussed
with the causes? Most often, according to the
notes, it's these blood clots orbits of plaque obstructing those
vital small vessels that supply the eye.
And this blockage, or reduced flow then leads to what the
notes call an ischemic episode. Correct, Ischemia just means a
period where there's reduced blood flow and therefore reduce
(05:50):
oxygen supply to the tissue, in this case the retina or the
optic nerve tissue. And the immediate result of that
temporary lack of oxygen is? Temporary loss of vision.
Simple as that. Pretty much.
And it's temporary because usually the obstruction itself
is transient. The clot might break up and move
on, or maybe a spasm resolves, blood flow gets spontaneously
restored. And vision comes back relatively
(06:11):
quickly. Exactly.
Vision returns to normal. The notes do mention that the
duration can vary quite a bit, sometimes just a few seconds,
other times several minutes. OK.
So moving on to what you actually see or feel, the
clinical features, the main one we've kept coming back to is
that sudden temporary vision loss, usually just in one eye,
(06:32):
though the notes say it can affect both.
Right. And to really lock it in your
memory, that distinct curtain like or shade like effect is the
classic description you'll oftenhear or read about.
It's a very helpful detail, definitely.
And the vision loss itself, can it vary in intensity?
Yes, it can be complete, like a total blackout in that eye.
Or it might be partial, maybe just affecting the top half or
(06:55):
the bottom half of the visual. Field And just to reiterate,
these episodes last seconds to minutes before fully resolving
on their own that spontaneity iskey.
It is. Associated symptoms, according
to the notes, can sometimes include things like flashes of
light, maybe some blurry vision during the episode, or even a
feeling of pressure behind the affected eye.
But the crucial detail, and thishelps differentiate it perhaps,
(07:18):
is that Vision usually returns completely to normal after the
episode passes, no lasting deficit from the event itself.
That's the typical pattern, yes.OK, so if someone experiences
sudden temporary vision loss, how do doctors know for sure
it's amorosis, fugacs and not one of the many other things
that can cause sudden visual disturbances?
(07:40):
This must be where the differential diagnosis comes in.
Precisely. It's a critical step.
The source notes list several conditions that can look similar
and absolutely need to be ruled out.
What sort of things are on that list?
Things like ocular migraine or retinal migraine, which are
related but distinct. Retinal detachment, that's an
emergency vitreous haemorrhage, which is bleeding inside the
eye. Angle closure.
(08:01):
Glaucoma, another urgent condition, optic neuritis, which
is inflammation of the optic nerve and something called
ocular ischemic syndrome, which is more chronic.
Poor blood flow. Wow, that's quite a list.
So how do doctors sort through that?
How do they differentiate? Well, a really comprehensive
evaluation is essential, the notes describe.
This involves taking a thorough medical history, paying close
(08:23):
attention to those cardiovascular risk factors we
talked about earlier makes sense.
Then a detailed ophthalmic examination to actually look at
the eye structure itself, visualfield testing to map out any
vision loss, and various imagingtechniques.
Right, like the Doppler scans orMRI.
Exactly. Things like carotid Doppler,
ultrasound, maybe an MRI or CT angiography.
(08:45):
And the aim of all this investigation?
What are they trying to achieve?It's really twofold.
First, assess the patient's overall vascular status.
Hunt for blockages, sources of emboli, that sort of thing.
Find the upstream. Problem.
Find the upstream problem, yes, and 2nd, definitively exclude
those other potential causes on the differentialist.
The eye exam, for instance, helps rule out things happening
(09:07):
inside the eye itself, like a detachment or a haemorrhage.
Got it. And just briefly on the
epidemiology, who gets this and how often?
The notes mention UK figures. Yes, they do mention that
specific prevalence just for amorosis fugax itself isn't
perfectly defined in the source notes we have OK, but they give
an estimate for TI as in general, which as we know
(09:29):
amorosis fugax often falls under.
And they estimate around 46,000 annual cases of TI as in England
alone so. It's not uncommon.
Not at all, and while it can occur at various ages, it
mirrors the risk factors become significantly more common in
people over the age of 60. Right.
So digging into those investigations a bit more than
(09:49):
How exactly do doctors figure out the underlying cause?
The investigation section in thenotes lays out the steps quite
clearly. It does.
It usually starts with, as we mentioned, a detailed medical
history and a physical examination.
They're actively looking for signs of underlying vascular
disease or those risk factors welisted.
Then come blood tests. What are they specifically
checking for in the bloods in this context?
(10:10):
They'll check things like cholesterol levels, blood
clotting factors to see if the blood is too prone to clotting
and maybe markers that could indicate systemic inflammation
or other vascular issues. It helps build that overall
picture of cardiovascular health.
And imaging studies, you mentioned carotid ultrasound,
MRI, CT angiography. What's the main focus there?
(10:31):
Imaging is absolutely crucial because they're trying to
pinpoint the source of that temporary blockage if possible.
A carotid ultrasound is very common.
It looks directly for plaque buildup in those big arteries in
the neck, a really frequent source of emboli going to the
eye. OK, MRI and CT angiography give
even more detailed pictures of blood vessels, helping to
(10:53):
identify abnormalities or blockages elsewhere, maybe
higher up or in the brain circulation.
What about checking the heart? Is that usually part of the work
up? Often, yes, a cardiac
evaluation, maybe with an ECG oran echocardiogram and ultrasound
of the heart is needed because the heart itself can be a source
of emboli. They're looking for things like
irregular heartbeats, valve problems, things that could
(11:14):
generate clots. And of course the eye itself
gets a proper look too. Oh definitely.
A detailed ophthalmic examination is standard.
That includes checking visual acuity, how well you see the
chart, visual fields, and doing a fundoscopy, which means
looking right inside the eye at the retina and the optic nerve
head. And that helps confirm it looks
(11:34):
like amorosis Fugacs and rule out primary eye problems.
Exactly, and depending on what all these initial tests find,
the notes mention additional tests might be needed as well.
Right, tailored to the individual.
Precisely. And this whole investigation
process, it really connects backto that central idea, Amorosis
Fugacs is usually a sign of a deeper systemic issue.
(11:55):
The tests are looking upstream at the blood vessels, the heart,
the whole system, not just focusing narrowly on the eye.
It's about finding the root cause of the disruption.
So once they've hopefully figured out the likely cause,
what's the plan? What's the management?
What do doctors actually do for someone who's had an episode of
Amorosis Fugacs? Well, the goals are very clear
(12:15):
from the source material. Number one, prevent future
vascular events, especially stroke and #2 preserve vision as
much as possible. And the focus isn't just on
treating the eye symptoms themselves then?
No, not primarily. The focus is squarely on
treating the underlying cause, whatever that may be, and
aggressively managing those cardiovascular risk factors we
(12:36):
identified earlier. That's absolutely key to
preventing future, potentially much more serious events.
So what does that treatment actually involve?
What kind of approaches do the notes describe?
It's really multi pronged based on the source.
First off, crucial lifestyle modifications.
Things like smoking cessation. Stopping smoking is huge,
(12:56):
Adopting a healthy diet, gettingregular exercise, the
foundations. Medications, I assume they play
a big role. Yes, medications are key, both
for controlling the risk factorsand preventing clots.
The notes list controlling bloodpressure, cholesterol levels and
diabetes effectively. Then there's often
anticoagulation therapy to reduce the overall risk of clot
formation and long term antiplatelet therapy.
(13:18):
Medications like aspirin or clopidogrel is very commonly
prescribed, particularly if an embolic cause like from
atherosclerosis is suspected or found.
And what if the cause is inflammatory, like that giant
cell arteritis he mentioned? Good point.
The notes specify that for inflammatory causes like GCA,
high dose steroids are really the cornerstone of treatment and
(13:39):
often these are needed long term.
Is surgery ever an option? Sometimes, yes.
In cases where there's severe narrowing or stenosis of the
carotid artery in the neck, thatcommon source of emboli we
talked about, then surgical intervention might be necessary,
like. Clearing out the plaque.
Exactly, a procedure called carotid endarterectomy to
physically remove the blockage. The notes also wisely mention
(14:02):
the importance of considering the status of the other carotid
artery as well, as atherosclerosis is often
bilateral. And follow up is essential.
I imagine this isn't A1 off treatment.
Absolutely critical regular monitoring is needed.
Treatment might need adjusting overtime and often it involves
collaboration between different specialists, maybe vascular
medicine, neurology, ophthalmology, to ensure all
(14:23):
aspects of the underlying issue are being addressed properly.
The notes give a few specific treatment details too, don't
they? For different causes they do.
For presumed carotid artery emboli, for instance, the
initial treatment often involvesa short course of high dose
aspirin, maybe for two weeks, followed by that long term
antiplatelet therapy. And if there are other reasons
(14:44):
for clots, perhaps coming from the heart, then long term
anticoagulation medications likewarfarin or newer agents might
also be appropriate. And going back to those steroids
for GCA, any other considerations there?
Yes, the source reminds us that when a patient is on high dose
steroids, especially long term, Co prescribing certain other
medications is important for protection.
(15:05):
Things like proton pump inhibitors or PPI's to protect
the stomach lining from ulcers which can be a side effect of
steroids, and also bisphosphonates which help
protect bone density because long term steroids can
unfortunately weaken bones. Right.
Managing the side effects of thetreatment itself.
Yeah. And reinforcing those lifestyle
factors, healthy diet, exercise,quitting smoking, reducing
(15:29):
alcohol. That sounds foundational
regardless of the specific medical treatment pathway.
They really are. They address the underlying
systemic vascular health that isso often the root issue here.
The notes also include the specific point about driving.
Oh yes, it mentions you should avoid driving for one month
after experiencing symptoms, andyou can only return to driving
if the visual symptoms have fully and permanently resolved.
(15:51):
That's an important practical point.
Definitely. And if unfortunately, despite
everything, someone is left withsome permanent visual deficits,
is there support mentioned? Yes, the notes mentioned the
availability of support through occupational therapy
interventions to help adapt to any vision loss and also
considering registration as visually impaired, which can
(16:12):
provide access to various resources and support services.
OK, so looking at the long term picture, then the prognosis,
Yeah. What happens after an episode of
Amyrosis Fugacs? What do the notes say about the
outlook? Well, it heavily depends on the
underlying 'cause that's identified and crucially how
effectively the individual's cardiovascular risk factors are
(16:32):
managed going forward. But a key point, the notes
emphasise, is that prompt evaluation and getting the right
management significantly reduce the risk of having subsequent
vascular events right. Yes, absolutely.
Getting it checked out and treated makes a big difference,
but on the flip side the warningis that there is a potential
increased risk of future TI As or even full strokes if those
(16:54):
underlying issues aren't investigated and treated
aggressively. So regular follow up, sticking
with those lifestyle changes, taking the prescribed
medications, all that is absolutely crucial for the long
term outlook and trying to prevent something worse down the
line. Couldn't agree more.
And finally, let's just touch onthe potential complications.
What are the bad outcomes if amorosis Fugacs isn't properly
(17:16):
addressed? The major complication, as we've
really been highlighting throughout this, is that
increased risk of subsequent TI as or most seriously a full
blown stroke. That's the big danger.
It is, and if the underlying vascular disease isn't treated
and is allowed to progress, it can unfortunately lead to severe
visual impairment or even permanent blindness in some
(17:37):
cases. So the message from the notes is
pretty stark. Immediate medical attention is
crucial when you experience these symptoms.
It's all about preventing these serious complications.
Exactly, and getting appropriate, timely treatment is
absolutely essential to reduce that risk of future vascular
events and protect both brain health and vision long term.
So there you have it. Amorosis Fugacs That temporary
(17:58):
visual warning sign, often described so vividly as a
curtain falling, is frequently linked to some pretty serious
underlying systemic vascular issues like atherosclerosis.
Yeah, and probably the single most important thing to take
away from these notes, the key message is that this symptom is
a significant red flag. It absolutely needs prompt
medical investigation to preventsomething potentially far more
(18:20):
serious like a stroke or permanent visual loss.
It's your body sending a clear warning signal.
It really makes you think, what does this tell us about
seemingly isolated symptoms? You know, how can paying close
attention to these transient events, like a temporary loss of
vision, be such a crucial early step in potentially preventing
(18:42):
major health crises down the line?
It really highlights how incredibly interconnected the
body systems are, doesn't it? Especially that vital vascular
network trouble in one small part can indicate a much wider
problem. Absolutely.
Well, these notes provided an excellent basis for this deep
dive, offering a really high yield look at such a crucial
topic. They were very well structured.
(19:02):
For those of you listening who might be preparing for exams or
maybe just want more high yield medical knowledge drawn directly
from relevant sources like these, do check out pass
themezrae.com. And for free resources as well
to help you keep learning and exploring these kinds of
topicsfreemestrae.com is also available for you.
Keep exploring, stay curious. We'll see you on the next deep
(19:22):
dive.
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