쉐도잉 연습: Cerebral Vascular Anatomy And Imaging - 영상으로 영어 말하기 배우기
레슨 만드는 중...
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Welcome back, friends. This is Dr. Rybinnik.
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Today we'll talk about cerebrovascular anatomy and vascular imaging.
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This video is rated MS for medical student, due to basic concepts, clear language and case based examples.
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Medical student participation is advised.
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I have no relevant financial conflicts to disclose except to say that the case presented here was modified for teaching purposes.
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Meet Mr. S.E.
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He is an 83 year old man with multiple vascular risk factors including hypertension, dyslipidemia, type 2 diabetes, and coronary artery disease.
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He suddenly develops disorientation, right sided visual disturbance, and minor right sided weakness.
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Because of his disorientation, some of the history was obtained from the family.
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He was trying to use his old phone at the time, and couldn’t quite figure out how to unlock it, something he does without issue several times per day.
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Family denied him having recent illness, prior thromboembolism On arrival to the emergency department… He is awake, alert, oriented to self and place but not time He has mild word finding difficulties and makes paraphasic errors.
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He called my pen a “den”.
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But his repetition is perfectly preserved, and he was able to say “no ifs, ands, or buts. ” He has an obvious complete right homonymous hemianopia (field cut).
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There is no weakness on my examination.
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In this talk, we will focus on localization and not on pathology, so let me ask you this… Assuming these symptoms are caused by a vascular lesion, what vascular territory is likely affected?
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Keep the answer to yourself, and we’ll revisit at the end.
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That reminds me, we have to review some vascular anatomy.
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Pretend this patient is looking directly at you.
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Patient’s left is on your right.
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You can see the arch of the aorta on the bottom giving rise to anterior and posterior circulation vessels.
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Common carotid arteries typically arise from the brachiocephalic trunk on the right, and aortic arch itself on the left.
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They bifurcate into external carotids (with branches in the neck) and the internal carotids that ascend to the brain.
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Vertebral arteries arise from subclavian branches of the aorta and supply the posterior circulation.
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Now let’s take a look at the intracranial vasculature and the circle of Willis.
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The two vertebral arteries we spoke about are visible here with an important perforator called Posterior Inferior Cerebellar Artery (or PICA), which, you guessed it, mostly supplies the posterior inferior cerebellum and lateral medulla.
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Vetebrals then join together to form the basilar artery, with major branches including Anterior Inferior Cerebellar Artery (or AICA) and Superior Cerebellar Artery (or SCA).
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At its tip, the basilar artery bifurcates into posterior cerebral arteries.
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It sort of looks like a palm tree.
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From the posterior circulation, posterior communicating arteries connect the PCAs to internal carotid arteries and the anterior circulation.
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ICAs then bifurcate into the middle cerebral and anterior cerebral arteries.
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And anterior cerebral arteries are connected by the anterior communicating artery.
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By the way, there is quite a bit of variability in the vasculature.
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If you are watching this talk with two other people, turn to your right, turn to the left.
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Statistically, only one of you has a complete circle of Willis.
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Speaking of the cirle of Willis, time to identify blood vessels in a real normal patient.
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The patient is facing you and slightly up, and by convention the patient’s left is on your right.
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Pictured here are two common vascular studies – brain MR angiogiogram without contrast on the left, and head CT angiogram with contrast on the right.
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Let’s start with the posterior circulation.
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Vertebrals are… here.
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PICA must be… here, since comes off of the vertebral artery.
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The two vertebrals join to form the basilar… here.
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The two major brainches of the basilar are… AICA, and SCA.
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They are faintly seen on the MRA, and I’m not seeing AICA on the CTA.
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The basilar terminates into… PCAs.
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Meanwhile in the anterior circulation, ICAs split into ACAs and MCA.
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And now, the neck vasculature. Same orientation as before.
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MRA of the neck with gadolinium contrast is on the left and CTA of the neck with iodine-based contrast is on the right.
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Incidentally, you might have picked up on the fact that intracranial MRA does not need contrast and neck MRA does. That is because intracranial vasculature is fixed inside the skull but breathing and swallowing introduces motion artifacts in the neck vessels.
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There is also more tissue to go through to capture vessels.
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So, if you don’t inject contrast, you generally get a blurry mess.
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Ok, back to the vessels. Every time I call out a vessel name, point it out.
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Aortic arch… gives rise to brachiocephalic trunk on the right, which branches into the common carotid, and then internal carotid. On the patient’s left, the common carotid arises directly from the aortic arch. Common carotid bifurcates into the external carotid with branches in the neck and the internal carotid.
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Posterior circulation originates from the subclavian arteries, which given rise to the vertebrals.
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Speaking of vascular imaging, the most detailed vessel study is the conventional (also known as the digital subtraction) angiogram.
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This study is the gold standard but also unfortunately invasive.
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These imagines are obtained but injecting contrast from a catheter located inside the internal carotid artery.
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The patient’s right side is imaged first… and then the left.
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After each arterial run, you see the venous phase when blood exits the head.
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So we briefly reviewed 3 imaging modalities: MR angiogram, CT angiogram and conventional angiogram. All these imaging studies essentially paint the vessel lumen. MR angiogram tends to be safer because it does not require radiation or contrast. It may even be safe in pregnancy.
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MR angiogram can also be ordered with an MRI of the brain making it more informative.
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But, it’s slow and tends to overestimate the degree of stenosis.
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MRA is excellent in non-emergent and outpatient setting.
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CTA is very rapid and potentially more accurate with slightly higher resolution.
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So, it’s well suited to emergency situations like stroke codes.
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But it involves radiation and iodine-based contrast which rarely causes acute kidney injury and anaphylaxis. So, CTA is potentially less safe.
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Finally, conventional cerebral angiogram is the gold standard, but also the most invasive and expensive technique.
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Nowadays, non-invasive imaging produces results approximating conventional angiography.
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You may notice that I am omitting ultrasound technologies like carotid duplex and transcranial doppler. Those are excellent for screening and follow-up monitoring because they are cheap and provide realtime physiologic data.
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But, ultrasound sees a limited portion of the vascular tree and is technologist dependent, which limits its usefulness in diagnosis.
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Now onto the main event, vascular territories.
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For this last section of the talk, please refer to the color legend on the right.
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Anterior cerebral artery supply the medial frontal lobe, highlighted in yellow.
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So, ACA territory infarctions cause: Contralateral leg weakness, by damaging the medial primary motor cortex of the frontal lobe when leg fibers reside.
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Contralateral lower extremity sensory loss, by damaging the medial primary sensory cortex in the parietal lobe An unmotivated state called abulia And anterograde amnesia, by damaging the cingulate cortex which is part of the memory circuit Picture in your mind a patient who is appears more forgetful, withdrawn, and slow to respond and dragging a weak lower extremity when walking.
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Middle cerebral artery territories in red are by far the largest in the brain. If your brain is 1200cc, then half is being supplied by the MCAs. MCA territory infarction may include: Contralateral hemiparesis, from damage to the primary motor cortex and descending motor pathways. Internal capsule for example pictured here.
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Contralateral facial paresis, again from damage to corticobulbar fibers Contralateral gaze paresis, from damage to the frontal eye fields.
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Basically, if you infarct the left frontal lobe, you would not be able to look to the right, causing a right gaze paresis and left gaze deviation.
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Aphasia, with damage to dominant frontal and temporal lobes where expressive and receptive language pathways reside.
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Contralateral hemisensory deficits with damage to the primary sensory cortex in the parietal lobe and ascending sensory pathways Field cut with damage of both temporal and parietal optic radiations And finally neglect with damage of the non-dominant parietal lobe A patient with MCA occlusion does not necessarily have to have all these deficits.
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But if you now that aphasia is MCA territory, maybe that would prompt you to look for field cut and gaze paresis.
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A quick note: The head of caudate is supplied by a tiny branch off of the ACA called the recurrent artery of Heubner.
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Don’t memorize that name. Why is that important?
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Well, if you see a comma-shaped infarct like this, both ACA and MCA territories are affected.
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Which means that their parent vessel, the ICA was probably involved.
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An embolus likely traveled to the ICA terminus and transiently occluded both the ACA and MCA.
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Posterior cerebral artery supplies the inferior medial temporal lobe and the occipital lobe. But here is the trouble with the PCA.
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PCA supplies the thalamus. Thalami are the switchboards of the brain that receive and send projections to all the lobes and then some.
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So, PCA strokes can mimic MCA strokes. Patients get contralateral hemisensory loss from damage to sensory nuclei in the posterior thalamus, contralateral hemianopia from occipital lobe damage, rarely neglect with non-dominant thalamic damage. Thalamic neglect is clinically indistinguishable from parietal lobe neglect but improves much more quickly.
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Transcortical aphasia with dominant thalamic damage.
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Transcortical aphasias are less severe than the classical Broca’s and Wernicke’s with intact repetition. And global cognitive issues likely behavioral abnormalities, confusion, and even memory difficulties.
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To make things even more difficult, PCA is the terminal branch of the basilar so it supplies the midbrain.
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Midbrain is brainstem. Overlaid in blue are sample strokes.
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Damaging the motor fibers in the cerebral peduncle causes contralateral hemiparesis.
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Contralateral ataxia can result from damage to the red nucleus, which is part of the cerebellar pathway.
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And damaged oculomotor nucleus causes ipsilateral CN3 palsy.
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Thankfully, superior cerebellar artery is easy.
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It supplies anterior superior cerebellum, and infarctions here cause ipsilateral ataxia (the cerebellar fibers are damaged after double crossing).
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The basilar artery supplies… wait for it… the base of the brain, well mostly the pons and some anterior medulla to be precise.
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Damaging the anterior medial pons results in contralateral hemiparesis and facial paresis.
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Intranuclear ophthalmoplegia is caused by interrupting the medial longitudinal fasciculus – the connection between the pontine paramedian reticular formation (horizontal gaze center) and the oculomotor nucleus in the midbrain. Basically, when looking in a particular direction one eye goes out but the other does not follow because it never gets the command.
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Spinothalamic tract damage causes contralateral hemisensory loss.
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Patients with damaged lateral pons and cerebellar peduncles will have contralateral ataxia.
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Finally, there are several cranial nerve nuclei that when lesioned will produce ipsilateral lesions.
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Pontine paramedian reticular formation damage will cause gaze weakness.
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And lower motor neuron type facial paresis and sensory loss results from damage to 7th 5th cranial nerve nuclei in the lateral pons.
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There is a lot going on in the pons, so I tried to illustrate possible strokes with green highlights.
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Medial pontine stroke cause weakness and intranuclear ophthalmoplegia, and lateral pontine strokes cause everything else. Bottom line, if you see a patient with ataxic hemiparesis on one side, start looking for eye movement abnormalities, like gaze deviation to the side of weakness or intranuclear ophthalmoplegia. AICA is a major perforator off the basilar artery.
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It supplies the lateral pons, cerebellar peduncles, and the anterior inferior cerebellum.
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So, like super cerebellar artery stroke, AICA stroke can cause ipsilateral ataxia.
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It can also damage lateral pons causing facial sensory loss from trigeminal nucleus damage, and Horner syndrome for sympathetic damage. However, AICA has an interesting party trick – strokes can cause hearing loss. Hearing pathways are bilateral in the CNS, so it is impossible to cause a stroke from a central lesion.
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But AICA gives rise to labyrinthine artery which supplies the inner ear.
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Don’t bother memorizing it. It is just a fun fact but incredibly rare.
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I am a stroke neurologist and saw this only once in a decade.
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Your emotional ordeal, like this talk will be over as soon as we discuss the medulla.
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Here, the lateral medulla is where the action is.
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The lateral medulla and the posterior inferior cerebellum is supplied by the posterior inferior cerebellar artery, which is a branch of the vertebral.
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So, if PICA is involved, you can bet that vertebral artery lesion is likely responsible.
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The lateral medullar contains: The contralateral spinothalamic tract Ipsilateral cerebellar pathways in the inferior cerebellar peduncle and vestibular nuclei Ipsilateral trigeminal nucleus Ipsilateral sympathetics Nucleus of solitary tract that controls special sensation like taste And nucleus ambiguous which donates motor fibers to cranial nerves 9 and 10.
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So a lateral medullary lesions will cause contralateral hemisensory loss, ipsilateral ataxia, ipsilateral facial numbness, Horner, taste loss and dysarthria/dysphagia.
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Note what is missing from this list: Weakness.
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Medial medulla is supplied by the basilar artery and considering that you probably have PTST from all that pontine review, it should be fairly obvious what would happen when the basilar artery is involved.
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People with lateral medullary stroke will be ataxic, numb, dysarthric but not be weak.
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Congratulations, we are done!
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And now for a quick review with MRI diffusion weighted imaging examples of major strokes.
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You are going to have to help out with this: PICA strokes causes… ataxic, dysarthric patient with a droopy eyelid on the same side and hemisensory loss on the opposite side. They will have difficulty swallowing.
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AICA stroke causes… a patient to have ipsilateral ataxia and maybe some ipsilateral hearing loss What happens when you knock out one of these basilar perforators and affect the anteromedial pons? That’s right, contralateral weakness and maybe intranuclear ophthalmoplegia if the lesion reaches far enough dorsally.
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SCA stroke causes… Correct. Ipsilateral ataxia.
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In practice it is very difficult to differentiate AICA and SCA strokes.
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But who even cares? Both AICA and SCA are branches of the basilar artery – giant perforators of sorts. So stroke in both of these territories will likely be caused by the same mechanisms and have the same treatments.
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PCA strokes will cause which deficits? That’s a trick question.
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It depends on whether or not midbrain is involved.
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Most commonly, this type of stroke will just affect the occipital lobe and the thalamus.
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So, when you see a patient with a field cut, look for cognitive deficits.
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Carotid occlusion will cause a large stroke comprising of ACA and MCA territories.
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Remind me what does a patient with an ACA stroke look like?
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That’s right, abulic, amnestic and dragging a leg when walking.
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And what are the deficits of a patient presenting with a right MCA syndrome like pictured here? Right.
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Contralateral weakness involving the face, gaze paresis, field cut and neglect.
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Remember that with MCA occlusion does not have to present as a complete MCA syndrome.
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When a division (M2 branch) is occluded, only half of the MCA will be affected. You get the idea.
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I guess in the end you start thinking about the beginning… Patient S. E.
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So, which one of these is the vascular territory of our patient’s stroke?
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Remember that he had disorientation, mild word finding difficulties, paraphasic errors, and right homonymous hemianopia.
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Well someone has been paying attention. Its an acute left PCA stroke, which involves the inferior medial temporal lobe and the occipital lobe, and the the thalamus.
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Looking at this patient’s CTA, you can plainly see that his left posterior cerebral artery is occluded. No surprise there.
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But there is just one more thing.
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You have been at least partially oriented during this talk.
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So you remember that PCA is posterior circulation. Posterior circulation is comprised of subclavians off of the aorta the left and brachiocephalic trunk on the right, and their vertebral artery branches that eventually join together to form the basilar artery.
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Is there another problem with the patient’s posterior circulation?
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How about now?
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Yes our 83 may had an acute left posterior cerebral artery occlusion because of an artery-to-artery embolism from a left vertebral artery origin plaque causing severe stenosis.
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And that’s all I have for now. I feel like I should end with my customary disclaimer that this is an oversimplification. It’s a good beginner’s guide with some intermediate stuff sprinkled in. Thank you for indulging me, and we’ll talk again soon. Bye.
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이 레슨의 어휘와 말하기 포인트
이 C1 수준 말하기 레슨은 영상 “Cerebral Vascular Anatomy And Imaging”을(를) 바탕으로 합니다. 가장 자주 반복되는 단어는 다음과 같습니다: artery, stroke, posterior, damage, contralateral. 이 영상에는 섀도잉할 문장 152개와 단어 2752개가 있습니다. 말하는 구간의 길이는 23:44입니다. 화자는 분당 약 116단어의 일정한 속도로 말해서 섀도잉하기에 편한 속도입니다. 영어에서 가장 많이 쓰이는 3,000단어에 속하는 단어가 64%뿐이라 어휘가 어려운 편입니다.
이 영상의 핵심 어휘
영상에서 가장 어려운 단어 15개를 발음, 뜻과 함께 정리했습니다.
| 단어 | 발음 | 뜻 |
|---|---|---|
| artery 명사 | /ˈɑɹ.təɹ.i/ | 동맥 |
| posterior 형용사 | /poʊˈstɪɹ.i.ɚ/ | 후부의, 뒤의 |
| nucleus 명사 | /ˈnuː.kli.əs/ | 핵심, 핵 |
| cortex 명사 | /ˈkɔɹtɛks/ | 피질 |
| neglect 동사 | /nɪˈɡlɛkt/ | 소홀히 하다, 등한히 하다 |
| deficit 명사 | /ˈdɛfəsɪt/ | 적자 |
| cerebellum 명사 | /ˌsɛrəˈbɛləm/ | 소뇌 |
| midbrain 명사 | 중간뇌 | |
| occipital 형용사 | /ɑkˈsɪp.ət.l̩/ | (의학)후두부 |
| thalamus 명사 | /ˈθæləməs/ | 시상 |
| arch 명사 | /ɑɹt͡ʃ/ | 아치 |
| aorta 명사 | /eɪˈɔɹtə/ | 대동맥 |
| aphasia 명사 | /əˈfeɪzɪə/ | 실어증 |
| trunk 명사 | /tɹʌŋk/ | 그루 |
| infarct 명사 | /ɪnˈfɑɹkt/ | 경색 |
영상에 나오는 구동사
| 단어 | 뜻 |
|---|---|
| go out 동사 | 나가다 |
따라 말해 볼 만한 문장
영상에 나오는 짧고 완결된 문장으로, 일상 대화에서 그대로 쓸 수 있습니다:
- Today we'll talk about cerebrovascular anatomy and vascular imaging.
- Patient’s left is on your right.
- Is there another problem with the patient’s posterior circulation?
이 영상의 문법
화자가 가장 많이 쓰는 문형을 영상 속 실제 표현과 함께 정리했습니다.
| 문형 | 영상 속 표현 |
|---|---|
| 수동태 be + 과거분사 — 누가 하는지보다 무슨 일이 일어나는지에 초점 | is rated · is advised · was modified |
| 관계절 who / which + 절 — 사람이나 사물에 대한 추가 정보 | cortex which is · nucleus, which is · artery, which is |
주의할 발음
화자는 don't, we'll, couldn't 같은 축약형과 약화된 형태를 8번 사용합니다. 들리는 대로 짧게 발음하세요.
- “th” 소리: pathway /ˈpæθˌweɪ/, thalamus /ˈθæləməs/, thalamic /θəˈlæ.mɪk/
- “sh”와 “zh” 소리: circulation /ˌsɝkjʊˈleɪʃən/, lesion /ˈliːʒən/, occlusion /əˈkluː.ʒən/, disorientation /dɪsˌɔ.ɹi.ɪnˈteɪ.ʃn̩/, deviation /ˌdiː.viˈeɪʃən/
- 긴 단어 — 강세 위치에 주의: posterior /poʊˈstɪɹ.i.ɚ/, contralateral /ˌkɑntɹəˈlætəɹəl/, cerebellar /ˌsɛɹ.əˈbɛl.ɚ/, ipsilateral /ˌɪpsɪˈlætəɹəl/, anterior /ænˈtɪɹ.i.ɚ/
한국어 화자가 어려워하는 소리:
- /f/ — ㅍ(/p/)으로 바꾸지 말고 윗니를 아랫입술에 대기: inferior /ɪnˈfɪɹ.i.ɚ/, frontal /ˈfɹʌn.təl/, fiber /ˈfaɪ.bɚ/, deficit /ˈdɛfəsɪt/, bifurcate /ˈbaɪfɚˌkeɪt/
- /v/ — ㅂ(/b/)과 구별하기: vertebral /vɚˈti.bɹəl/, vascular /ˈvæskjələ/, vasculature /ˈvæskjʊlət͡ʃə(ɹ)/, invasive /ɪnˈveɪsɪv/, deviation /ˌdiː.viˈeɪʃən/
- /z/ — ㅈ이 아니라 성대를 울리는 /s/: basilar /ˈbæz.əl.ɚ/, pons /ˈpɑnz/, gaze /ɡeɪz/, aphasia /əˈfeɪzɪə/, reside /ɹɪˈzaɪd/
이 영상으로 연습하는 방법
- 먼저 말하지 않고 영상을 끝까지 듣고 모르는 단어를 적어 둡니다.
- 보통 속도로 한 문장씩 섀도잉하고, 화자의 리듬과 맞을 때까지 반복합니다.
- 자신의 목소리를 녹음해 원본과 비교하고, artery, posterior, nucleus 같은 단어에 특히 주의합니다.
쉐도잉이란? 영어 실력을 빠르게 키우는 과학적 방법
쉐도잉(Shadowing)은 원래 전문 통역사 훈련을 위해 개발된 언어 학습 기법으로, 다언어 학자인 Dr. Alexander Arguelles에 의해 대중화된 방법입니다. 핵심 원리는 간단하지만 매우 강력합니다: 원어민의 영어를 들으면서 1~2초의 짧은 지연으로 즉시 소리 내어 따라 말하는 것——마치 '그림자(shadow)'처럼 화자를 따라가는 것입니다. 문법 공부나 수동적인 청취와 달리, 쉐도잉은 뇌와 입 근육이 동시에 실시간으로 영어를 처리하고 재현하도록 훈련합니다. 연구에 따르면 이 방법은 발음 정확도, 억양, 리듬, 연음, 청취력, 말하기 유창성을 크게 향상시킵니다. IELTS 스피킹 준비와 자연스러운 영어 소통을 원하는 분들에게 특히 효과적입니다.