跟读练习: Cerebral Vascular Anatomy And Imaging - 通过视频学习英语口语
选择练习模式
每种模式都会打开全屏练习室。
152 句
如果句子过短或过长，请点击 Edit 进行调整。
1
Welcome back, friends. This is Dr. Rybinnik.
2
Today we'll talk about cerebrovascular anatomy and vascular imaging.
3
This video is rated MS for medical student, due to basic concepts, clear language and case based examples.
4
Medical student participation is advised.
5
I have no relevant financial conflicts to disclose except to say that the case presented here was modified for teaching purposes.
6
Meet Mr. S.E.
7
He is an 83 year old man with multiple vascular risk factors including hypertension, dyslipidemia, type 2 diabetes, and coronary artery disease.
8
He suddenly develops disorientation, right sided visual disturbance, and minor right sided weakness.
9
Because of his disorientation, some of the history was obtained from the family.
10
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.
11
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.
12
He called my pen a “den”.
13
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).
14
There is no weakness on my examination.
15
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?
16
Keep the answer to yourself, and we’ll revisit at the end.
17
That reminds me, we have to review some vascular anatomy.
18
Pretend this patient is looking directly at you.
19
Patient’s left is on your right.
20
You can see the arch of the aorta on the bottom giving rise to anterior and posterior circulation vessels.
21
Common carotid arteries typically arise from the brachiocephalic trunk on the right, and aortic arch itself on the left.
22
They bifurcate into external carotids (with branches in the neck) and the internal carotids that ascend to the brain.
23
Vertebral arteries arise from subclavian branches of the aorta and supply the posterior circulation.
24
Now let’s take a look at the intracranial vasculature and the circle of Willis.
25
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.
26
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).
27
At its tip, the basilar artery bifurcates into posterior cerebral arteries.
28
It sort of looks like a palm tree.
29
From the posterior circulation, posterior communicating arteries connect the PCAs to internal carotid arteries and the anterior circulation.
30
ICAs then bifurcate into the middle cerebral and anterior cerebral arteries.
31
And anterior cerebral arteries are connected by the anterior communicating artery.
32
By the way, there is quite a bit of variability in the vasculature.
33
If you are watching this talk with two other people, turn to your right, turn to the left.
34
Statistically, only one of you has a complete circle of Willis.
35
Speaking of the cirle of Willis, time to identify blood vessels in a real normal patient.
36
The patient is facing you and slightly up, and by convention the patient’s left is on your right.
37
Pictured here are two common vascular studies – brain MR angiogiogram without contrast on the left, and head CT angiogram with contrast on the right.
38
Let’s start with the posterior circulation.
39
Vertebrals are… here.
40
PICA must be… here, since comes off of the vertebral artery.
41
The two vertebrals join to form the basilar… here.
42
The two major brainches of the basilar are… AICA, and SCA.
43
They are faintly seen on the MRA, and I’m not seeing AICA on the CTA.
44
The basilar terminates into… PCAs.
45
Meanwhile in the anterior circulation, ICAs split into ACAs and MCA.
46
And now, the neck vasculature. Same orientation as before.
47
MRA of the neck with gadolinium contrast is on the left and CTA of the neck with iodine-based contrast is on the right.
48
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.
49
There is also more tissue to go through to capture vessels.
50
So, if you don’t inject contrast, you generally get a blurry mess.
51
Ok, back to the vessels. Every time I call out a vessel name, point it out.
52
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.
53
Posterior circulation originates from the subclavian arteries, which given rise to the vertebrals.
54
Speaking of vascular imaging, the most detailed vessel study is the conventional (also known as the digital subtraction) angiogram.
55
This study is the gold standard but also unfortunately invasive.
56
These imagines are obtained but injecting contrast from a catheter located inside the internal carotid artery.
57
The patient’s right side is imaged first… and then the left.
58
After each arterial run, you see the venous phase when blood exits the head.
59
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.
60
MR angiogram can also be ordered with an MRI of the brain making it more informative.
61
But, it’s slow and tends to overestimate the degree of stenosis.
62
MRA is excellent in non-emergent and outpatient setting.
63
CTA is very rapid and potentially more accurate with slightly higher resolution.
64
So, it’s well suited to emergency situations like stroke codes.
65
But it involves radiation and iodine-based contrast which rarely causes acute kidney injury and anaphylaxis. So, CTA is potentially less safe.
66
Finally, conventional cerebral angiogram is the gold standard, but also the most invasive and expensive technique.
67
Nowadays, non-invasive imaging produces results approximating conventional angiography.
68
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.
69
But, ultrasound sees a limited portion of the vascular tree and is technologist dependent, which limits its usefulness in diagnosis.
70
Now onto the main event, vascular territories.
71
For this last section of the talk, please refer to the color legend on the right.
72
Anterior cerebral artery supply the medial frontal lobe, highlighted in yellow.
73
So, ACA territory infarctions cause: Contralateral leg weakness, by damaging the medial primary motor cortex of the frontal lobe when leg fibers reside.
74
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.
75
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.
76
Contralateral facial paresis, again from damage to corticobulbar fibers Contralateral gaze paresis, from damage to the frontal eye fields.
77
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.
78
Aphasia, with damage to dominant frontal and temporal lobes where expressive and receptive language pathways reside.
79
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.
80
But if you now that aphasia is MCA territory, maybe that would prompt you to look for field cut and gaze paresis.
81
A quick note: The head of caudate is supplied by a tiny branch off of the ACA called the recurrent artery of Heubner.
82
Don’t memorize that name. Why is that important?
83
Well, if you see a comma-shaped infarct like this, both ACA and MCA territories are affected.
84
Which means that their parent vessel, the ICA was probably involved.
85
An embolus likely traveled to the ICA terminus and transiently occluded both the ACA and MCA.
86
Posterior cerebral artery supplies the inferior medial temporal lobe and the occipital lobe. But here is the trouble with the PCA.
87
PCA supplies the thalamus. Thalami are the switchboards of the brain that receive and send projections to all the lobes and then some.
88
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.
89
Transcortical aphasia with dominant thalamic damage.
90
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.
91
To make things even more difficult, PCA is the terminal branch of the basilar so it supplies the midbrain.
92
Midbrain is brainstem. Overlaid in blue are sample strokes.
93
Damaging the motor fibers in the cerebral peduncle causes contralateral hemiparesis.
94
Contralateral ataxia can result from damage to the red nucleus, which is part of the cerebellar pathway.
95
And damaged oculomotor nucleus causes ipsilateral CN3 palsy.
96
Thankfully, superior cerebellar artery is easy.
97
It supplies anterior superior cerebellum, and infarctions here cause ipsilateral ataxia (the cerebellar fibers are damaged after double crossing).
98
The basilar artery supplies… wait for it… the base of the brain, well mostly the pons and some anterior medulla to be precise.
99
Damaging the anterior medial pons results in contralateral hemiparesis and facial paresis.
100
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.
101
Spinothalamic tract damage causes contralateral hemisensory loss.
102
Patients with damaged lateral pons and cerebellar peduncles will have contralateral ataxia.
103
Finally, there are several cranial nerve nuclei that when lesioned will produce ipsilateral lesions.
104
Pontine paramedian reticular formation damage will cause gaze weakness.
105
And lower motor neuron type facial paresis and sensory loss results from damage to 7th 5th cranial nerve nuclei in the lateral pons.
106
There is a lot going on in the pons, so I tried to illustrate possible strokes with green highlights.
107
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.
108
It supplies the lateral pons, cerebellar peduncles, and the anterior inferior cerebellum.
109
So, like super cerebellar artery stroke, AICA stroke can cause ipsilateral ataxia.
110
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.
111
But AICA gives rise to labyrinthine artery which supplies the inner ear.
112
Don’t bother memorizing it. It is just a fun fact but incredibly rare.
113
I am a stroke neurologist and saw this only once in a decade.
114
Your emotional ordeal, like this talk will be over as soon as we discuss the medulla.
115
Here, the lateral medulla is where the action is.
116
The lateral medulla and the posterior inferior cerebellum is supplied by the posterior inferior cerebellar artery, which is a branch of the vertebral.
117
So, if PICA is involved, you can bet that vertebral artery lesion is likely responsible.
118
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.
119
So a lateral medullary lesions will cause contralateral hemisensory loss, ipsilateral ataxia, ipsilateral facial numbness, Horner, taste loss and dysarthria/dysphagia.
120
Note what is missing from this list: Weakness.
121
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.
122
People with lateral medullary stroke will be ataxic, numb, dysarthric but not be weak.
123
Congratulations, we are done!
124
And now for a quick review with MRI diffusion weighted imaging examples of major strokes.
125
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.
126
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.
127
SCA stroke causes… Correct. Ipsilateral ataxia.
128
In practice it is very difficult to differentiate AICA and SCA strokes.
129
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.
130
PCA strokes will cause which deficits? That’s a trick question.
131
It depends on whether or not midbrain is involved.
132
Most commonly, this type of stroke will just affect the occipital lobe and the thalamus.
133
So, when you see a patient with a field cut, look for cognitive deficits.
134
Carotid occlusion will cause a large stroke comprising of ACA and MCA territories.
135
Remind me what does a patient with an ACA stroke look like?
136
That’s right, abulic, amnestic and dragging a leg when walking.
137
And what are the deficits of a patient presenting with a right MCA syndrome like pictured here? Right.
138
Contralateral weakness involving the face, gaze paresis, field cut and neglect.
139
Remember that with MCA occlusion does not have to present as a complete MCA syndrome.
140
When a division (M2 branch) is occluded, only half of the MCA will be affected. You get the idea.
141
I guess in the end you start thinking about the beginning… Patient S. E.
142
So, which one of these is the vascular territory of our patient’s stroke?
143
Remember that he had disorientation, mild word finding difficulties, paraphasic errors, and right homonymous hemianopia.
144
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.
145
Looking at this patient’s CTA, you can plainly see that his left posterior cerebral artery is occluded. No surprise there.
146
But there is just one more thing.
147
You have been at least partially oriented during this talk.
148
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.
149
Is there another problem with the patient’s posterior circulation?
150
How about now?
151
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.
152
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.
FOR YOU
推荐视频
C12
12 句
Behind the Scenes: Diagnostic Angiogram with Dr. Oliveira | Riverside Neuroscience
IELTS PrepTOEFL PrepUniversity Students
C28
146 句
Anatomy - Carotid Artery (Carotid artery disease, aneurysm, dissection, amourosis fugax)
IELTS PrepTOEFL PrepUniversity Students
C14
28 句
SVINutes: Collateral Circulation
IELTS PrepTOEFL PrepUniversity Students
C13
186 句
Embryology of the Nervous System
IELTS PrepTOEFL PrepUniversity Students
C17
23 句
Your Brain on Drugs: Marijuana
IELTS PrepTOEFL PrepUniversity Students
C11
43 句
🏥 Locating Organs with Surface Landmarks: Do You Know Where Key Organs Are?
IELTS PrepTOEFL PrepUniversity Students
C12
173 句
What is it? Exercise-induced episodic gait disorder in a young boy
IELTS PrepTOEFL PrepUniversity Students
C13
30 句
Identifying and treating large vessel occlusion stroke due to intracranial atherosclerotic disease
IELTS PrepTOEFL PrepUniversity Students
C13
52 句
Human Anatomy Eye
IELTS PrepTOEFL PrepUniversity Students
C12
56 句
RCoA Primary Examination: SOE Physics Question Example
IELTS PrepTOEFL PrepUniversity Students
C11
448 句
If You Can Understand This News Article, Your English is Excellent!
IELTS PrepTOEFL PrepUniversity Students
C11
28 句
What is Nuclear Medicine | Dr. Paulien Moyaert
IELTS PrepTOEFL PrepUniversity Students
本课的词汇与口语要点
这节 C1 级别的口语课以视频“Cerebral Vascular Anatomy And Imaging”为素材。 视频中反复出现的词有：artery, stroke, posterior, damage, contralateral。 这段视频共有 152 个句子、2752 个单词可供跟读。 讲话部分时长为 23:44。 说话人语速平稳，每分钟约 116 个词，很适合跟读。 只有 64% 的单词属于英语最常用的 3,000 词，词汇难度较高。
视频中的重点词汇
视频中最难的 15 个单词，附发音和释义：
| 单词 | 发音 | 释义 |
|---|---|---|
| artery 名词 | /ˈɑɹ.təɹ.i/ | 動脈 /动脉 |
| posterior 形容词 | /poʊˈstɪɹ.i.ɚ/ | 後面的 /后面的, 尾部的 |
| lobe 名词 | /ləʊb/ | 一坨, 一團 /一团 |
| basilar 形容词 | /ˈbæz.əl.ɚ/ | 基底的 |
| carotid 名词 | /kəˈɹɑt.ɪd/ | 頸動脈 /颈动脉 |
| cerebellar 形容词 | /ˌsɛɹ.əˈbɛl.ɚ/ | 小腦的 /小脑的 |
| anterior 形容词 | /ænˈtɪɹ.i.ɚ/ | 前部 |
| nucleus 名词 | /ˈnuː.kli.əs/ | 核心, 核 |
| cerebral 形容词 | /səˈɹi.bɹəl/ | 大腦的 /大脑的 |
| vertebral 形容词 | /vɚˈti.bɹəl/ | 脊椎的 |
| vascular 形容词 | /ˈvæskjələ/ | 脉管的, 导管的 |
| inferior 形容词 | /ɪnˈfɪɹ.i.ɚ/ | 低劣, 低賤 /低贱 |
| angiogram 名词 | 血管造影 | |
| pons 名词 | /ˈpɑnz/ | 橋腦 /桥脑, 腦橋 /脑桥 |
| ataxia 名词 | /əˈtæksɪə/ | 共濟失調 /共济失调 |
视频中出现的短语动词
| 单词 | 释义 |
|---|---|
| figure out 动词 | 弄清楚 |
| follow up 动词 | 跟進 /跟进 |
| go out 动词 | 出, 出口 |
| knock out 动词 | 昏迷 |
值得反复跟读的句子
视频中简短而完整的句子，可以直接用在日常对话里：
- 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?
视频中的语法
说话人最常用的结构，并附上视频中的原话：
| 结构 | 视频中的用法 |
|---|---|
| 被动语态 be + 过去分词 — 强调发生了什么，而不是谁做的 | is rated · is advised · was modified |
| 定语从句 who / which + 从句 — 补充说明人或事物 | cortex which is · nucleus, which is · artery, which is |
需要注意的发音
说话人用了 8 次缩略和弱读形式，例如 don't, we'll, couldn't。请按听到的简短形式来说。
- “th” 音: pathway /ˈpæθˌweɪ/, thalamus /ˈθæləməs/, thalamic /θəˈlæ.mɪk/
- “sh” 和 “zh” 音: circulation /ˌsɝkjʊˈleɪʃən/, lesion /ˈliːʒən/, occlusion /əˈkluː.ʒən/, disorientation /dɪsˌɔ.ɹi.ɪnˈteɪ.ʃn̩/, deviation /ˌdiː.viˈeɪʃən/
- 长单词——注意重音位置: posterior /poʊˈstɪɹ.i.ɚ/, contralateral /ˌkɑntɹəˈlætəɹəl/, cerebellar /ˌsɛɹ.əˈbɛl.ɚ/, ipsilateral /ˌɪpsɪˈlætəɹəl/, anterior /ænˈtɪɹ.i.ɚ/
中文母语者容易读错的音：
- /v/ — 不要读成 /w/，上齿轻触下唇: vertebral /vɚˈti.bɹəl/, vascular /ˈvæskjələ/, vasculature /ˈvæskjʊlət͡ʃə(ɹ)/, invasive /ɪnˈveɪsɪv/, deviation /ˌdiː.viˈeɪʃən/
- 词尾辅音 — 要读清楚，后面不要加元音: lobe /ləʊb/, carotid /kəˈɹɑt.ɪd/, nucleus /ˈnuː.kli.əs/, pons /ˈpɑnz/, gaze /ɡeɪz/
- /r/ 和 /l/ 的区别: contralateral /ˌkɑntɹəˈlætəɹəl/, cerebellar /ˌsɛɹ.əˈbɛl.ɚ/, ipsilateral /ˌɪpsɪˈlætəɹəl/, cerebral /səˈɹi.bɹəl/, lateral /ˈlætəɹəl/
如何用这段视频练习
- 先完整听一遍视频，不要开口，记下不认识的单词。
- 用正常速度逐句跟读，每句重复到你的节奏与说话人一致为止。
- 录下自己的声音并与原声对比，特别注意 artery, posterior, lobe 这类单词。
什么是跟读法？
跟读法 (Shadowing) 是一种有科学依据的语言学习技巧，最初开发用于专业口译员的培训，并由多语言者Alexander Arguelles博士普及。这个方法简单而强大：您在听英语母语原声的同时立即大声重复——就像是一个延迟1-2秒紧跟说话者的影子。与被动听力或语法练习不同，跟读法强迫您的大脑和口腔肌肉同时处理并模仿真实的讲话模式。研究表明它能显着提高发音准确性，语调，节奏，连读，听力理解和口语流利度——使其成为雅思口语备考和真实英语交流最有效的方法之一。