Topic 4 - extra cranial cerebral vessels Flashcards

1
Q

Which neck vessels supply which part of the brain?

A
  • the anterior aspect of the brain supplied by the carotid circulation
  • the posterior brain supplied by the vertebral circulation.
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2
Q

Where does each neck vessel originate?

A
  • The right carotid arises from the innominate artery
  • the left carotid artery arises directly from the aorta
  • The vertebral arteries both arise from their respective subclavian arteries, which originate from the innominate artery on the right and directly from the aorta on the left.
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3
Q

What is the anatomical position of the internal carotid artery?

A

• The internal carotid artery arises lateral and posterior to the external carotid artery and as it courses upward and posteriorly, it crosses the external carotid to become medial and deep to it.

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4
Q

What are the branches of the internal carotid artery?

A
  • The first branch of the internal carotid artery is the ophthalmic artery as it passes through the cavernous sinus.
  • The internal carotid arteries then branch into the middle and anterior cerebral arteries.
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5
Q

What are the stages of cellular changes that occur in the formation of atherosclerosis

A

Early fatty streak development
Early fibroatheroma
Advancing Atheroma: Thin-Cap Fibroatheroma and Its Rupture
Complex lesion development

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6
Q

Outline early fatty streak development

A

• begins in early teenage years
• initiated by lipid incorporation into the arterial wall which initiates inflammation.
• This attracts various cells including monocytes, which become macrophages and then absorb lipids to become foam cells.
Can be reversed

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7
Q

Outline early fibroatheroma

A
  • occurs in persons in their teens and 20s
  • The progression of inflammation promotes the accumulation of lipid and necrosis of the surrounding tissue.
  • This necrotic lesion then forms a fibrous cap and this creates lesions which are not of haemodynamic significance.
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8
Q

Outline advancing atheroma

A
  • occurs in persons aged >55 years.
  • In this stage of plaque development, a thin-cap fibroatheroma (TCFA) develops and may rupture
  • This allows the internal contents of the plaque to be exposed and thrombus forms.
  • This creates a plaque which thromboses the artery in some cases or releases a thrombus from the plaque which will travel distally to occlude a smaller artery and cause ischaemia.
  • This type of lesion is termed a ‘vulnerable plaque’.
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9
Q

What is vaso vasorum and why are they significant in advanced plaque formation?

A

Small blood vessels that supply the walls of larger arteries and veins
may grow into the atheroma and haemorrhage which will further increase the lesion size and promote thrombus formation

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10
Q

Outline complex lesion development

A
  • Many ruptures of thin fibrous caps are clinically silent in that they heal by forming fibrous tissue matrices of cells, collagen fibers, and extracellular space but may rupture again with thrombus formation
  • as the sequence of rupture, thrombosis and repair occurs to increase the size of the plaque.
  • Calcification may also increase, causing larger deposits which may become exposed to the lumen and become a further site of thrombus formation.
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11
Q

What are some risk factors that promote the progression of atheroma?

A

smoking, diabetes, kidney disease and hypertension

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12
Q

What are the different causes of stroke?

A
  • ischemia (85%) caused by occlusion from atherosclerosis or emboli released from atheroma or the heart
  • cerebral haemorrhage (15%) of the intracranial arteries.
  • Small artery occlusions within the brain may also cause ischemic infarcts (lacunar infarcts)
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13
Q

What defines a stroke?

A
  • symptoms last for more than 24hrs

* residual functional deficit persists or only partially resolves

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14
Q

What defines a TIA?

A
  • symptoms last for less than 24hrs
  • symptoms completely resolve
  • TIA’s occur in about 10% of stroke patients
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15
Q

What is a crescendo TIA?

A

Patients with multiple episodes of TIA within a 7day period

considered at high risk of stroke no matter what other risk factors may be present.

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16
Q

What is Amaurosis Fugax?

A

also known as Transient Monocular Blindness (TMB) . It occurs in one eye and it typically resolves in a short period of time.
There may be several pathologies related to TMB but emboli from carotid plaque is most common.

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17
Q

What are some terms that can be be used to define symptoms that last longer than 24hrs but completely resolve?

A

Reversible Ischemic Neurologic Deficit (RIND) and ‘stroke in evolution’

18
Q

What symptoms does an MCA stroke have?

A
  • facial asymmetry
  • arm weakness
  • speech deficits
  • hemiplegia (paralysis) of the contralateral side, affecting the lower part of the face, arm, and hand while largely sparing the leg
  • contralateral (opposite-side) sensory loss in the same areas
  • contralateral homonymous hemianopia—visual-field deficits affecting the same half of the visual field in both eyes.
19
Q

What are the symptoms of an ACA stroke?

A

It’s the vessel least commonly affected by strokes.
• contralateral leg weakness and sensory loss.
• behavioral abnormalities and incontinence also may occur.

20
Q

What are the symptoms of a PCa stroke?

A

• feeds the medial occipital lobe and inferior and medial temporal lobes.
• Vision is the primary function of the occipital lobe
• so a stroke affecting PCA distribution commonly causes visual deficits—specifically contralateral homonymous hemianopia.
• MCA stroke also may cause this symptom
Larger PCA strokes also may cause contralateral hemiparesis and hemi¬sensory loss.
Large left PCA strokes may result in aphasia, where¬as right PCA strokes may cause neglect.

21
Q

What are the symptoms of cerebellar stroke?

A
  • Cerebellar strokes commonly impair balance and coordination. Assess for ataxia (incoordination)
  • may cause vertigo, nausea and vomiting, headache, nystagmus, and slurred speech.
22
Q

Describe the management of asymptomatic carotid stenosis in terms of the major surgical trials

A

The significantly higher overall risk of stroke or death associated with carotid angioplasty/stenting (CAS) than with CEA
controversial management problem.
the Asymptomatic Carotid Artery Surgery study showed a benefit for carotid endarterectomy for internal carotid artery stenoses of 60% diameter narrowing or above
this threshold for intervention is often kept higher.
Typically, a cut point of 80% is selected.

23
Q

List the major non-atherosclerotic lesions of the carotid arteries

A
Dissection
Giant cell arteritis
Aneurysm
carotid body tumour
kinks and coils
fibromuscular dysplasia
24
Q

Define dissection

A
  • separation of the intimal layer occurs in arterial dissection.
  • Carotid artery dissection may occur by blunt trauma or heavy exertion, or spontaneously.
  • Spontaneous dissection may be associated with fibromuscular dysplasia or cystic medial degeneration.
25
Q

Define giant cell arteritis

A
  • covers a number of conditions which can involve arteries in the thorax, abdomen and cerebrovascular circulation.
  • Of these conditions, temporal arteritis and Takyashu’s arteritis are often associated with inflammation of the aorta and its proximal branches.
  • Uniform thickening of the arterial wall in the carotid or subclavian arteries may be seen on ultrasound in Takyashu’s arteritis
  • temporal arteritis may show a ‘halo’ around the temporal artery due to inflammation.
26
Q

Describe carotid aneurysm

A
  • Carotid artery aneurysm is uncommon but may occur in the common or internal carotid arteries.
  • The most common cause of aneurysm in these arteries is from atheroma although trauma and previous surgery may also be related.
  • TIA and stroke are the most common complications of aneurysm.
27
Q

Describe a carotid body tumour

A
  • neoplasms of the tissue derived from neural crest cells and are termed paragangliomas.
  • usually occurs at the carotid body in the bifurcation of the carotid artery
  • present as a mass below the angle of the mandible and may cause tinnitus, dysphagia or hoarseness.
  • These tumours are visible on ultrasound with wide separation of the ICA and ECA forming a characteristic ‘hourglass’ appearance.
  • Surgical resection is appropriate treatment for these tumours.
28
Q

Describe how carotid kinks and coils affect cerebrovascular circulation

A
  • The presence of significant stenosis from kinking or coiling of the carotid artery is a rare occurrence and is usually associated with atheroma formation at the site of the curvature.
  • The symptoms relate to those of carotid occlusive disease and they are usually managed surgically in conjunction with an endarterectomy
29
Q

How does fibromuscular dysplasia affect the carotids?

A
  • abnormal growth and connective tissue deposition in the media of the artery, forming a series of thickened ridges which displays a ‘string of beads’ appearance.
  • It is more common in women between 40-60years of age, with symptoms of TIA and amaurosis fugax or stroke.
30
Q

What is vertebrobasilar ischemia?

A
  • identifies a number of conditions which impair the posterior circulation
  • blood flow may be disturbed by embolic occlusion, external compression or stenosis
  • The symptoms which result may range from dizziness and vertigo to diplopia, paresthesias, tinnitus or drop attacks.
  • These symptoms are not specific to vertebrobasilar disease and a number of other conditions must also be excluded
31
Q

What can cause vertebrobasilar ischemia?

A
  • Stenosis of the vertebral artery may result in thrombus formation and thus occlusion of the artery
  • while stenosis of the subclavian artery can cause a fall in blood pressure in the subclavian artery and hence the vertebral artery.
  • Compression by osteophytes in the cervical spine may also cause flow disturbances in the posterior circulation as the head is moved and these cause transient and reproducible symptoms with rotation or flexion and extension of the neck.
32
Q

What is the subclavian steal effect?

A
  • In severe cases of subclavian stenosis the pressure reduction in the subclavian artery is great enough to cause retrograde flow in the vertebral artery and basilar artery thus causing symptoms of ischemia.
  • This effect is sometimes referred to as a ‘steal’ or ‘subclavian steal’
  • these terms should not be confused with the patient who shows a clear set of clinical symptoms which constitute the ‘subclavian steal syndrome’.
33
Q

What is the medical management for stroke patients?

A
  • medicated to reduce thrombosis formation, hypertension and blood lipids, with anti platelet, anti hypertensive and anti-lipid (statin) medications.
  • Patients may be sent for routine surveillance of their carotid atheroma to monitor plaque progression as a marker for the level of treatment they require.
34
Q

What are the two types of surgical management available for stroke patients?

A
  • The Carotid Thromb-endarterectomy (TEA)

* The Eversion Endarterectomy (EEA)

35
Q

What is a carotid thromb endarterectomy?

A
  • involves a longitudinal incision in the artery and the removal of the diseased segment.
  • The incision is then stitched closed but in some arteries, this causes a ‘pinching’ of the artery and so a ‘patch’ of either synthetic material or vein is sown into the incision to increase the circumference of the artery.
36
Q

What is an Eversion Endarterectomy (EEA)

A
  • involves a transverse incision through which the atheroma is removed from the ica, cca and eca.
  • The atheroma is removed from the cut end of the artery while pulling back or everting the artery to assist atheroma removal and the arteries are then re-sown.
  • This places stitches around the circumference of the artery and thus does not constrict the artery radially
37
Q

Briefly discuss carotid angioplasty and stenting

A
  • Angioplasty with stent placement has become increasingly common for carotid stenosis
  • there remains debate over the trials which compare stenting and endarterectomy.
  • Definitive studies which show the equivalence of stenting to endarterectomy have yet to be fully published but there are an increasing number of surgeons favouring the endarterectomy based on the results published so far.
38
Q

How can the CCA appear after an endarterectomy?

A
  • wall irregularity, which is the result of removing the atheroma and is of no clinical consequence.
  • there can be hyperplasia.
  • The region is slightly dilated and is the result of either a patch being stitched into the operated site or the bifurcation being moved to the region of the carotid bulb so that a patch is not required.
39
Q

Consider a patient that has right-sided weakness and slurred speech. Which ICA would you expect to demonstrate severe disease and why?

A

In a right handed person, the left hemisphere normally controls the right side of the body and the power of speech.
In a left handed person, speech is often but not always controlled by the right hemisphere.
In reality, many patients who have carotid disease related to speech impairment, may have lesions on either side.

40
Q

What is a normal appearance of the artery wall after CEA?

A

irregularity on the far wall.
This is commonly seen after this procedure and this thickened appearance is not normally of clinical significance to the patient.

41
Q

What ay happen to a vessel distal to a CEA?

A

kinking