2. Vascular Neurology Flashcards
(233 cards)
1
Q
ABCD2 score is used for?
A
Identification of risk factors that predict stroke after TIA.
2
Q
ABCD2 score points?
A
Age of 60 years or more (1 point).
Initial BP: SBP ≥ 140 or DBP ≥ 90 (1 point).
Clinical symptoms:
1 point for speech impairment without weakness.
2 points for unilateral weakness.
Duration of symptoms:
0 points for < 10 minutes.
1 point for 10 to 59 minutes.
2 points for 60 minutes or more).
Diabetes (1 point).
3
Q
Stroke risk after low risk TIA based on ABCD2 score?
A
0-3 points: Low Risk.
2-Day Stroke Risk: 1.0%
7-Day Stroke Risk: 1.2%
90-Day Stroke Risk: 3.1%
4
Q
Stroke risk after moderate risk TIA based on ABCD2 score?
A
4-5 points: Moderate Risk.
2-Day Stroke Risk: 4.1%
7-Day Stroke Risk: 5.9%
90-Day Stroke Risk: 9.8%
5
Q
Stroke risk after high risk TIA based on ABCD2 score?
A
6-7 points: High Risk.
2-Day Stroke Risk: 8.1%
7-Day Stroke Risk: 11.7%
90-Day Stroke Risk: 17.8%
6
Q
Picture? And presentation?
A
Restricted diffusion in the pons and the cerebellum.
Quadriplegia and impaired horizontal gaze - locked-in syndrome.
7
Q
Vertical gaze impairment lesion localization?
A
Midbrain lesions.
8
Q
Maximum NIHSS score?
A
42
9
Q
tPA/Alteplase dose?
A
The dose is 0.9 mg/kg, with a 10% bolus and the rest over 1 hour, with a maximum dose of 90 mg.
10
Q
tPA trial for the 3-hour window?
A
FDA approved on the basis of the National Institute of Neurological Disorders and Stroke (NINDS) tPA trial.
Published 1995.
11
Q
tPA trial for the 4.5-hour window?
A
The European Cooperative Acute Stroke Study 3 (ECASS3), intravenous tPA is safe and beneficial up to 4.5 hours after the onset of symptoms.
12
Q
Locked-in syndrome?
A
Caused by a basilar occlusion.
Bilateral infarcts at the base of the pons, affecting the long tracts but preserving the reticular activating system.
Patients are awake, consciousness is preserved, and they can blink and move their eyes vertically; however, they are quadriplegic, unable to speak, and with impairment of horizontal eye movements.
13
Q
Top of the basilar syndrome?
A
Infarcts of various structures including the midbrain, thalamus, and temporal and occipital lobes.
The manifestations are complex and varied, including combinations of behavioral abnormalities, alteration of consciousness, pupillary manifestations, disorders of ocular movements, visual field defects, and motor and/or sensory deficits.
14
Q
Venous sinus thrombosis clinical presentation?
A
Headache in about 90% of cases in adults.
Seizures in 40% of patients (higher than arterial strokes).
Increased ICP - due to occlusion of venous drainage, hemorrhagic infarct and edema.
Diplopia due to 6th CN palsy - nonlocalizing and may be a manifestation of increased ICP.
Focal neurologic findings depending on the area affected along the thrombosed venous sinus.
> Thrombosis of the deep venous system may lead to deep venous infarcts, including bilateral thalamic infarcts.
> Superior sagittal sinus thrombosis can lead to infarcts in the parasagittal cortex bilaterally along the sinus.
15
Q
Picture? Vessel occluded?
A
Wallenberg’s or lateral medullary syndrome - right lateral medulla and cerebellum infarct.
Caused by occlusion of the PICA, and is often associated with occlusion of the vertebral artery.
16
Q
Wallenberg’s or lateral medullary syndrome involved structures and manifestations?
A
• Vestibular nuclei, causing vertigo, nystagmus, nausea, and vomiting.
• Descending tract and nucleus of the 5th CN, producing impaired sensation on the ipsilateral hemiface.
• Spinothalamic tract, producing loss of sensation to pain and temperature in the contralateral hemibody.
• Sympathetic tract, manifesting with ipsilateral Horner’s syndrome with ptosis, miosis, and anhidrosis.
• Fibers of the 9th and 10th CN, presenting with hoarseness, dysphagia, ipsilateral paralysis of the palate and vocal cord, and decreased gag reflex.
• Cerebellum and cerebellar tracts, causing ipsilateral ataxia and lateropulsion.
• Nucleus of the tractus solitarius, causing loss of taste.
Patients may present with combinations of these manifestations and not always with a complete syndrome.
Hiccups is typically seen in this syndrome, but may not be explained by a lesion to a specific structure in the brainstem.
17
Q
Vertebral artery dissection? Most common site of dissection?
A
Can cause lateral medullary syndrome.
The most common site of a vertebral dissection is at the level of C1-C2, where the artery is mobile as it is leaving the transverse foramina to enter the cranium.
18
Q
Vertebral artery dissection? Imaging modalities?
A
Catheter angiogram - gold standard, will demonstrate the narrowing of the vessel, the extension of the dissection with an intimal flap, or double lumen. Potential risk of causing or worsening an existing dissection.
CTA and MRA with contrast have replaced a catheter angiogram for the diagnosis of dissection of the cervical arteries.
MRA with a time-of-flight sequence: assess the flow at the site of the dissection; however, it does not provide information about the vessel wall.
MRI with fat-suppression technique: assess the vessel wall and surrounding tissues, and very useful in nonocclusive dissections, when conventional angiogram will not give information about the vessel wall.
19
Q
NINDS trial stats?
A
Symptomatic ICH occurred in 6.4% of the tPA group, compared with 0.6% in placebo group.
tPA group had improved clinical outcomes and were at least 30% more likely to have minimal or no disability at 3 months.
The mortality at 3 months was 17% in the tPA group and 21% in the placebo group.
The earlier the administration, the better the prognosis and the lower the risk of hemorrhage.
20
Q
ECASS3: tPA between 3 and 4.5 hours additional exclusion criteria?
A
NIHSS >25.
Age >80.
History of both stroke and diabetes.
Any anticoagulant use, regardless of prothrombin time or INR.
21
Q
Amaurosis fugax?
A
Transient monocular blindness.
Painless visual loss: a “shade” or “curtain” moving in the vertical plane, with a rapid onset and brief duration of a few minutes.
Vision is most commonly recovered completely.
However, the presentation of amaurosis fugax in a patient with an underlying ICA stenosis, may herald the occurrence of a stroke.
22
Q
Amaurosis fugax causes?
A
Atherosclerotic stenosis of the ipsilateral ICA.
Transient occlusion of the retinal or ophthalmic arteries (the retinal artery originates from the ophthalmic artery, which is a branch of the ICA).
Other rate causes include giant cell arteritis, and embolism from other source.
23
Q
Differentiate AICA from PICA strokes?
anterior inferior cerebellar artery
A
1- Ipsilateral deafness occurs with AICA infarcts.
(Hearing loss attributed to involvement of the lateral pontomedullary tegmentum.
Audiologic evaluations have also suggested an inner ear and cochlear injury, which could be explained by involvement of the labyrinthine artery, which is a branch of the AICA).
2- By imaging, AICA infarcts affect the cerebellum more ventrally as compared with PICA infarcts.
24
Q
Picture? Mechanism?
A
Bilateral thalamic infarction, which can be seen with occlusion of the artery of Percheron.
The P1 segment of the PCA gives rise to interpeduncular branches that will provide vascularization to the medial thalamus. Most frequently, these branches arise from each PCA separately and will give perfusion to the thalamus on their respective side. In some cases, a single artery called the artery of Percheron will arise from the P1 segment on one side and will supply the medial thalami bilaterally. This is a normal variant. If an occlusion of the artery of Percheron occurs, the result will be an infarct in the medial thalamic structures bilaterally.
Thrombosis of the deep venous structures may produce venous infarcts in the thalamus, but this is not seen with superior sagittal sinus thrombosis.
25
The recurrent artery of Heubner? Origin? Supplies?
A branch of the ACA - largest deep penetrating branch.
Supplies the anterior limb of the internal capsule, the inferior part of the head of the caudate, and the anterior part of the globus pallidus.
26
The pericallosal artery origin?
One of the subdivisions of the ACA, running along the corpus callosum.
27
Lacunar stroke? Mechanism? Risk factors?
Occurs from occlusion of a small penetrating artery, as a consequence of chronic hypertension.
Diabetes and hyperlipidemia also play a role but to a lesser degree.
These small vessels develop lipohyalinosis with vessel wall degeneration and luminal occlusion.
Atherosclerosis of the parent vessel may occlude the opening of these small penetrating branches, or predispose to the entry of embolic material that will occlude them.
28
Lacunar infarcts? Locations?
Putamen.
Caudate nuclei.
Thalamus.
Basis pontis.
Internal capsule.
Deep hemispheric white matter.
29
Lacunar stroke syndromes?
• Pure motor, usually involving face, arm, and leg equally, and the most frequent location is in the territory of the lenticulostriate branches, affecting the posterior limb of the internal capsule, but has also been described with lacunes in the ventral pons.
• Pure sensory, with hemisensory deficit involving the contralateral face, arm, trunk, and leg from a lacune in the thalamus.
• Clumsy-hand dysarthria occurs more frequently from a lacune in the paramedian pons contralateral to the clumsy hand, but it may also occur from a lacune in the posterior limb of the internal capsule.
• Ataxic hemiparesis, in which the ataxia is on the same side of the weakness, but out of proportion to the weakness, and this occurs from lacunes in the pons, midbrain, internal capsule, or parietal white matter.
30
Lacunar stroke “stuttering”?
The clinical manifestations of lacunar infarcts may have a sudden onset; however, it is not infrequent to see a stepwise "stuttering" progression of the neurologic deficits over minutes, and sometimes over hours to even days.
31
Lenticulostriate branches origin? Supplies?
Arise from the trunk of the MCA before its bifurcation
Provide vascular supply to the putamen, part of the head and body of the caudate nucleus, the outer globus pallidus, the posterior limb of the internal capsule, and the corona radiata.
32
Superior division of MCA stroke? Presentation?
Hemiparesis affecting mainly arm and face, probably from ischemia to the lateral hemispheric surface.
Eye deviation occurs from unopposed action originating from the other frontal eye fields.
Broca's or motor aphasia.
33
Aphasia types in MCA and MCA branches strokes?
Broca's or motor aphasia occurs from ischemia in the territory of the superior division of the MCA affecting the dominant inferior frontal gyrus.
Ischemia in the territory of the inferior division of the MCA in the dominant hemisphere will cause Wernicke's aphasia.
A left MCA trunk occlusion will likely produce a global aphasia (will also produce ischemia in the lenticulostriate arteries' territory presenting with hemiparesis or hemiplegia affecting face, arm, and leg).
An infarct of the lenticulostriate branches will not present with cortical findings such as aphasia.
34
ACA branches and supply?
ACA supplies the anterior three-quarters of the medial surface of the frontal lobe.
Deep penetrating branches originate from the ACA (proximal and distal to the Acomm), and the recurrent artery of Heubner is the largest of these deep branches.
These penetrating vessels supply the anterior limb of the internal capsule, the inferior part of the head of the caudate nucleus, and the anterior part of the globus pallidus.
35
ACA stroke presentation?
Given that both ACAs communicate via the Acomm, an occlusion proximal to the Acomm may not produce significant clinical manifestations in the setting of a normal complete circle of Willis.
An infarction occurring from an ACA occlusion distal to the Acomm presents with:
1- Contralateral sensorimotor deficits of the lower extremity, sparing the arm and face.
2- Urinary incontinence due to involvement of the medial micturition center in the paracentral lobule.
3- Deviation of the eyes to side of the lesion.
4- Paratonic rigidity occur sometimes.
36
An anterior communicating artery occlusion significance?
Does not produce clinical manifestations in patients with otherwise normal perfusion dynamics.
37
The vascular supply of the thalamus?
Originates mainly from the posterior circulation through four major arteries:
1. The tuberothalamic artery: (aka polar artery) originates from the Pcomm and supplies the anterior portion of the thalamus, especially the ventral anterior nucleus.
2. The thalamoperforating or paramedian artery originates from P1/PCA and supplies the medial aspect of the thalamus, especially the dorsomedial nucleus.
3. The thalamogeniculate artery originates from P2/PCA and supplies the lateral aspect of the thalamus, including the ventral lateral group of nuclei.
4. The posterior choroidal artery arises from P2/PCA and provides vascularization to the posterior aspect of the thalamus, where the pulvinar is located.
38
Picture? Artery involved?
Superior cerebellar artery (SCA) stroke - right cerebellar hemisphere superiorly. CT scan at the level of the midbrain.
39
Vascular supply of cerebellum and brainstem in general?
The SCA supplies most of the superior half of the cerebellar hemisphere, including the superior vermis, the superior cerebellar peduncle, and part of the upper lateral pons.
The anterior inferior cerebellar artery (AICA) supplies the inferolateral pons, middle cerebellar peduncle, and a strip of the ventral cerebellum between the posterior inferior cerebellar and superior cerebellar territories.
The posterior inferior cerebellar artery (PICA) supplies the lateral medulla, most of the inferior half of the cerebellum and the inferior vermis.
40
The inferior division of the MCA? Structures supplied? Stroke presentation?
Supplies the inferior parietal and lateral temporal lobe regions.
Stroke syndrome:
1- Wernicke's (receptive) aphasia, in which the patient may speak fluently but does not make sense, and is not able to understand spoken language or follow commands. This occurs from ischemia of the posterior aspect of the superior temporal gyrus.
2- Agitation and confusion.
3- Cortical sensory deficits in the face and arm.
4- Visual defects in the contralateral hemifield.
41
Picture?
MRA: absence of basilar artery, probably from an occlusion.
42
What basilar occlusion can cause?
- Pontine infarct and will possibly result in a locked-in syndrome.
- Possibly could cause extensive brainstem infarction resulting in brain death.
43
Basilar occlusion mechanism?
- Local thrombosis of the basilar artery itself.
- Thrombosis of both vertebral arteries.
- Thrombosis of a single vertebral artery when it is the dominant vessel.
- Embolism can occur as well, frequently lodging distally in the vessel.
44
Parinaud’s syndrome? Clinical findings? Lesion location?
Characterized by:
- Supranuclear paralysis of eye elevation.
- Defect in convergence.
- Convergence-retraction nystagmus.
- Light-near dissociation.
- Lid retraction.
- Skew deviation of the eyes.
The lesion is localized in the dorsal midbrain and is classically seen with pineal tumors compressing the quadrigeminal plate; however, it can occur from midbrain infarcts.
45
Picture?
Absence of the ICA on the left side. The left MCA is still partially seen and is being supplied via the anterior communicating artery.
46
The anterior choroidal artery? Origin? Supplies?
Arises from the ICA just above the origin of the Pcomm (or supraclinoid ICA segment).
Supplies the internal segment of the globus pallidus, part of the posterior limb of the internal capsule, and part of the geniculocalcarine tract.
As it penetrates the temporal horn of the lateral ventricle, it supplies the choroid plexus and then joins the posterior choroidal artery from the posterior circulation.
47
Picture?
Occlusion of the main trunk of the left MCA, which is not filling with contrast beyond the occluded segment.
The ICA is visualized up to its terminus. The ACA is also visualized and the A1 segment is patent.
48
ACA segments?
A1 segment: extends from the ICA terminus to the Acomm artery.
A2 segment: extends from the Acomm artery to the bifurcation into pericallosal and callosomarginal arteries.
A3 segment: includes the distal branches after this bifurcation.
49
Picture? Mechanism?
Watershed infarction, between the superficial and deep territories of the MCA.
Occur when there is reduction of blood supply between two vascular territories; this region being susceptible to ischemia.
This reduction of blood flow can occur in the setting of systemic hypotension, especially with an underlying stenosis proximal to both territories, ie carotid stenosis.
50
Picture?
Hyperdense left MCA sign.
51
Hyperdense left MCA sign? Specificity? Sensitivity? Mimics?
loss of the insular ribbon, attenuation of the lentiform nucleus, and hemispheric sulcal effacement.
In a patient with a presumed stroke, the hyperdense MCA sign has good specificity and positive predictive value for atheroembolic occlusions of the affected vessel, and it is associated with poor prognosis.
This sign lacks sensitivity but is helpful when a strong clinical suspicion exists.
Mimics of hyperdense MCA sign, aka pseudohyperdense sign, include vascular calcification, increased hematocrit, and intravenous contrast.
52
Early signs (within 6 hours) of ischemic stroke on CT scan?
Hyperdense left MCA sign.
Loss of the insular ribbon.
Attenuation of the lentiform nucleus.
Hemispheric sulcal effacement.
53
“Person-in-a-barrel” syndrome?
Occurs in severe cases of bilateral watershed infarcts, in which the patient can only move the distal part of the extremities.
Watershed infarcts manifest clinically with proximal weakness, affecting the proximal upper and proximal lower extremities, with weakness at the shoulder and at the hip. This occurs because the watershed regions correlate with the homuncular representation of the proximal limbs and trunk.
54
Medial medullary syndrome?
Caused by occlusion of the vertebral artery or one of its medial branches.
Infarct affecting the pyramid, medial lemniscus, and emerging hypoglossal fibers.
- Contralateral arm and leg weakness sparing the face (from corticospinal tract involvement prior to its decussation).
- Contralateral loss of sensation to position and vibration.
- Ipsilateral tongue weakness.
55
Giant cell arteritis?
Older adults, typically > 50 years of age.
Inflammation of the temporal artery predominantly but may also affect other branches of the ECA.
Headaches, associated with generalized constitutional symptoms, jaw claudication, and tenderness of the scalp around the temporal artery.
May overlap with polymyalgia rheumatica, and patients will also present with proximal muscle pain and achiness.
Labs: leukocytosis and very elevated sedimentation rates and C-reactive protein levels.
The diagnosis is based on a biopsy of the temporal artery demonstrating granulomatous inflammation.
Blindness may occur from ocular ischemia, and these patients should be treated ASAP with steroids while arranging for a temporal artery biopsy.
56
Millard–Gubler syndrome?
The lesion is localized in the pons and affects the corticospinal tract before its decussation (which occurs at the level of the pyramids), as well as the VII cranial nerve nucleus and/or fibers.
Manifested by contralateral hemiplegia with ipsilateral facial palsy.
>> When there is also conjugate gaze paralysis toward the side of the brainstem lesion, it is called Foville syndrome.
57
Intracranial aneurysms etiology?
Most often acquired and sporadic.
In associations with various conditions:
1- AVMs.
2- AD polycystic kidney disease.
3- Aortic coarctation.
4- Fibromuscular dysplasia.
5- Marfan’s syndrome.
6- Ehlers–Danlos syndrome.
Can also be familial. Screening with CTA or MRA is recommended in patients with two or more family members with an intracranial aneurysm or history of SAH.
58
Factors associated with increased risk of cerebral aneurysmal rupture and SAH?
1- Size: higher with diameters of 7 mm or higher, and the risk rises with increasing size.
2- Aneurysmal growth: growing aneurysm on imaging, or new symptoms from aneurysm growth (new cranial nerve palsy or mass effect).
3- Aneurysm location: posterior circulation aneurysms are at higher risk for rupture as compared to anterior circulation aneurysms.
4- Smoking.
5- Uncontrolled hypertension.
6- Patients with previous aneurysmal rupture are at higher risk for SAH.
59
Treatment of unruptured aneurysms?
Conservatively (imaging surveillance and observation) in patients with low risk of aneurysmal rupture).
Endovascular treatment (coiling).
Surgical treatment (clipping).
>> In selected aneurysms, endovascular coil embolization is associated with reduced procedural morbidity and mortality as compared to surgical clipping; however, the recurrence risk may be higher.
60
Occipital/PCA strokes in the dominant hemisphere manifestations?
- Homonymous hemianopia in the contralateral side. Typically, spares central vision because of collateral blood supply to macular cortical representation.
- Alexia (inability to read).
- Anomia.
- Achromatopsia (color anomia).
- Classical alexia without agraphia (with left occipital infarcts involving the splenium of the corpus callosum): patient cannot see what is placed in the right visual hemifield, and whatever can be seen in the left visual hemifield will be represented in the right occipital cortex, but due to corpus callosum involvement this information cannot be connected with language centers in the left hemisphere.
61
Benedikt’s syndrome?
Infarction in the right mesencephalic tegmentum in its ventral portion, involving the ventral part of the red nucleus, the brachium conjunctivum, and the fascicle of the third cranial nerve.
Ipsilateral third nerve palsy with contralateral involuntary movements such as tremor and choreoathetosis.
62
Results of the Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) trial?
Randomized patients with a recent TIA or stroke with a 50% to 99% stenosis of a major intracranial artery to warfarin or aspirin.
The primary end point was ischemic stroke, intracranial hemorrhage (ICH), or death from vascular causes other than stroke.
Concluded that warfarin was associated with higher rates of adverse events and provided no benefit over aspirin.
63
Warfarin INR target?
Between 2.0 and 3.0, except in the setting of mechanical valves, in which the target INR is 2.5 to 3.5.
64
Gaze deviation with stroke?
MCA stroke: the frontal eye fields may be involved, and patients will have gaze deviation toward the hemisphere involved. This occurs because the contralateral frontal eye fields will be unopposed, “pushing” the eyes to the side of the infarct.
Pontine stroke: eyes deviate toward the hemiparetic side.
65
The Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial?
Studied the effect of atorvastatin 80 mg daily in patients with a recent (within 6 months) TIA or stroke, with LDL between 100 and 190 mg/dL.
The conclusion was that 80 mg of atorvastatin daily reduces the overall incidence of strokes and cardiovascular events.
66
SAMMPRIS (Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis) trial?
Compared best medical therapy versus intracranial stenting in patients with intracranial stenosis (70% to 99% stenosis) and recent stroke or TIA, demonstrating that medical therapy is superior.
The rate of early stroke was high in the stent group, and lower than expected in the medical therapy group.
Medical management in the study included aspirin 325 mg daily and clopidogrel 75 mg daily for 90 days, optimal management of risk factors (target systolic BP <140 mm Hg, and <130 mm Hg in diabetics, and target LDL <70 mg/dL), and lifestyle modifications.
67
Alberta Stroke Program Early CT Score (ASPECTS)?
A grading system to assess early ischemic changes in patients with acute ischemic strokes of the anterior circulation.
Two axial cuts are obtained on the CT, one at the level of the basal ganglia and thalamus, and another more cranial cut where these structures are not appreciated.
10 regions of interest, of which 4 are deep and defined as the caudate, the internal capsule, the lentiform nucleus, and the insular region, and 6 regions are cortical. These regions are assigned a point, which is subtracted if there is early ischemic change in that specific region.
A normal looking CT scan will obtain a maximum of 10 points, and a score of 0 is consistent with diffuse ischemic injury of the entire MCA territory.
An ASPECTS score of 7 or less correlates with increased dependence and death.
68
Segments of the ICA? by Bouthillier et al.
- The cervical (C1) segment: begins at the level of the CCA and ending where the ICA enters the carotid canal in the petrous bone. It has no branches.
- The petrous (C2) segment: runs within the carotid canal in the petrous bone. Vidian and caroticotympanic branches arise from this segment.
- The lacerum (C3) segment: runs between where the carotid canal ends and the superior margin of the petrolingual ligament (this ligament runs between the lingula of the sphenoid bone and the petrous apex and is a continuation of the periosteum of the carotid canal).
- The cavernous (C4) segment: begins at the superior margin of the petrolingual ligament, runs within the cavernous sinus, and ends at the proximal dural ring formed by the junction of the medial and inferior periosteum of the anterior clinoid process. Meningohypophyseal trunk, inferolateral trunk, and capsular arteries arise from this segment.
- The clinoid (C5) segment: runs between the proximal dural ring and the distal dural ring where the ICA becomes intradural. Small segment - no branches.
- The ophthalmic (C6) segment: begins at the distal dural ring ending proximal to the origin of the Pcomm artery. Gives two major branches, the ophthalmic artery and the superior hypophyseal artery.
- The communicating (C7) segment: begins proximal to the origin of the Pcomm artery extending to the ICA bifurcation. Gives off the Pcomm artery and the anterior choroidal artery.
69
A more simple and practical classification divides the internal carotid into?
- Cervical segment.
- Petrous segment.
- Cavernous segment.
- Supraclinoid segment.
70
Symptomatic carotid stenosis treatment according to the North American Symptomatic Carotid Endarterectomy Trial (NASCET)?
Symptomatic carotid stenosis of 70% to 99% should be revascularized - the 2-year ipsilateral stroke rate was 26% with medical treatment versus 9% with CEA.
Symptomatic stenosis of 50% to 69% may also benefit from CEA, with greater impact in men versus women, in those with previous strokes versus TIAs, and with hemispheric versus retinal symptoms.
Stenosis of less than 50% or carotid occlusions, there is no evidence to support that surgical treatment is better than medical therapy. The treatment should be medical management.
71
Asymptomatic carotid disease treatment? Trials?
CEA has proven benefits over medical treatment in patients with more than 60% stenosis as demonstrated in the Asymptomatic Carotid Atherosclerosis Study (ACAS), and in the Asymptomatic Carotid Surgery Trial (ACST), however, the numbers needed to treat were high, and the benefit may not be significant in the real world, depending also on the experience of the surgeon.
In ACAS, the absolute risk reduction was 1.2% per year with a number needed to treat of 85 favoring the surgical group.
In ACST, the absolute risk reduction was 1.1% with a number needed to treat of 93 favoring surgery over medical therapy.
72
Risk of stroke after TIA?
Around 10% to 15% of patients who suffer a TIA will have a stroke within 3 months, and the risk is higher soon after the TIA, with 50% of the strokes occurring within 48 hours.
73
Guidelines recommend the following workup for TIAs:
- Neuroimaging within 24 hours, preferably an MRI with DWI.
- Noninvasive vascular imaging of the extracranial arteries.
- Noninvasive imaging of the intracranial vasculature if it is considered that this will alter management.
- Patients should be evaluated as soon as possible.
74
Picture? Mechanism?
Deep intracerebral hemorrhage, most likely caused by hypertension.
This occurs from rupture of deep perforating arteries, which suffer changes caused by chronic hypertension, leading to lipohyalinosis, making these vessels susceptible to sudden closure (causing lacunar infarctions) or rupture (causing hemorrhage).
75
Hemorrhages showing a fluid–fluid level?
Anticoagulation associated hemorrhage.
76
Intracerebral hemorrhage (ICH) accounts for approximately —-%? of all strokes.
10%.
77
The most common 2 causes of spontaneous ICH?
Hypertension, most common, 75% of cases.
Followed by cerebral amyloid angiopathy.
78
Hypertensive ICH most common locations?
Commonly originates in deep subcortical structures such as:
- Putamen.
- Caudate.
- Thalamus.
As well as in:
- Pons.
- Cerebellum.
- Periventricular deep white matter.
79
Charcot Bouchard microaneurysms have been classically associated with?
Hypertensive ICH; however, they are not found consistently and are described only in a small number of patients.
80
Cerebral amyloid angiopathy pathogenesis?
Results from the deposition of amyloid protein (congophilic material) in the media and adventitia of cerebral vessels, especially in cortical and leptomeningeal vessels.
This process is associated with cortical and lobar hemorrhages, which may be recurrent.
Since the angiopathy is diffuse, there are recurrent and multiple hemorrhages, and commonly MRI with gradient echo sequences will show multiple small areas of hypointensity suggesting prior hemosiderin deposition from prior microhemorrhages.
81
Moyamoya disease? Pathogenesis?
Noninflammatory, nonatherosclerotic vasculopathy that affects the intracranial circulation, leading to arterial occlusions and prominent arterial collateral circulation.
82
Moyamoya disease? Presentation?
It presents most commonly in children and adolescents, with a second peak in the fourth decade of life, but with a much lower frequency.
Clinical manifestations include TIAs and strokes, as well as ICHs.
In childhood the presentation is predominantly ischemic, with strokes and TIAs, which may be precipitated by hyperventilation.
In adults, the presentation is most frequently ICH.
Other manifestations include headaches, seizures, movement disorders, and cognitive deterioration.
83
The diagnosis of moyamoya disease? Imaging? Histopathology?
Based on the angiographic findings, characterized by progressive bilateral stenosis of the distal ICAs, extending to proximal ACAs and MCAs, and the development of extensive collateral circulation at the base of the brain, with the “puff of smoke” appearance.
Histopathologically, there is intimal thickening by fibrous tissue of the affected arteries, with no inflammatory cells or atheromas.
84
Treatments of Moyamoya disease?
There is no curative treatment for this condition. Revascularization procedures may improve perfusion, angiographic appearance, and ischemic manifestations; however, they may not impact the frequency of hemorrhagic events.
Medications such as antiplatelets, vasodilators, calcium-channel blockers, and steroids have been used with equivocal results.
Anticoagulation is not helpful and usually avoided given the hemorrhagic complications.
85
Picture?
Amyloid angiopathy - multiple small rounded areas of gradient echo susceptibility throughout the brain, representing microhemorrhages with hemosiderin deposition.
86
Amyloid angiopathy Histopathology?
Histologically, there is deposition of Congo-red positive amyloid material in the media and adventitia of small- and medium-sized vessels. This causes weakening of the vessel walls.
87
Genetics associations with amyloid angiopathy?
There are associations of amyloid angiopathy with apolipoprotein E4 and E2, as well as with Alzheimer’s disease.
88
Dejerine–Roussy syndrome?
Caused by a thalamic infarct, in which the lesion affects the sensory relay nuclei.
Present with severe deep and cutaneous sensory loss of the contralateral hemibody, usually the entire hemibody and up to the midline. In some cases, there may be dissociation of sensory loss, often affecting position sense more than other sensory functions.
With time, some sensation returns, but the patient may develop severe pain, allodynia, and paresthesias of the affected body part.
89
The anterior and the posterior choroidal arteries origins?
The anterior choroidal arteries arise from the anterior circulation, more specifically from the ICA slightly distal to the origin of the Pcomm artery.
The posterior choroidal arteries arise from the posterior circulation, more specifically from the PCAs.
90
The vertebral artery origin?
The vertebral arteries originate from the subclavian arteries on their respective sides.
91
The vertebral artery segments? Vascular supply in general?
V1 segment: extends from the subclavian artery to the transverse foramen of C5-C6.
V2 segment: runs within the transverse foramina of the cervical vertebra from C5-C6 to C2.
V3 segment: extends from the transverse foramen of C2 and turns posterolaterally around the arch of C1, between the atlas and the occiput. It is extracranial.
V4 segment: begins where the vertebral artery enters the dura at the foramen magnum and joins the contralateral vertebral artery to form the basilar artery. Gives off the PICA and the ASA. Both vertebral arteries will join to form the basilar artery.
The posterior circulation provides the vascular supply to the brainstem, cerebellum, the thalamus, and the occipital lobes.
92
Picture?
Hemorrhagic infarct from left transverse sinus thrombosis.
93
CVST associated infarct pathogenesis?
Occlusion of the venous sinuses will lead to venous infarction and localized edema. The affected tissue becomes engorged, swollen, and the parenchyma will suffer ischemia, leading to infarct and hemorrhage, which is also influenced by the impaired venous drainage.
Given the occlusion of venous drainage and in the setting of parenchymal edema, the content of the intracranial volume will tend to rise, leading to intracranial hypertension.
94
CVST manifestations?
Characterized by the presence of headache, and depending on the extent of the disease, focal neurologic deficits, altered mental status, seizures, and coma will be present, in severe cases progressing to herniation and death.
95
CVST Risk factors/causes?
Oral contraceptives use.
Pregnancy and puerperium.
Cancer.
Nephrotic syndrome.
Connective tissue disorders.
Hematologic conditions such as antiphospholipid antibody syndrome.
Trauma.
Dehydration.
Genetic prothrombotic conditions such as protein C and S deficiency, antithrombin deficiency, factor V Leiden mutation, prothrombin mutation, and homocysteinemia.
Infectious causes (otitis, mastoiditis, sinusitis, meningitis).
96
CVST associated infarct diagnosis?
CT scan and MRI of the brain will show hemorrhagic infarcts that are not in a strictly arterial distribution.
MRV will demonstrate the absence of signal in the thrombosed venous sinus.
97
CVST treatment?
In patients with venous sinus thrombosis, an etiologic factor should be investigated, since it may be a treatable condition.
Treatment involves stabilization of the patient and anticoagulation to stop the thrombotic process. Studies comparing anticoagulation with placebo have shown no increased or new cerebral hemorrhages with anticoagulation, even in patients with pre-existing hemorrhagic infarcts.
Treatment of intracranial hypertension may be needed, sometimes requiring surgical decompression.
Endovascular intervention for thrombolysis and clot removal should be reserved for patients with severe neurologic impairment, stupor or coma and intracranial hypertension, including those with no improvement or worsening despite anticoagulation.
98
EC/IC bypass study?
Patients were randomized to medical therapy versus EC/IC bypass surgery, demonstrating higher rates of stroke in the bypass arm.
EC/IC bypass is not recommended for the management of intracranial atherosclerotic stenosis.
99
Claude’s syndrome?
Manifested by ipsilateral third nerve palsy, and contralateral ataxia and tremor.
The lesion affects the dorsal red nucleus and the third nerve fascicle, and is in the midbrain tegmentum more dorsally located than the lesion seen in Benedikt’s syndrome, which is caused by a ventral mesencephalic tegmental lesion.
Patients with Claude’s syndrome, as compared to Benedikt’s syndrome, have more ataxia but no involuntary choreoathetotic movements.
100
Picture?
Left transverse sinus thrombosis.
101
CHA2DS2VASc score, points?
Congestive heart failure (1 point).
Hypertension (1 point).
Age ≥75 years (2 points).
Diabetes mellitus (1 point).
Stroke/TIA/thromboembolism (2 points).
Vascular disease (previous MI, PAD or aortic plaque) (1 point).
Age 65 to 74 years (1 point).
Sex category (female) (1 point).
The maximum score is 9 points.
102
HAS-BLED score?
Used for the assessment of risk of hemorrhage.
1 point is assigned each for hypertension, abnormal renal or liver function (1 point each), stroke, bleeding history or predisposition to bleeding, labile INRs, elderly (age >65 years), and drug use (1 point for antiplatelets or NSAIDs, and 1 point for excessive alcohol intake).
A HAS-BLED score of >2 is considered high and associated with risk of major bleeding.
103
Cerebral venous sinuses?
Drainage of venous blood occurs through veins into dural venous sinuses, which eventually drain into the internal jugular veins.
The dural venous sinuses are venous channels enclosed between dural layers, and they have no valves.
The major venous sinuses are the superior sagittal sinus, the inferior sagittal sinus, the straight sinus, the transverse sinuses, sigmoid sinuses, and the cavernous sinuses.
104
Cerebral venous sinuses illustration?
105
The deep venous system?
Drains the periventricular white matter, basal ganglia, and thalamic regions and is composed of deep veins that drain toward the straight sinus.
106
The internal cerebral vein?
Formed by the junction of the thalamostriate and septal veins, run posteriorly encountering the contralateral internal cerebral vein and emptying into the great cerebral vein of Galen.
107
The basal vein of Rosenthal?
A deep vein that drains the base of the forebrain, travels posteriorly between the midbrain and the temporal lobe on each side, and also empties into the great cerebral vein of Galen, located beneath the splenium of the corpus callosum.
108
The great cerebral vein of Galen?
It joins the inferior sagittal sinus forming the straight sinus, which will then run toward the confluence of the sinuses.
109
The cavernous sinuses?
Are on both sides of the sella turcica and receive blood from facial and orbital structures, including the ophthalmic veins.
The cavernous sinuses drain into the superior and inferior petrosal sinuses.
The superior petrosal sinus connects the cavernous sinus with the transverse sinus on each side.
The inferior petrosal sinus connects the cavernous sinus with the sigmoid sinus or the jugular bulb on each side, but this sinus may be hypoplastic or absent in some cases.
110
Superficial veins over the convexity of the brain?
Drain into the superior sagittal sinus, the transverse sinus, or the middle cerebral vein, which runs along the Sylvian fissure.
Between these structures there are anastomotic veins:
The superior anastomotic vein of Trolard: large anastomotic vein that connects the Sylvian vein to the superior sagittal sinus.
The inferior anastomotic vein of Labbe: large vein traveling over the temporal lobe convexity connecting the Sylvian vein to the transverse sinus.
111
Emissary veins?
Connect scalp veins with the dural venous sinuses.
112
CADASIL stands for?
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.
113
When to suspect CADASIL?
History of multiple strokes without traditional vascular risk factors, a history of migraines, subsequent development of dementia, and a family history of strokes and dementia suggesting a hereditary condition.
114
CADASIL genetics and pathogenesis?
CADASIL is inherited in an autosomal dominant fashion,
This condition is associated with a missense mutation in the gene NOTCH3 on chromosome 19.
The gene product is a transmembrane receptor expressed mainly in vascular smooth muscle, and the mutation leads to accumulation of this protein in the vascular walls, especially in small arteries and capillaries.
115
CADASIL clinical manifestations?
Patients present with migraines with aura, stroke episodes, seizures, pseudobulbar palsy, and progressive cognitive decline leading to the development of dementia.
The strokes are recurrent and predominantly lacunes, caused by small vessel disease.
Some patients present with psychiatric manifestations, especially depression and emotional lability.
116
CADASIL MRI typical findings?
T2 hyperintensities in the subcortical white matter and basal ganglia.
117
Picture?
A blood vessel with a thick wall, which contains a basophilic granular material. This pathologic finding is characteristic of CADASIL.
118
CADASIL diagnosis?
The diagnosis could be made based on detection of the NOTCH3 mutation, or with skin biopsy demonstrating pathologic changes.
119
Weber’s syndrome?
A combination of an ipsilateral third nerve palsy with contralateral hemiplegia.
This is caused by a midbrain lesion.
Third nerve palsy, manifested by limited adduction and upward movements of the eye, therefore presenting with diplopia on upward gaze and when looking to the other side.
The contralateral hemiplegia is caused by the lesion affecting the corticospinal tract before its decussation at the level of the pyramids.
120
Picture?
Cavernous malformation - typical “popcorn-like” appearance, with a dark rim on T2 consistent with hemosiderin.
121
Intracranial vascular malformations include:
1- Arteriovenous malformations (AVMs).
2- Cavernous malformations.
3- Venous angiomas.
4- Capillary telangiectasias.
5- Dural arteriovenous fistulas (DAVF).
122
Cavernous malformations?
Clusters of vascular channels, composed of dilated thin-walled vessels, with no smooth muscle or elastic fibers, and with no intervening brain parenchyma separating the vascular structures.
MRI,l: typical “popcorn-like” appearance, with a dark rim on T2 consistent with hemosiderin; gradient echo may show evidence of cavernous malformations when not evident on T2-images.
Typically incidental and found in asymptomatic patients; however, they may present with seizures and occasionally with hemorrhage, with manifestations depending on the location of the lesion.
Hemorrhage from cavernous malformation is of lesser severity and lower pressure as compared to hemorrhage from AVMs.
123
AVMs?
Congenital vascular lesions consisting of a tangle of dilated vessels (nidus) in which arteries and veins communicate without an intervening normal capillary bed in between.
Can be seen on CT but CTA provides better vascular visualization.
MRI demonstrates the vascular lesion with flow voids and regions of previous hemorrhage, as well as its relationship with the parenchyma.
Catheter angiography is the gold standard diagnostic study to evaluate the vascular structure, pattern of vascular feeders, and drainage.
AVMs present most commonly with intracerebral hemorrhage, with other typical presentations including seizures and headache.
124
Dural arteriovenous fistulae (DAVF)?
Acquired vascular lesions in which there is arteriovenous shunting typically supplied from meningeal or dural arterial branches, with drainage toward a dural venous sinus.
The meningeal arterial supply (not pial arterial supply) as well as the absence of a parenchymal nidus distinguishes DAVFs from AVMs.
Associated with increased venous pressure and arterialization of the draining veins and the etiopathogenesis may be related to a venous sinus occlusion (from venous sinus thrombosis, trauma, or previous craniotomy), leading to increased venous pressure and eventual formation of the arteriovenous shunt.
DAVF may present with pulsatile tinnitus, headaches, seizures, and focal neurologic deficits from increased venous pressure and abnormal vascular hemodynamics. Intracranial hemorrhage can also occur.
125
Venous angiomas or developmental venous anomalies?
Thin-walled venous structures with normal intervening brain tissue.
These are asymptomatic with a very low risk of hemorrhage.
MRI demonstrates a conglomerate of vessels in a “caput medusa” pattern.
126
Capillary telangiectasias?
Abnormally dilated capillaries that are separated by normal brain tissue.
They are typically found incidentally and rarely become symptomatic.
127
The common carotid artery divides into external and internal carotid arteries, typically at the level of?
C4, below the angle of the jaw.
128
“Bovine aortic arch”?
In which the left common carotid has the same origin with the innominate artery, and in some cases the left common carotid will originate from the innominate artery.
129
Picture?
Spinal dural arteriovenous fistula (DAVF) - a lesion with T2 hyperintensity in the spinal cord, with perimedullary flow voids.
130
Spinal dural arteriovenous fistula (DAVF)? Stats?
The most common type of spinal vascular malformation.
DAVF is more frequently encountered in men and above 50 years of age.
131
Spinal dural arteriovenous fistula (DAVF)? Pathogenesis and location?
An acquired condition, and the arteriovenous shunting site is located within the dura mater near a spinal nerve root, where a radiculomeningeal artery connects with a radicular vein.
This arterialization leads to increased venous pressure, venous congestion, and intramedullary edema, manifesting as a progressive myelopathy.
The typical location is in the lower thoracic and lumbar regions, and this type of lesion rarely produces hemorrhage.
132
Spinal dural arteriovenous fistula (DAVF)? Presentation?
Patients present with pain, weakness, and sensory symptoms below the level of the lesion, as well as gait disturbance.
The myelopathic syndrome is usually gradually progressive with occasional intermittent exacerbations and/or remissions. Some patients may have acute worsening of symptoms.
133
Spinal dural arteriovenous fistula (DAVF)? Imaging?
MRI: enlargement of the cord with hyperintensity on T2 seen over several levels, with perimedullary flow voids.
Spinal angiogram: (the gold standard diagnostic test) detects this abnormality, and localizes the level of the feeding artery.
134
Spinal dural arteriovenous fistula (DAVF)? Treatment goal and techniques?
The treatment goal is to stop the progression of the condition, and the prognosis depends on the degree of disability and duration of the symptoms prior to the treatment.
Treatment involves endovascular embolization with liquid embolic agents and/or surgical disconnection of the lesion.
Surgical treatment has a higher success rate with low recurrence, as compared to endovascular embolization.
A common approach is a combined treatment with endovascular embolization followed by surgical resection.
135
Picture?
ICH in the right anterior temporal lobe.
Hemorrhage is approximately 1 week old. Early subacute.
136
The basis to estimate timing of hemorrhage on MRI?
Initially hemorrhage is composed of plasma and red blood cells, with the presence of intracellular oxyhemoglobin,
which is then converted to deoxyhemoglobin,
subsequently oxidized to methemoglobin.
Later, cell lysis occurs with the presence of extracellular hemoglobin,
which is then converted to hemosiderin.
Estimation of the timing of the ICH is based on the presence of these different types of blood products.
137
Hyperacute ICH on MRI?
<12 hours.
The predominant blood product is oxyhemoglobin.
Isointense on T1 sequences.
Hyperintense on T2 sequences.
138
Acute ICH on MRI?
12 hours to 2 days.
Deoxyhemoglobin is the predominant blood product.
Isointense on T1.
Hypointense on T2.
139
Early subacute ICH on MRI?
2 to 7 days.
Intracellular methemoglobin.
Hyperintense on T1.
Hypointense on T2.
140
Late subacute ICH on MRI?
8 days to 1 month.
There is extracellular methemoglobin.
Hyperintense on T1 and T2 sequences.
141
Chronic ICH on MRI?
>1 month, and probably for years.
There is hemosiderin.
Isointense or hypointense on T1.
Hypointense on T2 sequences.
142
ICH timing table?
143
Saccular intracranial aneurysms? Prevalence? Risk of rupture?
Acquired lesions which are found in approximately 3.2% of the general population.
The majority of intracranial aneurysms do not rupture, and only approximately 1 in 200 to 400 will rupture.
However, it is the most common cause of nontraumatic SAH (80% to 85% of cases).
The majority of intracranial aneurysms are solitary; however, 15% to 30% of patients have multiple aneurysms.
144
The most frequent locations of intracranial aneurysms are:
Anterior communicating artery (30%).
Posterior communicating artery (25%).
Middle cerebral artery bifurcation (20%).
Internal carotid artery bifurcation (7.5%).
Basilar apex (7%).
Pericallosal artery (4%).
Posterior inferior cerebellar artery origin (3%).
Other locations include the ophthalmic artery origin, anterior choroidal artery origin, SCA, AICA, and cavernous ICA.
145
Carotid-cavernous fistula (CCF)? Pathogenesis?
A tear in the cavernous segment of the ICA allows arteriovenous shunting to the cavernous sinus, causing increased pressure within this sinus, with drainage toward a superior ophthalmic vein and impairing the venous drainage of the eye.
Symptoms are secondary to increased pressure within the cavernous sinus (with involvement of the cranial nerves traveling within this sinus and causing ophthalmoplegia), and increased pressure in the venous system draining the eye, impairing venous drainage (leading to chemosis, proptosis, increased intraocular pressure, retinal ischemia with vision loss).
Increased intracranial pressure can occur, as well as increased intracranial venous pressure which can lead to intracerebral or subarachnoid hemorrhage (about 5% of patients).
146
Different CCFs classifications?
Etiology (traumatic vs. spontaneous).
Hemodynamic factors (high flow vs. low flow).
Anatomic factors (direct vs. indirect).
147
Traumatic vs. spontaneous CCF?
Traumatic CCFs are the most common, associated with head or facial trauma, and most frequent in young males. In general, most traumatic CCFs are direct and high flow.
Spontaneous CCFs are typically encountered in older female patients, and may be caused by either feeders to from the ICA or external carotid artery to the cavernous sinus, or spontaneous tear within the cavernous ICA segment, occasionally from rupture of a cavernous ICA aneurysm.
148
Direct vs. indirect CCF?
With direct CCFs the shunt is of high flow, causing an acute presentation with rapid progression of symptoms.
Indirect CCFs are low flow, with insidious onset and gradual progression of symptoms. In indirect CCFs, the feeders may be from either the internal or the external carotid artery.
149
CCF diagnosis?
Cerebral angiography is the gold standard for diagnosis, demonstrating arteriovenous shunting at the cavernous sinus, with drainage to the superior ophthalmic vein or to other venous structures.
150
CCF treatment?
The goal of treatment is to occlude the fistula, and hopefully preserve flow in the internal carotid artery.
Endovascular embolization is the treatment of choice, and can be performed transarterially through the tear in the ICA (in a direct fistula) or the feeders (in an indirect fistula), or transvenously using a transfemoral venous approach with navigation through the inferior petrosal sinus or the facial and superior ophthalmic veins to reach the cavernous sinus.
Coils and liquid embolics are used through either endovascular route to occlude the shunting site.
After successful embolization, chemosis and proptosis improve rapidly, and cranial nerve impairment may improve over days to weeks. Improvement of visual deficits depends on the duration and severity of pre-existing deficits prior to treatment.
A last resort endovascular approach is the sacrifice of the involved ICA after making sure that the patient can tolerate permanent occlusion of this vessel.
Surgical treatment is only indicated if endovascular approach is not possible or not successful, and may involve ligation of the involved carotid artery.
Conservative management (external manual compression of the involved carotid artery at the neck several times per day for 4 to 6 weeks) may be useful in certain indirect CCFs, but is generally not effective.
151
DAVFs have been classified according to?
DAVFs have been classified according to the pattern of venous drainage.
The presence of cortical venous drainage is associated with increased risk of intracranial hemorrhage and nonhemorrhagic neurologic complications.
152
Dural arteriovenous fistulae (DAVF) Borden classification?
Type I: direct drainage from meningeal arteries to a dural venous sinus which has normal antegrade flow. The most benign.
Type II: shunts between meningeal arteries and a dural venous sinus, with retrograde flow into subarachnoid or cortical veins.
Type III: drainage from meningeal arteries to subarachnoid or cortical veins.
Types II and III have cortical venous drainage, and are “aggressive” DAVFs associated with risk of neurologic symptoms including hemorrhage.
153
DAVFs diagnosis?
CTA and MRI/MRA may suggest the presence of a DAVF, by detecting abnormal flow voids, vascular dilatations, and/or cluster of vascular channels near a dural venous sinus.
Cerebral angiography is the gold standard for the diagnosis, and provides information on arterial supply and venous drainage.
154
DAVFs treatment?
Endovascular embolization is the most widely used therapy for DAVFs, and can be performed transarterially or transvenously, typically with liquid embolic materials, with occasional adjunct use of coils.
Given the efficacy of endovascular embolization, surgery is reserved for cases in which endovascular approach is not feasible or not successful.
155
Early studies to support endovascular thrombectomy?
MR CLEAN study published in 2014.
Four studies published in 2015 (ESCAPE, EXTEND-IA, SWIFT PRIME and REVASCAT).
Demonstrated benefit of endovascular thrombectomy using stent-retriever devices in anterior circulation LVO strokes presenting within 6 hours from the onset of symptoms, with significant improvement of clinical outcomes.
156
2015 guidelines for endovascular therapy with a stent-retriever device, patients meeting the following criteria?
- Modified Rankin score of 0 to 1 prior to the stroke.
- Acute ischemic stroke with intravenous tPA therapy within 4.5 hours from onset.
- Occlusion causing the stroke involving the ICA or proximal MCA (M1 segment).
- Age 18 or older.
- NIHSS score of 6 or higher.
- ASPECTS of 6 or higher.
- Treatment can be initiated within 6 hours from the onset of symptoms.
157
Which year did FDA approve Dabigatran for stroke prevention in nonvalvular atrial fibrillation?
2010.
158
Which year did FDA approve Rivaroxaban for stroke prevention in nonvalvular atrial fibrillation?
2011.
159
Which year did FDA approve Apixaban for stroke prevention in nonvalvular atrial fibrillation?
2012.
160
Dabigatran MOA?
Direct thrombin inhibitor (DTI), available as a prodrug which is metabolized to its active form.
161
Dabigatran bioavailability?
It has poor oral bioavailability, and the medication is coated with tartaric acid to improve absorption.
162
Dabigatran absorption and half life?
Once absorbed, the peak level is reached in 1 to 2 hours and the half-life is 14 to 17 hours.
163
Dabigatran metabolism?
The drug is 80% cleared renally, with the rest being metabolized in the liver. Therefore patients with low creatinine clearance require dose adjustments.
164
Dabigatran side effects?
This medication can however cause dyspepsia and may be associated with the risk of GI hemorrhage.
165
Dabigatran vs Warfarin study?
In the RE-LY study, Dabigatran 110 mg twice a day was noninferior to warfarin for prevention of strokes and systemic embolism in nonvalvular atrial fibrillation, with lower rates of major hemorrhage; and Dabigatran 150 mg twice daily was superior to warfarin with similar rates of major hemorrhage.
166
Dabigatran FDA approved dosing?
The FDA approved Dabigatran 150 mg twice daily, with a 75 mg twice daily dose for patients with creatinine clearance of 15 to 30 mL/min.
167
Rivaroxaban MOA?
Factor Xa inhibitor.
168
Rivaroxaban bioavailability?
Easily absorbed and preferably with food.
169
Rivaroxaban absorption and half life?
Reaches peak levels in 2 to 4 hours and has half-life of 5 to 9 hours.
170
Rivaroxaban metabolism?
Two-thirds are metabolized in the liver with one-third excreted unchanged in the urine.
171
Rivaroxaban vs Warfarin study?
In ROCKET AF trial, Rivaroxaban was noninferior to warfarin for preventing stroke and systemic embolism in nonvalvular atrial fibrillation, with similar risks of bleeding, but lower risks of intracranial and fatal hemorrhages.
172
Rivaroxaban FDA approved dosing?
It is 95% protein bound, allowing once daily dosing. Rivaroxaban is administered in a dose of 20 mg once daily with a meal, or 15 mg daily in case of creatinine clearance 15 to 50 mL/min.
173
Apixaban MOA?
Factor Xa inhibitor.
174
Apixaban absorption and half life?
With peak levels at 3 to 4 hours, and half-life of 8 to 15 hours.
175
Apixaban metabolism?
It is metabolized in the liver by CYP450 3A4, and 25% is renally excreted.
176
Apixaban vs Warfarin study and dosing?
In ARISTOTLE trial, Apixaban 2.5 mg or 5 mg twice daily was superior to warfarin for preventing stroke and systemic embolism in nonvalvular atrial fibrillation. Apixaban also was associated with lower risk of major bleeding including intracranial hemorrhage, and lower mortality rates.
177
Dabigatran reversal agent?
Idarucizumab. A monoclonal antibody fragment that binds free and thrombin-bound Dabigatran neutralizing its activity.
Activated charcoal can be considered within 2 hours of the intake of Dabigatran, Rivaroxaban or Apixaban.
Hemodialysis has also been considered with Dabigatran.
178
Central nervous system vasculitis (CNSV) categories?
1) Primary angiitis of the central nervous system (PACNS).
2) Secondary CNSV includes:
a) Idiopathic systemic vasculitides.
b) Systemic vasculitides associated with autoimmune diseases.
c) Systemic vasculitis 2/2 nonautoimmune conditions, such as infections, drugs, or cancer.
179
CNS vasculitis mimics? in which there is no inflammation but the vessels may appear abnormal on angiographic studies
Atherosclerosis.
Reversible cerebral vasoconstriction syndrome (RCVS).
CADASIL.
Antiphospholipid syndrome.
180
PACNS? Definition and gender distribution?
Inflammation of small- and medium-sized parenchymal and leptomeningeal arteries involving the brain and/or spinal cord.
It is present similarly in males and females, with presentation at a median age of 50 years.
181
PACNS? Presentation?
Headache is the most common symptom, usually insidious and/or chronic; however, thunderclap headache is very rare in PACNS, distinguishing it from RCVS in which thunderclap headache is a classic presentation.
Ischemic strokes and altered cognition are also common presentations in PACNS.
182
The following three criteria have to be met to make the diagnosis of PACNS?
Acquired otherwise unexplained neurologic or psychiatric deficit.
Classic angiographic or histopathologic features of CNS angiitis.
No evidence of systemic vasculitis or any disorder that could mimic the angiographic or pathologic features.
183
Probable vs. Definite PACNS diagnosis?
A probable diagnosis is made in those with high probability cerebral angiogram with abnormal MRA and abnormal CSF analysis but without biopsy confirmation.
A definite diagnosis requires biopsy confirmation of vessel wall inflammation.
184
Three main histopathologic patterns in PACNS?
Granulomatous angiitis of the CNS.
Lymphocytic PACNS.
Necrotizing CNSV.
185
PACNS CSF?
CSF analysis is required in the work up of PACNS, showing abnormalities in the majority of cases, including elevated WBCs and protein.
CSF is also important to exclude other diagnoses including infections and cancer.
In RCVS the CSF is usually normal but may be slightly abnormal.
186
PACNS MRI of the brain?
May demonstrate ischemic infarcts, areas of gadolinium enhancement in the parenchyma or meninges, and nonspecific hyperintensities in the deep gray and white matter.
187
PACNS DSA?
Cerebral angiogram is helpful, demonstrating the characteristics “beading” which represents areas of narrowing and dilatation.
However, cerebral angiogram is not the gold standard for diagnosis and the “beading” pattern is nonspecific, seen also in atherosclerosis, vasospasm and infectious or radiation vasculopathy.
Similar angiographic findings are seen in RCVS; however, these resolve within 3 months.
188
PACNS gold standard test?
Brain biopsy is the gold standard for the diagnosis of PACNS, demonstrating vessel wall inflammation.
However, the sensitivity of brain biopsy is low, and this could be secondary to various factors, including sampling error and frequent inability to obtain involved brain.
The yield of the biopsy may increase by obtaining tissue from an identified lesion on MRI.
189
Treatment of PACNS?
High-dose steroids with or without cyclophosphamide.
Once remission is achieved, azathioprine or mycophenolate mofetil can be utilized for maintenance.
The evidence to guide treatment is limited, and mostly based on retrospective observational data and expert opinion recommendations.
190
Reversible cerebral vasoconstriction syndrome (RCVS)? Characteristics and gender distribution?
More common in women than in men.
Characterized by headaches with or without other neurologic symptoms, with vasoconstriction of cerebral arteries that resolve spontaneously within 12 weeks.
191
RCVS presentation?
Typically present with headache, most commonly an acute headache or thunderclap headache, which usually resolves but may recur within 1 to 4 weeks.
Nausea and vomiting as well as photo and phonophobia are not uncommon.
After the acute headache or in between episodes of acute headache the patient may have a moderate degree of persistent headache which also tends to resolve within a month.
Patients may develop focal neurologic symptoms and seizures, which are usually transient.
RCVS may be complicated by cortical SAH, ischemic stroke, or IPH, in which case neurologic deficits may be persistent and the severity correlates with the area involved and severity of the parenchymal damage.
192
RCVS associated conditions?
PRES - it is possible that both overlap or represent different manifestations in the spectrum of the same condition.
Preeclampsia and eclampsia.
193
RCVS precipitant factor and triggers?
Vasoactive drugs: amphetamines, cocaine, cold medicines with decongestants, triptans, ergot alkaloid derivatives, and other adrenergic and serotoninergic drugs.
Triggers such as strenuous activity, sexual activity, Valsalva, and/or stressful or emotional situations.
194
RCVS imaging?
CT and MRI may be completely normal, or demonstrate small cortical SAH, ischemic stroke and/or IPH.
Noninvasive or cerebral angiography may demonstrate “beading” pattern with areas of narrowing and dilatation representing vasoconstriction, which is typically dynamic and may change over the course of the illness.
The diagnosis of RCVS is confirmed with the reversibility of these angiographic findings, which occur at some point within 12 weeks. These findings can be assessed and followed up with noninvasive imaging, including transcranial Doppler.
195
RCVS CSF?
CSF findings may be completely normal, or may demonstrate findings consistent with SAH, or slight elevations in protein and WBCs, which resolve spontaneously.
196
RCVS BIOPSY?
Brain biopsy is not indicated, and only obtained when suspecting central nervous system vasculitis.
In RCVS the biopsy should not demonstrate vessel wall inflammation.
197
RCVS management?
Symptomatic with supportive care as necessary.
Vasodilators such as calcium-channel blockers and magnesium sulfate are typically used.
Inciting factors and drugs should be avoided.
Steroids are not indicated, and actually have been reported to worsen the clinical course.
198
RCVS prognosis?
Prognosis is good with complete resolution of symptoms; however, residual deficits may persist in cases of ischemic stroke or intraparenchymal hemorrhage.
199
Carotid angioplasty and stenting (CAS) vs. Carotid endarterectomy (CEA) trials?
The SAPPHIRE (Stent and Angioplasty with Protection in Patients at High Risk for Endarterectomy).
The CREST (Carotid Revascularization, Endarterectomy vs. Stent Trial).
200
The SAPPHIRE (Stent and Angioplasty with Protection in Patients at High Risk for Endarterectomy) study?
Randomized high surgical risk patients with symptomatic (≥50%) or asymptomatic (≥80%) carotid stenosis to CEA or CAS.
High surgical risk criteria included significant cardiac disease, severe pulmonary disease, contralateral carotid occlusions, contralateral laryngeal nerve palsy, previous radical neck surgery or radiation therapy to the neck, recurrent stenosis after endarterectomy, and age >80 years.
This study showed initially lower rates of stroke or death in the CAS group, but no differences in long-term outcomes between both groups.
201
The CREST (Carotid Revascularization, Endarterectomy vs. Stent Trial) study?
Randomized patients with symptomatic (>50%) or asymptomatic (≥60%) carotid stenosis to CEA or CAS.
Demonstrated no significant difference between the groups in primary events (periprocedural stroke, death or MI, and ipsilateral stroke up to 4 years).
However, there was a higher rate of periprocedural stroke in the CAS group and higher rate of periprocedural MI in the CEA group.
A differential outcome based on age was noticed, with CAS favoring patients younger than 70 years of age, and CEA favoring patients older than 70 years of age.
202
When deciding revascularization option for patients with carotid stenosis, several factors should be taken into account, including?
- Comorbidities that may increase the surgical risk and anesthesia risk (severe cardiac and pulmonary disease).
- Anatomic factors (aortic arch anatomy, high carotid bifurcation, obesity with difficult neck access).
- Previous or pre-existing conditions (contralateral carotid occlusion, contralateral laryngeal nerve palsy, previous radical neck surgery or radiation).
203
Selecting CEA vs. CAS?
It is reasonable to select CEA over CAS when revascularization is indicated in older patients with vascular anatomy that would not be favorable for endovascular treatment.
It is also reasonable to select CAS over CEA in patients with neck anatomy unfavorable for CEA.
It may be reasonable to consider CAS in patients at high risk of surgical complications related to the comorbidities, contralateral carotid occlusion, previous radical neck surgery or radiation, and contralateral laryngeal nerve palsy.
Long-term benefit in terms of stroke prevention appear to be similar in patients undergoing CAS and CEA.
204
Quadriplegia, inability to speak, limited horizontal gaze, with preserved consciousness, vertical gaze, and blinking?
Locked-in syndrome
205
Vertigo, nystagmus, nausea, hiccups, hoarseness, dysphagia, ipsilateral paralysis of the palate and vocal cord, decreased gag reflex, impaired sensation on the ipsilateral hemiface, loss of sensation to pain and temperature in the contralateral hemibody, ipsilateral ataxia and lateropulsion, and ipsilateral Horner's syndrome?
Wallenberg's syndrome
Caused by a lateral medullary infarction (associated with posterior inferior cerebellar artery or vertebral artery occlusion)
206
Ipsilateral hearing loss, vertigo, ipsilateral ataxia, ipsilateral Horner's syndrome, sensory deficit in the ipsilateral hemiface, and contralateral hemibody?
Anterior inferior cerebellar artery infarct
207
Contralateral hemibody sensory loss with subsequent development of pain, allodynia, and paresthesias. Results from a thalamic lesion?
Dejerine-Roussy syndrome
208
Finger agnosia, right-left disorientation, agraphia, and acalculia?
Gerstmann's syndrome
209
Normal variant with vascular supply to both medial thalami?
Artery of Percheron
210
Deep branch from ACA that supplies anterior limb of the internal capsule, inferior part of head of caudate nucleus, and anterior part of globus pallidus?
Recurrent artery of Heubner
211
Caused by chronic hypertension, and associated with the pathogenesis of lacunar strokes?
Lipohyalinosis
212
Infarct between two vascular territories. Produces the "person-in-a-barrel" syndrome, characterized by proximal weakness?
Watershed infarcts
213
Infarct in the posterior circulation from thrombus lodging in the distal basilar. Symptoms: Behavioral abnormalities, altered level of consciousness, and abnormalities of ocular motion?
Top of the basilar syndrome
214
Right hemiparesis, right homonymous hemianopsia, and aphasia?
Left MCA syndrome
215
Left hemiparesis, left homonymous hemianopsia, and left hemineglect?
Right MCA syndrome
216
Thalamus, contralateral hemisensory loss?
Pure sensory lacunar syndrome
217
Posterior limb of internal capsule, contralateral motor deficits. Also described with ventral pons lacunes?
Pure motor lacunar syndrome
218
Paramedian pons, "clumsy hand, and dysarthria?
Clumsy-hand dysarthria lacunar syndrome
219
Pons, midbrain, or internal capsule, weakness with ataxia out of proportion to weakness?
Ataxic hemiparesis lacunar syndrome
220
NOTCH3?
CADASIL: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy
221
Dilated thin-walled vessels, with no smooth muscle or elastic fibers, and no intervening brain parenchyma. Popcorn appearance on MRI?
Cavernous malformation
222
Thin-walled venous structure with normal intervening brain tissue?
Venous angioma
223
Abnormally dilated capillaries, normal intervening brain tissue?
Capillary telangiectasia
224
Nidus, with arteries and veins communicating without an intervening normal capillary bed in between?
Arteriovenous malformation
225
Hemorrhage in the putamen, caudate, thalamus, pons, cerebellum, and deep white matter?
Hypertensive intracranial hemorrhage
226
Associated with lipohyalinosis and Charcot-Bouchard microaneurysms?
Hypertensive intracranial hemorrhage
227
Lobar hemorrhages.Multiple microhemorrhages on MRI gradient echo. Congo-red positive amyloid material, seen as apple-green birefringence with polarized light?
Cerebral amyloid angiopathy
228
"Puff of smoke"?
Extensive collateral circulation seen in Moyamoya disease, in which there is bilateral stenosis of the distal internal carotid arteries and intracranial arteries of the circle of Willis
229
Ipsilateral third nerve palsy and contralateral hemiplegia?
Weber's syndrome (midbrain lesion)
230
Ipsilateral third nerve palsy and contralateral involuntary movements?
Benedikt's syndrome (lesion in the ventral portion of the mesencephalic tegmentum)
231
Ipsilateral third nerve palsy and contralateral ataxia and tremor?
Claude's syndrome (lesion in the dorsal portion of the mesencephalic tegmentum)
232
Ipsilateral seventh nerve palsy with contralateral hemiplegia?
Millard-Gubler syndrome (lesion in the pons)
233
Limited upward gaze, convergence retraction nystagmus, light-near dissociation, lid retraction, and skew deviation of the eyes?
Parinaud's syndrome (lesion affecting the quadrigeminal plate)
