Ischemic Stroke & Transient Ischemic Attack 2 Flashcards

Bradley's Neurology in clinical practice Current Diagnosis & Treatment Neurology UpToDate

1
Q

a) Which 3 major cerebrovascular disorders does stroke encompass and b) which is the most common?

A

a) The 3 major cerebrovascular disorders are:
1) Ischemic stroke
2) Primary intracerebral hemorrhage
3) Spontaneous subarachnoid hemorrhage

b) The most common is Ischemic stroke (70-80%)

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2
Q

Definition of TIA

A

TIA is a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia with the ABSENCE OF INFARCTION ON BRAIN IMAGING

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3
Q

Definition of stroke

A

Ischemic stroke is defined as an infarction of central nervous system tissue (brain, spinal cord, or retinal cell death) attributable to ischemia, based on neuropathologic, neuroimaging, and/or clinical evidence (ie, persistence of symptoms or findings) of permanent injury

AHA/ ASA 2013

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4
Q

Μηχανισμοί δημιουργίας ισχαιμικού εγκεφαλικού επεισοδίου

A

1) Θρόμβωση
2) Εμβολή
- αρτηριο-αρτηριακή
- καρδιο-αρτηριακό έμβολο (κολπική μαρμαρυγή, στένωση μιτροειδούς, έμφρακτο μυοκαρδίου, μύξωμα, θρόμβος στην αριστερή κοιλία κ.α.)
- έμβολο από τη φλεβική κυκλοφορία μέσω καρδιακού ελλείμματος (π.χ. ανοικτό ωοειδές τρήμα)

3) Μείωση συστηματικής πίεσης διηθήσεως (καρδιακή ανεπάρκεια, πτώση αρτηριακής πίεσης, καταπληξία κ.α.)
4) Αρτηριακός σπασμός (κακοήθης υπέρταση, υπαραχνοειδής αιμορραγία, λοιμώξεις, τοξική επίδραση ουσιών, ΚΕΚ)

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5
Q

Σύσταση εμβόλων

A

Τμήμα αθηρωματικής πλάκας
++
έμβολα αέρος, λίπους, καρκινικά κύτταρα, υλικό από ενδοφλέβια λήψη τοξικών ουσιών, βακτηριακό υλικό

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6
Q

Causes of ischemic stroke
TOAST classification

A

1) large artery atherosclerotic disease
2) small-vessel or penetrating artery disease (lacunes)
3) cardiogenic embolism
4) cryptogenic (undetermined etiology)
6) uncommon causes (Current / table 10-3)

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7
Q

Algorithm for evaluating patients with a clinical diagnosis of stroke

A

AHA/ASA 2021

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8
Q

Hematologic testing in stroke evaluation

A

Hematologic testing for arterial hypercoagulable states (eg, antiphospholipid syndrome and hyperhomocysteinemia) is indicated for many patients with cryptogenic stroke, particularly for patients who are young, have a history of lupus or symptoms compatible with lupus, or have features suggestive of antiphospholipid syndrome such as unexplained venous or arterial thrombotic events, miscarriages, or unexplained thrombocytopenia

In addition to testing for the antiphospholipid syndrome, additional testing for hypercoagulable states associated with venous thrombosis (eg, Factor V Leiden mutation, prothrombin gene mutation, protein S deficiency, protein C deficiency, and antithrombin deficiency) is suggested by some experts for patients with evidence of a cardiac or pulmonary right-to-left shunt

For patients with cryptogenic stroke and systemic or constitutional symptoms suggestive of vasculitis, screening tests include erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), serum cryoglobulins, antinuclear antibody (ANA), antineutrophil cytoplasmic antibody (ANCA), and complement levels.

Another consideration is testing ADAMTS13 activity, particularly in patients with low platelet counts; in rare cases, ischemic stroke may be the presenting finding or occur during remission in individuals with thrombotic thrombocytopenic purpura (TTP), which is caused by deficient activity of the ADAMTS13 protease

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9
Q

Early CT signs of ischemic stroke in the MCA territory

A
  • loss of gray/white-matter differentiation
  • sulcal effacement (εξάλειψη)
  • effacement of the Sylvian fissure
  • obscuration of the lentiform nucleus
  • The intracranial large vessel segments are occasionally hyperdense in the noncontrast CT (dense MCA sign, Sylvian fissure dot sign, dense basilar artery) before the infarction becomes visible
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10
Q

Clues from stroke topography in source identification

A

Isolated superficial cerebral or cerebellar infarction suggests an embolic mechanism from a large artery, heart, or aorta

● Cortical or large subcortical infarcts in multiple vascular territories suggest a proximal source of embolism from the heart or aorta

Infarcts of varying age in a single vascular territory suggest a large artery source of embolism

● Infarcts along the boundary regions between the major cerebral arteries (ie, border zone or watershed regions) suggest the stroke mechanism is low flow (hypoperfusion) or multiple small emboli

Small subcortical infarcts suggest lacunar infarction from small vessel disease

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11
Q

In how much time can ischemic changes be found in CT scan

A

In a systematic review involving 15 studies where noncontrast CT scans were performed within six hours of stroke onset, the prevalence of early infarction signs was 61 percent (standard deviation ±21 percent)
The sensitivity of noncontrast CT for signs of brain infarction increases over time from stroke onset.

Uptodate

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12
Q

ischemic changes found in MRI according to stroke phase

A

Hyperacute
* DWI can detect abnormalities due to infarction within 3 to 30 minutes of onset
* after 6 hours, high T2 signal will be detected, initially more easily seen on FLAIR
* T1 hypointensity is only seen after 16 hours and persists.

Acute (24h to 1 week)
During the first week, the infarcted parenchyma continues to demonstrate high DWI signal and low ADC signal, although by the end of the first week ADC values have started to increase.
The infarct remains hyperintense on T2 and FLAIR, with T2 signal progressively increasing during the first 4 days.
After day 5 the cortex usually demonstrates contrast enhancement on T1 C+

Subacute (1-3 weeks)
ADC demonstrates pseudonormalization typically occurring between 10-15 days
In contrast, DWI remains elevated due to persistent high T2/FLAIR signal (T2 shine through)
Cortical enhancement is usually present throughout the subacute period.
T1 weighted sequences continue to show hypointensity throughout the area of infarct

Chronic (more than 3 weeks)
T1 signal remains low with intrinsic high T1 in the cortex if cortical necrosis is present
T2 signal is high.
Cortical contrast enhancement usually persists for 2 to 4 months.
Importantly if parenchymal enhancement persists for more than 12 weeks the presence of an underlying lesion should be considered.
ADC values are high. DWI signal is variable, but as time goes on signal progressively decreases.

Radiopedia

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13
Q

Patients with ischemic stroke and DWI-negative-stroke

A

Nearly 7%

DWI is reported to fail in the detection of ischemic strokes involving:

  • posterior circulation infarction: 5x more likely to be DWI-negative than anterior circulation ischemia, especially within the first 48 hours
  • small strokes, particularly small brainstem infarcts
  • hyperacute ischemia: within 3 hours of symptom onset
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14
Q

CT perfusion findings in acute stroke

A

On CT perfusion imaging, the penumbra is identified by tissue demonstrating mismatch between cerebral blood flow or cerebral blood volume and mean transit time (μέσος χρόνος διέλευσης) (MTT; a measure of the time it takes for blood to pass through small vessels).

The three parameters typically used are:

1) mean transit time (MTT) or time to peak (TTP) of the deconvolved tissue residue function (Tmax)
2) cerebral blood flow (CBF)
3) cerebral blood volume (CBV)

Normal perfusion parameters are:
gray matter
MTT: 4 s
CBF: 60 mL/100 g/min
CBV: 4 mL/100 g

white matter
MTT: 4.8 s
CBF: 25 mL/100 g/min
CBV: 2 mL/100 g

In acute stroke:
The CBV, and to a lesser extent CBF, differentiates penumbra and core infarct:

core
increased MTT/Tmax
markedly decreased CBF
markedly decreased CBV

penumbra
increased MTT/Tmax
moderately reduced CBF
near-normal or increased CBV

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15
Q

CT Perfusion limitations

A

delayed cerebral tissue iodine saturation could occur in the setting of
* ipsilateral cervical internal carotid artery stenosis
* low cardiac output and
* cardiac arrhythmia

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16
Q

Χρησιμότητα διακρανιακού υπερηχογραφήματος στο ΙΑΕΕ

A

1) ανάδειξη μεγάλης στενωτικής βλάβης μεγάλης αρτηρίας και παρακολούθηση της εξέλιξης της
2) υπόδειξη ανοικτού ωοειδούς τρήματος με τη δοκιμασία φυσαλίδων

17
Q

What percentage of stroke is of atherosclerotic origin?

A

14-25% of strokes

18
Q

Which are the most common sites of atherosclerosis?

A

The most common sites of atherosclerosis are:

1) the junction of the common and internal carotid artery
2) the middle cerebral artery stem
3) the vertebral arteries at the origin and vertebrobasilar junction
4) the mid-basilar artery

19
Q

Mechanism of ischemic stroke most commonly seen in large artery atherosclerosis

A

Plaque rupture with subsequent artery-to-artery embolization

** Less frequently, when the degree of stenosis is greater than 90%, flow failure may develop as a mechanism of stroke

20
Q

Modalities for vessel imaging

A
  • Ultrasonography
  • CT angiography
  • Magnetic resonance angiography without or with contrast
  • Catheter-based digital subtraction angiography
21
Q

What is the gold standard for establishing the extent of vascular disease in TIA or evolving stroke

A

Conventional angiography or intra-arterial digital subtraction angiography

22
Q

A main dissadvantage of MRA

A

It overestimates the degree of stenosis related to disturbed signal from turbulent flow

23
Q

Patients with recent stroke or TIA (within 30 days) attributable to severe stenosis (70%–99%) of a major intracranial artery management

A

The addition of clopidogrel 75 mg/d to aspirin for up to 90 days is reasonable to further reduce recurrent stroke risk

24
Q

Patients with a stroke or TIA caused by 50% to 99% stenosis of a major intracranial artery management

A

Aspirin 325 mg/d is recommended in preference to warfarin to reduce the risk of recurrent ischemic stroke and vascular death

25
Q

In patients with a TIA or nondisabling ischemic stroke within the past 6 months and ipsilateral severe extracranial (70%–99%) carotid artery stenosis management

A

Carotid endarterectomy (CEA) is recommended to reduce the risk of future stroke, provided that perioperative morbidity and mortality risk is estimated to be <6%.

26
Q

Patients with recent TIA or ischemic stroke and ipsilateral moderate (50%–69%) extracranial carotid stenosis as documented by catheter-based imaging or noninvasive imaging, management

A

CEA is recommended to reduce the risk of future stroke, depending on patient-specific factors such as age, sex, and comorbidities, if the perioperative morbidity and mortality risk is estimated to be <6%.

27
Q

Algorithm for approach to symptomatic and asymptomatic carotid stenosis

A
28
Q

Choice of method of revascularization

A

In patients ≥70 years of age with stroke or TIA in whom carotid revascularization is being considered, it is reasonable to select CEA over CAS to reduce the periprocedural stroke rate

In patients in whom revascularization is planned within 1 week of the index stroke, it is reasonable to choose CEA over CAS to reduce the periprocedural stroke rate

In patients with symptomatic severe stenosis (≥70%) in whom anatomic or medical conditions are present that increase the risk for surgery (such as radiation-induced stenosis or restenosis after CEA) it is reasonable to choose CAS to reduce the periprocedural complication rate

29
Q

Patients unlikely to benefit from revascularization (and thus should be excluded)

A

● Stenosis less than 50 percent.

● Severe comorbidity due to other surgical or medical illness.

Stroke associated with persistent, severe neurologic deficits and disability that precludes preservation of useful function.

Near occlusion of the symptomatic ipsilateral internal carotid artery; note that distinguishing between a very high-grade stenosis and near occlusion is not necessarily straightforward; the management of such patients should be individualized along with expert guidance.

For patients with total occlusion, revascularization is not an option!

30
Q

When should revascularization be performed in patients with TIA or nondisabling stroke (when indicated)

A

It is reasonable to perform the procedure within 2 weeks of the index event rather than delay surgery to increase the likelihood of strokefree outcome

31
Q

Patients with recently symptomatic extracranial vertebral artery stenosis management

A

Intensive medical therapy (antiplatelet therapy, lipid lowering, BP control) is recommended to reduce stroke risk

** the usefulness of stenting is not well established

32
Q

Patients with a stroke or TIA and evidence of an aortic arch atheroma management

A
  1. Intensive lipid management to an LDL cholesterol target
    <70 mg/dL is recommended to prevent recurrent stroke
  2. Antiplatelet therapy is recommended to prevent recurrent stroke
33
Q

Patients with ischemic neurologic symptoms caused by cervical artery dissection evaluation

A

AHA 2024

34
Q

Patients with ischemic neurologic symptoms caused by cervical artery dissection management

A

AHA 2024

35
Q

What are carotid webs and which is the best imaging modality

A

Carotid webs are rare vascular pathologies of the internal carotid artery.
They are nonatherosclerotic fibrous bands that arise along the posterior margin of the carotid bulb.
Histopathologically, they are characterized by fibroelastic thickening of the arterial intima (variant of fibromuscular dysplasia).

They are regarded as a high-risk factor for ischemic stroke of undetermined etiology!
it is detected in up to 9.5% of patients <65 years of age with anterior circulation stroke of unknown cause

CT/MR angiography

36
Q

Patients with carotid web in the distribution of ischemic stroke and TIA, without other attributable causes of stroke management

A

Antiplatelet therapy is recommended to prevent recurrent ischemic stroke or TIA

37
Q

Patients with fibromuscular dysplasia and a history of ischemic stroke or TIA without other attributable causes management

A

FMD is a nonatherosclerotic segmental disease of small or medium-sized arteries that can result in arterial stenosis, occlusion, intraluminal thrombus, aneurysm, or dissection.
It can involve the extracranial carotid, vertebral and renal arteries.
Appearance of a “string of beads” on angiography

Antiplatelet therapy, BP control, and lifestyle modification are recommended for the prevention of future ischemic events.

38
Q

Patients with vertebrobasilar dolichoectasia and a history of ischemic stroke or TIA without other attributable causes management

A

Vertebrobasilar dolichoectasia is characterized by the fusiform dilatation and elongation and tortuosity of the vertebral and basilar arteries. Vertebrobasilar dolichoectasia is associated with traditional ischemic stroke risk factors such as increasing age, hypertension, and male sex.

The use of antiplatelet or anticoagulant therapy is reasonable for the prevention of recurrent ischemic events