Ischemic Stroke & Transient Ischemic Attack 2 Flashcards
Bradley's Neurology in clinical practice Current Diagnosis & Treatment Neurology UpToDate
a) Which 3 major cerebrovascular disorders does stroke encompass and b) which is the most common?
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%)
Definition of TIA
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
Definition of stroke
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
Μηχανισμοί δημιουργίας ισχαιμικού εγκεφαλικού επεισοδίου
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)
Σύσταση εμβόλων
Τμήμα αθηρωματικής πλάκας
++
έμβολα αέρος, λίπους, καρκινικά κύτταρα, υλικό από ενδοφλέβια λήψη τοξικών ουσιών, βακτηριακό υλικό
Causes of ischemic stroke
TOAST classification
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)
Algorithm for evaluating patients with a clinical diagnosis of stroke
AHA/ASA 2021
Hematologic testing in stroke evaluation
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
Early CT signs of ischemic stroke in the MCA territory
- 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
Clues from stroke topography in source identification
● 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
In how much time can ischemic changes be found in CT scan
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
ischemic changes found in MRI according to stroke phase
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
Patients with ischemic stroke and DWI-negative-stroke
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
CT perfusion findings in acute stroke
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
CT Perfusion limitations
delayed cerebral tissue iodine saturation could occur in the setting of
* ipsilateral cervical internal carotid artery stenosis
* low cardiac output and
* cardiac arrhythmia