ADD-ONS / SCALES
TOAST classification of stroke
Created 23/03/2021, last revision 30/01/2023
- the exact etiology of ischemic stroke has implications for prognosis and management
- a system for classifying ischemic stroke subtypes mainly based on etiology has been developed for the Trial of Org 10172 in Acute Stroke Treatment (TOAST)
- TOAST classification identifies five subtypes of stroke:
- 1 – large-artery atherosclerosis (LAA)
- 2 – cardioembolic stroke (CE)
- 3 – small-vessel disease (SVD) / penetrating artery disease (PAD)
- 4 – a stroke of other determined cause
- 5 – a stroke of undetermined cause (cryptogenic stroke)
- 1 – large-artery atherosclerosis (LAA)
- diagnosis is based on clinical features and data obtained from brain imaging (CT/MRI), vessel imaging (CTA/MRA, neurosonology, DSA), cardiac imaging, and laboratory tests
- representation of each group depends on the mean age of the patients’ sample
- cryptogenic stroke and TOAST 4 predominate at a younger age
- arteriolopathy and cardioembolic strokes predominate at an older age (increased occurrence of AFib and cardiac diseases)
- other improved classification systems have been introduced:
- SSS-TOAST (2005)
- CISS (2011)
- CCS (2007)
- ASCO (2009)
- ASCOD (2013)
→ ischemic stroke diagnosis and classification
TOAST 1 – Large Artery Atherosclerosis (macroangiopathy)
- medium-sized and large arteries are affected
- stroke is caused by atherothrombosis or thromboembolism
- significant stenosis (> 50%) or occlusion of relevant extra- or intracranial artery due to atherosclerosis
- cortical lesion on brain CT/MRI
- subcortical lesion > 1.5 cm on brain CT/MRI (originally published)
- it is known that even smaller lesions can be caused by branch arteries atherosclerosis (see CISS classification)
- it is known that even smaller lesions can be caused by branch arteries atherosclerosis (see CISS classification)
Issues discussed regarding TOAST 1
- a specific and probably underdiagnosed etiology is thromboembolism from an unstable (complicated) non-stenosing (< 50%) plaques in CCA, ICA, aorta, and intracranial arteries [Harloff, 2010]
- in addition, minor infarcts resulting from atherosclerotic plaques in the ostium of perforating arteries should be included here – branch artery disease (BAD) / branch occlusive disease (BOD)
- BAD can be detected using high-resolution MRI
- this concept is already presented in the CISS and SSS-TOAST classification
- the importance of plaque composition and morphology is increasingly recognized.
- demonstration of intraplaque hemorrhage (IPH), thrombus, thin or ruptured fibrous cap, or a large lipid-rich and/or necrotic core (visible on high-resolution MRI) are associated with an increased risk of cerebrovascular events regardless of the severity of the stenosis [Kopczak, 2020] [Kamel, 2019
- these findings may support an atherothrombotic etiology (TOAST 1)
- no significant atherosclerosis in major brain arteries
- presence of potential cardioembolic source (especially any high-risk factor)
TOAST 2 – Cardioembolic stroke
- at least one potential and significant cardioembolic source must be identified
- cardiac sources are divided into high-risk and medium-risk groups based on their propensities for embolism
- some high-risk sources:
- clinical and brain imaging findings are similar to TOAST 1
- a stroke in a patient with a medium-risk cardiac source of embolism and no other cause of stroke is classified as a possible cardioembolic stroke
- presence of significant stenosis in relevant extra- and/or intracranial arteries
TOAST 3 – Small artery disease (arteriolopathy, microangiopathy)
- lacunar strokes
- leukoaraiosis
- clinical presentation: lacunar stroke / subcortical ischemic encephalopathy
- + traditional vascular risk factors (hypertension, dyslipidemia, diabetes, etc.)
- brainstem or subcortical lesion on CT/MRI (diameter < 1.5 cm)
- leukoencephalopathy on CT/MRI
(→ FAZEKAS scale, ARWMC scale)
- distinguish non-arteriolopathic occlusion of perforating arteries
- atherosclerosis of the parent artery near perforator origin – Branch Artery Disease (BAD) / Branch Occlusive Disease (BOD)
- infarcts tend to be larger than in classic arteriolopathy
- high resolution MRI can be used for diagnosis
- embolization (from proximal arterial segments or from the heart)
- atherosclerosis of the parent artery near perforator origin – Branch Artery Disease (BAD) / Branch Occlusive Disease (BOD)
- presence of significant stenosis in relevant extra- and/or intracranial arteries
- presence of a significant cardioembolic source
- hemisferal infarction on CT/MRI
TOAST 4 – Stroke of other determined etiology
- dissection
- vasospasm
- primary (idiopathic)
- secondary (a consequence of complicated migraine, VSP provoked during angiography or by drugs, etc.)
- reversible vasoconstriction syndrome (RCVS)
- moya-moya angiopathy
- multiple etiologies (e.g., Grange syndrome, ACTA2 mutations, vasculitis, etc.)
- metabolic diseases
- Fabry disease
- homocystinuria
- migraine (probably due to vasospasm)
-
genetically linked diseases of the connective tissue
-
Marfan syndrome
-
Ehlers-Danlos syndrome
-
- Sneddon syndrome
- non-inflammatory thrombotic angiopathy affecting small to medium-sized arteries, clinically stroke + livedo racemosa
- carotid artery web
- Grange syndrome
- dolichoectasia (usually in the basilar artery)
- more often in older patients
- CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy)
- CARASIL
- CARASAL
- Fabry
- MELAS
- HANAC (Hereditary angiopathy with nephropathy, aneurysms, and muscle cramps)
- HERNS (Hereditary endotheliopathy with retinopathy, nephropathy, and stroke) → more here
- Susac syndrome (retino-cochleo-cerebral vasculopathy)
- COVID-19
- often in younger patients, in up to 1/3 of cases asymptomatic) [Shahjouei, 2021] [Fridman, 2020]
- 36% in age <55 yrs, 46% < 65 y [Shahjouei, 2021]
- predominantly embolic mechanism with large artery occlusion (LVO) due to a hypercoagulable state [Shahjouei, 2021] [Yaghi, 2020]
- more severe course
- ↑ D-dimers
- often in younger patients, in up to 1/3 of cases asymptomatic) [Shahjouei, 2021] [Fridman, 2020]
- hypercoagulable states
- primary – most often antiphospholipid syndrome and APC resistance
- secondary
- oncohematological diseases (e.g., leukemia, polycythemia vera)
- thrombotic thrombocytopenic purpura (TTP)
- non-specific intestinal inflammation
- nephrotic syndrome
- hemoglobinopathies (typically sickle cell disease)
- hematological malignancies
- hyperviscosity syndrome (HVS)
- pulmonary AV malformations (PAVM)
- Patent Ductus Arteriosus (PDA) (Panagopoulos, 2019)
- angiography (including cardiac catheterization) → complications of endovascular procedures
- carotid surgery
- surgery using ECC (Extra Corporeal Circulation)
- air and fat embolism (see below)
- fat embolism
- typically occurs after trauma (long bone fractures) and surgery (including plastic surgery with fat removal)
- air embolism (microscopic x macroscopic)
- a consequence of the incorrect insertion of a venous catheter into an artery [Riebau, 2004]
- improper extraction of the central venous catheter (CVC) [Brockmeyer, 2009]
- repeated IV applications in combination with pulmonary AV shunt or PFO
- during catheterization
- embolization of cholesterol particles from plaques should be assessed as TOAST 1 → Cholesterol Embolization Syndrome (CES)
- spontaneous x iatrogenic
- various mechanisms ( e.g., vasospasm, cardioembolism in endocarditis)
-
oral contraceptives (usually in combination with a hypercoagulable state and/or smoking)
-
cocaine, crack, amphetamines, LSD, and heroin (drugs frequently cause IC hemorrhages)
-
sympathomimetics, ergotamine, sumatriptan
TOAST 5 – Stroke of undetermined etiology
- cause of a stroke could not be determined with sufficient confidence
- ≥2 potential causes of stroke identified (such as AFib in a patient with carotid stenosis > 50%, significant carotid stenosis + microangiopathy, etc.)
- cryptogenic stroke (CS) – no etiology determined despite extensive evaluation
- incomplete diagnostic evaluation