An ischemic lesion refers to an area of damaged tissue resulting from insufficient blood supply, typically due to reduced or blocked blood flow to a specific region. Ischemia occurs when there is an inadequate supply of oxygen and nutrients to tissues, leading to cell injury or death. The lack of blood flow can be caused by various factors, including blood vessel blockages, blood clots, or other conditions that compromise normal blood circulation.
Ischemic lesions can occur in different organs and tissues throughout the body, and they are often associated with conditions such as:
Ischemic Stroke: A blockage or clot in the blood vessels supplying the brain can lead to an ischemic stroke, causing damage to brain tissue.
Peripheral Artery Disease (PAD): Narrowing or blockage of arteries in the limbs can cause ischemia in the muscles, leading to pain, cramping, and tissue damage.
Medical imaging techniques, such as magnetic resonance imaging (MRI) or computed tomography (CT) scans, can be used to visualize ischemic lesions in various organs. Treatment often involves addressing the underlying cause of the reduced blood flow, such as removing blood clots, opening narrowed arteries, or managing conditions that contribute to ischemia.
Ischemic lesions on diffusion-weighted imaging (DWI) are common after acute spontaneous intracerebral hemorrhage (ICH) but are poorly understood for large ICH volumes (> 30 mL). Rivera-Lara et al. hypothesized that large blood pressure drops and effect modification by cerebral small vessel disease markers on magnetic resonance imaging (MRI) are associated with DWI lesions.
This was an exploratory analysis of participants in the Minimally Invasive Surgery Plus Alteplase for Intracerebral Hemorrhage Evacuation phase 3 trial with protocolized brain MRI scans within 7 days from ICH. Multivariable logistic regression analysis was performed to assess biologically relevant factors associated with DWI lesions, and relationships between DWI lesions and favorable ICH outcomes (modified Rankin Scale 0-3).
Of 499 enrolled patients, 300 had MRI at a median of 7.5 days (interquartile range 7-8), and 178 (59%) had DWI lesions. The incidence of DWI lesions was higher in patients with systolic blood pressure (SBP) reduction ≥ 80 mm Hg in the first 24 h (76%). In adjusted models, factors associated with DWI lesions were as follows: admission intraventricular hematoma volume (p = 0.03), decrease in SBP ≥ 80 mm Hg from admission to day 1 (p = 0.03), and moderate-to-severe white matter disease (p = 0.01). Patients with DWI lesions had higher odds of severe disability at 1 month (p = 0.04), 6 months (p = 0.036), and 12 months (p < 0.01). No evidence of effect modification by cerebral small vessel disease on blood pressure was found.
In patients with large hypertensive intracerebral Hemorrhage, white matter disease, intraventricular hemorrhage volume and large reductions in SBP over the first 24 h were independently associated with DWI lesions. Further investigation of potential hemodynamic mechanisms of ischemic injury after large intracerebral Hemorrhage is warranted 1)
Ischemic lesion classification is generally based on the etiology, timing, vascular territory, and imaging characteristics of the lesion. Below are common ways to classify ischemic lesions:
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### 1. By Etiology (TOAST Classification) The TOAST classification is widely used in stroke studies and clinical practice. It divides ischemic lesions into five subtypes:
1. Large-artery atherosclerosis (LAA): Caused by stenosis or occlusion of a large extracranial or intracranial artery due to atherosclerosis.
2. Cardioembolism (CE): Arising from emboli originating in the heart (e.g., atrial fibrillation, valvular disease).
3. Small vessel occlusion (SVO): Also known as lacunar infarction, caused by occlusion of small penetrating arteries.
4. Stroke of other determined etiology: Rare causes such as arterial dissection, vasculitis, or hypercoagulable states.
5. Stroke of undetermined etiology (cryptogenic): Includes cases where no clear cause is identified or multiple causes are present.
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### 2. By Timing - Hyperacute (0–6 hours): Characterized by restricted diffusion on MRI but minimal changes on CT. - Acute (6–24 hours): Edema and hypoattenuation may appear on CT, with DWI changes persisting on MRI. - Subacute (1–7 days): Edema peaks, and mass effect is visible on imaging. - Chronic (>1 week): Gliosis and volume loss may develop; infarcted area may appear hypointense on T1-weighted MRI and hyperintense on T2.
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### 3. By Vascular Territory - Anterior Circulation: Includes the middle cerebral artery (MCA), anterior cerebral artery (ACA), and their branches. - Posterior Circulation: Involves the vertebrobasilar system, including the posterior cerebral artery (PCA), brainstem, and cerebellum. - Borderzone/Watershed Areas: Occurs in regions between major vascular territories, often due to hypoperfusion.
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### 4. By Imaging Characteristics - Diffusion Restriction: Seen on diffusion-weighted imaging (DWI), indicating cytotoxic edema. - Hypoattenuation: Seen on non-contrast CT, representing tissue infarction. - Perfusion Abnormalities: On CT or MRI perfusion imaging, showing mismatch areas suggestive of salvageable tissue.
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### 5. By Size - Lacunar Infarcts: Small (<15 mm), involving deep structures (e.g., thalamus, internal capsule). - Non-Lacunar Infarcts: Larger, involving cortical and/or subcortical areas.
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### 6. By Pathophysiological Mechanism - Embolic: Sudden occlusion by emboli (cardiac or arterial origin). - Thrombotic: Gradual occlusion due to local thrombus formation. - Hypoperfusion: Resulting from systemic hypotension or arterial stenosis. - Watershed Infarction: Located in borderzones between vascular territories.
Acute ischemic lesions seen on brain magnetic resonance imaging (MRI) are associated with poor spontaneous intracerebral hemorrhage prognosis, but drivers for these lesions are unknown. Rapid hemoglobin decrements occur in the initial days after ICH and may impair brain oxygen delivery. Poyraz et al. investigated whether acute hemoglobin decrements after ICH are associated with MRI ischemic lesions and poor long-term ICH outcomes.
Consecutive patients with acute spontaneous intracerebral hemorrhage enrolled into a single-center prospective cohort study were assessed. Change in hemoglobin levels from admission to brain MRI was defined as the exposure variable. The presence of MRI ischemic lesions on diffusion-weighted imaging was the primary radiographic outcome. Poor 6-month modified Rankin Scale score (4-6) was assessed as our clinical outcome. Separate regression models assessed relationships between exposure and outcomes adjusting for relevant confounders. These relationships were also assessed in a separate prospective single-center cohort of patients with ICH receiving minimally invasive hematoma evacuation.
Of 190 patients analyzed in our primary cohort, the mean age was 66.7 years, the baseline hemoglobin level was 13.4 g/dL, and 32% had MRI ischemic lesions. Greater hemoglobin decrements were associated with MRI ischemic lesions (adjusted odds ratio [OR] 0.77 for every 1 g/dL change, 95% confidence interval [CI] 0.60-0.99) and with poor 6-month outcomes (adjusted OR 0.73, 95% CI 0.55-0.98) after adjusting for demographics, ICH and medical disease severity, and antithrombotic use. In our separate cohort of 172 surgical patients with ICH, greater hemoglobin concentration decrements similarly associated with MRI ischemic lesions (adjusted OR 0.74, 95% CI 0.56-0.97) and poor 6-month outcomes (adjusted OR 0.69, 95% CI 0.48-0.98).
Greater hemoglobin decrements after acute ICH are associated with ischemic lesions on brain MRI and poor long-term outcomes. Further work is required to clarify drivers for these relationships and whether anemia treatment and prevention can be used to improve ICH outcomes 2).
This study's design enables researchers to establish associations between hemoglobin changes and outcomes in ICH, but it does not determine causality, as it is observational. Further experimental or interventional studies would be required to clarify causal mechanisms or assess the efficacy of anemia treatment in improving outcomes.