Cerebral Infarct and Brain Injury

Brain Injury Overview

• Acute neuronal injury can result from hypoxia, ischemia, hypoglycemia, or trauma.
• "Red Dead Neurons" appear within 6-12 hours following acute injury due to necrosis.
• Gliosis is a histopathologic marker indicated by astrocyte hypertrophy and hyperplasia, producing more glial fibrillary acidic protein (GFAP).
• Axonal injuries are prominently observed in anterior horn cells.

Neuronal Staining

• Necrotic neurons display eosinophilic staining due to RNA loss within the cytoplasm.
• This contrasts with normal neurons, leading to a distinct red appearance in necrotic cells.

Ischemia Types

• Global Cerebral Ischemia: Results from widespread decreased oxygen due to reduced blood flow; conditions include cardiac arrest, shock, and severe hypotension.
• Focal Cerebral Ischemia: Occurs in localized brain areas due to vessel disease and arterial occlusions from thrombotic events, often associated with atherosclerosis.

Stroke Statistics

• Ischemic strokes account for approximately 85% of all strokes, significantly more common than hemorrhagic strokes.

Outcomes of Global Ischemia

• Minor ischemia might cause transient confusion without major derangements.
• Severe ischemia can lead to widespread neuronal death and significant neurological deficits if the patient survives.

Severe Global Ischemia Implications

• Patients may experience deep coma or meet brain death criteria, characterized by flat EEG, absent respiratory drive, and reflexes, along with no cerebral perfusion.
• "Respirator brain" indicates necrosis and extensive damage due to cycles of edema and vasocompression, leading to brain autolysis.

Vulnerable Brain Areas

• Areas particularly susceptible to damage during hypotension include the pyramidal cell layer of the hippocampus (CA1 area) and the Purkinje cell layer of the cerebellum.
• "Watershed" or border-zone areas are especially affected by decreased perfusion pressure, often resulting in permanent tissue injury after hypotension.

Reperfusion and Hemorrhagic Changes

• Reperfusion can lead to bleeding into nonviable tissue, especially in embolic CNS infarcts.
• Hemorrhagic manifestations occur due to reestablishment of blood flow to compromised areas, complicating the injury.

Gross Morphology of Ischemia

• Ischemia may present as a swollen brain with widened gyri and narrowed sulci, with potential herniation of brain tissue.

Infarct Progression

• Hyperacute to acute conditions lead to thrombi from atherosclerosis, representing "white strokes" characterized by pallor.
• Common sites for thrombosis include carotid bifurcation and middle cerebral artery.

Embolic Sources

• Cardiac sources, such as myocardial infarction and atrial fibrillation, are major contributors to embolic strokes.
• Middle cerebral artery is the primary site for embolization.

Other Embolic Causes

• Fat emboli can result from large bone fractures, leading to widespread white matter hemorrhages.
• Air emboli may arise from penetrating injuries or intravenous air injection.
• Tumor emboli can originate from various malignant neoplasms.

Lacunar Infarcts

• Small vessel occlusions result in lacunar infarcts, visible as small, healed lesions.
• Most often caused by hypertension-related atherosclerosis, leading to deep infarcts affecting the internal capsule and thalamus.

Risk Factors for Stroke

• Non-modifiable: age, gender (male), race (African American), genetic predisposition.
• Modifiable: hypertension, heart disease, diabetes, smoking, obesity, hypercholesterolemia, and history of transient ischemic attacks (TIA).

Clinical Features of Non-Hemorrhagic Stroke

• Symptoms typically develop rapidly and may evolve over hours, with potential for gradual improvement.
• Immediate thrombolytic treatment can mitigate long-term damage.
• Occlusions in the middle cerebral artery frequently cause contralateral paralysis, motor and sensory defects, along with aphasias.

Hemorrhage and Ischemic Infarcts

• Hemorrhage risks in occlusive ischemic infarcts are influenced by factors such as vascular integrity and ischemia-reperfusion injury.