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.

This quiz covers the effects of cerebral infarct on brain areas and function, including acute neuronal injury, gliosis, and axonal injury. It explores the consequences of brain injury on the central nervous system.