What is Cerebral Infarction?
Cerebral infarction, commonly known as a
stroke, occurs when there is a disruption of blood supply to a part of the brain, leading to tissue death. This can result from either a blockage (ischemic stroke) or a bleed (hemorrhagic stroke). In histological terms, this manifests as a series of cellular and structural changes in the affected brain tissue.
Histological Features of Cerebral Infarction
The histological features of cerebral infarction vary depending on the time elapsed since the onset of the infarction. Acute Phase (First 24-48 hours)
During the acute phase, affected neurons and glial cells show signs of
necrosis. Neurons become shrunken and eosinophilic, a condition known as "red neurons." There is also an influx of inflammatory cells, primarily neutrophils, into the infarcted area.
Subacute Phase (Days 3-7)
In the subacute phase,
macrophages and microglia begin to phagocytize the necrotic tissue. This phase is characterized by a dense infiltration of these immune cells. Astrocytes also start proliferating around the infarcted area, initiating the process of gliosis.
Chronic Phase (Weeks to Months)
In the chronic phase, the infarcted area undergoes liquefactive necrosis, leaving a cystic cavity surrounded by a dense glial scar composed mainly of astrocytes. Ongoing phagocytosis and tissue remodeling continue, and the cavity may become filled with cerebrospinal fluid.
Hematoxylin and Eosin (H&E) Staining
H&E staining is commonly used to identify red neurons and inflammatory cells in the acute phase. It provides good contrast between cellular and extracellular structures.
Immunohistochemistry
Immunohistochemistry can be employed to identify specific cell types and proteins. For example, staining for
GFAP (Glial Fibrillary Acidic Protein) highlights astrocytes, while Iba1 staining can be used to identify microglia and macrophages.
Special Stains
Luxol Fast Blue can be used to detect myelin loss in the affected area. Periodic Acid-Schiff (PAS) staining can highlight glycogen deposits and necrotic debris.
Pathophysiological Mechanisms
The pathophysiological mechanisms underlying cerebral infarction involve complex interactions between vascular, cellular, and molecular factors. Ischemia leads to a lack of oxygen and glucose, causing
cellular hypoxia and subsequent energy failure. This activates a cascade of events, including the release of excitatory neurotransmitters like glutamate, leading to excitotoxicity and further cellular damage.
Clinical Relevance
Understanding the histological changes in cerebral infarction is crucial for
diagnosis and treatment. Histopathological analysis can help determine the age of the infarction, the extent of tissue damage, and the effectiveness of therapeutic interventions. It also provides insights into potential targets for neuroprotective strategies.
Conclusion
Cerebral infarction is a complex condition with distinct histological features that evolve over time. By employing various staining techniques, histologists can gain valuable insights into the cellular and structural changes that occur during and after an infarction. This knowledge is essential for improving diagnosis and developing more effective treatments for stroke patients.
