patoloji-ders-notlari

Title

Serdar Balcı

Injury in central nervous system

Serdar BALCI, MD

CNS

• Anatomy is important
  • Signs, symptoms and clinical features depend on anatomy
• Histology and reaction patterns are different
• Have unique tumors and diseases

PATTERNS OF INJURY IN THE NERVOUS SYSTEM

Features of Neuronal Injury

• Within 12 hours of an irreversible hypoxic-ischemic insult
  • acute neuronal injury
    • Changes in cell body
    • Changes in axons
    • Changes in body seconder to axonal injury
  • breakdown of the blood-brain barrier
    • cerebral edema

Shrinkage of the cell body, pyknosis of the nucleus, disappearance of the nucleolus, and loss of Nissl substance, with intense eosinophilia of the cytoplasm (“red neurons”)

**Nucleus assumes the angulated shape of the shrunken cell body **

Acute hypoxic-ischemic injury in cerebral cortex, where the individual cell bodies are shrunken, along with the nuclei. They also are prominently stained by eosin (“red neurons”).

Robbins Basic Pathology

Injured axons undergo swelling and show disruption of axonal transport

Swellings (spheroids) can be recognized on H&E stains and can be highlighted by silver staining or immunohistochemistry.

Axonal spheroids are visible as bulbous swellings at points of disruption, or altered axonal transport.

Robbins Basic Pathology

Axonal injury

-leads to cell body enlargement and rounding

-peripheral displacement of the nucleus

-enlargement of the nucleolus

-peripheral dispersion of Nissl substance (central chromatolysis)

C: With axonal injury there can be swelling of the cell body and peripheral dispersal of the Nissl substance, termed chromatolysis.

Robbins Basic Pathology

Other diseases also cause changes in neurons

• Specific intracellular inclusions
  • Neurodegenerative diseases
    • Lewy bodies in Parkinson disease
    • Tangles in Alzheimer disease
  • Pathogenic viruses
• Neuronal processes
  • thickened and tortuous In some neurodegenerative diseases
  • dystrophic neurites
• Age
  • cytoplasm and lysosomes
  • accumulate complex lipids (lipofuscin)

Astrocytes in Injury and Repair

• Principal cells responsible for repair and scar formation in the brain
• Gliosis
• Astrocytes undergo both hypertrophy and hyperplasia
• Nucleus enlarges and becomes vesicular
• Nucleolus becomes prominent
• Gemistocytic astrocyte
  • Previously scant cytoplasm expands and takes on a bright pink hue, and the cell extends multiple stout, ramifying processes

Robbins and Cotran Pathologic Basis of Disease

Fibroblasts

Participate in healing after brain injury to a limited extent

Except in penetrating brain trauma or around abscesses

Fibrillary astrocytes

Long-standing gliosis

Cytoplasm of reactive astrocytes shrinks in size

Cellular processes become more tightly interwoven

Rosenthal fibers

Thick, elongated, brightly eosinophilic protein aggregates found in astrocytic processes in chronic gliosis and in some low-grade gliomas

Oligodendrocytes

• Produce myelin
• Limited spectrum of specific morphologic changes in response to various injuries
• Progressive multifocal leukoencephalopathy
  • viral inclusions
  • smudgy, homogeneous-appearing enlarged nucleus

Microglial cells

Bone-marrow–derived cells

Function as the resident phagocytes of the CNS

Activated by tissue injury, infection, or trauma

Proliferate and become more prominent histologically

• Take on the appearance of activated macrophages
  • In areas of demyelination, organizing infarct, or hemorrhage
• Rod cells
  • Neurosyphilis or other infections, they develop elongated nuclei
• Microglial nodules
  • Aggregates of elongated microglial cells at sites of tissue injury
• Neuronophagia
  • Collections congregating around and phagocytosing injured neurons

Ependymal cells

• Cytomegalovirus
  • can produce extensive ependymal injury
  • typical viral inclusions