patoloji-ders-notlari

Title

Serdar Balcı

Santral Sinir Sisteminde Hasar

Dr. Serdar BALCI

Santral Sinir Sistemi

• Anatomi önemli
  • Belirti, bulgu ve klinik özellikler
• Histoloji ve reaksiyon paternleri farklı
• Kendine özgü tümör ve hastalıkları var

SANTRAL SINIR SISTEMI HASAR PATERNLERI

Nöron hasarı

• Geri dönüşsüz hipoksik-iskemik atağın ilk 12 saati:
  • Akut sinir hasarı
    • Hücredeki değişiklikler (perikaryon)
    • Aksonlardaki değişiklikler
    • Akson hasarına ikincil perikaryondaki değişiklikler
  • Kan-beyin bariyerinin yıkılması
    • Serebral ödem

Hücrede büzüşme, piknozis, nükleol kaybı, Nissl cisimciği kaybı, sitoplazmada belirgin eozinofili (kırmızı nöron)

Nükleus da büzüşen hücre gibi köşeli şekil alır

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