patoloji-ders-notlari

Title

Serdar Balcı

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

Robbins and Cotran Pathologic Basis of Disease

Traumatic Diseases of CNS

Serdar BALCI, MD

Central Nervous System Trauma

• Significant cause of death and disability
• Severity and site of injury affect the outcome
  • injury of several cubic centimeters of brain parenchyma
    • frontal lobe → clinically silent
    • spinal cord → severely disabling
    • brain stem → fatal

Penetrating trauma

Blunt trauma

Open injury

Closed injury

• The magnitude and distribution of lesions depend on

  • shape of the object causing the trauma
  • force of impact
  • whether the head is in motion at the time of injury

• External signs may not correlate with severity of brain injury

• Injuries may involve the parenchyma, the vasculature, or both

• Repetitive episodes of trauma can lead to later development of neurodegenerative processes

  • Muhammed Ali

• Association of trauma with the risk of Alzheimer disease

• Trauma-associated degeneration

  • chronic traumatic encephalopathy
  • intraneuronal tau protein inclusions

Traumatic Parenchymal Injuries

• When an object impacts the head
• Coup injury
  • **Injury occur at the site of impact **
• Contrecoup injury
  • opposite the site of impact on the other side of the brain
• Both coup and contrecoup lesions are contusions
  • rapid tissue displacement
  • disruption of vascular channels
  • subsequent hemorrhage
  • tissue injury
  • edema
• Crests of the gyri are the part of the brain that is most susceptible to traumatic injury
• Contusions are common in regions of the brain overlying rough and irregular inner skull surfaces
  • orbitofrontal regions and the temporal lobe tips
• Penetration of the brain
  • bullet
  • skull fragment from a fracture
  • laceration, with tissue tearing, vascular disruption, and hemorrhage

Contusions, wedge-shaped, widest aspect closest to the point of impact

Acute contusions are present in both temporal lobes, with areas of hemorrhage and tissue disruption

Robbins Basic Pathology

In contrast with ischemic lesions, in which the superficial layer of cortex may be preserved, trauma affects the superficial layers most severely

Robbins Basic Pathology

• Few hours of injury
  • blood extravasates throughout the involved tissue
  • across the width of the cerebral cortex
  • into the white matter
  • subarachnoid spaces
• Functional effects are seen earlier
• Morphologic evidence of injury takes about 24 hours to appear
  • nuclear pyknosis, cytoplasmic eosinophilia, cellular disintegration
• Inflammatory response to the injured tissue follows its usual course, with neutrophils preceding the appearance of macrophages

Old traumatic lesions have a characteristic macroscopic appearance

**-depressed, retracted, yellowish brown patches involving the crests of gyri **

Robbins Basic Pathology

Autopsy Pathology: A Manual and Atlas

Remote orbital surface contusions

Diffuse axonal injury

Trauma can also cause more subtle but widespread injury to axons within the brain

Movement of one region of brain relative to another is thought to disrupt axonal integrity and function

Angular acceleration, even in the absence of impact, may cause axonal injury as well as hemorrhage

50% of patients who develop coma shortly after trauma are believed to have white matter damage and diffuse axonal injury

Concussion

reversible altered consciousness from head injury in the absence of contusion

loss of consciousness, temporary respiratory arrest, and loss of reflexes

neurologic recovery is complete, amnesia for the event persists

The pathogenesis of the sudden disruption of nervous activity is unknown

Traumatic Vascular Injury

• CNS trauma directly disrupts vessel walls
  • epidural, subdural, subarachnoid, or intraparenchymal
  • occur alone or in combination
  • Subarachnoid and intraparenchymal hemorrhages most often occur at sites of contusions and lacerations

Robbins Basic Pathology

Epidural Hematoma

• Dural vessels are vulnerable to traumatic injury
  • Middle meningeal artery
• Infants
  • traumatic displacement of the easily deformable skull may tear a vessel, even in the absence of a skull fracture
• children and adults
  • tears almost always stem from skull fractures
• **Blood accumulates under arterial pressure **
• Dissect the tightly applied dura away from the inner skull surface
• Produce a hematoma that compresses the brain surface

Epidural hematoma covering a portion of the dura

Robbins Basic Pathology

Subdural Hematoma

• Rapid movement of the brain during trauma
• Tear the bridging veins that extend from the cerebral hemispheres through the subarachnoid and subdural space to the dural sinuses
• Bleeding into the subdural space
• Elderly
  • Patients with brain atrophy, the bridging veins are stretched out, and the brain has additional space within which to move, accounting for the higher rate of subdural hematomas
• Infants also are susceptible
  • bridging veins are thin-walled

Robbins Basic Pathology

Manifest within the first 48 hours after injury

Most common over the lateral aspects of the cerebral hemispheres and may be bilateral

Acute subdural hematoma

Collection of freshly clotted blood apposed to the contour of the brain surface

Without extension into the depths of sulci

Underlying brain is flattened

Subarachnoid space is often clear

Venous bleeding is self-limited

Breakdown and organization of the hematoma take place over time

**Evolving subdural hematoma. The semiliquid membrane-bound mass of blood in the subdural space **

Autopsy Pathology: A Manual and Atlas

Subdural hematomas organize

1 week → lysis of the clot

2 weeks → growth of granulation tissue from the dural surface into the hematoma

1 to 3 months → fibrosis

Autopsy Pathology: A Manual and Atlas

Large organizing subdural hematoma attached to the dura

Organized hematomas are attached to the dura, but not to the underlying arachnoid

subdural membranes

Fibrosing lesions may retract, leave a thin layer of connective tissue

Subdural hematomas commonly rebleed

chronic subdural hematomas

From the thin-walled vessels of the granulation tissue, leading to microscopic findings consistent with hemorrhages of varying age

Robbins Basic Pathology