Brain and Behavior

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Brain and Behavior
2010-04-06 15:44:31
Neuronal Injury

Exam 1 Material
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  1. Label the indicated areas of the healthy cell

  2. What pathology is affecting theses cells. What are the major characteristics?
    This picture shows features of hypoxic/ischemic changes of neurons. The neurons have smudged and pyknotic nuclei, collapsed and flame-shaped eosinophilic cytoplasm with accentuated (artificial) pericellular space. Neurons most susceptible to hypoxia are in the hippocampus (Sommer’s sector) and the cerebellum (Purkinje cells).
  3. Ischemic brain edema is a combination of what two major types of edema? what are the major differences between the two?
    • cytotoxic (cellular) and vasogenic. Cytotoxic edema evolves over minutes to hours and may be reversible, while the vasogenic phase occurs over hours to days, and is considered an irreversibly damaging process.
    • Acute hypoxia initially causes cytotoxic edema, followed within the next hours to days by the development of vasogenic edema as infarction develops. The delayed onset of vasogenic edema suggests that time is needed for the defects in endothelial cell function and permeability to develop.
  4. What is cytotoxic edema?
    Cytotoxic edema is characterized by swelling of all the cellular elements of the brain. In the presence of acute cerebral ischemia, neurons, glia and endothelial cells swell within minutes of hypoxia due to failure of ATP-dependent ion (sodium and calcium) transport.
  5. What mechanism follows cytotoxic edema?
    As the ions are unabled to be pumped out of the cell due to the loss of ATP dependent ions pumps, rapid accumulation of sodium within cells occurs with an increase in water (water follows to maintain osmotic equilibrium.) The acute depletion of ATP leads to neuronal damage from excessive accumulation of glutamate. This process called excitotoxicity, involves activation of glutamate receptors, accumulation of cytosolic calcium, activation of calcium-triggered cascades, generation of oxygen free radicals, and mitochondrial failure.
  6. Cells undergoing necrotic cell death show ??
    mitochondrial swelling, dilation of the endoplasmic reticulum, and extensive vacuolization of the cytoplasm. The chromatin becomes coarse and clumpy, which is followed by loss of nuclear staining. The cells swell and eventually lyse, releasing their contents into the surrounding tissue and triggering an inflammatory response.
  7. Vasogenic Edema is characterized by??
    an increase in extracellular fluid volume due to increased permeability of brain capillary endothelial cells to macromolecular serum proteins (e.g., albumin.) Vasogenic edema can displace the brain hemisphere and, when severe, lead to cerebral herniation.
  8. What is chromatolysis? When would this occur?
    Chomatolysis can occur when there is damage to a neuronal axon. The cell body will swell the nucleus will move to an eccentric postion, the RER dipereses and moves to the periphery of the cell, and all synapses are lost from the cell body. This represents and increase in the RNA and associates enzymes that provide polypeptides and enzymes for the repair of the axon.

  9. What process is occuring in this cell? What are the defining characteristics?
    • Central chromatolysis
    • Cell bodies swollen, nuclear displacement
    • RER at the periphery

  10. What process is occuring in this cell? What are the defining characteristics?
    • neurophagonia
    • Macrophages encircle the dead neuron.
  11. Neurofibrillary tangles are common in Alzheiemers disease or in the cerebral hemispheres of aging patients.
  12. Accumulation of vaculoles in the cytoplasm of neurons. Common in elderly patients and patients with Alzheimers
  13. Lewy bodies
    • Histologically these inclusion bodies have a central rounded, concentrically
    • laminated core of hyaline that is eosinophilic with a peripheral pale halo.
    • They may be single or multiple. They are
    • found in the substantia nigra and the locus
    • ceruleus of patients with idiopathic Parkinson’s
    • disease.
  14. Hirano bodies:

    • Hirano bodies
    • Sections stained with H&E can demonstrate
    • elongated eosinophilic structures [10-30 x 8-15
    • microns]. These inclusion bodies are dense hyaline
    • masses composed primarily of actin. They are
    • seen in the elderly and increased in Alzheimer’s
    • disease.
  15. When the axon is seperated fro the cell body, the distal part of the axon undergoes ??
    Wallerian degeneration
  16. Name the process that occurs when axons become atrophic in the distal end and degenerate towards the cell body.
    "Dying back" occurs in the PNS mostly but also the CNS
  17. Pick bodies These inclusion bodies are large, silver positive cytoplasmic structures consisting of neurofilaments and microtubules. There is a distinct type of change in the neuronal perikarya, which becomes distended (balloon cell neurons, globose cells) and the nucleus is pushed off to the side. Pick bodies are characteristic of Pick’s disease.
  18. A lesion of the axon may lead to_______
    • (1) degeneration occurs at the nerve terminals of the injured neuron
    • (2) Wallerian degeneration occurs at the distal segment of the axon (3) the myelin sheath fragments leaving myelin debris (4) phagocytic cells infiltrate the site of the lesion (5) the neuronal cell body undergoes central chromatolysis (6) in the presynaptic neuron, terminals retract from the dendrites of the injured neuron (7) the cell body of the presynaptic neuron can undergo retrograde transneuronal degeneration (8) in the postsynaptic neuron anterograde transneuronal degeneration can occur
  19. What kind of nerve injury does this describe?

    There is a block in conduction of the impulse down the nerve fiber and recovery
    takes place without Wallerian degeneration.

    What can cause this?
    • Neurapraxia
    • Most likely a biochemical lesion caused by a concussion or shock-like injury to the nerve fiber. Common examples: peroneal paralysis from prolonged cross-legged position; radial or Saturday night paralysis caused by compression of the axilla.
  20. This injury involves loss of the relative continuity of the axon and its
    covering of myelin but preservation of the connective tissue framework of the nerve. Wallerian
    degeneration due to the loss of axonal continuity usually the result of a more severe crush or
    contusion injury. Since there is maintenance of the connective tissue framework, the potential
    for regeneration is excellent.
  21. This results from more severe contusion, stretch, or laceration and not only the
    axons, but the investing connective tissues lose their continuity. Transecting a nerve will
    cause a neurotmetic lesion in which endoneurial and perineurial connective tissue layers as well
    as the axons are disrupted. Regenerating axons may reach the distal stump but often fail to find
    their preinjury pathways and produce a functional regeneration.
  22. Why can't axons regenerate in the CNS?
    • Astrocytes, which are absent in the PNS, proliferate and promote scarring-- a process known as reactive gliosis. The scar is a physical barrier to axon growth.
    • Extracellular matrix proteins (laminin and fibronectin) that promote axon growth are not present in the CNS
    • Growth Associated Proteins (GAPs) are present in developing axons but absent in the adult CNS