CNS Pathology 1.ppt

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CNS Pathology 1.ppt

  1. 1. <ul><li>CENTRAL NERVOUS SYSTEM </li></ul><ul><li>neurocytology </li></ul><ul><li>a) cells include neurons, glia, meninges and cells composing vasculature </li></ul><ul><li>NEURONS : </li></ul><ul><li>a) composed as either i) aggregates </li></ul><ul><li>- such as nuclei or ganglia </li></ul><ul><li>ii) elongated columns </li></ul><ul><li>- such as in spinal column or iii) layers </li></ul><ul><li>- of cerebral cortex </li></ul>
  2. 2. b) vary in structure, size and cytoplasmic composition c) features consistent to neurons are: i) microtubules ii) neurofilaments iii) Golgi apparatus and iv) rER d) Mature neurons do not divide i) loss of neurons with age ii) neurons of CNS do not regenerate over long distances iii) infarcts that transect internal capsule  permanent motor deficits
  3. 3. <ul><li>e) CNS neurons do not remyelinate </li></ul><ul><li>i) MS causes permanent deficits </li></ul><ul><li>Anatomy </li></ul><ul><li>a) centrally, round nucleus contains prominent nucleolus </li></ul><ul><li>b) cytoplasm is abundant </li></ul><ul><li>i) ribosome-studded ER forms prominent basophilic granules known as Nissl bodies </li></ul><ul><li>ii) some neurons, of the substantia nigra and locus ceruleus contain pigment termed neuromelanin </li></ul>
  4. 4. Normal Neuron
  5. 5. Pigmented Neuron neuromelanin 
  6. 6. <ul><li>Neurons react to injury in several ways: </li></ul><ul><li>a) chromatolysis </li></ul><ul><li>i) injured neurons swell, cytoplasm expands and Nissl substances disperse near the plasma membrane </li></ul><ul><li>ii) nucleus becomes eccentric </li></ul><ul><li>iii) these processed (i and ii) are known as chromatolysis and is common response to injury </li></ul><ul><li>- may be reversible or progress to irreversible damage </li></ul>
  7. 7. <ul><li>Chromatolysis </li></ul><ul><li>Swollen </li></ul><ul><li>Nissl margination </li></ul><ul><li>Pale cytoplasm </li></ul><ul><li>Eccentric nucleus </li></ul>
  8. 8. b) atrophy i) loss of neurons in brain – aging process ii) may be global or regional iii) single neurons may shrivel and become hyperchromatic (e.g., “Creutzfelt-Jacob disease”) c) neuronophagia (phagocytic response) i) injuries that kill neurons create debris and elicit phagocytosis by brain macrophages or microglial cells
  9. 9. <ul><li>Atrophy (Creutzfeld-Jacob disease) </li></ul><ul><li>Injured neurons shrivel and </li></ul><ul><li>Are hyperchromatic </li></ul>Spongiform changes 
  10. 10. d) intraneuronal inclusions i) diverse neuronal and cytoplasmic inclusions affect neurons (e.g., viral encephalitides and degenerative diseases) - cytomegalovirus induces inclusions (both nucleus and cytoplasm) (intranuclear) with prominent clear “halos” - rabies encephalitis induce cytoplasmic “Negri body”, which resemble RBC
  11. 11. cytomegalovirus
  12. 12. Negri Body
  13. 13. <ul><li>- Lewy bodies of Parkinsons disease </li></ul><ul><li>- Cowdry bodies as seen in herpetic infections </li></ul><ul><li>- Neurofibrillary tangles (intracytoplasmic) </li></ul><ul><li>Astrocytes </li></ul><ul><li>Support neurons and promote repair </li></ul><ul><li>a) star shaped glial cells </li></ul><ul><li>i) outnumber neurons throughout CNS </li></ul>
  14. 14. b) 2 prominent types: i) fibrillary astrocytes (white matter) ii) protoplasmic astrocytes (grey matter) iii) Glial Fibrillary Acidic Protein (GFAP) or silver impregnation stain demonstrate processes extending in all directions from cell body, some terminating as foot process on blood vessels
  15. 15. iv) proliferate locally in response to injury (trauma, abscess, tumors, infarcts and hemorrhages). This process is referred to as “astrocytosis” or “gliosis” - most important histopathologic indicator of CNS injury, regardless of etiology - evolves over hours to days and presence commensurate with severity of injury. - result in “glial scar”
  16. 16. - Astrocytes undergo hypertrophy (e.g., cell swelling – edema) and hyperplasia - cytoplasm expands to bright pink (gemistocytic Astrocytes) - long standing gliosis associated with Rosenthal fibers (bright, thick, elongated eosinophilic structures). Also associated with cerebellar pilocytic astrocytoma and reactive brain structures adjacent to craniopharyngioma
  17. 17. Astrocyte proliferation GFAP Silver carbonate
  18. 18. v) astrocytes may undergo neoplastic transformation resulting in most common primary brain tumor named “glioma” or “astrocytoma” c) corpora amylacea i) 5-50  m basophils and amorphous structures which accumulate with normal aging in the subpial and subependymal regions - extracellular that evolve within processes of Astrocytes ii) represent degenerative change in astrocyte iii) composed of polyglucosan
  19. 19. Corpora amylacia 
  20. 20. d) Alzheimer type II Astrocytes i) unrelated to Alzheimer disease ii) occurs most often in patients with long standing: - hyperammonia (due to liver disease) - Wilsons disease - hereditary metabolic diseases of urea cycle
  21. 22. ii) Glia - Astrocytes : found throughout CNS (grey and white matter). - act as BBB - metabolic buffers - repair and scar formation iii) Oligodendrocytes - myelination ( on multiple axons) - damage mediated via acquired demyelination diseases (e.g., MS) - may harbor viral inclusions iv) Ependymal cells - line ventricular system
  22. 23. <ul><li>Regulate fluid transport (CSF) </li></ul><ul><li>a) single layer of cells line the four ventricular chambers, aquaduct of Sylvius, central canal of spinal cord and filum termianle. </li></ul><ul><li>b) during gestation, some viral infectious target ependymal cells which may result in congenital hydrocephalus </li></ul><ul><li>c) ependymomas </li></ul><ul><li>i) usually arise within ventricles but may also appear in spinal cord and filum terminale </li></ul>
  23. 24. Ependyma 
  24. 25. <ul><li>v) Microglia </li></ul><ul><li>- primary function to serve as fixed macrophages </li></ul><ul><li>- proliferate with injury </li></ul><ul><li> and develop elongated nuclei (“rod cells”) </li></ul><ul><li>Reactions of neurons to injury </li></ul><ul><li>a) several forms: degeneration and cell death (necrosis and apoptosis) </li></ul><ul><li>i) acute neuronal injury ( red neuron) </li></ul><ul><li>- result from acute CNS hypoxia/ischemia (12-24 hrs) </li></ul><ul><li>- or any insult which results in cellular death </li></ul>
  25. 26. Microglia
  26. 27. - cell body atrophy - pyknosis of nucleus - loss of Nissl substance - intense eosinophilia of cytoplasm ii) Subacute and Chronic neuronal injury (degeneration) - result of a progressive disease - seen early as reactive gliosis (i.e., best early indicator) (early cell loss often difficult to determine!!)
  27. 28. iii) Axonal reaction - refers to axonal regeneration - associated with  protein synthesis - extensively studied in motor neurons of experimental animals

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