Week 16 Pathology

Nervous system

  • Neurons – transmit action potential. Have body, axon and dendrites.
  • Glia – eg astrocytes, oligodendrocytes, ependyma. They have structural and metabolic interactions with neurons.
  • Oligodendrocytes make myelin
  • Ependymal cells line ventricular system and make CSF
  • Microglia – macrophage system in CNS.


Nerve regeneration.

  • Axonal reaction occurs in cell body in anterior horn
  • Increased protein synthesis –> axonal sprouting–> enlargement and rounding up of cell body–> peripheral displacement of nucleus–> enlargement of nucleolus–> dispersion of Nissl substance from centre to periphery.




  • Ischaemic – thrombosis/embolism
    • Atherosclerosis
      • Common sites – carotid bifurcation, MCA origin, basilar artery. Associated with HTN and DM.
    • Global hypoperfusion/hypotension
    • ¬†Appearance
      • 1st 6hrs – little can be observed
      • By 48hrs – pale soft tissue and swollen, corticomedullary junction becomes blurred.
      • Neutrophils migrate. Macrophages and activated microglia come and are predominant for the next 2-3wks. The macrophaged may persist in the lesion for months to years.
      • 2-10d brain is gelatinous and friable, border between normal and abnormal becomes clear.
      • 10d to 3wks the tissue liquifies and then becomes a fluid filled cavity.
      • Several months – astrocytes form a dense feltwork of glial fibres and new cappilaries
  • Haemorrhagic – 60s. And female is common
    • Hypertensive 50% of clinically significant bleeds
      • Putamen 50-60% Thalamus, pons, cerebellar hemispheres
    • Ruptured aneurysm
      • Saccular/berry aneurysm – congenital, 90% occur in anterior circulation, near branch points.
      • ACA and ant communicating – 40%
      • Post communicating artery and MCA – 20%
      • MCA – 34%
      • Few mm to 2-3cm diameter, sac made of thickened hyalinised intima.
      • Any size has 1.3% risk of bleeding per year
      • Aneurysms greater than 10mm diameter have 50% risk of bleeding per year
      • Sometimes associated with strain, orgasm–> severe headache and LOC.
      • 25-50% die at first rupture.
      • Early post SAH period increased risk of further ischaemic injury from vasospasm of other vessels.


Cerebral oedema

  • Vasogenic
    • Due to increased vascular permeabilty and decreased lymphatic drainage
  • Cytotoxic
    • Cell injury to endothelial, neuronal or glial cell.