Clinical Pathology · MU Sofia

125. Cerebrovascular disease.

Covers the three main pathogenic mechanisms behind cerebrovascular disease: thrombotic occlusion, embolic occlusion and vascular rupture. It then describes global and focal cerebral ischaemia, including the three microscopic phases of neuronal injury and the haemorrhagic versus non-haemorrhagic infarct types. The intracranial haemorrhage section covers hypertensive, amyloid, aneurysmal and malformation-related bleeding, with a clinical case example and a short memory aid on the typical sites of hypertensive bleeds.

Inside: 1 section · 1 labelled picture · 16 flashcards · 4 min

Topic 125 of 138 in the MU Sofia syllabus for Clinical Pathology (Medicine, Year 4). The free AceMed note covers it in 1 section, about 653 words (4 min of reading), with 16 flashcards.

In this note

  1. Cerebrovascular disease

Cerebrovascular disease

Three major pathogenic mechanisms:

  • Thrombotic occlusion
  • Embolic occlusion
  • Vascular rupture

The term stroke is given to all three conditions when symptoms begin acutely.

The brain is highly oxygen dependent, loss of perfusion (as all of the above cause) leads to significant negative consequences. Deprivation of oxygen can be functional (e.g. high altitude, anemia, CO poisoning) or ischemia.

Global cerebral ischemia

  • Can be due to hypotension, possibly due to shock of all kinds
  • If insult is mild, may only be transient confused state
  • Most susceptible neurons are the pyramidal cells of hippocampus and neocortex
  • More severe cases can cause widespread neuron death leading to brain death
  • Morphologically we see brain swelling, widened gyri, decreased sulci, and poor demarcation between gray and white matter
  • Microscopically, there are three types of neuron changes in response to ischemia
  • Early changes - neuronal cell change (red neurons) with microvacuolization, cytoplasmic eosinophilia and nuclear pyknosis and karyorrhexis
  • Sub acute changes - necrosis of tissue, influx of macrophages, vascular proliferation, and reactive gliosis
  • Repair - removal of necrotic tissue, loss of organization and gliosis
  • In global cerebral ischemia we also see border zone infarcts, wedge shaped areas at distal portions of arterial territories that are damaged

Focal cerebral ischemia

  • This is caused by arterial occlusion, it is what we think of when we think stroke
  • Cardiac thrombi most common source of emboli
  • Two categories, hemorrhagic and non hemorrhagic infarcts (red and white necrosis).
  • Hemorrhagic infarcts result from reperfusion of ischemic tissue producing multiple petechial hemorrhages
  • Nonhemorrhagic result from absolute occlusion
  • The morphologic changes for non hemorrhagic infarcts show a pale soft and swollen brain early, before it becomes gelatinous and friable, followed finally by liquefaction, leaving a fluid filled cavity. Microscopically, the pattern is as we described above for global ischemia (early changes, sub acute changes, and repair).
  • Hemorrhagic infarcts have parallel macro and microscopic morphology but with the addition of blood extravasation and resorption.

Acute middle cerebral artery infarct (shaded area): swollen, soft territory with blurred grey-white boundary; the oedema pushes the brain across the midline (arrow).

Image: “MCA-Stroke-Brain-Humn-2A” by Marvin 101, CC BY-SA 3.0, via Wikimedia Commons.

Intracranial hemorrhage

  • Associated with hypertension, structural lesions and tumors, subarachnoid hemorrhages are commonly due to ruptured aneurysms while subdural or epidural hemorrhages due to trauma
  • Primary brain parenchymal hemorrhage
  • Mostly due to small intraparenchymal vessel rupture due to hypertension

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