Cerebrovascular Disease Pathology Study Guide

Cerebrovascular Disease
Examples of normal white matter versus severe white matter lesions with and without small vessel disease. Normal white matter and severe white matter lesions of the parietal deep white matter with and without small vessel disease. A-Ai, normal appearing white matter and a normal white matter artery (Aii). B, white matter lesion indicated by widespread pallor of the central white matter with typical sparing of the subcortical U-fibres (arrow); Bi, higher magnification of white matter lesion exhibiting severe rarefaction, i.e., myelin and axonal loss; Bii, white matter arterioles from white matter lesion area exhibting arteriolosclerosis with hyalinisation (arrows) of vessel walls. C, white matter lesion with severe white matter pallor; Ci, magnifies image of severe white matter rarefaction; Cii, white matter arteriole with enlarged perivascular space but no small vessel disease-related fibrosis or hyalinisation. Of note, this case exhibited severe tau pathology in the overlying cortex, suggesting Wallerian-like degeneration to be the cause for white matter damage. Images captured from serial sections. Histological stain Luxol fast blue was used for images A, Ai, B, Bi, C and Ci; H&E stain was used for Aii, Bii and Cii. Scale bars represent 1mm in A, B and C and 20μm in Ai, Aii, Bi, Bii, Ci and Cii. Is the time ripe for new diagnostic criteria of cognitive impairment due to cerebrovascular disease? Consensus report of the International Congress on Vascular Dementia working group BMC Medicine. Not Altered. CC.

Cerebrovascular Disease Pathology Video

Cerebrovascular Disease

Cerebrovascular disease is a significant source of morbidity and mortality due to cerebrovascular impairment and neurologic dysfunction.

Cerebrovascular disease is typically the result of:

  • Ischemia (85% of cases)
  • Hemorrhage (15% of cases)

Since serum glucose serves as their primary energy source, neurons are especially vulnerable to ischemia, and may undergo necrosis within 3-5 minutes.

  • Cerebrovascular Disease
    Cerebrovascular Disease. Brain infarct INFARCT.jpg: Lucien Monfils derivative work: Suraj - Not altered. CC BY-SA 3.0

Global Cerebral Ischemia

Global cerebral ischemia is ischemia that effects the entire cerebral tissue.

Important causes of global cerebral ischemia include:

  • Minimal perfusion (e.g. atherosclerosis)
  • Abrupt reduction in blood flow (e.g. cardiogenic shock)
  • Persistent hypoxia (e.g. anemia)
  • Hypoglycemia episodes (e.g. insulinoma)

Clinical findings of global cerebral ischemia depend on the length and severity of the trauma.

  • Mild global ischemia causes momentary confusion that quickly goes away
  • Severe global ischemia causes diffuse necrosis and may result in a vegetative state condition
  • Infarcts in watershed regions which may effect memory, sensory, and motor functions
  • Global Cerebral Ischemia
    Global Cerebral Ischemia. CT-scan of the brain with a RIGHT MCA infarct. Lucien Monfils - Not altered. CC BY-SA 3.0

Ischemic Stroke

An ischemic stroke can cause regional ischemia that causes focal neurologic impairments that continue longer than 24 hours.

Transient ischemic attack (TIA) is the name given to an incident if the symptoms last less than 24 hours.

Subtypes of ischemic strokes include:

  • Thrombotic (e.g. atherosclerotic plaque rupture)
  • Embolic (e.g. from thromboemboli from the heart in atrial fibrillation)
  • Lacunar (e.g. from hyaline arteriolosclerosis, an adverse effect of hypertension)

Symptoms of ischemic stroke depend on the region of brain involvement.

  • A pure motor stroke results from the interior capsule being involved
  • Thalamus causes a pure sensory stroke

Histologic findings (if obtained) for strokes show:

  • An early microscopic observation is an eosinophilic alteration in the cytoplasm of neurons (red neurons) (12 hours after infarction)
  • Coagulative necrosis (24 hours)
  • Neutrophil infiltration (days 1-3)
  • Microglial cell infiltration (days 4-7)
  • Granulation tissue (weeks 2-3)

Liquefactive necrosis is the outcome of ischemic stroke.

Liquefactive necrosis results in the development of a cystic area filled with fluid that is encircled by gliosis.

  • Ischemic Stroke
    Ischemic Stroke. Dense artery sign in a patient with middle cerebral artery infarction shown on the left. Right image after 7 hours. Hellerhoff - Not altered. CC BY-SA 3.0.

Intracerebral Hemorrhage

An intracerebral hemorrhage is due to brain parenchyma bleeding.

Symptoms of intracerebral hemorrhage include:

  • Headache
  • Nausea
  • Vomiting
  • Altered mental status (AMS)
  • Coma

Intracerebral hemorrhage may result from:

  • Lenticulostriate vessel rupture
  • Aneurysm rupture

The most typical location of the brain involved by intracerebral hemorrhage is the basal ganglia.

Intracerebral hemorrhage hemorrhages may be caused by hypertension.

Hypertension treatment decreases the risk of intracerebral hemorrhage by half.

  • Intracerebral Hemorrhage
    Intracerebral Hemorrhage. Spontaneous ICH with hydrocephalus on CT scan[8] Yadav YR, Mukerji G, Shenoy R, Basoor A, Jain G, Nelson A - Yadav YR, Mukerji G, Shenoy R, Basoor A, Jain G, Nelson A . Not altered. CC BY 2.0

Subarachnoid Hemorrhage

Subarachnoid hemorrhage is hemorrhage that involves the subarachnoid area of the brain.

Subarachnoid hemorrhage symptoms include:

  • Sudden “thunder clap” headache
  • Worst headache of life
  • Suddenly neck stiffness

A spinal tap in a patient with subarachnoid hemorrhage reveals xanthochromia (yellow hue due to bilirubin breakdown).

In subarachnoid hemorrhage, a spinal tap reveals xanthochromia (yellow hue due to bilirubin breakdown).

Causes of subarachnoid hemorrhage include:

  • Berry aneurysm rupture (85% of cases)
  • Arteriovenous (AV) abnormalities
  • Anticoagulation complication
  • Subarachnoid Hemorrhage
    Subarachnoid Hemorrhage. Autopsy of a case with subarachnoid hemorrhage. The arachnoid mater is left in place on the exterior surface, containing extensive hemorrhage that also fills the sulci, as detailed in magnified image. Mikael Häggström, M.D. Not altered. CC0