Cerebral Vascularization
I. Origins
A. Anterior Circulation
1. Aorta to common carotids, internal carotid to middle and cerebral arteries
B. Posterior Circulation
1. Aorta to vertebral arteries, vertebral to basilar, basilar gives off superior cerebellar and posterior cerebral arteries
II. Circle of Willis
A. Components
1. basilar
2. posterior cerebral
3. posterior communicating
4. middle cerebral
5. anterior cerebral
6. anterior communicating
B. Clinical Significance
1. multiple bifurcations and anastomoses
a. ensure perfusion during changing circumstances (e.g., flexing the neck, occlusion due to embolism or thrombus, etc.)
b. common site of occlusion (thrombus, embolism, or sclerosis) or hemorrhage due to aneurysm
2. “Normal” doesn’t mean that the circle is complete!
III. Territories of ACA, MCA, and PCA and Typical Signs (Syndromes) Associated with Cerebrovascular Accidents (CVAs)
A. Anterior Cerebral Artery, distal to communicating artery
1. contralateral hemiparesis (movement difficulty) and hemisensory loss involving primarily leg and foot
2. inability to identify objects correctly
3. apathy & personality changes—“frontal lobe syndrome”
B. Middle Cerebral Artery
1. contralateral hemiparesis and hemisensory loss involving mainly face and arm
2. aphasia (if left hemisphere is affected)
3. contralateral visual loss due to damage to optic radiation (visual tract)
C. Posterior Cerebral Artery
1. contralateral homonymous hemianopia with some macular sparing (damage to calcarine cortex, macular sparing occurs because occipital pole receives collateral blood supply from middle cerebral artery)
2. visual agnosia (ischemia of left occipital lobe)
3. impairment of memory (possible damage to medial temporal lobe)
D. Internal Carotid Artery
1. may cause no signs or may cause many signs—signs are usually those of middle cerebral artery occlusion, including contralateral hemiparesis and hemianesthesia
2. partial or complete visual field defect on side ipsilateral to lesion because emboli may be dislodged and translocate to retinal vessels
E. Vertebral Artery or Basilar Artery
1. because of the diffuse blood supply provided by the vertebral and basilar arteries, symptoms and signs of occlusion to either of these may be quite varied but may include any and all of the following:
a. ipsilateral pain and temperature sensory loss of face; contralateral pain and temperature sensory loss of body
b. episodes of hemianopia or complete cortical blindness
c. ipsilateral loss of gag reflex, dysphagia, hoarseness (resulting from lesions of nuclei of glossopharyngeal & vagus nerves)
d. vertigo, nystagmus, nausea, vomiting
e. ipsilateral ataxia, other cerebellar signs
f. hemiparesis (unilateral or bilateral)
g. coma
Cerebrovascular Accidents (CVAs)
I. Most Common Types
A. Intracerebral hemorrhage
1. bleeding into cerebral tissue
2. common causes
a. aneurysm
b. traumatic brain injury
B. Cerebral ischemia
1. occlusjion of blood flow leads to infarct
2. 3 primary causes of infarcts
a. thrombosis: blocks flow at site of formation
i. fat, blood clot, air bubble, etc.
b. embolism: plug forms, breaks and travels to anastamosis
c. arteriosclerosis: narrowing of vessels because of plaques (fat deposits)
II. Time course of a CVA
A. “First wave”
1. death of tissue in immediate area (infarct)
2. damage will occur, can’t really protect those cells
B. “Second wave”
1. death in tissue surrounding infarct (penumbra—Latin for “partial shadow”)
2. damage can be halted, minimized
3. sequence of events:
a. ischemia: O2 and glucose severely depleted
hemorrhage: penumbra cells flooded with excess O2, Ca2+, etc.
b. penumbra cells bombarded by waste products from dead or dying cells in area of infarct
c. K+ increase outside penumbra neurons—Na+-K+ pumps can’t keep up
d. blood-brain barrier broken, fluid accumulates in area
e. K+ increase plus edema cause glia to dump their glutamate and other NTs
f. excess glutamate overstimulates penumbra neurons (Na+-K+ pumps pressed even harder, fall farther behind)
g. Na+, Ca2+, and Zinc ions accumulate within neurons, causing swelling, breakdown of function, rupture of cell membranes
h. glia proliferate, remove waste products, phagocytize debris, create scar tissue (walling off damaged area if possible)
C. Important issues:
1. unconsciousness can occur in 5-10 seconds when blood flow is interrupted; after 3-4 minutes of arterial deprivation, neurons begin to die
2. cortical neurons are the most sensitive, brainstem neurons are more protected—if cortical neurons are totaled but brainstem neurons survive, person ends up in a “persistent vegetative state” and this may be demonstrated with an EEG.
III. Treatment Options (Acute)
A. Decrease overstimulation of penumbra neurons with GABAergic drugs or glutamate blockers; Ca2+ channel blockers, block entry of zinc
B. Cool brain from 37° to 29°--but must be done as soon as possible and continued for 24 hrs for maximum benefit.
C. Administer “clot-busting” drugs (e.g.tPA) in case of ischemia but NOT hemorrhage
D. Other considerations
1. diaschisis may occur: when one area depends on another area for input and the area depended upon is damaged, the area that needs the input to function correctly may shut down. In other words, diaschisis has occurred in the healthy tissue as a result of damage to a connected area.
2. To prevent or minimize diaschisis, stimulants should be administered, however stimulants are counterproductive when trying to reduce overactivity of neurons in the penumbra.