CVD and Ischemia Flashcards
IMC 606
Blood vessels involved in
Anterior Circulation
internal carotid, anterior cerebral, middle cerebral, ophthalmic arteries
Blood vessels involved in
Posterior Circulation
vertebral, basilar, posterior cerebral arteries (and their branches)
Define
Focal neurological deficit
A deficit that is associated with a specific area of dysfunction/lesion. Examples include: hemi/quadrant anopia, loss of tactile sensation for part of the body, UMN deficits for part of the body, Broca or Wernicke aphasia.
Pathological stages of plaque formation in atherosclerosis
Deposition of fat in the intima of vessels – macrophages migrate into area and secrete cytokines to initiate an inflammatory reaction – smooth muscle cells proliferate and connective tissue is deposited – plaque continues to grow in size
What are the pathophysiologic stages of occlusion in small vessels?
Lipohyalinosis involves endothelial damage followed by thickening of the vessel wall. This can cause vessel occlusion or formation of microaneurysms.
What are risk factors for lipohyalinosis?
Hypertension, diabetes, aging are major risk factors.
What vessels are involved in lipohyalinosis
Long, narrow vessels such as lenticulostriates, thalamic perforators, and basilar branches
What is a lacunar stroke?
Lacunar strokes are infarcts of small, penetrating blood vessels that result in small lesions deep in the brain.
Where do lacunar strokes occur?
They occur along long, narrow penetrating vessels that supply regions such as basal ganglia, internal capsule, diencephalon.
What process contributes to lacunar strokes?
Lipohyalinosis contributes to infarcts of these vessels affected by hypertension, diabetes, and age.
What is a TIA?
A temporary decrease in blood flow to part of the brain lasting typically about 5 minutes. It may be caused by an embolism that eventually dissolves or a thrombosis.
How can SAH be distinguished from meningitis?
SAH does not involve fever and would show RBCs in an LP. CT/MRI may also be helpful to show blood in sulcal spaces vs meningeal inflammation.
Pathological process in
Thombosis
Atherosclerosis – fat deposition, fibrosis, occlusion
Pathologic Process in
Small Vessel Occlusion/ Lacunar Infarct
Lipohyalinosis – endothelial damage, vessel thickening, occlusion
Pathologic process in
Embolism
Dislodged objects circulating in bloodstream
Pathologic Process in
Arterial Dissection
Separation of intima and media layers with expanding hematoma
Risk factors in
Thrombosis
Hypertension, diabetes, hyperlipidemia, smoking, inflammation
Risk factors in
Small Vessel Occlusion/ Lacunar Infarct
Hypertension, diabetes, aging
Risk factors in
Embolism
Common sources: Heart and internal carotid artery
Risk factors in
Arterial Dissection
Hypertension, trauma, atherosclerosis
Treatment for
Thrombosis
tPA, thrombectomy
Treatment for
Small Vessel Occlusion/ Lacunar Infarct
Control hypertension
Treatment for
Embolism
Anticoagulants, AF control
Treatment for
Arterial Dissection
thrombectomy
3 criteria for brain death
lack of brain function, lack of cranial nerve function, and loss of all brainstem reflexes
What is the caloric test?
involves infusion of cold/warm water into the external ear canal that stimulates movement of endolymph and thereby elicits the vestibulo-ocular reflex
Why is the caloric test used to test brain death?
assesses function of a large portion of the brainstem from medulla to midbrain that contains the pathway for this response
What reflexes do we test to assess brainstem function?
Pupillary light reflex
Corneal reflex
Oculo-cephalic
What does the pupillary light reflex test?
Midbrain function
What does the corneal reflex test?
Pons function
What does the oculo-cephalic reflex or caloric test assess?
Medulla function
Location of
Intracerebral Hemorrhage (aneurysm, AVM)
Subcortical – basal ganglia, thalamus, brainstem, cerebellum
Location of
Subarachnoid Hemorrhage
Subarachnoid space
Location of
Berry or fusiform aneurysm
Circle of Willis, vessel branch locations
Any location
Location of
AVM
Subcortical or subarachnoid
Risk factors for
Intracerebral hemorrhage
Hypertension causing microaneurysms, AVM, trauma, tumor
Risk factors for
Subarachnoid hemorrhage
Trauma
Aneurysm
Treatments for
Aneurysms
Clipping/ Coiling
Treatments for
AVM
BP control
Treatment of
Intracerebral Hemorrhage
BP control
Treatment for
Subarachnoid hemorrhage
BP control
Symptoms of
Intracerebral Hemorrhage
Focal signs, headache, nausea, confusion
Symptoms of
Subarachnoid hemorrhage
Worst headache ever, stiff neck
What is the first step in evaluating a patient with symptoms of stroke and what methods can be used to assess it?
The first step is to determine whether the stroke resulted from hemorrhage or infarct. Methods to assess this involve non-contrast CT (first choice), LP, CT/MRI angiography.
How are hemorrhagic strokes treated?
Hemorrhagic strokes are treated by controlling blood pressure. Aneurysms can be clipped or coiled.
What are some complications of these strokes?
Hemorrhage can result in hydrocephalus if ventricular blockage occurs and cerebral vasospasm due to irritability of blood, which can be treated with nimodipine.
How does cerebral blood flow respond to changes in systemic arterial pressure?
CBF remains constant from 50 – 150 mmHg of systemic arterial pressure.
This ensures that the brain, which utilizes 20% of the energy output of the body, has adequate supply of O2 and glucose to function normally
Explain
Excitotoxicity
Excitotoxicity occurs from exposure to low O2 levels/ischemia
Explain
How ischemia causes excitotoxicity
Excitotoxicity occurs from exposure to low O2 levels/ischemia. Under this condition, oxidative metabolism is reduced and glycolysis is insufficient to produce enough ATP to maintain the Na/K pump. As a result, intracellular Na levels rise, cytotoxic edema occurs, electrical activity eventually ceases, the neurons depolarize, and glutamate is released from terminals. Glutamate binds to AMPA and NMDA postsynaptic receptors allowing prolonged Ca++ entry into neurons. The wave of intracellular Ca++ activates degradative proteins and free radicals.
In which CNS locations are neurons most sensitive to ischemia ?
Hippocampus, cerebellum, cortex
