Mechanisms of Cerebral Injury
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| Hypoxia and Ischemia | Brain accounts for 20% of body oxygen consumption
Depletion of oxygen occurs within 10 sec of cessation of blood flow
Conversion to anaerobic metabolism occurs within 2-4 minutes
ATP supplies exhausted within 4-5 minutes
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| Hypoxia | From reduced atmospheric pressure, anemia, carbon monoxide poisoning, congenital heart defects
Hypoxia in small amounts can be tolerated over long term
Capable of anaerobic metabolism, enough oxygen to prevent large scale acidosis
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| Ischemia | Severe or total loss of blood supply
Can be to the entire brain (cardiac arrest) or to a focal area (stroke)
Small focal areas have advantage of collateral circulation
Global or Focal
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| Collateral Circulation | if 1 vessel is blocked due to a stroke, cells that are further away, but close to another blood vessel can get blood supply from other vessel feeding area nearby. It’s getting a lower pressure of blood, but it’s getting some.
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| Global Ischemia | Blood flow inadequate to meet the metabolic needs of the entire brain
Cardiac arrests, shock, or severe dysrhythmias
Failure of Na/K ATPase pump causes neuronal edema
Calcium influx causes release of intracellular digestive enzymes
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| Global Ischemia (cont) | Anatomy of blood vessels leads to watershed zones
Farthest from large arteries
Profound lowering of blood pressure in these areas
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| Excitotoxicity Amino Acids | Injury to neurons can be caused by overstimulation of receptors for excitatory amino acids (GLUTAMATE, aspartate)
This is overstimulation of receptors– most commonly glutamate
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| Excitotoxicity Cont'd NMDA | NMDA-subtype of glutamate receptors, opens and allows sodium and calcium to enter the cell-results in prolonged action potentials, swelling
iontropic receptor which allows na and ca to passively move into cell– edema & prolonged action potential
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| Excitotoxicity Calcium | Calcium initiates the calcium cascade-series of intracellular signals that leads to release of intracellular enzymes-free radical formation, fragmentation of DNA, nuclear breakdown
sm amts allow neurotransmitters to be released= of intracellular enzymes
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| Excitotoxicity excess Glutamate | Astrocyte dysfunction: normal astrocytes remove extracellular glutamate
Cell damage: intracellular glutamate concentration is 16 times that of the extracellular space. Large amounts released from damaged cells
Microneurons much more affected
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| Excess Glutamate and O2 | Astrocytes suck up glutamate after it’s released, so if they’re damaged, there’s a build up and will continually send the signal to the next neuron which will cause that to continually fire, which will increase ATP need and there’s not enough O2 already
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| Reperfusion Injury | Return of oxygen to ischemic cells can lead to oxygen free fradical formation, and allows inflammatory cells to enter the ischemic area
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| Reperfusion Injury | Leads to lipid peroxidation of the cell membrane, which activates the arachadonic acid cascade, leading to more free radical formation
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| Reperfusion Injury | Increase in inflammatory cells due to alteration in BBB, leads to further edema, neutrophil chemoattraction
Trauma and inflammation promote platelet aggregation, causing further decreases in localized blood flow
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| Nimodipine (Nimotop) Pharm | Calcium channel blocker that is preferential for cerebral blood vessels. Approved for prophylaxis vs brain injury after intracranial aneurysm rupture
Being investigated for prevention of some of the deleterious effects of excess glutamate/excitotoxicity
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| Intracranial Pressure | Cranial cavity: brain (80%), blood (10%), and CSF (10%)
Rigid skull does not allow for expansion
Normal ICP 0-15mmHg (lateral ventricles)
Small changes with respiratory movements, coughing, straining, or sneezing
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| Intracrania Pressure s/s | ICP above 20mmHg is seen as pathologic and should be treated
Initial Symptoms: Headache-worst ever, projectile vomiting, papilledema-seen thru opthlamascope
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| Cushing's Triad | Bradycardia, hypertension (with widening pulse pressure), and irregular respiratory pattern
Pulse pressure: difference between sys and diastole– so systolic will raise and diastolic won’t
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| Monroe-Kellie's Hypothesis | Vol of each of 3 comparts (brain, blood, CSF) can vary slightly without causing and marked increase in ICP. Increase in one compartment will be compensated by a decrease in one or both of the other compartments.
Path ICP caused by vol ch in any of the 3
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| Modified Monroe-Kellie Hypothesis | Of the 3 comparts, brain tissue is least able to compensate.
Initial ICP changes buffered by CSF shunting to the spinal cord.
Only small amount of blood, blood flow tightly regulated
CSF most easily compensated by shunting
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| Cerebral Perfusion Pressure (CPP) | CPP=MABP-ICP
Nml CPP is 70-100
Brain ischemia 50-70: Pressure in cavity might be so high that any osmotic or oncotic pressure may not be high enough to overcome pressure that’s pushing back. No exchange of nutrients, and maybe not any blood.
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| Artificially raise Blood Pressure | Can artificially raise BP: vasoconstrictors to allow more perfusion
BP can raise ICP too– but it’s relatively small
If hemorrhagic stroke– don’t want the higher BP– may break an embolism
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| Brain Herniation General | Increases in pressure can push areas of the brain around these septa to areas that are less dense
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| Two Septa | Falx Cerebri: between hemispheres
Tentorium Cerebelli: above cerebellum
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| Types of Brain Herniation: cingulate | Cingulate Herniation (subfalcine herniation): Cingulate gyrus beneath the falx cerebri. Greatest danger from compression of blood vessels
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| Types of Brain Herniation: Uncal | Uncal Herniation (transtentorial herniation): : Medial aspect of temporal lobe protrudes over the tentorial edge. Ipsilateral pupil dilatation. Can interfere with RAS
Ipsilateral: pupil dilated with ICP, they maybe have herniation of that side
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| Types of Brain Herniation: Central | Central Herniation: Downward displacement of hemispheres, basal ganglia, diencephalon and midbrain through tentorial incisura. Slowly dilating pupils
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| Types of Brain Herniation: Tonsillar | Tonsillar Herniation: Cereballar tonsils through foramen magnum, compression of medulla. Less common but high mortality in short period of time. See changes in HR, BP, constricted pupils, ataxic breathing.
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| Cerebral Edema | Increase in tissue volume secondary to abnormal fluid accumulation
Seen as pathologic but does not necessarily disrupt brain function unless ICP is increased
Three types: Interstitial, Vasogenic, and Cytotoxic
Types correlating to compartments
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| Institial Cerebral Edema | Movement of CSF across the ventricular wall. Results in sodium (and therefore water) in the periventricular white matter. Seen with impaired CSF flow. around the ventricles: a bit more compressible.
problems will be in ventricles
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| Vasogenic Edema | Occurs when BBB is impaired. Transfer of proteins and water to interstitial space. Occurs more in white matter. Can cause herniations
Rupture in blood vessel, infection causing capillaries to become more leaky, etc
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| Cytotoxic Edema | Increase in fluid matter in intracellular space, mostly gray matter. Caused by water intoxication, severe ischemia, hypoxia, acidosis, and brain trauma.
Cause: water intox, dilutional hyponatremia
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| Treatment for Cerebral Edema | Corticosteroid therapy for localized edema (such as inflammation around a tumor).
Controversial in use of generalized edema
Unsure of mechanism of action, but appears to stabilize the cell membrane and scavenger free radicals
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| Mannitol (Osmitrol) | Osmotic diuretic, IV only.
Pulls water into the vasculature from the brain tissue
DO NOT give if cerebral vasculature is compromised
If hemorrhage, brain inj that rupture vessels, etc– mol will flow into ECF and will attract more water and make it wors
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| Hydrocephalus | Apendymals: coriod plexus in 2 lateral vent & will travel down into 3rd vent, thru aqueduct into 4th vent & has openings that allow it to free float down spinal cord & around the brain
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| Noncommunicating Hydrocephalus | (obstructive): obstruction in the ventricular system prevents CSF from reaching absorption point (arachnoid villi)
Congenital malformation, tumor, inflammation, hemorrhage, infection
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| Communicating Hydrocephalus | Bad reab of CSF from villi into the venous
From too few villi, postinf scarring, obst of villi
Adenomas of choroid plexus can cause increased CSF production-uncomm
Adenomas: cancerous growth on cells that make CSF– making too much CSF arachnoid villi c
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