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Mech Cerebral Injury

Mechanisms of Cerebral Injury

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
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
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
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.
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
Global Ischemia (cont) Anatomy of blood vessels leads to watershed zones Farthest from large arteries Profound lowering of blood pressure in these areas
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
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
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
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
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
Reperfusion Injury Return of oxygen to ischemic cells can lead to oxygen free fradical formation, and allows inflammatory cells to enter the ischemic area
Reperfusion Injury Leads to lipid peroxidation of the cell membrane, which activates the arachadonic acid cascade, leading to more free radical formation
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
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
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
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
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
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
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
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.
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
Brain Herniation General Increases in pressure can push areas of the brain around these septa to areas that are less dense
Two Septa Falx Cerebri: between hemispheres Tentorium Cerebelli: above cerebellum
Types of Brain Herniation: cingulate Cingulate Herniation (subfalcine herniation): Cingulate gyrus beneath the falx cerebri. Greatest danger from compression of blood vessels
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
Types of Brain Herniation: Central Central Herniation: Downward displacement of hemispheres, basal ganglia, diencephalon and midbrain through tentorial incisura. Slowly dilating pupils
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.
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
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
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
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
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
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
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
Noncommunicating Hydrocephalus (obstructive): obstruction in the ventricular system prevents CSF from reaching absorption point (arachnoid villi) Congenital malformation, tumor, inflammation, hemorrhage, infection
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
Created by: Marissagostanian