The document discusses hypoxic and ischemic encephalopathy, which is caused by lack of oxygen or blood flow to the brain. This leads to energy failure in neurons, which causes the sodium-potassium pump to fail and glutamate to be released excessively. This results in cellular edema, calcium influx, and cell death through various mechanisms including free radicals and mitochondrial injury. Certain neurons, like those in the hippocampus and cortex, are more vulnerable to damage due to their high energy demands. Pathological patterns include hippocampal sclerosis, cortical necrosis, and border zone lesions. Cerebrovascular accidents like cerebral infarction and hemorrhage can also cause hypoxic or ischemic injury through mechanisms like atherosclerosis or bleeding from aneurysms.
Copyright:
Attribution Non-Commercial (BY-NC)
Available Formats
Download as DOCX, PDF, TXT or read online from Scribd
The document discusses hypoxic and ischemic encephalopathy, which is caused by lack of oxygen or blood flow to the brain. This leads to energy failure in neurons, which causes the sodium-potassium pump to fail and glutamate to be released excessively. This results in cellular edema, calcium influx, and cell death through various mechanisms including free radicals and mitochondrial injury. Certain neurons, like those in the hippocampus and cortex, are more vulnerable to damage due to their high energy demands. Pathological patterns include hippocampal sclerosis, cortical necrosis, and border zone lesions. Cerebrovascular accidents like cerebral infarction and hemorrhage can also cause hypoxic or ischemic injury through mechanisms like atherosclerosis or bleeding from aneurysms.
The document discusses hypoxic and ischemic encephalopathy, which is caused by lack of oxygen or blood flow to the brain. This leads to energy failure in neurons, which causes the sodium-potassium pump to fail and glutamate to be released excessively. This results in cellular edema, calcium influx, and cell death through various mechanisms including free radicals and mitochondrial injury. Certain neurons, like those in the hippocampus and cortex, are more vulnerable to damage due to their high energy demands. Pathological patterns include hippocampal sclerosis, cortical necrosis, and border zone lesions. Cerebrovascular accidents like cerebral infarction and hemorrhage can also cause hypoxic or ischemic injury through mechanisms like atherosclerosis or bleeding from aneurysms.
Copyright:
Attribution Non-Commercial (BY-NC)
Available Formats
Download as DOCX, PDF, TXT or read online from Scribd
The document discusses hypoxic and ischemic encephalopathy, which is caused by lack of oxygen or blood flow to the brain. This leads to energy failure in neurons, which causes the sodium-potassium pump to fail and glutamate to be released excessively. This results in cellular edema, calcium influx, and cell death through various mechanisms including free radicals and mitochondrial injury. Certain neurons, like those in the hippocampus and cortex, are more vulnerable to damage due to their high energy demands. Pathological patterns include hippocampal sclerosis, cortical necrosis, and border zone lesions. Cerebrovascular accidents like cerebral infarction and hemorrhage can also cause hypoxic or ischemic injury through mechanisms like atherosclerosis or bleeding from aneurysms.
Copyright:
Attribution Non-Commercial (BY-NC)
Available Formats
Download as DOCX, PDF, TXT or read online from Scribd
Download as docx, pdf, or txt
You are on page 1of 2
Hypoxic and Ischemic Encephalopathy- Pathology of Stroke
Brain is sensitive because it works by oxidative phosphorylation
Brain has no energy stores and most injury is caused by hypoperfusion Causes of energy shortage: ischemia, cerebral perfusion, hypoxia, hypoglycemia, and anemia Usually is from cardiac arrest or shock (severe hypotension) Traumatic brain injury or increased intracranial pressure is a cause of HIE in adults and children A rise of 10 mmHg (systolic) in the brain will cause brain capillaries to collapse There is a pump in the membrane of neurons that works against the concentration gradients that is the source of neuronal membrane excitability (Na in and K out) o In energy failure there is a depolarization of the membranes (fainting) o If energy failure persists then there will be permanent neuronal damage o Glu is dumped into the synaptic cleft (at toxic levels) o Na channels open which causes a mass influx into the cell which results in cellular edema o Ca also rushes in and there is activation of cytolytic enzymes and other free radicals which results in cell death o Damage- energy failure, glutamate, mitochondrial injury free radicals, lactic acidosis, edema o Reperfusion, while maintaining brain function, allows the aforementioned damages to occur as well Neurons are more sensitive than glial cells to damage because neurons have higher energy demands o Some neurons are more vulnerable- hippocampus, 3-5 cortical layers, purkinje cells, and striatal cells Pathological Patterns of HIE o Hippocampal sclerosis Patients with epilepsy or after cardiac arrest Purkinje cell sparing without hypoglycemia Segment of pyramidal layers are missing Causes Korsakoff amnesia- loss of episodic memory (long/short are preserved) o Laminal Cortical Necrosis (Pseudolaminar necrosis) and Thalamic injury Korsakoff (due to dorsal nu of thal involvement) or PVS – state when wakefulness may be present but awareness is not; Diffuse cortical, thalamic, or combined neuronal loss/white matter damage (with intact brainstem) – bilateral o Border zone (watershed) lesions- does not affect hippocampus o Total Cerebral and Brainstem Damage Unresponsiveness, absent brainstem reflexes, no spontaneous respiration, flat EEG, no circ, non perfused brain Imaging shows hypodesnity due to disintegration Cerebral infarcts involving brainstem Cerebrovascular Accident o Cerebral Infarct- atherosclerosis, small vessel disease (HTN), emoblism Evolution: (1) Cerebral Necrosis (2) Edema (3) Caviation (months) Micro: (1) inflammation and axonal swelling (AA and FA) (2) neovascularization at 2 weeks; monocytes enter the infarct and disgest neurons and turn into lipid laden macrophages (3) macrophage reaction at 3- 4 weeks (4) gemistocytic astrocytes and glial scare (2 months) Embolic infarcts can look hemorrhagic but their primary process is an infarct (clot lyses and then causes bleeding) Lacunar infarcts from small vessel disease (HTN/diabetes)can cause cystic problems; affects deeper nuclei (basal ganglia/thalamus); can be just as bad as more massive infarcts Cerebral Autosomal Dominant Arteriopathy with subcortial infarcts and ischemic encephalopathy (CADASIL = notch 3 gene), coll 4A1 defects, cerebral amyloid angiopathy Vascular dementia (multi-infarct) Ischemic penumbra- central zone where the necrosis/death is irreversible; surrounded by a gray zone where recovery may be possible (this surrounding zone is the penumbra) o Cerebral Hemorrhage- HTN, arterial aneurysms, AVM, Angiopathy, Coagulopathy Caused by small vessel disease- vessels lose elasticity so their strength is greatly diminished since strength is due to elasticity not stiffness Affects basal ganglia, thalamus, and lateral ventricles; also pons, cerebellum, and central white matter Vascular lesions can cause infarction and hemorrhage Intracranial Aneurysm (Saccular/Berry Aneurysms)- located at the junction of bifurcation of vessels Can enlarge and cause tumor like symptoms Can rupture (BAD) Subarachnoid hemorrhage will cause increase in intracranial pressure Risks – polycystic Kidneys, coarc, and female AVM- tangle of veins and arteries that are delicate and can hemorrhage and cause seizures/focal defecits Cerebral Amyloid Angiopathy- parenchymal brain damage; amyloid/fibring deposit in walls of arteries and makes them fragile o