Neuropath Flashcards
Hypoxic injury
Loss of ribonucleoproteins and desaturation of cytoskeletal proteins leads to cytoplasmic eosinophilia and nuclear pykknosis
Red neurons
Neuron shrinks and becomes eosinophilia
Astrocytes responds to
Injury by proliferation of cytoplasmic process and intermediate filaments
Reactive gliosis by astrocytes
Analogous to fibrous scar
Oligodendrocytes injury results in
Demyelinating disease (MS)
Microglia
Antigen presenting cell
Can sometimes appear as rod cells
Neuron response to injury
Shrinkage Cell Body
Nuclear and nuclei degeneration
Breaks down in blood brain barrier with acute injuries
Astrocytes response to injury
Primarily responsible for repair and scar formation
Rosenthal fibers
Rosenthal fibers
Thick eosinophilic protein aggregates seen in chronic gliosis
Microglia cells response to injury
Microglia nodules
Neuropnphagia (eating of neurons) at injured site
Ependymal Cell Response to injury
Certain pathogens cause extensive ependymal injury with viral inclusions
Cerebral Edema Etiology
1) Disrupted blood brain barrier; increased vascular permeability (vasogenic)
2) Increase in water content secondarily to glial or endothelial injury (cytotoxic)
Cerebral edema causes
Compressed ventricle
Brain shifting
Swollen gyro
Narrowed sulci
Cerebral Edema: Brain Swelling leads to
Brain swelling leads to increased intracranial pressure
Present as Severe headache vomiting papilledema (swelling of optic disc)
Brain herniation
Displacement of brain tissue from one intracranial compartment to another-may result from brain swelling, tumor
3 types of brain herniation
Subfalcine (cingulate)
transtentorial (uncinate)
Tonsillar (the worst)
Uncinate will compress
CN 3
Hydrocephalus
Accumulation of excess CSF within ventricular system
Expanded ventricles with increased crainial pressure
Hydrocephalus caused by
Decreased CSF resorption (CSF flow obstructed by: Tumor, hemorrhage or inflammation)
-Increased CSF production (tumors of choroid plexus)
Cerebrovascular Diseases Mechanism
“Stroke”
1) thrombus occluded vessels
2) Moving thrombus (embolus) occluded vessels
3) Rupture of blood vessel
Stroke
Acute non epileptic neurological deficit lasting > 24 hours
Strokes result from 2 major processes
Occlusion/hypoxia
Hemorrhage
Brain hemorrhages
Intra-parenchymal hemorrhage
Subarachnoid hemorrhage
Vascular malformations
Most frequently affected with brain infarction
Middle cerebral artery
Brain infection risk factors
Hypertension, smoking, diabetes
Atherosclerosis is the most common underlying cause
Acute infarction
24-36 hours
Neurons become eosinophils
Neutrophils infiltrate into brain parenchyma
Subacute infarction
3rd-5th day
Involved tissue becomes softer in consistency
Macrophages with foamy cytoplasm begin to infiltrate
Chronic infarction
Weeks to months
Softening and liquefaction results in smooth walled cystic cavity
Loss of brain tissue
Intraparenchymal hemorrhage
Basal ganglia most commonly affected
Pons thalamus and cerebellum also affected
Subarachnoid hemorrage
Severe headaches
Rupture saccular berry anyersms
Most arise at artisan bifurcations of the circle of Willis
Vascular malformations hemorrhage
Arteriovenous malformation most common
Collection of abnormal blood vessel
Sucharachnoid or parenchyma hemorrhage results in neurologic deficits
Epidural hematoma
Rupture of a meningeal artery-arterial bleeding
Lucid interval
In epidural hematoma blood between
Skull and dura mater
Subdural hematoma blood between
Dura and arachnoid membrane
subdural hematoma disruption of
Bridging veins-Venous bleeding
Acute- Whiplash shake a baby
Chronic-elderly with brain atrophy
Concussion
Loss of consciousness with full recovery
Contusion
Disruption and hemorrhage of superficial brain caused by blunt trauma
Laceration
Tearing of brain parenchyma
Coup lesion
Impact site that hits the bone in contusion