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Flashcards in Neuropathology I Deck (19):

What is eosinophilia of the perikaryon? What are frequent causes? How soon after the insult can this change be seen?

pink/red neuron.
pyknotic nuclei
often caused by hypoxia or hypoxic-ischemia. excitotoxic aas like glutamate may be effectors of the lesion
recognizable 6-8 hrs after the insult.
represents acute neuronal necrosis.


What is neuronal atrophy?

non-eosinophilic shrinkage of cell body with nucler hyperchromasia or pyknosis. direct or indirect mechanisms.


When do we see simple atrophy? What are some features?

excessive lipofuscin (brown dots)
common in degenerative diseases


What is transynaptic atrophy

retrograd or anterograde. retrograde: problem with axonal transmission. anterograde: problem with reception of info from the dendrites


What is chromatolysis? How common is it?

rarely encountered in routine autopsy or surgical samples
enlarged neurons. rounded with peripheral displacement of the nucleus and enlargement of the nucleolus. cytoplasm has a homogenous granular appearance from dispersion of the nissl substance.


What is central chromatolysis?

spares a peripheral rim of Nissl substance. usually a regenerative response to axonal damage. repair most likely successful if it occurs in central neurons with peripheral axons.


What is perikaryal swelling?

swelling due to storage of metabolites. Don;t confuse with chromatolysis!


In what diseases do we see nuerofibrillary tangles?

Alzheimers (progressive supranclear palsy and postencephalitic PD)


What other main inlcusions may be seen in the perikaryon? (PD, Pick's diseases, measles enecephalitis, rabies)

lewy bodies in PD, Pick bodies in Pick disease, Lafora bodies, viral inclusions (esp. in measles encephalitis, herpes, ctyomegalovirus), Negri and Lyssa bodies in rabies.


When is phagocytosis of dead neurons prominent?

hypoxi-ischemic lesions and viral disease. usually the microglial cell


What is Wallerian-like degeneration and when is it seen?

CNS counterpart of true Wallarian degeneration. common central axon lesion. occurs after infarcts or traumatic lesions have destroyed neuronal perikaryia or their axonal projections


What is dying back degeneration?

loss of the distal axon following an insult, then progressive loss of more proximal segements, starting with the distal regions (and dying back).


What are spheroids?

axonal swellings: focal enlargements of axons due to trauma, ischemic, or metabolic insults


What are the two types of speroids? Difference between the types Waht are they associated with?

reactive (prolif of normal cellular things, like organelles, lysosomes, or mitochondria). Reactive usually from trauma or focal infarction. Dystropic (one of the above plus smooth membranous and visicular proliferations with electron dense material of unknown origin) usually not clinically significant but seen in aged.
symptomatic dystrophic lesions usually seen diffusely in rare metabolic/degenerative diseases (neuroaxonal dystrophies
(remember, these are axonal issues)


What are the 2 lesions of myelin sheaths?

primary demyelination and spongy degenration or change. Primary: myelin sheath lost with preservation of the axon. spongy: intramyelinitc edema- lots of metabolic-toxic diseases


What is neutropil?

feltwork that fills the spaces between cell bodies of gray matter. small unmyelonated axons, dentrides, synapses, and glial processes


What are neuritic plaques?

seen in neutropil: amyloid, degenerating or regenerating axons


What is spongy change?

seen in gray matter. due to neuronal loss, resprption of spheroids, cytotoxic/vasogenic edema, or change of prion diseases (emphasized)


What are the astrocytic reactions?

hypertrophy, storage, inclusions, neoplasia