CNS Flashcards
what is necessary to ensure the differentiation of neural and epidermal tisse
closure of the neural tube (fully)
which direction do neuron migrate in the brain, and where
from the central lumen to the outer edge (white matter)
in cerebellum this continues 2 mths after birth
name the 3 primary vesicles of the developing brain and the additional 2 secondary ones
- pro, mesen and rhombencephalon
- telen and diencephalin
name the 2 biggest sulci on the brain
tentorium cerebelli
falx cerebri
what is the nissyl substance
rER in the cytoplasm of neurons
what is substantia nigra
neuromelanin pigm used as a NT in primates
what marker can be identified by IHC on astrocytes
GFAP
what is the role of astrocytes
BBB uptake and recycle NT maintain pH support metabolic needs help neuronal migration
describe the diff stages of microglia
inactive - rammified
active - rod, comma nuc, mphages
de-activated (when finished), granular - gitter cells
what is malacia
gross appearance of necrosis of the brain
where in the brain can you find poss fibrosis
nowhere - meninges can tho
why are neurones easily damage
v active
cant differentiate of prolif
axons and dendrites extend far from the soma
constantly inhib or stim
why do red hypoxic neurones occur
over excitment, inc ca++ prod or just in hypoxic states**
what is the neuronal response to oxidatie stress
chromatolysis (massive pale cytoplasm in soma, tiny peripheral nucleus)
how do you describe an inc in astrocyte number and vole
number = astrogliosis vol = astrocytosis
what are the 2 forms of myeline damage/degen
1ry - if the oligo is damaged –> dysfct myelin (leukodystrophy)
2ry - if its the myelin thats damaged
bane the 4 types of CNS oedema
- cytotoc - altered cyto metab, ballooning degen
- vasogenic - vascular damage + extracellular fluidin WM
- hydrostatic - inc fluid in Ventricles + extra-cellular WM
- hypo-osmotic - intra + extra fluid in W+G matter
what are the general affects of vascular pathology in brain, seen by what
asymetrical
malacia and haem+ (probs)
acute, non-progressive neural issues
what is penumbra
the area around an area of complete ischaemia, which will suffer repurfusion injury if too quick
how can an infarct be caused in the brain
- mis injection of carotid a causing thrombembolism
- rupture of f-cartilagenous disk
- ichaemia due to reduced blood from stenosis of a caused by calcinosis sidero (in t. media=blue)
how can path access the brain
- retrograde axonal transm (rabies, listeria)
- deposit IC at the BBB (FCoV)
- infec endothelial cells (CSF)
- within other cells (toxo, viruses)
- accum wi vessels (bact)
what are the characteristics of viral inf
- targeted areas
- neuronophagic nodules
- glial nodule (n-phagic nodules but wo a neuron involved)
- non-supperative
how do you tell diff PM of rabies and pseudorabies, as both get non-supp polioencephalomyelitis
rabies = IC inclusion and negri bodies in hippocampus (Carnivores) or perkinje cells (herbiv) pseudorabies = swine herpes 1 = IN inclusions
what is swine polioecephalomyelitis trophic for
LMN