Neuro 6-9
hemorrhagic stroke (2 types)
-occurs when a blood vessel within brain burst -results in blood spilling into/around brain -can be from HTN/aneurysms -intracerebral hemorrhage if vessel is bleeding into brain tissue => brain cells die -subarachnoid hemorrhage if vessel is bleeding into subarachnoid space => surrounding aa. spasm => reduced flow to brain. often from burst aneurysm
oligodendrocyte myelination process
-oligodendrocyte recognize cell-surface proteins on axons -leading edge of processes flatten out to warp around axon multiple times -cytoplasm extruded => compaction leaving behind tightly rolled myelin sheath continuous w/ oligodendrocyte for nourishment
CNS glia
-oligodendrocytes -astrocytes -ependymal cells -microglia
vertebral aa.
-pair of aa. (R/L) -4 parts: V1-V4 -runs from subclavian a. to pontomedullary junction of brainstem becoming basilar a.
internal carotid a.
-pair of aa. (R/L) -4 parts: cervical, petrous, cavernous, cerebral -runs from common carotid a. bifurcation (into internal and external carotids) to intracranial space becoming anterior and middle cerebral aa.
confluence of sinuses
-point posteriorly where sinuses all come together -blood flows from various sinuses here and then travels laterally via transverse sinuses
intracranial hematomas
-pooling of blood within various spaces including -epidural -subdural -subarachnoid
cerebellar aa.
-posterior inferior cerebellar a. (PICA) comes off vertebral aa. -anterior inferior cerebellar a. (AICA) is 1st branch of basilar a. -superior cerebellar a. is last branch of basilar a. -each supplies respective parts of cerebellum
intracranial branches of vertebral aa.
-posterior inferior cerebellar aa. (PICA) emerge from individual vertebral aa. (serves posterior, inferior cerebellum) -anterior spinal aa. branch off vertebral aa. right before they become basilar a. (meet up and serves anterior spine) -posterior spinal aa. branch from PICA or vertebral aa. (each serve posterior spine)
myelin basic protein (MBP)
-potential target of T-cells (or other leukocyte) => immune-mediated demyelinating dz (ie multiple sclerosis in CNS and Guillain-Barre in PNS)
oligodendrocytes
-predominant CNS glia in white matter responsible for myelinating axons -has central body w/ multiple (50's) processes that branch to myelinate individual neuron axons (unlike schwann, a single oligo can myelinate multiple axons) -arranged in regularly spaced rows w/ processes radiating out towards axons
protein 0 (PO)
-protein that can be mutated to contribute to hereditary demyelinating dz (ie Alexander and Canavan dz)
neuronal tumors
-rare 1' CNS tumor -neurons do not divide -these must revert to undifferentiated stem cells to proliferate -often not aggressive and easy to tx
artery watersheds
-regions receiving dual blood supply from most distal branches of 2 aa. -supply from vessels do NOT overlap (no anastomosis) -this area vulnerable to hypoperfusion as most distal sections are first to fall if pressure decreases
astrocyte K+ buffer
-repolarization of neuron requires extrusion of K+ -repetitive AP's => elevated extracellular K+ => compromised fxn -astrocytes can uptake excess K+ and through its syncytium (network) distribute excess K+ to low [K+] areas ("spatial buffering") -high K+ may also signal astrocytes to increase glucose metabolism => more lactate for neurons (due to high K+ suggesting high activity)
cerebellum development
-rhombic lip forms as cells proliferate where roof plate meets alar plate (A) -these lips increase in size and eventually fuse together => rudimentary cerebellum (B) -cerebellum grows dorsal to 4th ventricle -eventually have cerebellum separated from pons by 4th ventricle (C&D)
superficial cerebral vv.
-run along surface of brain
superior sagittal sinus
-runs along superior aspect of falx cerebri
cervical internal carotid a.
-runs from common carotid a. bifurcation (into internal and external carotids) -enters cranium via carotid canal of temporal bone (between green circles)
petrous internal carotid a.
-runs within carotid canal of temporal bone (between green circles)
schwann cell myelination process
-schwann cell attracted to axons via specific surface proteins -they then flatten/extend out to engulf axon and wrap around multiple times -they then extrude cytoplasm => compaction => schwann cell + myeline sheath consisting 1' of lipid membrane and protein (very little cytoplasm)
PNS glia
-schwann cells -satellite cells
radicular aa.
-segmental a. of spinal cord (SC) -enters at every level -emerges from spinal aa. (S) at each level -supplies dorsal and ventral roots ONLY (if continuous on to SC is a segmental medullary a.)
segmental medullary aa.
-segmental a. of spinal cord (SC) -enters at variable level (not every level) -emerges from spinal aa. (S) at variable levels -supplies anterior/posterior spinal aa. (continues past dorsal/ventral roots)
arteria radicularis magna (great anterior segmental medullary a.)
-segmental a. of spinal cord (SC) -supplies lower T/upper L spine to cauda equina (white arrow) -only on one side (typically L) and blockage => paralysis
cerebellar vv.
-serves cerebellum (see mid-sagittal X-section)
internal cerebral vv.
-serves inside of brain (see mid-sagittal X-section) -drains into great cerebral v.
microglia recruitment
-small injury to brain parenchyma can be handled by microglia alone -larger lesions => microglia secreting IL's to attract T's/macs to CNS -T's/macs cross BBB by secreting IL's to loosen endothelial tight junctions -once in microglia act as APCs to T's => immune response -oligodendrocytes especially vulnerable to immune response and T/mac attack can overwhelm its ability to produce myelin -proliferating macs => mitotic figures that can be mistaken for neoplasm
dural venous sinuses
-spaces between meningeal and periosteal layers of cranial dura -fxn as venous blood channels -composed to dura lined w/ endothelial cells NOT tunics (unlike nm blood vessels)
demyelinating dz's
-specific proteins critical for myelination in CNS/PNS -mutations in genes responsible for these proteins => hereditary demyelinating dz -immune cells can attack these proteins => immune-mediated demyelinating dz -results in poor AP conduction (or none at all)
astrocyte network
-star shaped cells w/ coordinated network across entire brain/spinal cord (recall glia limitans and true BBB) -communication occurs via gap junctions -each w/ multiple processes that contact dendrites, cell bodies, and some axons/synapses
telencephalon vesicle derivatives
-structures: cerebrum (cerebral hemispheres, cortex, white matter, basal nuclei) -canals: lateral ventricles (1 per hemisphere)
diencephalon vesicle derivatives
-structures: diencephalon (thalamus, hypothalamus, epithalamus) and retina -canal: third ventricle (recall communicates w/ lateral ventricles via interventricular foramen AKA foramen of Monro)
myelencephalon vesicle derivatives
-structures: medulla oblongata of brainstem -canal: 4th ventricle -CSF now leaves ventricular system => subarachnoid space (recall lateral and median apertures) OR central canal to spinal cord (recall inferior apex of 4th ventricle)
mesencephalon vesicle derivatives
-structures: midbrain of brainstem -canal: cerebral aqueduct = passageway draining cerebrum (recall between 3rd and 4th ventricle)
metencephalon vesicle derivatives
-structures: pons of brainstem and cerebellum -canal: 4th ventricle (diamond shape) between pons and cerebellum
CNS vasculature location
-subarachnoid space
dorsal root ganglion development
-subset of neural crest migrates ventrally -accumulates adjacent to neural tube = dorsal root ganglion -eventually gives off 2 processes emerging from either side -processes move towards one another and fuse (bottom pic) = unipolar dorsal sensory root
cerebral internal carotid a.
-terminal segment after exiting cavernous sinus -bifurcates into anterior and middle cerebral aa. (each supplying respective parts of brain)
cavernous internal carotid a.
-travels through cavernous sinus
cerebral arterial circle (circle of willis)
-ventrally located arterial anastomosis formed by... -anterior cerebral aa. (A1) -anterior communicating a. -end portion of internal carotid aa. (before bifurcation => anterior/middle cerebral aa.) -posterior cerebral aa. -posterior communicating aa. -if one of the above is blocked, flow from the others can preserve brain perfusion to avoid sx of ischemia (note: circle encloses pituitary gland)
saccular ("berry") aneurysms
-weak spot in arterial wall => bulges occurring in aa. of circle of willis (often at branching points) -due to degeneration of tunica media => tunica intima bulges -can be incidental finding or via autopsy -sacks eventually enlarge until ruptures
great cerebral v.
-where internal cerebral vv. come together and enter dura
meningioma
-~1/3 of 1' CNS tumors -benign neoplasm of arachnoid origin
gliomas
-~1/3 of 1' CNS tumors -glia cells naturally proliferate => aggressive tumor w/ poor prognosis
varied 1' CNS tumors
-~1/3 of 1' CNS tumors -varied origin -most prevalent = pituitary adenoma and schwannomas
1st part of vertebral a. (V1)
-1st largest branch of subclavian a. -ascends between anterior scalene and longus colli mm. -enters transverse foramen (TF) of C6 as V2
posterior spinal aa.
-2x longitudinal aa. of spinal cord (SC) -emerge from each vertebral a. (earlier than anterior spinal aa.) -each descend within posterolateral sulcus of SC (not midline) -collectively supply posterior 1/3 of SC
cerebral aa.
-3 pairs that supply telencephalon (cerebrum) -internal carotid aa. bifurcate => anterior/middle cerebral aa. -basilar a. bifurcates => posterior cerebral aa. -each supply respective parts of brain
anterior cerebral a.
-3 sections: A1-A3 (only need to know A1/2) -A1 runs from internal carotid a. bifurcation to anterior communicating a. (within circle of willis) -A2 continues distal to anterior communicating a. midline between hemispheres -eventually gives off branches that travel up medial aspect of hemispheres to serve... -superior/medial frontal lobe -superior/medial parietal lobe -corpus callosum (also basal ganglia and part of internal capsule) -lesions of this a. => motor/sensory deficit of contralateral LE
posterior cerebral a.
-4 sections: P1-4 (only need to know P1/2) -P1 runs from bifurcation of basilar a. to posterior communicating aa. (within circle of willis) -P2 continues distal to posterior communicating a. to supply... -inferior temporal lobe -occipital lobe -posterior corpus callosum -part of thalamus/hypothalamus -lesions of this a. => visual, some CN, and memory deficits
brain 1' vesicle formation
-AFTER neurulation -neural tube temporarily occludes => pressure => 3 dilations occur near rostral end of neural tube => 1' vesicles... -prosencephalon (forebrain) -mesencephalon (midbrain) -rhombencephalon (hindbrain)
transient ischemic attack (TIA)
-a. supplying brain is blocked for short time -blood flow slows/stops => sx including... -numbness/weakness -vision loss -aphasia -loss of balance -a. then becomes unblocked OR alternate route opens up -sx resolve as nm blood flow is restored
end aa.
-aa. that are the sole route to a destination -blockages here CANNOT be circumvented (unlike within circle of willis where blood can go around if blocked) -strokes here results in deficits distal to lesion
CNS gliablast development
-after all neuroblasts produced, neuroepithelial cells begin making gliablasts -these later differentiate into various glia for CNS
veins of spinal cord
-all run w/ SC aa. w/ same name -HOWEVER there is a 3rd posterior spinal v. that runs along midline of posterior spine w/o accompanying a.
homunculi vasculature
-anterior cerebral aa. travel between hemispheres up and over top to serve medial/superior regions, responsible for BLE/torso (to blue dotted line) -middle cerebral aa. travel out laterally then up to serve lateral regions, responsible for BUE/face (to blue dotted line) -NO anastomosis occurs between them -strokes in either a. will affect motor/sensory within their respective distribution on OPPOSITE side of lesion
spinal watershed
-anterior spinal a. supplies larger (2/3) anterior SC, including ventral horns/columns (gray/white matter) = motor area -posterior spinal a. supplies smaller (1/3) posterior SC, including dorsal horns/columns (gray/white matter) = sensory area -both meet to form watershed zone (DO NOT anastomose)
conduction velocity classifications
-applies to both sensory and motor fibers -A = fastest -C = slowest -often applies to myelinated fibers BUT slowest fibers (C) are unmyelinated
hypophyseal (H) aa.
-arise from internal carotid a. -supplies pituitary gland that lies inside circle of willis
labyrinthine (L) a. (AKA internal auditory a.)
-arises from anterior inferior cerebellar a. (AICA) or sometimes basilar a. -travels w/ CN VIII to serve inner ear
astrocytic influence on NTs
-astrocytes present at synapses, affecting NT metabolism -plays a role in synthesis of neuroactive compounds -terminates synaptic transmission by uptaking NT's -takes up glutamate and converts to glutamine which is recycled by neurons back to glutamate
neoplastic astrocytes (+marker)
-astrocytes' ability to proliferate => most prevalent origin of CNS tumors (80% of all gliomas) -reactive and neoplastic astrocytes stain strongly for glial fibrillary acidic protein (GFAP, intermediate filament isoform)
middle cerebral a.
-begins at bifurcation of internal carotid a. -runs above insular lobe laterally through Sylvian fissure (between frontal/parietal and temporal lobes) -splits into superior and inferior branches -superior branch supplies lateral frontal/parietal lobes (all except superior 2-3 cm) -inferior branch supplies lateral temporal lobes (also basal ganglia and part of internal capsule) -lesion of this a. => motor/sensory deficit of contralateral face/arm (including aphasia)
transverse sinuses
-begins at confluence of sinuses -runs laterally and dives inferior -becomes sigmoid sinus (where it gets bendy)
cerebral artery watersheds
-between anterior cerebral a. and middle cerebral a. -between middle cerebral a. and posterior cerebral a.
cerebral hemisphere development
-bilateral evaginations of telencephalon grow -cells proliferate => R/L cerebral hemispheres (increasing in size)
CNS neuron/glia embryonic origin
-both CNS neuron/glia directly derived from embryonic neural tube
PNS neurons/glia embryonic origin
-both PNS neuron/glia indirectly derived from embryonic neural tube via neural crest
sulcal a.
-branch of anterior spinal aa. (white arrow) -enters fissure before branching to supply anterior 2/3 of SC
superior/inferior petrosal sinuses
-cavernous sinus (green circle) drains into beginning and end of sigmoid sinus via superior/inferior petrosal sinuses (both running over petrous portion of temporal bone)
ventral motor root development
-cell bodies in basal plate (becoming ventral horn) give off outgrowing motor axons -these migrate to marginal layer => white matter -axons eventually emerge out in a bundle = ventral motor neuron
glia cells
-cells that support neuron fxn -may also be active partners in shaping nervous system fxn (playing a role in signal transmission)
gyri/sulci development
-cerebral hemispheres continue to grow -eventually limited by cranial vault -begins to forms convolutions (gyri) and grooves (sulci) -these increase surface area in the limited amount of space -results in increased space for more cells
chiari malformation
-condition where brain tissue extends into vertebral canal -can be due to small/misshapen skull => brain growth forcing it downward
anterior communicating a.
-connects 2x anterior cerebral a. rostrally -part of circle of willis
posterior communicating aa.
-connects posterior cerebral aa. to internal carotid aa. -part of circle of willis
sigmoid sinuses
-continuations of transverse sinuses (bendy bits going down) -transitions to internal jugular v. at jugular foramen between temporal and occipital bones
astrocytic barriers
-contributes to true BBB via astrocytic end-feet inducing tight junctions in capillary endothelium + contribution to physical barrier -astrocytic end-feet form glia limitans (recall between pia and parenchyma)
spinal nerve formation
-dorsal sensory root meets up w/ ventral motor root => trunk of spinal nerve
cauda equina development
-early in development spinal cord extends down through entire vertebral canal -eventually vertebral canal growth >>> spinal cord => gap between ends -results in spinal nerve roots lengthening as they travel from conus medullaris (inferior most spinal cord) to vertebral canal exits at IV foramen = cauda equina -at birth conus medullaris at IV disc L2/3 -adults conus medullaris at IV disc L1/2
microglia
-endogenous immune cell of CNS (smallest glia) -at rest make up small % of CNS glia (~5%) -each have processes that cover unique territory (processes DO NOT overlap w/ neighboring microglia) -proliferates rapidly in response to injury/dz => "reactive microglia"
2nd part of vertebral a. (V2)
-enters transverse foramen (TF) of C6 -ascends through TF until exiting out of TF of C2 as V3
3rd part of vertebral a. (V3)
-exits transverse foramen (TF) of C2 -travels through TF of C1 -curves posteromedially along groove for vertebral a. on superior, posterior arch of C1 (atlas) -pierces atlantooccipital membrane (AOM) and dura/arachnoid mater -now in subarachnoid space as V4
rachischisis
-failure of caudal neuropore closure => spinal bifida -often seen w/ anencephaly -infant can live w/ this BUT will be paralyzed from point of deficit caudally (note: "craniospinal rachischisis" = one that extend all the way up to cranium)
anencephaly
-failure of cranial neuropore closure (mid in pic) -results in developing brain/spinal cord to be exposed to amniotic fluid => nervous tissue degeneration -brainstem persists => infant able to carryout basic fxns -fatal -folate supplements may reduce risk
holoprosencephaly
-failure of telencephalon to develop into 2 hemispheres -has 4 degrees of severity
neuroblast differentiation
-neuroblast arrives to mantle layer as single cell body -two processes emerge opposite each other -short grows towards neural tube lumen eventually becoming dendrites -long grows towards marginal layer eventually becoming axon => myelination => white matter -Nissl substance (recall like ribo's) form around cell body => gray matter -now is a multipolar neuroblast
principle cell types of nervous system
-neurons -glia -neural stem cells (progenitor cells)
neurulation steps
-notochord secretes proteins => neuroectoderm invagination => "neural plate" (purple) -invagination continues until neural folds (margins) meet (green) -non-neural surface ectoderm fuses => epidermis of back (blue) -neural folds detach and migrate => neural crest -neural plate fuses => neural tube (precursor to CNS)
4th part of vertebral a. (V4)
-now in subarachnoid space -ascends through foramen magnum to intracranial space -R/L vertebral aa. merge near pontomedullary junction of brainstem (green circle) -forms basilar a. (green highlight)
pontine (P) aa.
-numerous small branches off basilar a. -lie over pons to serve that area -stroke here => compromised neural pathways throughout pons
stroke
-obstruction/rupture of a. supplying brain -sx include... -aphasia -memory loss -unilateral paralysis -can be ischemic vs hemorrhagic
ophthalmic (O) a.
-1st branch of internal carotid aa. distal to cavernous sinus -enters optic canal w/ optic n. -serves globe and orbit of eye -occlusions here => blindness
microcephaly
-"small brain" -lack of proper brain growth -may still form gryi/sulci (more than lissencephaly) -results in decreased mental capacity due to decreased brain mass
lissencephaly
-"smooth brain" -disrupted brain growth such that no gyri/sulci form -results in decreased mental capacity due to decreased surface area
1' vs 2' CSN tumors
-1' = those that arise from CNS cells -2' = mets from elsewhere (often lungs, breast, melanoma) -2' >>> 1' in occurance
axon diameter classifications
-1' applies to sensory fibers -group I = largest -group IV = smallest -often applies to myelinated fibers BUT smallest fibers (IV) are unmyelinated
CNS glucose routes
-1' fuel of brain -direct route = diffusion from blood to BECF => neurons where oxidized -indirect route = taken up by astrocytes => glycogen for storage OR metabolized to lactate to diffuse into neuron where oxidized -astrocytic glycogen stores last ~5-10 min to protect against fluctuating blood [glucose] (note: glucose yields more ATP than lactate)
microglia embryonic origin
-CNS glia -originates from mesoderm -derived from hematopoietic stem cells via mononuclear phagocytic cell line -related to phagocytes like macs
astrocyte types
-CNS glia -protoplasmic astrocytes = short, branching processes more in gray matter around soma (cell bodies) -fibrous astrocytes = fewer, straight processes more in white matter w/ axons
microglia development
-CNS glia derived from mesenchymal cells (mesoderm) -microglia appear shortly after other glia form
ependymal cell development
-CNS glia derived from neuroepithelial cells -some neuroepithelial cells will NOT become gliablasts and instead remain near lumen of neural tube -these become ependymal cells lining lumen of neural tube (later becoming ventricles)
astrocyte development
-CNS glia derived from neuroepithelial cells => gliablasts -some gliablasts migrate to mantle layer and associate w/ cell bodies in gray matter => astrocytes
oligodendrocyte development
-CNS glia derived from neuroepithelial cells => gliablasts -some gliablasts migrate to marginal layer and associate w/ axons in white matter => oligodendrocytes
astrocyte CNS injury
-CNS injury => hypertrophy/plasia of astrocyte => "reactive astrocytes" -they then form astrocytic scars (glial scars) where cells were destroyed (fibroblast-like activity)
pituitary gland development
-Rathke's pouch = ectoderm from primitive oral cavity (red) -infundibulum = neuroectoderm of diencephalon (blue) -Rathke's extends up to meet infundibulum -Rathke's detaches from oral ectoderm and grows/fuses w/ infundibulum -Rathke's => anterior lobe of pituitary made of epithelial cells -infundibulum => stalk and posterior lobe of pituitary made of neurons
PNS nerve fiber classifications
-NT's released = pharm classes -info transmitted/where to: sensory vs motor + visceral vs somatic = anatomic classes -axon diameter/speed of impulse = physiologic classes
satellite cells
-PNS glia -small cuboidal cells that form layer over neuronal cell bodies in PNS ganglia -provide support to neuron = nourishment, electrical insulation, regulating microenvironment
schwann cells 1' fxn
-PNS glia -single schwann cell wraps single segment of intermediate to large axon => myelination -small axons are embedded by schwann cells but NOT myelinated
neural tube flexures
-formation of brain in relatively fixed space => forces that bend neural tube -cervical flexure between myelencephalon and spinal cord -pontine flexure between metencephalon and myelencephalon -cephalic flexure within mesencephalon -all result in postnatal brain taking its final shape
basilar a. branches
-from proximal to distal.... -anterior inferior cerebellar aa. (AICA) -labyrinthine aa. (L) -pontine aa. (P) -superior cerebellar aa. (SCA) -terminal end spits into posterior cerebral aa.
neurons
-generate electrical signal to transmit info throughout nervous system -manipulated ion gradients for membrane/action potentials -synthesized NTs -requires controlled environment to properly transmit APs
hindbrain development
-hindbrain architecture is modified by 4th ventricle -dorsal neural tube everted at sulcus limitans -alar plate => sensory nuclei now lateral and dorsal (blue circles) -basal plate => motor nuclei now ventral and medial (red circles)
axon regeneration
-if axon transected the proximal cut end will form end bulb -detached distal end will undergo Wallerian degeneration (neuron/schwann/myeline degraded and digested by neuron/schwann/macs) -schwann cells of proximal end bulb will proliferate => upregulate cytoskeletal growth factors => regeneration -will downregulate synapse maintenance fxns => muscle atrophy (note: crush injuries heal faster than complete transection bc CT framework still somewhat in place)
cauda equina clinical use
-in adults spinal cord stops at IV disc L1/2 -everything below is cauda equina = good site for LP to extract CSF (note: good landmark = iliac crest for L4)
hydrocephalus
-increased CSF in ventricular system -often from blockage in cerebral aqueduct => build up in lateral and 3rd ventricles
reactive microglia
-injury/dz => microglia activation -rapidly proliferates -retracts processes => elongates nuclei -becomes motile, phagocytic phenotype -while reactive secretes toxin that damages neurons
watershed stroke (infarct)
-ischemia/blockages that occur in a watershed -results in unique neuro sx that can be used to dx/localize stroke -increased risk in pts w/ CVD => increase likelihood of clot/reduced flow in these watersheds -can be cortical vs sub-cortical
lenticulostriate (LS) aa.
-long, small diameter vessels -arise from middle cerebral aa. -travel up to deep nuclei of cerebrum -serves basal ganglia and internal capsule -very susceptible to damage from HTN (bc very thin) -end-a. that do NOT have collateral supply -occlusions here=> stereotyped stroke sx (strokes in these aa. are common)
anterior spinal aa.
-longitudinal a. of spinal cord (SC) -emerges from each vertebral a. -meet up and descend within ventral median fissure of SC -supplies anterior 2/3 of SC
spinal cord horns development
-mantle layer grows => alar (dorsal) and basal (ventral) plates divided by sulcus limitans -notochord (ventral to neural tube) releases SHH (sonic hedgehog) inducing ventral neural tube => floor plate -floor plate releases SHH inducing basal plate => ventral horns (motor) -overlying dorsal ectoderm releases BMP (bone morphogenic protein) inducing dorsal neural tube => roof plate -roof plate releases BMP inducing alar plate => dorsal horns (sensory)
homunculus
-mid cerebrum has 2x vertical gyri = motor/sensory homunculi -voluntary motor homunculus = anterior (green highlight) -sensory homunculus = posterior (blue highlight) -each are organization of motor/sensory fibers based on location in gray matter of cortex (note: motor and sensory both have similar organizational patterns) -medial/superior regions = BLE/torso -lateral regions = BUE/face
ischemic stroke (2 types)
-most common type of stroke -occurs when a. to brain is blocked -embolic stroke if clot/fragment forms outside of brain (typically heart/large a.) and moves into an a. supplying brain -thrombotic stroke if blockage originates inside a brain a.
brain 2' vesicle formation
-most rostral and caudal vesicles further subdivide => 2' vesicles -prosencephalon (forebrain) => telencephalon and diencephalon -rhombencephalon (hindbrain) => metencephalon (pons & cerebellum) and myelencephalon (medulla)
inferior sagittal sinus
-near where great cerebral v. enters dura (green arrow) -runs along inferior aspect of falx cerebri
straight sinus
-near where great cerebral v. enters dura (green arrow) -runs along posterior/inferior aspect of falx cerebri
neuropore closure
-neural folds initially meet in cervical region (~day 22) -further fusion occurs bi-directionally (cranial and caudal) -neuropores = openings on either end of neural tube -cranial neuropore closes ~day 25 -caudal neuropore closes ~day 28 -failure of closure => neural tube defects
spinal cord mantle/marginal layer development
-neural tube initially single cell thick -cell proliferate => thick pseudostratified neuroepithelium -neural tube closes then some neuroepithelial cells migrate peripherally becoming neuroblasts => mantle layer => neuronal cell bodies in gray matter -axons emerge from neuroblasts in mantle layer outward => marginal layer => white matter