Mkgrady8 Neuro 1 Blood Supply To The Cns

Front 1

why does the CNS need so much O2 and glucose

Back 1

the CNS stores little O2 and glycogen (only about 2 minute supply of glycogen) which places high constant demand for blood derived O2 and glucose; neurons have an absolute requirement for O2 and glucose, i.e., in essence, the CNS lack anaerobic metabolism; neurons have a high metabolic rate (due to ion pumps); adult CNS is 2% of body weight but at rest uses 20% of body's O2 consumption, 15% of cardiac output, and 25% of glucose consumption; goes through a lot of CSF

Front 2

metabolic rate in gray matter versus white matter

Back 2

4 times higher in gray; density of caps and extent of cerebral blood flow (CBF) is higher in gray that in white

Front 3

what happens to the brains food supply when you are fasting

Back 3

after 2-3 days the liver synthesizes ketone bodies from fatty acid breakdown; the brain uses these ketone bodies as fuel thus cutting its requirement for glucose with the brain getting 30% of its energy from ketone bodies; after 40 days this goes up to 75%; insulin is not required for transport of glucose across the neuron plasma membranes

Front 4

how long can your neurons survive being cut off from blood

Back 4

under normal circumstances the CNS extracts 50% of O2 and 10% of glucose from blood representing a safety factor of 3 times its required O2 and 7 times its required glucose; 10 secs of brain ischemia --> unconsciousness; a few minutes of ischemia leads to necrosis of neural tissue; irreversible brain damage occurs if cerebral blood flow is sustained at less than 15 ml/100gm brain tissue/min; this is 1/3 of the normal CBF

Front 5

how does the brain respond to mild to moderate ischemia

Back 5

insufficient O2 and glucose --> inadequate energy supply; reversible shutdown of neuronal activity; reversible regional brain dysfunction

Front 6

how does the brain respond to severe ischemia

Back 6

inadequate energy supply --> influx of water, Na, and Cl (cytotoxic edema), influx of Ca (irreversible cellular injury), and anaerobic metabolism (minimal capacity, accumulation of lactic acid and H+ compromises neuronal integrity)

Front 7

how does the brain respond to advanced ischemia

Back 7

all of the things from severe ischemia lead to impaired ion pump function --> increased extracellular K+ --> release of glutamate and aspartate which bind to NMDA receptors --> excessive CA2+ influx; influx of Na and Ca --> destruction of cell components, formation of free radicals, eicosanoids, and leukotrienes

Front 8

autoregulation of CBF

Back 8

important concept= THE CNA TAKES A 'ME FIRST' APPROACH TO THE BODY'S BLOOD SUPPLY; mechanisms= 1. response to cerebral perfusion pressure 2. response to metabolites 3. nervous innervation of cerebral vessels 4. vasoactive substances released by astrocytes

Front 9

response to cerebral perfusion pressure

Back 9

cerebral blood vessels dynamically alter their diameter in response to changes in perfusion pressure to help maintain appropriate CBF; these adaptive changes may take up to 60 secs to occur; may become impaired following brain trauma; this is a GLOBAL mechanism i.e. involves blood flow to the entire brain; cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) - intracranial pressure (ICP); ICP is normally 5-15 mm Hg; when CPP increases (usually from increased MAP), cerebral vessels constrict (i.e. cerebral vascular resistance increases); when CPP decreases (due to decreased MAP and/or increased ICP, cerebral vessels dilate thereby helping to keep CBF constant; CBF rate to the CNS is normally 50-65 ml/100gm/min over a wide range of mean arterial blood pressures (50-150 mm Hg), constant CPP is maintained even with chronic hypertension, inadequate CBF can occur with hypotension; when MAP falls below 50 mmHg, O2 extraction increases so ischemia may not occur until MAP approaches 30 mmHg

Front 10

response to metabolites

Back 10

this is a LOCAL, not global, mechanism; cerebral blood vessels dilate in response to increases in CO2 or H+ levels (and to decreases in O2 levels) in brain extracellular fluid; inverse changes have opposite effects; CO2 increases CBF indirectly via H+= CO2 + H2O --> H2CO3 (carbonic anhydrase) --> H+ + HCO3- (bicarbonate ion); increased concentrations of H+ causes a dose dependent vasodilation of cerebral vessels (up to 2 fold increase in local CBF); cerebral hemodynamic changes influenced more by CO2 and H+ than by O2; there is dynamic regional variation of CBF to meet local metabolic demands up t o100% change in local CBF; increased local blood flow associated with increased neuronal activity is largely due to energy requirements of synaptic neurotransmission (arises from net ion fluxes from synaptic neurotransmission being much higher than net ion fluxes form action potentials, ATP is used to pump ions against their concentration gradient)

Front 11

nervous innervation of cerebral arteries

Back 11

this innervation is provided by autonomic and central fibers (e.g. serotonergic); serotonin is a vasoconstrictor for many cerebral vessels; sympathetic innervation is from cervical sympathetic ganglia, has little influence on local blood flow except when arterial pressures become extremely high --> sympathetic innervation constricts larger diameter cerebral arteries to restrict excessive CBF which can help prevent hemorrhage of small diameter arteries

Front 12

vasoactive substances released by astrocytes

Back 12

CNS caps are surrounded by 'endfeet' processes of astrocytes which release nitric oxide and other vasoactive substances to elicit local dilation

Front 13

4 main arterial supplies to the brain

Back 13

2 internal carotid arteries (internal carotid arterial system) for the anterior circulation; 2 vertebral arteries (vertebral-basilar arterial system) for the posterior circulation; about 80% of CNS blood volume is from carotids

Front 14

arterial supply to the spinal cord

Back 14

one anterior spinal artery and 2 posterior spinal arteries; numerous segmental (radicular; medullary) arteries which supplement blood supply in spinal arteries

Front 15

vertebral basilar arterial system: the vertebral arteries where so they come from, where do they do, what are their names

Back 15

vertebral arteries are branches of subclavian arteries; ascend vertically through transverse foramen of C6 to C1 vertebrae; pierce posterior atlanto-occupital membrane, dura, and arachnoid mater, and enter posterior fossa via foramen magnum; source of blood supply to brainstem and cerebellum; gives rise to= POSTERIOR SPINAL ARTERIES (MAY BRANCH OFF PICA) (supplies posterior medulla and posterior spinal cord), ANTERIOR SPINAL ARTERY (supplies medial medulla and anterior spinal cord), and POSTERIOR INFERIOR CEREBELLAR ARTERIES (PICA) (supplies posterior and inferior parts of the cerebellum, lateral medulla, and (along with AICA) supplies the choroid plexus in the 4th ventricle), infarction leads to lateral medullary syndrome)

Front 16

lateral medullary syndrome; medial medullary syndrome

Back 16

lateral medullary syndrome= a result of infarct in the posterior inferior cerebellar arteries (PICA); ipsilateral cerebellar signs, contralateral loss of pain and temp, vestibular signs; PICA supplies the inferior cerebellar peduncle, the vestibular nuclei, and the spinothalamic tract which is why you have these symptoms; medial medullary syndrome= anterior spinal artery supplies the pyramidal tract (descending motor fibers (corticospinal tract) so contralateral motor deficits (this is above the desuccation)), medial lemniscus (ascending somatosensory tract that has already crossed so you will have contralateral sensory deficits), and hypoglossal nucleus (paralysis of the ipsilateral side of the tongue)

Front 17

vertebral basilar arterial system: basilar artery

Back 17

2 vertebral arteries join at caudal pons to form basilar artery on ventral surface of pons; basilar artery terminates at midbrain as left and right posterior cerebral arteries which supply caudal regions of cerebral hemispheres; ANTERIOR INFERIOR CEREBELLAR ARTERIES (AICA)= supplies anterior and inferior parts of cerebellum; LABYRINTHINE (INTERNAL ACOUSTIC) ARTERIES= supplies inner and middle ear (usually branches off the AICA, can also originate from the basilar artery), infarction leads to impaired auditory and vestibular function; PONTINE ARTERIES= supplies the pons, paramedian and short/long circumferential pontine arteries; SUPERIOR CEREBELLAR ARTERIES= supplies superior portion of the cerebellum and rostral pons/caudal midbrain, aneurysm leads to compression of cranial nerve III (extraocular muscle palsy and dilated pupil)

Front 18

relation of AICA and facial nerve

Back 18

AICA wraps around VII so a vasospasm can induce Bell's palsy (disruption of neuronal signals through VII, ipsilateral paralysis of the face)

Front 19

blood supply to medulla

Back 19

vertebral artery; anterior and posterior spinal arteries; PICA

Front 20

blood supply to pons

Back 20

pontine arteries from basilar artery; AICA and superior cerebellar artery

Front 21

blood supply to cerebelum

Back 21

cerebellar arteries

Front 22

blood supply to midbrain

Back 22

branches of posterior cerebral artery, superior cerebellar artery, and basilar artery

Front 23

vertebral-basilar arterial system: posterior cerebral artery

Back 23

basilar artery terminates as left and right POSTERIOR CEREBRAL ARTERY (PCA); branches of PCA supply occipital lobes (think vision for deficits) and inferior/medial aspect of temporal lobe

Front 24

internal carotid arterial system

Back 24

internal carotid arterial system supplies that part of the brain (anterior 2/3 of brain) not supplied by the vertebral-basilar system; left common carotid artery arises directly from aortic arch; right common carotid artery arises from brachiocephalic artery; internal carotid arteries enter cranium via carotid canal of temporal bone and travel to middle cranial fossa through superior part of the cavernous sinus

Front 25

branches of the internal carotid artery

Back 25

ophthalmic artery, anterior choroidal artery, posterior communicating artery; terminates by bifurcating into 2 major paired cerebral arteries= anterior cerebral artery and middle cerebral artery

Front 26

ophthalmic artery: supplies what, interruption of blood causes what

Back 26

supplies retina and optic nerve (think blindness in associated eye for deficits); gives rise to central artery of the retina; there are extracranial-intracranial anastomoses between ophthalmic artery and external carotid artery; interruption of blood supply leads to sudden loss blindness in affected eye

Front 27

anterior choroidal artery: supplies what

Back 27

optic tract, choroid plexus in the lateral ventricles (along with the posterior choroidal artery from the basilar artery), cerebral peduncles, posterior limb of internal capsule, globus pallidus (caudal part) (part of basal ganglia), lateral geniculate nucleus (part of thalamus concerned with vision) and other deep forebrain and midbrain structures (hippocampal formation, amygdala, red nucleus, others)

Front 28

posterior communicating artery does what

Back 28

communicates with posterior cerebral artery and is part of the circle of willis

Front 29

anterior cerebral artery: supplies what

Back 29

medial aspect of frontal and parietal lobes

Front 30

middle cerebral artery: supplies what

Back 30

often considered to be a continuation of internal carotid (it's the fattest and straight off from internal carotid, this also means that a thrombus is way more likely to take this path than to take anterior or posterior cerebral); branches supply insula and lateral surface of cerebral hemisphere (frontal, parietal, and temporal)

Front 31

what are the branches of the cerebral arteries and what do they supply

Back 31

the 3 paired cerebral arteries (anterior, middle, and posterior) have 2 general categories of branches= cortical (circumferential) branches that innervate the more superficial aspects of the cerebral hemispheres and the central (ganglionic branches) that innervate the deeper structures of the brain (central branches also arise from the circle of willis)

Front 32

arteries on the surface of the brain and spinal cord travel in what

Back 32

the subarachnoid space

Front 33

central (ganglionic branches) arise from what, supply what, divide into what

Back 33

arise from anterior, middle, and posterior cerebral arteries to supply deep forebrain structures such as diencephalon, basal ganglia, and internal capsule; medial striate arteries (largest= recurrent artery of Heubner) branch of ANTERIOR cerebral artery that supplies parts of caudate, putamen, and medial parts of anterior limb of internal capsule; lateral striate (lenticulostriate) arteries branch of MIDDLE cerebral artery that supplies internal capsule (posterior limb, genu, lateral parts of anterior limb), globus pallidus, and putamen, these terminal arteries are especially susceptible to damage from hypertension; these striate arteries enter base of forebrain at anterior perforated substance

Front 34

clinical application: capsular hemiplegia

Back 34

ipsilateral descending fibers from motor cortical areas to brainstem and spinal cord travel through the posterior limb of internal capsule; occlusion of LATERAL STRIATE arteries and/or ANTERIOR CHOROIDAL artery can damage posterior limb of internal capsule resulting in contralateral profound CAPSULAR HEMIPLEGIA (weakness/impaired motor control of contralateral body) and contralateral somatosensory loss for body; if genu is damaged, contralateral side of face is involved (lower half for motor, all for somatosensory); due to a lesion of internal capsule posterior limb; somatotopy of ascending somatosensory fibers in internal capsule is similar to that of descending motor fibers

Front 35

posterior limb of internal capsule supplied by

Back 35

most of the posterior limb is supplied by LATERAL STRIATE ARTERIES; caudal portions supplied by ANTERIOR CHOROIDAL ARTERY

Front 36

branches of cerebral arteries

Back 36

basilar, PCA, VA, M1, M2, A1, A2, ICA

Front 37

ACA branches

Back 37

A1, A2, A3; the lower the number the more proximal it is; the more proximal a hemorrhage or clot the more damaging it will be

Front 38

A1: extends from where to where, what comes off it

Back 38

extends from internal carotid artery to the anterior communicating artery; most of the small medial lenticulostriate arteries arise from A1

Front 39

A2: extends from where to where, gives rise to what

Back 39

extends from A1 to bifurcation that forms the pericallosal and callosomarginal arteries; gives rise to recurrent artery of Heubner (90% from A2, 10% from A1) and, more distally, to orbitofrontal artery and frontopolar artery

Front 40

A3: extends from where to where, gives rise to what

Back 40

also termed the pericallosal artery; this is the main terminal branch of the ACA; gives rise to the callosal marginal artery (present distinctly about 60% of the time)

Front 41

MCA branches

Back 41

M1, M2, M3, M4; same numbering as before

Front 42

M1: gives rise to what and extends to what

Back 42

this proximal unbranched segment gives rise to the lateral lenticulostriate arteries, and extends until the beginning of the insula

Front 43

M2: where is it

Back 43

within insula, after first branching of MCA

Front 44

M3: extends from what to what

Back 44

extends laterally from the insula to the lateral fissure

Front 45

M4: extends from what to what

Back 45

extends in all directions distal to the lateral fissure with branches traveling in sulci to supply the lateral aspects of the frontal and parietal lobes; so every MCA you see coming out of the lateral fissure are M4 and the ones going superior are called M4 superior and the ones going inferior are called M4 inferior; Wernicke (language center on the superior temporal gyrus) is on the left side of the brain and is supplied by the M4 inferior branches; Brockas (language center) is also on the left side of the brain and is supplied by the M4 superior branches; global aphasia if there is a more proximal blockage that nocks out both superior and inferior M4s

Front 46

PCA branches

Back 46

P1, P2, P3, P4

Front 47

P1: extends from what to what

Back 47

from the basilar artery to the posterior communicating artery

Front 48

P2: extends from what to what, supplies what

Back 48

extends from P1 to the posterior midbrain; supplies brainstem and thalamus

Front 49

P3: extends from what to what

Back 49

the posterior aspect of midbrain to the calcarine fissure

Front 50

P4: extends from what to what

Back 50

termination fo PCA in calcarine sulcus (gives rise to calcarine artery)

Front 51

anastomoses between internal carotid and vertebral-basilar systems: why are they there, what are the 2 main ones

Back 51

serve to help equalize blood pressure in internal carotid and vertebral-basilar artery systems and between left and right hemispheres; can provide alternative partial sources of blood in event of an occluded artery; 2 major sites of anastomoses between internal carotid and vertebral-basilar systems= CIRCLE OF WILLIS AND WATERSHED ZONES

Front 52

circle of willis: teritory

Back 52

encircles the optic chiasm and pit on the ventral surface of the diencephalon; connects the anterior cerebral arteries, anterior communicating artery, internal carotid arteries, posterior communicating arteries, posterior cerebral arteries

Front 53

what happens in an anterior communicating artery aneurysm

Back 53

bitemporal hemianopsia from damage to optic chiasm

Front 54

what happens in posterior comminucating artery aneurysm (posterior)

Back 54

cranial nerve III palsy

Front 55

watershed zones: where are they, what are they, what can happen here

Back 55

on lateral surface of cerebral cortex at the edge of the territories supplied by cerebral arteries (so there is the ACA-MCA watershed (trunk part of motor center), the MCA-PCA watershed, and the ACA-PCA watershed) there is relatively low arterial blood pressure; this is a region of increased susceptibility to ischemia with systemic hypotension (of heart attack), resulting in borderzone or watershed infarcts

Front 56

intracranial arterial collateral circulation

Back 56

these are minor connections and the number and location vary from person to person; if a person has more of these they are less prone to the negative effects of a stroke

Front 57

meningeal arteries (what supplies the meninges)

Back 57

supply the dura; most blood supply is from arteries that do not perfuse the CNS; the primary blood source is the MIDDLE MENINGEAL ARTERY a branch of the maxillary artery; unlikely to hemorrhage unless there is skull trauma (like a skull fracture) because the dura is super strong; these are in the epidural space so they would cause an epidermal hematoma

Front 58

extracranial arterial collateral circulation

Back 58

just like intracranial, these are relatively minor and vary from person to person

Front 59

arteries of the spinal cord: descending vertebral arteries

Back 59

ANTERIOR SPINAL ARTERY= each vertebral artery gives rise to anterior spinal branch that merge to form anterior spinal artery, runs length of spinal cord along anterior median fissure to supply anterior 2/3 of spinal cord (so anterior and lateral areas so motor and pain); POSTERIOR SPINAL ARTERIES= each vertebral artery (or PICA) gives rise to one posterior spinal artery, runs length of the spinal cord in dorsolateral sulci to supply posterior 1/3 of spinal cord (including the dorsal column and the dorsal horn) (what info is in the dorsal column? fine sensory and proprioception); the vasocorona is a network of anastomoses between the anterior and posteriors

Front 60

blood supply in vasocorona may be sufficient to

Back 60

support lateral white matter if spinal artery becomes occluded so much less likely to have a CVA in the spinal cord (lots of redundant blood sources) than in the brain (very few)

Front 61

arteries of spinal cord: segmental (radicular, medullary) arteries originate from where, go where, divide into what, supply what

Back 61

originate from numerous peripheral arteries (vertebral, deep cervical, ascending cervical, posterior intercostal, DESCENDING AORTA lumbar, and lateral sacral arteries); pass through intervertebral foramina and divide into anterior and posterior radicular arteries in subarachnoid space near the ventral (anterior) and dorsal (posterior) roots; they supply vertebrae, spinal meninges, and spinal arteries

Front 62

arteries of spinal cord: segmental (radicular, medullary) arteries where and how many, what is the big one to know

Back 62

typically 1-2 cervical, 2-3 thoracic, and 1-2 lumbar segmental arteries; ARTERY OF ADAMKIEWICZ (from intercostal or lumbar artery) also known as the ARTERY OF THE LUMBAR ENLARGEMENT is a large anterior radicular artery that is the major source of blood supply to inferior spinal cord; artery of adamkiewicz is usually on left side, entry into spinal column occurs at variable levels (mid thoracic to upper lumbar vertebrae)

Front 63

source of blood supply to cervical levels

Back 63

from the anterior and posterior spinal arteries; the blood supply from the vertebral arteries to the spinal arteries is sufficient to only supply cervical levels

Front 64

source of blood supply to the thoracic, lumbar, and sacral levels

Back 64

segmental arteries that anastomose with the spinal arteries

Front 65

clinical point: spinal cord vascular assidents

Back 65

very rare because lots of collateral and redundant sources of blood supply in spinal cord

Front 66

collateral circulation and areas of susceptibility in spinal cord

Back 66

most levels have extensive collateral circulation of blood supply but some levels have little collateral circulation so they are susceptible to infarct following occlusion of supplying segmental artery; T1 to T4 (esp T4), L1; this is why you can have paraplegia without damage to the spinal cord (blood supply has been cut off)

Front 67

venous drainage of brain

Back 67

is indirect; caps empty into small veins located either deep to the pia mater of in the subarachnoid space; cerebral veins do not travel adjacent to arteries; veins in the CNS drain either directly into the systemic circulation (spinal cord and medulla) or into dural sinuses (cerebral areas) that in turn empty into the internal jugular veins; sinuses are encased in dura

Front 68

2 groups of veins drain into dural sinuses

Back 68

superficial cerebral veins= drain external structures like cerebral cortex, brainstem, cerebellum, and feed into superior sagittal sinus; deep cerebral veins= drain internal structures like basal ganglia, diencephalon, internal capsule, and eventually feed into straight (rectus) sinus

Front 69

major route of venous drainage of brain

Back 69

flow of venous blood from dural sinuses to internal jugular vein; inferior sagittal sinus and the great cerebral vein of Galen --> straight (rectus) sinus; at occipital pole the superior sagittal sinus joins straight and occipital sinuses at CONFLUENCE OF SINUSES --> left and right transverse sinuses --> left and right sigmoid sinuses --> left and right internal jugular veins

Front 70

minor route of venous drainage of brain

Back 70

cavernous, anterior intercavernous and posterior intercavernous sinuses from which arises superior petrosal sinus which drains into the transverse sinus and the inferior petrosal sinus which drains into the internal jugular veins; HE SAID WE DIDN'T NEED TO KNOW THESE; JUST KNOW THAT EVERYTHING DRAINS INTO THE INTERNAL JUGULAR

Front 71

dural sinuses can also receive blood from face and scalp via

Back 71

EMISSARY VEINS which connect intracranial venous sinuses with veins outside the cranium; they are valveless veins that permit blood to flow in both ways (usually flows away from the brain); these are possible routes of infection of the meninges since bac infections of the nose and upper lip (triangle of danger) can be transmitted by venous blood into cavernous sinus via the superior inferior ophthalmic veins

Front 72

venous drainage of spinal cord

Back 72

spinal cord venous blood drains directly to systemic circulation via numerous irregular plexiform channels (i.e. no dural sinuses); these channels are drained by radicular veins --> epidural venous plexuses (located between dura and vertebral periosteum) --> external venous plexus and other systemic veins; HE DIDN'T NAME THESE VEINS JUST SAID THERE ARE MANY ROUTES AND THAT THEY FOLLOW SIMILAR PATHS AS THE ARTERIES

Front 73

characteristics of brain veins: distribution of arteries vs veins, valves, venous routes

Back 73

distribution of veins differs from that of arteries; there are no valves in cerebral veins or dural sinuses; venous drainage routes have extensive anastomoses with each other and for this reason occlusion of cerebral veins usually has no clinical consequences

Front 74

characteristics of spinal cord veins: distribution of arteries vs veins, valves

Back 74

distribution is similar to that of spinal arteries; no valves so the direction of venous blood flow between the spinal cord and periphery depends on differences in blood pressure; this is a common route of metastasis from the periphery to the CNS

Front 75

clinical correlations localization of function: which cerebral arteries supply broca's area?

Back 75

left superior M4

Front 76

clinical correlations localization of function: which cerebral arteries supply the primary motor cortex? contralateral, ipsilateral, or bilateral deficits with unilateral lesion?

Back 76

upper half of the body is more lateral precentral gyrus and that is supplied by the superior M4; lower half of the body (trunk, leg, foot) is more medial precental gyrus and that is supplied by anterior cerebral artery; depends on the place but you got this

Front 77

clinical correlations localization of function: which cerebral arteries supply the primary somatic sensory cortex? contralateral, ipsilateral, or bilateral deficits with unilateral lesion?

Back 77

upper half of the body is more lateral postcentral gyrus and that is supplied by the superior M4; lower half of the body (trunk, leg foot) is more medial postcental gyrus and that is supplied by anterior cerebral artery; so if there is a block of left M2 then symptoms= contralateral (right side) motor and sensory deficits to the upper body, also have lost broca and wernicke so global aphagia

Front 78

clinical correlations localization of function: which cerebral arteries supply wernicke's area? which cerebral arteries supply the primary auditory cortex?

Back 78

wernicke's= left inferior M4; primary auditory cortex (areas 41, 42)= both inferior M4s

Front 79

clinical correlations localization of function: which cerebral arteries supply the primary visual cortex?

Back 79

posterior cerebral artery

Front 80

arteriovenous malformation

Back 80

developmental disorder where there is mixing of the venous and arterial blood supply; usually the tangled mass of blood vessels in the brain is asymptomatic; it can grow and then cause symptoms which depend on the location but are usually headache and epilepsy

Front 81

cerebral venous sinus thrombosis: is what, how do you see it, symptoms

Back 81

a rare form of CVA involving a thrombosis of the dural venous sinuses; incidence= 7/million annually (very rare); first yr of life; 3rd decade for females; mortality= untreated is 30-50% and treated is 5-20%, 40% of children have long term impairment; use CT and MRI with contrast to image the thrombosis; symptoms= headache, signs of CVA (not always unilateral), elevated intracranial pressure/papilledema (decreased CSF resorption can result from sinus thrombosis --> increase in intracranial pressure), seizures; a sinus thrombosis may break off to cause a pulmonary embolism (10%)

Front 82

cerebral venous sinus thrombosis: risk factors

Back 82

thrombophilia, nephrotic syndrome, chronic inflammatory diseases, pregnancy and postpartum, meningitis, dehydration, trauma to dural sinuses, medical procedures to head/neck

Front 83

increases in ICP: due to what

Back 83

volume of intracranial space is constant once cranial sutures fuse early in infancy; by volume intracranial contents are= neural tissue and extracellular fluids (80%), CSF (8%), blood (12%), once cranial vault volume is fixed if any of these intracranial constituents increases in volume it will do so at the expense of the other 2 (this concept is called the MONRO-KELLIE DOCTRINE); in addition there will be a concomitant increase in intracranial pressure; edema, tumors, aneurysms, hematomas, and hydrocephalus; valsalva maneuver or a sneeze causes a transient increase in ICP; ICP is normally 5-15 mm Hg

Front 84

medical dangers of increase in ICP

Back 84

1. may cause PHYSICAL TRAUMA to neural tissue through compression (the cerebellum may herniate into the foramen magnum or forebrain structures may herniate into the tentorial incisure (tentorial notch); 2. likely to DECREASE BLOOD PERFUSION OF THE BRAIN, small increases in ICP may exceed venous blood pressure and cause collapse of cerebral veins which will produce vascular congestion and further increase in ICP, this may lead to low levels of cerebral perfusion pressure (CPP) resulting in ischemia and necrosis (CPP=MAP-ICP so when ICP exceeds MAP there is no cerebral blood flow and brain ischemia occurs)

Front 85

this reduction in CPP will initiate a brain mediated ischemic response which is

Back 85

activation of a vasomotor center in the reticular formation of medulla and caudal pons --> activates preganglionic sympathetic neurons int he spinal cord --> raises MAP above ICP in order to reinstate perfusion of the brain; this response is called the CUSHING REACTION (or reflex)

Front 86

associated with the cushing reaction is the CUSHING TRIAD which consists of

Back 86

1. systemic hypertension with an increase in pulse pressure (due to cushing reaction) 2. bradycardia (due to baroreceptor reflex) 3. respiratory irregularities (brainstem is not getting enough blood); cushing triad is a late sign of increased ICP

Front 87

common symptoms and signs of elevated intracranial pressure

Back 87

headache (worse in am due to recumbent position in sleeping reducing gravity of edema), altered mental status, nausea and vomiting, papilledema, visual loss (compression of axons and decreased venous return=increased blind spot of unilateral blindness), diplopia (from downward traction on CN6=uni or bi CN6 palsy), cushing's triad

Front 88

types of CVA

Back 88

thrombotic stroke= blood clot (thrombus) blocks flow of blood in brain; embolic stroke= fatty plaque or blood clot (embolism) breaks away and flows to brain where it blocks an artery; cerebral hemorrhage= break in blood vessel (aneurysm) in brain

Front 89

stroke can lead to what

Back 89

infarction (ischemic) (85%) which is due to cerebrovascular disease or cardiogenic embolism; hemorrhage (15%) which can be intracerebral or subarachnoid

Front 90

evolution of cerebral infarct

Back 90

core of the area affected will die (ischemic necrosis) within a matter of minutes; more peripheral to it called the penumbra zone of the stoke can be saved if there is reperfusion within a few hrs; core expands out

Front 91

recovery of function

Back 91

damage to CNS is essentially irreversibly with current medical technologies due to innate mechanisms that inhibit developmentally mature neurons from dividing and inhibit axons from re establishing synaptic connections (e.g. inhibition of growth cones, absence of tropic factors); but the surviving brain is plastic and, depending on the nature of the lesion, has the potential for varying degrees of recovery of function via a variety of mechanisms and this is where rehab and therapies come into play (physical therapy, occupational therapy, speech therapy)

Front 92

the 3 compartments in the CSF

Back 92

neural tissue, blood, and CSF; postnatally no physical barriers between neural tissue and CSF (i.e. between neural tissue and the ventricular walls) these areas exchange fluid and macromolecules via diffusion; there are physical barriers between neural tissue and blood and between CSF and blood; the BBB is a barrier that hinders the free exchange of many substances in blood with extracellular fluid of CNS parenchyma

Front 93

BBB and the immune system

Back 93

under normal physiological conditions the immune system does not have access to the CNS as a result the CNS is said to be IMMUNOLOGICALLY PRIVILEGED; microglia play an immunological role within the CNS; in immunological diseases affecting the CNS the immune system breaches the BBB

Front 94

4 functions of BBB

Back 94

1. isolated and protects CNS neurons from neuroactive and neurotoxic substances in blood (such as neurotransmitters and iron) 2. barrier to diffusion of proteins and most water soluble drugs 3. freely permeable to gases such as CO2 and O2 and to most lipid soluble molecules (including alcohol and barbiturates) 4. glucose, certain aas, Na+, and nucleosides are actively transported across the BBB by specific carrier systems

Front 95

anatomical basis of BBB

Back 95

capillary endothelium; tight junctions between cap endothelial cells in the CNS thereby hindering the exchange of most substances; CNS caps are not fenestrated (except in the circumventricular regions) and have little pinocytotic capacity; estimated total length of brain caps= 650 km; estimated surface area= 12 m^2; tight junctions between cell layers of arachnoid mater creates a barrier between the subarachnoid space and dura mater

Front 96

'designated' breches in BBB

Back 96

some regions of the CNS need to monitor or secrete agents in the blood and a BBB would prevent this function; these regions are near the ventricles and are called the CIRCUMVENTRICULAR ORGANS; their caps do not have the anatomical properties of a BBB; a common feature of these areas is that they are highly vascularized; they stick out of the BBB; they monitor things like toxins and hormones

Front 97

blood-CSF barrier

Back 97

the blood-CSF barrier occurs within the extensively vascularized choroid plexus of the ventricles (only 1/5000 the surface area of the BBB); anatomical basis for the barrier is tight junctions between choroidal epi cells that line the choroid plexus; there are no tight junctions between the cuboidal ependymal cells of ventricular walls so there is no CSF-brain barrier

Front 98

disruption to integrity of BBB

Back 98

trauma (e.g. open head wound); compounds that alter osmotic pressure (eg intravenous mannitol), causing the BBB endothelial cells to transiently and reversibly shrink forming intercellular breaches in the BBB; inflammatory reactions (viral, e.g. HIV, and autoimmune responses e.g. multiple sclerosis)

Front 99

back doors around BBB

Back 99

bac can gain access to the CNS via valveless veins (e.g. spinal cord, triangle of danger in face); some viruses (e.g. herpes zoster) enter CNS via retrograde transport by somatosensory axons