neuro week 4

tonsillar herniation

"Coning": cerebellar tonsils herniate through the foramen magnum

TBI epidemiology

1.7 million 75% mild young males vehicle collisions, falls, violence, sports

cortical/external borderzone

ACA/MCA MCA/PCA

Balint syndrome (simultagnosia)

Bilateral lesion of Parietal lobe. Inability to perceive more than one object at a time. (cant recognize a bunch of dots making a number) Spatial localization reduced - hard time reaching for objects (optic ataxia) Don't move eyes much when focusing attention. hard time moving eyes to focus(oculomotor apraxia)

central herniation

Downward shift of the diencephalon through the tentorial notch/incisura

junctional adhesion molecules

Ig type

secondary TBI injury

NT release- ion channel activation, astrocyte swelling, edema Free-radical generation calcium mediated damage gene activation-caspases mitochondrial dysfunction inflammation mechanisms differ by type of primary injury

Arteriolosclerosis

Narrowing of small arterioles more in white matter thickened and hyalinized(pink,glassy) vessel walls widened perivascular spaces htn, diabetes are risk factors

communicating arteries

anterior- connects the anterior cerebral arteries posterior- ICA with posterior cerebral artery

1 month mortality of strokes

ischemic-5% hemorrhagic- 50%(half in first 2 days) SAH- 10-20% in first dfew days

Man in a Barrel Syndrome

watershed infarct

Blood-CSF barrier

*fenestrated endothelium* *thin basement membrane* single layer of cuboidal epithelial cells next to choroid plexus epithelium

Perimesencephalic SAH

-Nonaneurysmal SAH -hemorrhage confined to area around midbrain and pons(in front) -no definable cause based on angiography

Romberg test

-ask client to stand with feet at comfortable distance apart, arms at sides, and eyes closed -expected finding: client should be able to stand with minimal swaying for at least 5 seconds

Moyamoya

-progressive stenosis of intracranial ICA with proliferation of lenticulostriate collaterals -puff of smoke appearance on angiography -FLAIR ivy sign -child --> sickle cell, watershed infarct -adults --> bleed, aneurysm formation in posterior circulation -NF, Down's sx, prior radiation

ICP management teirs

1- head position, sedation, CSF drainage, 2- mannitol, hypertonic saline, hypothernia, paralysis 3- pentobarbital, decompressive craniectomy

SAH risk factors

1/3 age family Hx connective tissue disease, PCKD coarctation of the aorta 2/3 cigarettes HTN ETOH Cocaine HTN nost strongly correlated w/ rupture, correlated w/ development

pts post stroke

10% get worse 1% have recurrent stroke 34% silent ischemia on MRI

glasfow coma rankings

13-14 mild 9-12- moderate severe- 8 or less

IMPORTANCE OF tia

15% OF STROKES preceded by TIA dangerous in old, diabetic, HTN unilateral weakness lasting more than 1hr

edema peak in stroke

2-4 days starts after a couple hours

% of clots of cardiac origin

20% tend to be large or multifocal

severe TBI outcomes

20% mortality little improvement with time impaired cognition and function

neurological deficts begin at

20ml per 100g a min

CSF production

3-4x turnover a day 70% choroid plexus interstitial- virchow Robin spaces ependemya

CSF composition

50/50 intercranial and spinal 0-5 cells/MM-no RBC/PMN constant ion composition- hypertonic

ICP goals

<22 mmHG CPP- 60-70

cavernous sinus

A sinus containing venous blood located on each side of the body of the sphenoid bone, near the base of the brain, behind the bridge of the nose

superior sagittal sinus

A venous sinus located in the midline just dorsal to the corpus callosum, between the two cerebral hemispheres.

subventricular stem cells

A- neuroblasts B- slow dividing stem cells B1. subependymal. contact CSF via primary cilium B2 C- fast dividing transit amplifying stem cells

decreasers of CSF production

ANP, AVP, androgenics, acetazolamide, furosemide.,

Right MCA stroke(non-dominant)

Apraxia -idiomotor -eyelid -ideational(cant draw, cant use pen) Hemineglect -visual(wont acknowledge someone standing in that left visual field) -sensory(touch both sides, only recognize right sided touch)

gemistocytes

Astrocytes that respond to injury by increasing their cytoplasm. They may also become multinucleated.

Left superior MCA stroke

Brocas area -expressive aphasia FEF -ipsilateral(left) gaze deviation PMC/PSC -contralateral (right) hemiplegia & sensation loss

CPP formula

CPP = MAP - ICP approximates CBF

SAH diagnosis

CT if shortly after onset\ falls to 50%sensitivity at 7 days Lumbar puncture -xanthochromia at 12 hours to 2 weeks elevated RBC count in last tube angiography after confirmation(80-85%SUCCESS)

epidural hematoma radiography

CT- biconvex, lenticular/lentiform, hyperdense clot constricted by suture lines

CT vs MRI in stroke

CT- subtle and hours DWMRI- minutes. restricted diffusion of water

delayed cerebral ischemia treatment

Ca channel blocker (nimodipine)- prophylaxis hemodynamic therapy- after aneurism secured angioplasty intraarterial vasodilators

Amyloid angiopathy cerebral hemorrhage

Can cause intracranial, frequently lobar(esp posterior), hemorrhage. Amyloid deposits within media and adventitia of medium size and small cortical arteries. Not associated with systemic vascular amyloidosis. Affects elderly pften w/ dementia.

cerebral herniation

Central uncal subfalcine tonsillar

Lipohyalinosis

Defn: Process of lipids coating the inside of small arteries, gradually narrowing the lumen. disorganized, thickened tissue. fat deposition in the wall causes lacunar strokes HTN/diabetes

hydrocephalus management

Diamox(acetazolamide) lasix(furosemide) osmotic agents -limited effect surgical - shunting (ventriculor or lumbar) -3rd ventriculostomy -preferred usually need surgery

arachnoid granulations

Extensions of the arachnoid mater int dural sinuses, that allow excess CSF to be absorbed by the dural sinuses.

tenecteplase

Fibrinolytic better tpa

most common site of selective neuronal necrosis

Hippocampal CA1

Hypertensive intracerebral hemorrhage

Hyalinization of small vessels/fibrinoid necrosis/microanyeurisms Basal ganglia(putamen), thalamus, pons, cerebellum, lobar white mater - frequent locations - supplied by small penetrating arteries w/o collaterals associated with charcot-bouchard aneurisms

Common sites of atherosclerosis

ICA origin carotid siphon(bend in cavernous sinus) distal vertebral/proximal to mid bassilar

rebleeding risk

ICH 1/3 SAH- common w/o intervention

TBI management

ICP Monro-Kellie CBF/PP O2 negative predictors -SBP<90 age>40 PaO2<60 preserve CBF/MAP, minimize ICP

Monro-Kelly doctrine

ICV= Brain + Blood + CSF volume is fixed

no benefit in stroke

IV heparin steroids neuroprotective agents lowering BP

ICP management

MAss lesion- surgical removal Monro-Kellie -CSF drainage -elevate head (increase venous return) -hyperventilate (vasoconstriction, short term) hyperosmolar therapy -mannitol -hypertonic saline decompressive craniectomy reduce brain metabolism -drugs, EEG hypothermia

ICA syndrome

MCA+ ACA +(PCA-5%) opthalmic artery- amaurosis fugax- transient loss of vision of one eye

active transport in BBB

MDR family removes toxins

mechanism of primary injury in tbi

Macroscopic- shearing of WM tracts contusion intracranial hematoma swelling Microscopic -small vessel rupture cell membrane microporation ion channel dysfunction

Duret hemorrhage

Midline hematoma within tegmentum of rostral pons and midbrai. Associated with descending transtentorial herniation. Due to stretching or tearing of penetrating arteries. may be from herniation

berry aneurysm

Most often found in the circle of Willis in the brain circulation Consists of a small, spherical vessel dilation

Malignant Brain Edema Syndrome

Occurs in young population w/in minutes to hours of a head injury Caused by intracranial clot resulting in diffuse brain swelling w/ little or no brain injury Swelling is the result of hyperemia or vascular engorgement - results in increased pressure

ACA stroke

PMC/PSC-Lower extremities more affected than U.E/Face. Contralateral hemiplegia and sensory loss Paracentral lobule(sensory &motor) -urinary(more)/fecal incontinence(less) Prefrontal cortex/Anterior Cingulate cortex -abulia(decrease in motivation/willingness to do anything. delay or ignore commands)-lose one side -akinetic mutism(lose both/bilateral ACA) Anterior/superior frontal lobe(dominant side) -transcortical motor aphasia utilization behavior(compulsion to use object placed in front of them)

glia limitans

Physical barrier between nervous tissue and pia mater composed of astrocytic processes

posterior circulation stroke areas

Primary visual cortex/association area -contralateral homonymous hemianopia -alexia w/o agraphia -anomia Brainstem(impaired consciousness) thalamus- cognition/memory(right-neglect, left-apasia) -contralateral sensory loss/pain, decreased arousal(VPL/VPM) -Lateral geniculate nucleus -homonymous hemianopsia Left- temporal- memory peduncular hallucinosis

SAH complications

Rebeleeding - 24-48hrs (strop anticoag) -sudden deterioration, raise BP, unresponsive vasospasm- 3-10 days (ca channel blockers, balloon dilation, arterial vasodilators) hydrocephalus- bleed into ventricles, lethargy(extraventricular drain)- global deterioration, sleepy hyponatremia/electrolyte imbalance(isotonic/hypertonic saline)-global deterioration. dont treat w/ fluid restriction delayed cerebral ischemia- focal neurologic deficit. usually days after. ~4

gross signs of recent cerebral infarction

Softness(edema) discoloration, pale or hemorrhagic

cerebellar blood supply

Superior cerebellar artery Anterior inferior cerebellar artery Posterior inferior cerebellar artery off the vertebral, arteries

middle cerebral artery

Supplies entire lateral cortex Largest branch of internal carotid artery down the silvian fissure/lateral sulcus to supply latera frontal, temporal and pariatal lobes and basal ganglia

anterior cerebral artery

The arteries that supply oxygen to most medial portions of frontal lobes and superior medial parietal lobes; strokes here can affect leg use

Amaurosis fugax

Transient partial or complete loss of vision in one eye. curtian up and down

uncal herniation

Uncus of the temporal lobe is displaced downward Creates pressure on CN III, posterior cerebral artery, and RAS(fixed and dilated pupil). can push on corticospinal tracts- contralateral hemiparesis Mesial temporal structures (uncus, ± hippocampal gyrus) herniate over the tentorial edge

MCA-PCA watershed infarct

Vision -prosopagnosia(visual association) -Balint syndrome -optic ataxia

brocas area receives input from

Wernicke's and Anterior/Superior frontal lobe.

germinal matrix

a group of thin-walled blood vessels and cells within the subependymal layer of the fetal brain responsible for brain cell migration during fetal development

temporary loss of unilateral vision due to blockage

amaurosis fugax

Subhyaloid hemorrhage

an intraocular collection of blood that remains contained in a self-created, previously nonexistent space, usually between the posterior limiting layer of the vitreous and the retina.

secondary stroke prevention

antiplatelet therapy anti-HTN statins oral anticoag if afib endarterectomy if severe ICA stenosis smoking cessation

CSF clearance

arachnoid granulations and nerve sheaths

penumbra

area of brain tissue surrounding infarct that is ischemic but can be rescued if bloodflow is promptly restored.

regulators of cerebral blood flow

arterial CO2 Arterial O2 neuronal activity

mediators of BBB opening

astrocytes neurons bradykinan, 5-HT, thrombin, free radicles

return to play

asymptomatic at rest and w/ exertion cognitive baseline rehab stage 1-6

gross signs of remote infaction

atrophy cavitation tract degeneration gliotic rim hydrocephalous ex vacuo (compensatory ventricle enlargement)

genetic defects in cilia

bardet-Biedle (hydrocephalus) Joubert (cerebellar malformation) PCKD

pediatric germinal matrix and intraventricular hemorrhage

before 29 weeks fragile microvasculature poor hemostatic capability impaired autoregulation first few days of life- nonspecific findings dx- ultrasound

driver of ionic balance in CSF

bicarb from carbonic anhydrase

Xanthocromia

bilirubin in csf

Coup-contrecoup

blow to the head that causes a contusion at site of impact(coup) and hits brain to opposite side of head (contrecoup)

Transient Ischemic Attack (TIA)

brief episode of loss of blood flow to the brain, usually caused by a partial occlusion that results in temporary neurologic deficit (impairment); arbitrary timeline of less than 24 hrs. most less than an hour NO EVIDENCE OF ACUTE INFARCTION

adherens junction proteins

cadherin catenin bind to actin

inferior MCA stroke

can affect Wernicke's area (left) -receptive/fluent aphasia optic radiations -homonymous hemianopsia

acetazolamide inhibits

carbonic anhydrase

Acetazolamide

carbonic anhydrase inhibitor

Charcot-Bouchard aneurysms

caused by hyaline arteriosclerosis; can result in intracerebral hemorrhagic stroke A Charcot-Bouchard aneurysm is a rare brain microaneurysm, a bulge in the wall of a tiny (less than 300 micrometers in diameter) artery. It most frequently affects the lenticulostriate branches of the middle cerebral artery, which supply blood to the basal ganglia, thalamus, pons, and cerebellum in the brain associated w/ hypertensive hemorrage

autoregulation

changes in cerebral perfusion pressure from 60-150 have little effect on cerebral blood flow vessels will dilate until maximum dilation. then if MAP continues to drop they can collapse DILATION

BBB present except

choroid plexus, circumventricle organs (pineal gland)

tight junctions proteins

claudin and occludin, zonulla occuldin attach to actin

ICH enlargement

clinical deterioration poor outcome 1/3 of pts usually happens in 1st 12 hours

rim on CT from hemmorage

clot retraction

subdural hematoma radiography

concave/cresent. hyperdense diffuse. crosses suture lines- its below adhesions may be layered along falx or tentorium

bulging fontanel indicates

cranial sutures have separated due to increased icp

ICH happens because

damaged blood vessels, not anticoag anticoag makes bleed area larger

Traumatic contusion

deceleration causes brain to impact bony prominences blossom overtime

HTN effect on autoregulation

decompensate earlier in drops of MAP in regards to cerebral blood flow

surgical indications for depressed scalp fracture

depressed more than width of skull bone communitive- multiple fragments open fracture

axonal retraction ball

diffuse axonal injury

Subfalcine herniation

displacement of cingulate gyrus under the falx cerebri -> compression of branches of anterior cerebral artery -> ischemic injury of primary motor and/or sensory cortex -> weakness and/or sensory abnormalities in leg

hyponatremia from bleed

dont treat w fluid restriction give NS or hypertonic saline

deterioration after ischemic stroke

edema, hemorrhagic transformation,infarct extension, infection/fever

mechanism of atherosclerosis causing strock

embolic is most common can be hemodynamic

BBB structure

endothelial(primaru) - no fenestrations, lots of tight junctions -sparse pinocytosis pericytes- support/regulate astrocytic end-feet -indirect contribution

CSF-brain barrier

ependyma in ventricles pia in subarachnoid space

layers of head

epidermis dermis calvarial bone endosteal and meningeal dura (pachymeninx) arachnoid mater (trabeculae_subarachnoid space)+ pia mater = leptomeninx) pial BM glial limitans

types of intracranial hemorrhage

epidural, subdural, subarachnoid*, intracerebral* *stroke primary ICH, traumatic ICH, hemorrhagic transformation

Second Impact Syndrome

exponential increase in symptoms from a concussion following the immature return of an athlete back into competition prior to symptoms being resolved - may trigger malignant brain edema

chronic traumatic encephalopathy

form of dementia caused by repeated head trauma such as concussions. behavior, cognitive, motor, histological amyloid beta and tau pathology

stroke recovery

generally plateaus at 3 months

glucose transport across BBB

glut 1 facilitated diffusion

common places for emboli to lodge in brain

grey-white junctions inter-arterial watershed zones

ICH tx without clear benefit

hemostasis surgery for deep ich treating icp bp lowering

factors determining damage due to ischemia

how low blood flow gets how long it stays low collateral circulation

Watershed/borderzone infarct

hypotension/hypoperfusion at zones between arterial territories Internal borderzone is most common- superficial and deep perforating arteries of MCA

reverse cerebellar sign

hypoxic ischemic encephalopathy - will have diffuse gray-white matter de-differentiation with relatively normal perfusion to the posterior fossa. cerebellum brighter on CT pic with occipital subdural hematoma and deep nuclear grey is brighter than surrounding cortical tissue- ominous finding

Apraxia

impaired ability to carry out motor activities despite intact motor function and willingness to carry out task.

Prosopagnosia

inability to recognize familiar faces

secondary defense measure for brain w/ reduced perfusion

increase % O2 extraction. baseline is 30-40% can double

activators of CSF production

increased cerebral blood flow CO2 volatile anesthetics colinergics NTs

clopidogrel

inhibits ADP binding to platelet receptor

dipyridamole

inhibits phosphodiesterase

Asparin

inhibits thrombaxane

most common infarct area for watershed/borderzone

internal borderzone- deep and superficial perforating arterial territories of MCA (white matter)

carotid arteries

internal- has bulb and larger diameter. distal branches after cavernous sinus. anterior 2/3 of cerebral hemispheres. external- branches early

hemorrhagic transformation

is thought to occur as a result of blood vessel spasm around a blood vessel that has been occluded by a blood clot, which in time resolves, causing the blood clot to break apart and restoring blood flow to surrounding ischemic and infarcted brain tissue. During ischemia, tissues may become friable or fragile, and when normal blood flow or pressure is reestablished, this pressure may cause tissue damage or bleeding. or caused by clotbusting medication around 10% of strokes undergo hemorrhagic transformation. 1% are symptomatic. tissue is already dead. only associated with poor outcomes when exerts a mass effect..

global hypoxia mechanisms

ischemic - cardiac arrest, hypotension, high ICP hypoxic -hemmorage/anemia(quantity) or -RA, status epilepticus, CO posioning (dec O2) histotoxic - cyanide

brain bleeds most common cause

ischemic stroke- atherosclerosis(HTN) ICH- prolonged HTN, abnormal arteries (AMYLOID, Moyamoya, avm)

RACE AND stroke

ischemic- AA> HA > whites primary hemorrhagic Asian >> AA/HA > white SAH SAH- japan and Finland ICH/ischemic stroke >> age. SAH only slightly

mechanism of subdural hematoma

laceration of bridging vessel. accelleration/deceleration or rupture of parenchymal hematoma and bleeding into sub dural space.

characteristics of small vessel infarcts

lacunar, smaller territory

predictors of hemorrhagic transformation

large lesion cardioembolic source hyperglycemia thrombolytic tx

Tpa less effective

larger vessel, longer clot

CSF circulation

lateral ventricles -> foramen of Monroe third ventricle -> aqueduct of Sylvius 4th ventricle -> foramens of Lushka and Magendie subarachnoid space-> arachnoid granulations driven by hydrostatic pressure/CSF production arterial pulsations cilia

arteries supplying basal ganglia

lenticulostriate

subventricular zone

lining of lateral ventricles. contains neural stem cells

small vessel disease comprable to atherosclerosis

lipohyalinosis

small artery disease comparable to atherosclerosis

lipohyalinosis lenticulostriate arteries

diffuse cerebral edema

loss of autoregultion Vasogenic edema is defined as extracellular accumulation of fluid resulting from disruption of the blood-brain barrier (BBB) and extravasations of serum proteins, while cytotoxic edema is characterized by cell swelling caused by intracellular accumulation of fluid. loss of grey and white matter distinction

mild-moderate TBI outcome

low/no mortality > GCS 8 memory deficit behavioral disorder academic difficulty usually improves with time/adapt

microscopic findings of subacute phase cerebral infarction

macrophages proliferative capillaries

microscopic signs of chronic phase cerebral infarction

macrophages reactive astrocytes(astrocytosis/gliosis) cavitation

Choroid plexus functions

make CSF brain homeostasis trophic factors of stem cells immune-cytokine production

small vessel infarcts common cause and location

may be due to arteriolosclerosis preferentially affect - basal ganglia, thalamus, pons, hemispheric white matter

hypotension+ anemia/hypoxemia

may need earlier intervention w/ transfusion to maintain cerebral perfusion

proximal vessel clot tx

mechanical clot retrieval within 6 hours with or without TPA

function of CSF

mechanical support nutrient/waste from metabolism and synapses endocrine/paracrine

subdural hematoma facts

more lethal than epidural usually higher impact 24% of severe Head injuries usually vehicular anticoag is a risk factor- occurrence + mortality 50-90% mortality

epidural hematoma facts

more males 1-3 % of head trauma admissions usually temporal -skull fracture(absorbs a lot of impact) 20-55% mortality

cilia

motile- 9+2 primary- 9+ 0

hydrocephalus types

non-communicating (obstructive)- tumor, stenosis communicating(reduced absorption)- infection, subarachnoid hemorrhage- scarring of arachnoid villi overproduction of csf- rare, chorid plexus papilloma

ICP management principles

norma; <15 tx goal <22

Cerebral Venous Thrombosis

occurs when there is a blood clot in one of the dural sinuses; most common in women in their 30s superior sagittal sinus or cortical veins can result in ischemic stroke and intracerebral hemorrhage(increased venous pressure)

Classic epidural hematoma presentation

only 12% LOC lucid interval deterioration -coma -contralateral hemiparesis -ipsilateral pupil dilation

BBB transport

paracellular aqueous transcellular lipophilic transport proteins receptor mediated transcytosis absorptive transcytosis lipophilic mocules easily cross

Decompressive craniectomy

part of skull removed to allow the brain to swell lower mortality higher rate of severe disability

vascular sources of emboli

plaque rupture/thrombus peripheral vessels - neoplasm, fat emboli

glasgow coma scale

predicts severity of injury, not outcome Eye, motor and verbal components minimum score - 3 max-15

hemorrhagic infarct vs primary hemmorage

primary hemorrhage- big colt of blood. no brain tissue inside. 10% of strokes hemorrhagic infarct- revascularization into damaged blood vessels. blood seeps into brain tissue. about 10% of infarcts undergo hemorrhagic transformation. often from clot-busting medicine)

injury with TBI

primary- external force secondary-hours to days

delayed cerebral ischemia

progressive segmental narrowing of blood vessels at base of brain. vasospasm 1/3 of pts post SAH 4-10 days after Risks- large bleed, poor clinical grade at onset

inability to recognize faces

prosopagnosia

embryonic CSF and nanovesicles

protein/micro RNAs for stem cell prolif/diff/migration

MCA-ACA watershed infarct

proximal UE and Proximal LE weakness/hemiplegia and sensory loss. - man in a barrel syndrome

tissue window

pts imaging and symoptoms show small infarction but larger ischemic window. should treat even if its past normal 6 hour window

brain regions most susceptible to low blood flow

purkinje cells(cerebellum), hippocampus CA1, cortical layers 3,5,6 neurons die first, then glia, then vessels

most common intracerebral hemorrhage sites

putamen, basal ganglia, thalamus, pons, cerebellum, lobar white matter

SAH deterioration

rebleeding delayed cerebral ischemia(days after)-focal neurologic deficit(vasospasm) hydrocephalus electrolyte disturbance-hyponatremia

microscopic finds of acute phase cerebral infarction

red dead neurons(pyknotic nucleus, retracted from neuropil) neutrophils microvacuoles(in neuropil)

concussion tx

rest- 2nd injury b4 first has healed is bad avoid concentration/stimulation aviod medicines that can alter mental status thorough eval - neuropsychologist

diffuse axonal injury

rotational force hemorrhagic foci in corpus callosum, brainstem, corona radiata

ICH symptoms

same as stroke but with mass effect- AMS, headache, vomiting symptoms maximal at onset seizures if in cortex

abusive head trauma symptoms

seizures, not breathing/gasping, limp, unresponsive shear strain injury best case - minor to moderate disability

ischemic stroke vs intracerebral hemorrage

signs of increased intracranial pressure in ICH ischemic stroke has edema. large strokes will have latent significant edema- which can raise ISC. but onset will be delayed compared to hemorrhage.

Amyloid angiopathy cerebral hemorrhage

small arterioles, posterior lobar or lobar older dementia pts

Lacunar infarcts

small ischemic infarcts involving the deep brain structures (basal ganglia and pons) and subcortical white matter (internal capsule, corona radiata).k They are most often due to hypertensive aterioslclerosis of small, penetrating arterioles. May sound very similar to a Charcot-Bouchard aneursm with hemorrhage but this would appear hyperdense on CT whereas lacunar infarct would be dark and cavitary (lacuna)

lenticulostriate arteries

small, deep penetrating arteries that branch from the middle cerebral artery. basal ganglia and internal capsule susceptible to lacunar infarcts

choroid plexus ion directions

sodium, bicarb, chloride, water into csf potassium to blood

optic ataxia

spatial disorientation in which the patient is unable to accurately reach for objects using visual guidance

cerebellar ataxia

staggering, wide-based gait; difficulty with turns; uncoordinated movement with positive Romberg sign fail finger to nose

clot density on CT

subacute-isodense chronic- hypodense acute-hyperdense pic is isodense

glymphatic pathway

subarachnoid fluid following paraarterial routes through aquaporin 4 astrocytes to para venous route paravascular pathway/conductive bluk flow can clear out solutes

shaken baby triad/abusive head trauma

subdermal hematoma hypoxic-ischemic brain injury retinal hemorrhage mixed-density subdermal hematomas- multiple injuries over time

associated with abuse

subdural hematoma cerebral ischemia skull fractures + intracranial injury seizures, apnea retinal hemorrhage long bone or rib fracture

subdural vs epidural mechanics

subdural-shearing injury. brain moving within cranium. bridging veins lacerate from brain momentum/immovability. associated with retinal hemorrhage, increased ICP, cervical strain epidural- direct impact on skull- skull fracture lacerates middle meningeal artery(most common artery)

MCA strokes affect

superior division- PMC/PSC- contralateral hemiplegia and sensory loss, face and upper extremities. FEF- ipsilateral gaze deviation inferior division- Wernicke's area(left side MCA)

posterior cerebral artery

supplies occipital lobe, midbrain, thalamus, inferior temporal lobes

endoscopic 3rd ventriculostomy

target: tuber cinereum- into the prepontine cistern ETV

mechanism of epidural hematoma

tearing of meningeal artery. sometimes middle meningeal vein or dural sinus bleeding dissects between dura and brain

carotid endarterectomy

the surgical removal of the lining of a portion of a clogged carotid artery leading to the brain indicated in > 70% blockage in women >50% men no benefit w/o stroke or less than 50% blockage

cardiac sources of emboli

thrombus- Afib endocarditis-infections or noninfections calcific material from valve- rheumatic heart disease

Signs of SAH

thunderclap headache-max intensity within 1 min neck pain/stiffness CN deficit-esp 3(posterior communicating artery aneurism) loss of consciousness sentinel headache subhyaloid hemorrhage

cortical blindness

total or partial loss of vision in a normal-appearing eye caused by damage to the brain's occipital cortex PCA stoke sometimes pt will deny

nonfluent speech, intact comprehension and repitition.

transcortical motor aphasia -ACA

ICP Homeostasis

translocation of intra cranial venous blood to extracranial vessels translocation of CSF to extracranial vessels via acachnoid translocation of CSF to spinal subarachnoid space molding of brain to mass, reduction of ECF space brain shift / extrusion / herniation

concussion

traumatically-induced transient disturance of brain function.

global aphasia stroke

usually complete MCA

subarachnoid hemorrhage from trauma

usually in sulci most common form of SAH

site of clot formation in afib

usually left atrial appendage

Spontaneous subarachnoid hemorrhage

usually rupture of an aneurism at the base of the brain 3-5% of strokes usually cerebral aneurism usually circle of Willis branches or bifurcation of ICA

if ICP rises(autoregulation)

vessels dilate MAP constant usually impaired in anemia or hypoxemia (vessels alredy dilated)

watershed infarct vs superior sagittal venous thrombosis

watershed- see evidence at MCA/PCA and ACA/MCA superior sagittal VT- larger, less defined. clot at superior sagittal sinus.

CSF into venous system

when ICP > central venous pressure by 3-6 cm H@)

on imaging blood in the brain

will always have a signatre. use different MRI phases to determine age

IV tpa timing

within 4.5 hours increases likelihood of functional independence increases chance of ICH, but not mortality(those patients already had a poor prognosis) still only about 30% effective

hyperventilation to reduce ICP

works short term. but loses effectiveness over hours. then theres rebound if its prolonged response bunted in setting of ischemia (vessels already dilated)