The Brain Flashcards
gray matter is made of cell bodies or axons?
cell bodies
white matter is made of cell bodies or axons?
axons
what re the 3 types of neurons in the CNS?
- Mulitpolar
- pseudounipolar
- Bipolar
which type of neuron is most common in the CNS?
multipolar
name the glials cells in CNS. Which is most abundant?
astrocytes (most abundant)
ependymal cells
oligodendrocytes
microglia
what do astrocytes do?
repair neurons after injury
what do ependymal cells do?
form choroid plexus and produce CSF
what do oligodendrocytes do?
myelin sheath in CNS
what do microglial cells do?
act as macrophages and phagocytize neuronal debris
from what cells to most brain tumors arise?
Glial cells
Brain can be divided into which four areas?
cerebral hemispheres
dienchephalon
brainstem
cerebellum
name the four lobes of the cerebral cortex and name their function
frontal lobe: motor control
parietal lobe: somatic sensory cortex
Occipital lobe: vision cortex
temporal lobe: auditory / speech centers
what is wernickes area and where is it located?
part of the brain that understands speech. it is located in the temporal lobe
what is brocas area and where is it located?
where motor control for speech happens. Technically located in frontal lobe but is connected to wernicke’s area via neural pathway
besides the different cerebral lobes, what 3 other areas are located in the cerebral hemishpers?
hippocampus
Amygdala
Basal Ganglia
what is the funcition of the hippocampus
memory and learning
what is the function of the amygdala?
emotion, apetite, responds to pain and stress
basal ganglia function? What two areas make it up?
fine control of movement
made up of caudate nucleus and globus pallidus
What makes up the diencephalon?
Thalamus
hypothalamus
thalamus function?
relay station to direct information
hypothalamus function?
primary neurohumoral organ
brainstem is made up of what?
midbrain
pons
reticular activating system
medulla
midbrain function
auditory and visual tracts
pons function
autonomic integration
reticular activating system function
consciousness , arousal, sleep
medulla function
autonomic integration
Cerebellum function
equilibrum, muscle tone, coordinate voluntary muscle movement
name the cranial nerves
“Oh Oh Oh To Touch And Feel Very Good Velvet Ah Ha”
Olfactory
Optic
Occulomotor
Trochlear
Trigeminal
Abducens
Facial
Vestibulocochlear
Glossopharyngeal
Vagus
Accessory
Hypoglossal
Which cranial nerves are sensory vs motor?
SOME say marry money but my bro says big boobs matter most
sensory
sensory
motor
motor
both
motor
both
sensory
both
both
motor
motor
name each mucscle and which cranial nerve it is controlled by
blue: CN3
Orange: CN4
Green: CN6
LR6SO4
Everythign else is CN3
Starting at orange moving clockwise:
superior oblique muscle
lateral rectus m.
inf. oblique m.
sup rectus m.
medial rectus m.
inf. rectus m.
are cranial nerves part of central nervous system or peripheral nervous system? What is the implication?
all are part of peripheral nervous system except CN 2 optic nerve.
CN2 is the only CN surrounded by Duramatter
what is another name for Tic Douloureux? what does it cause?
trigeminal neuralgia. Causes excrutiating pain in the face
which cranial nerves control eye movement?
CN 3 4 and 6
name the branches of the facial nerve
To Zanzibar By Motor Car
Temporal
Zygomatic
Buccal
Mandibular
Cervical
Bells Palsy occurs when which cranial nerve is damaged?
CN 7
parasympathetic outflow comes from which cranial nerves?
3 7 9 & 10
vagus nerve is responsible for what percentage of total parasympathetic activity?
75%
what restricts the passage of large molecules and ions into the brain?
Blood Brain Barrier
Blood brain barrier can become dysfunctional at site of:
tumors, injury, infection, or ischemia
what parts of the brian is the BBB not present?
chemoreceptor trigger zone
post. pituitary
pineal gland
choroid plexus
parts of hypothalamus
BBB is poorly developed in which patient population?
neonates
how much CSF is usually present in the body?
about 150ml
what is CSF specific gravity?
1.002-1.009
how much CSF is produced every hour?
about 30ml/hr
what is normal CSF pressure?
5-15mmHg
where is CSF reabsorbed?
arachnoid villi in the sup. saggittal sinus
describe the pathway of CSF flow in the brain
Love My 3 Silly 4 Lorn Magpies
lateral ventricles
Monro (foramen)
3rd ventricle
Sylvius (aqueduct)
4th venticle
lushka (foramen)
magendie (foramen)
what are the two types of hydrocephalus? which is most common?
obstructive (most common)
communicating hydrocephalus
what causes obstructive hydrocephalus?
CSF Flow obstruciton in ventricular system
what are the two types of communicating hydrocephalus? Which type is super rare?
deceased CSF absorption in arachnoid villi
overproduction of CSF (very rare)
describe the normal cerebral blood flow for each section of the brain:
global
cortical
subcortical
global: 45-55ml/100g brain tissue/min or 15% CO
cortical: 75-80ml/100g brain tissue/min
subcortical: 20ml/100g brain tissue/ min
Describe the three critical thresholds for global CBF
CBF about 20ml/100g/min = evidence of ischemia
CBF about 15ml/100g/min = complete cortical supression
CBF < 15ml/100g/min = membrane failure and cell death
what are the 5 determinants of CBF?
- CMRO2
- CPP
- PaCO2
- PaO2
- Venous Pressure
name each line on the graph
red ICP
Orange PaCO2
blue Pa02
green CPP
what is normal CMRO2?
3.0-3.8ml/O2/100g brain tissue/ min
how much brain oxygen is used for electrical activity vs cellular integrity? Can you decrease CMRO2 more than 60%?
60% electrical activity
40% cellular integrity
No, even if brain is silent it still has to consume O2 for cellular integrity
for every 1 degree celsius decrease in body temp CMRO2 decreases by what percent?
7%
EEG suppression occurs at what temperture?
18-20 degrees C
what things decrease CMRO2?
hypothermia
volatile anesthetics
propofol
etomidate
barbiturates
what things increase CMRO2?
hyperthermia
seizure
ketamine
nitrous oxide
At what point can an increased temp decrease CBF?
at greater than 42 degrees C proteins will denature and CBF will decrease
how can you improve outcomes post anoxic brain injury?
by decreasing CMRO2
you should cool post out of hopsital v-fib cardiac arrest patients to what temp for how long to improve outcomes?
cool to 32-34 degrees celsius for 12-24hours
Cerebral autoregulation occurs between what MAPs?
50-150 or 60-160
what happens to CBF when MAP is less than 50
max vasodilation
CBF becomes pressure dependent
risk of cerebral hypoperfusion
what happens to CBF when MAP > 150
max vasoconstriciton
CBF becomes pressure dependent
risk of cerebral edema and hemorrhage
cerebral autoreguation is usually controlled by what?
products of local metabolism
myogenic mechanism
autonomic innervation
what things can abolish cerebral auto regulation
intracranial tumor
head trauma
volatile anesthetics
CBF consideration in HTN
classic teaching: HTN shifts cerebral auto regulation curve to the right
modern teaching: HTN shrinks window of cerebral autoregulation
either way: patients with systemic HTN are at the greatest risk of cerebral ischemia during hypotension
CBF will increase or decrease by how much for changes in PaCO2?
for every 1mmHg increase in PaCO2 CBF ^ by 1-2ml/100gtissue/min
same for decrease by 1, CBF decreases by 1-2
Max vasodilation occurs at what PaCO2?
80-100
max vasoconstriction occurs at what PaCO2?
PaCO2 about 25
there is a blank relationship between PaCO2 and CBF
linear
how do resp acidosis/akolosis affect CBF?
resp acidosis increase CBF
resp alkolosis decreae CBF
how does metabolic acidosis / alkolosis affect CBF? Why?
no effect on CBF becuase H+ ions do not cross the BBB
How does it from resp acidosis though???
is inverse steal an effective way to aide perfusion is ischemic brian tissue?
No, hyperventilation induce vasoconstriction in an efford to re-direct blood flow to ischemic brain tissue has NOT been shown to produce a clinical benefit. furthermore this practice could cause harm form cerebral ischemia from not enough CBF
what is the best practice for PaCO2 during ischemia?
mainatain normocapnia or very mild hopcapnia
PaCO2 30-35
PaO2 < 50-60 has what effect on CBF?
causes cerebral vasodilation to increase CBF
PaO2 > 60 has what effect on CBF?
any PaCO2 > 60 has no effect on CBF. Think about the CBF graph
how does venous volume affect CBF?
increased venous pressure decreases venous drainage which can lead to increased cerebral volume
name some conditions that impair venous drainage
jugular compression from improper head position (head flexion in sitting position)
^ intrathoracic pressure PEEP or coughing
vena cava thrombosis
vena cava syndrome
Name each type of herniation. Which is most common site of transtentorial herniation?
- Cingulate
- central
- uncal
- cerebellotonsilar
- upward
- transcalvarial
uncal is most common site of transtentorial herniation
how does uncal herniation manifest clinically? why?
with fixed dilated pupil.
this is because CN 3 crosses near tentorium and becomes compressed by the uncal herniation
what is psuedotumor cerebri?
idopathic intracranial HTN
Normal ICP
5-15
intracranial hyptension
> 20
gold standard to meaurse ICP
intraventricular catheter
other methods to meausre ICP
subdural bolt
catheter over convexity of cerebral cortex
ICP measurement is indicated in what glasgow score?
< or equal to 7
S/S of intracranial HTN
Headache
N/V
papilledema
pupil dilation and non-reactivity to light
focal neurologic deficit
seizure
coma
explain the Monroe-Kellie Hypothesis. What is one way to cope with increasing ICP?
brain blood and CSF are contained in the skull. IF one increases another must decrease or else pressure will rise.
CSF can be shunted into spinal column to mitigate rise in intracranial pressure up to a certain point
explain the deadly cycle that begins with increased ICP
^ICP > cerebral ischemia > decreased CPP > more ischemia
What are the three things that make up Cushing’s triad and explain how this is caused
- HTN
- bradycardia
- irregular respirations
An increased ICP leads to decreased CPP
Body tries to cope by increasing BP, which activates baroreceptors leading to bradycardia.
^ICP causes medulla compression leading to irregular respirations
List the 4 ways to treat increased ICP
- decrease CBV
- Decrease CSF
- Decrease cerebral edmea
- decrease cerebral mass
list ways to decrease CBV
mild hyperventialtion
avoid hypoxemia
avoid vasodilators
use vasoconstritors
elevate HOB to 30 degrees
avoid neck flexion
decrease intrathoracic pressure
how long do effects of hyperventilation last in regards to increaesed ICP? why?
6-20 hours because at this point pH of CSF equilibriates with PaCO2
even in traumatized brain the brain usually still maintains reactivity to
CO2
how can you decreaes CSF? what medications can be used for this?
drain with VP shunt or intraventricular catheter
lasix or acetazolamide also decrease CSF production
list two anesthetic drugs that are considered cerebral vasoconstrictors
propofol and thiopental considered to be vasoconstrictors because they decrease CMRO2
how can you decrease cerebral edema?
diuretics and steroids
how do you decrase cerebral mass?
surgical debulking or hematoma evacuation
mannitol is a blank diuretic
osmotic
is hypertonic saline considered a diuretic?
no
what happens is mannitol given when BBB is compromised
it will enter brain and cause cerebral edema
which two steroids can be used to decrease cerebral edema from mass lesions
decadron methylprednisolone
when thinking about neuro stuff and corticosteroids, what must you not forget about an effect of corticosteroids?
corticosteroids cause hyperglycemai and hyperglycemia is associted with worse outcomes in the setting of cerebral ischemia
are steroids also used for spinal cord injuries?
yes
what neuro conditions must steroids be avoided?
TBI and functional pituitary adenoma
Name the vessells
Better know em!
Is the pink ant. or post. cerebral ciruclation? Name the vessells
anterior.
is the yellow ant or post cerebral circulation? name the vessells
posterior
name the vessells
Orange: ant cerebral a.
purple: middle cerebral a.
green: post. cerebral a.
cerebral aterial ciruclation can be divided into blank and blank which converge at the blank
ant and post converge at circle of willis
anterior cerebral circulation is fed by the blank. they enter skull through the
internal carotid arteries
enter through foramen lacerum
post cerebral circulation is fed by blank and enter skull through the
vertebral arteries and enter through foramen magnum
Name the venous structures
cerebral cortex and cerebellum blood drains via
sup sagittal sinus and dural sinuses
basal brain structures blood drains via
inf. sagittal sinus, vein of galen, and straight sinus
blood flow from cerebral cortex and cerebellum converges with blood from basal brain structures at what point?
confluence of sinuses
all blood exits skull through:
paired jugular veins
ischemic strokes are usually caused by…
thromboembolic events like afib
what is a transient ischemic attack?
a mini stroke. focal neurologic deficit that spontaneously resolves within 24hrs.
it is a sign warning sign of cerebrovascular dz and impending stroke
list risk factors for ischemic stroke, which one is the most important?
HTN (most important)
smoking
DM
HLD
excessive alcohol intake
elevated homo-cysteine level
acute mgmt for ischemic stroke
emergent Non contrast CT
immediate evaluation of airway reflexes and ventilation (most still just need supplemental oxygen though)
PO aspirin
IV thrombolytic within 4.5 hours for eligible patient
embolectomy within 6hrs for elegible patient with large vein occlusion
why do you get non contrast CT with ischemic stroke?
it will reliably detect hemorrage within the first few hours, so if no bleeding you can rule that out and know most likely suffered ischemic stroke
why is HTN common post CVA? what should BP target be?
HTN supports CPP
targe BP < 185/110
why should you give fluids post ischemic stroke?
supports BP, CO, CPP, and CBF by decreasing viscosity
what happens to glucose durign cerebral hypoxia?
glucose gets converted to lactic acid
cerebral acidosis leads to destroyed brain tissue and brain outcomes
must monitor and treat serum glucose during ischemic stroke
What is the most common cause of subarachnoid hemorrhage?
aneurysm rupture
where do most cerebral aneurysms arise?
circle of willis
arterial bleedings is usually subarachnoid or subdural?
subarachnoid
venous bleeding is usually subarachnoid or subdural?
subdural
how do you calculate cerebral transmural pressure?
MAP-ICP
increase transmural pressure causes increased risk of…
aneurysm rupture
what is most common symptom of SAH?
intense headache “worse headache of my life”
Mobidity from SAH is associated with three key things
- obstructive hydrocephalus
- re-bleeding
- Vasospasm
what are the surgical treatment options for SAH?
aneurysm clipping or endovascular clipping
how soon should surgical repair take place following SAH?
24-48 hrs after initial bleed
what medication will patient need if an endovascular coil is placed?
heparinization
what medication should should you immediately give if SAH ruptures during surgery? What is the dose?
protamine 1mg per 100u heparin
intraop BP goal during SAH surgery
SBP 120-150
meticulous BP control during blank and blank is critical if patient has an aneurysm
induction and intubation
anesthetic treatment goals for aneurysm rupture during induction or intubation
decrease ICP and maintain CPP
when does cerebral vasospams occur?
delayed contraction of cerebral artery post SAH that can lead to cerebral infarct
How can SAH lead to vasospasm?
Hgb that contacts outside of cerebral arteries increase risk of vasospasm
there is a blank correlation between ammount of blood seen on CT with SAH and incidine of vasospasm
positive
gold standar to diagnose cerebral vasospasm
cerebral angiography
Cerebral vasospasm treatment
increase MAP to 20-30 above baseline
triple H: (basically just give fluids)
hypertension
hypervolemia
hemodilution (Hct 27-32, but little evidence for this)
what is the only CCB shown to decreae M&M from vasospasm? how does it work?
Nimodipine
it doesn’t dilate the spasm, but increases collateral flow
medicants to consider for medically refractory cerebral vasospams
verapamil
nicardipine
papaverine
milrinone
treatment for vasospasm that doesn’t resolve with any medication?
balloon angioplasty
what is cerebral salt wasting syndrome?
brain releases BNP which causes diuresis and sodium wasting
cerebral salt wasting treatmetn
isotonic crystalloids
cerebral salt wasting syndrome vs SIADH
SIADH presents with euvolemia or slightly hypervolemic and the treatment is fluid restriction
hyponatremia is most commonly caused by?
Cerebral salt wasting syndrome
Initial considerations for TBI
C-spine stabilization
airway protection
optimize hemodynamics
cerebral protection
what imaging should you get with TBI and why?
Head CT to rapidly determine if bleeding.
likely don’t need this if pt is totally neurologically intact and less than 60yrs old
GCS < X is consisent with TBI and an indication for intubation and mechanical ventilation?
8
when managing TBI what are your priorities as anesthesia provider?
ABCs first then, manage ICP
which patient population is uniquely challenging with head tramua?
anticoagulated patient
how can you reverse warfarin?
FFP
prothrombin complex concentrate
recombinant factor 7a
how can you reverse plavix?
platelets
some evidence that recombinant factor 7a can be used as well
intra-op anesthetic mgmt in TBI
keep MAP >70
decrease ICP
avoid prolonged hyperventilation
avoid steroids as they worsen neurologic outcomes
avoide nitrous oxide
which fluids should you use / avoid in TBI?
Use:
hypertonic saline: it restores intravascular volume and decreases brain water
avoid:
hypotonic fluids: increase cerebral edema
glucose containing solutions (only give glucose in hypoglycemic)
albumin is linked to poor outcomes
why avoid N20 in TBI?
you may not know if pneumothorax is present until after intubation and initiation of PPV, N20 can rapidly expand pneumothorax or cause pneumocephalus
what is a partial/focal seizure?
seizure activity is localized to a particular cortical region
what is generalized seizure?
seizure activity affects both hemispheres
what is jacksonian march?
when a partial seizure advances to generalized seizure
what is tonic phase of seizure?
whole body rigidity
what is clonic phase of seizure?
repetitive jerking motions
what is grandmal seizure?
generalized tonic-clonic activity
grandmal seizure acute treatment?
propofol, diazepam, thiopental
surgical tx of grandmal seizure
vagal n. stimulator or resection of foci
what happens with focal cortical seizure
localized to particular cortical region
usually no loss of consciousness
what happens during absence / petit mal seizure? more common in which patient population?
temporary loss of consciousness but remains awake
more common in children
what happens with akinetic seizure?
more common in what patient population
temp loss of consciousness and postural tone
can lead to fall and head injury
more common in children
what is status epilepticus?
seizure activity that lasts > 30min
Or
2 grandmal seizures with no regaining consciousness between
actue tx for status epilepticus?
phenobarbital, thiopental, phenytoin, benzos, propofol, even GA
impact of inhaled anesthetics on seizures?
have been implicated in causing seizures, but produce dose-dependent EEG supression
what are S/S of seizure when occuring under GA?
tachycardia
HTN
increasing EtCO2
can etomidate cause seizures?
commonly causes myoclonus, but this is not associated with increased EEG activity unless they have epilepsy
which medications can be used to increase EEG activity in patients with seizure disorder in order to locate seizure foci during cortical maping?
methohexital
etomidate
alfentanil
can atracurium cause seizures?
it’s metabolite is laudanosine which is a proconvulsant. this is only an issue in ICU with atracurium drip though
can cisatracurium cause seizures?
it also produces laudanosine like atracurium but produces much less
can meperidine cause seizures?
yes, because normeperidine can cause seizures
how to LAs affect seizure activity?
LAs decrease seizure threshold but properly executed regional does NOT increase risk of seizures.
Name anticonvulsant medications that work by blocking voltage gated sodium channels therby causing membrane stabalization
phenytoin
valporic acid
carbmazepine
which anticonvulsant medications inhibit voltage gated calcium channels in CNS > decreased neurotransmitter release?
gabapentin
pregabalin
which anticonvulsants cause hepatic enzyme induction. What is the main clinical consideration of this effect?
phenytoin
carbmazepine
NDNMB resistance
which anticonvulsants cause hepatic enzyme inhibition?
What is the main clinical consideration of this effect?
valporic acid
slows phenytoin metabolism
Phenytoin SE
dysrhythmias
Hypotension
gingival hyperplasia
aplastic anemia
nystagmus / ataxia
steven-johnson syndrome
birth defects
extravasion > purple glove syndrome
which medication eliminates the risk of purple glove syndrome from phenytoin?
fosphenytoin
valporic acid SE
hepatotoxicity
thrombocytopenia
displace phenytoin from plasma proteins
other than anticonvulsant effects, what is another use of carbmazepine?
trigeminal neuraliga
carbazepine SE
aplastic anemia
thrombocytopenia
liver dysfunction
leukopenia
ADH like effects
how are gabapentin and pregabalin metabolized?
excreted unchanged by kidneys
most common SE of gabapentin and pregabalin?
dizziness
somnolence
when can gabapentin and pregabalin cause resp depression?
when combined with opiods
why should you taper gabapentin and pregabalin as opposed to abrupt withdrawl?
abrupt withdrawl can cause seizure in patients with a hx of seizures
conditions gabapentin / pregabalin are usefeful for besides anticonvulsants effects?
diabetic neuropathy
postherpetic neuraliga
reflex sympathetic dystrophy
describe pathophys of alzheimers dz
diffuse beta amyloid rich plaques and neurofibrillary tangles in teh brain that lead to dysfunctional synaptic transmission and apoptosis
how can you treat alzheimers?
restore Ach concentration in the brain
what medications are used to treat alzheimers
cholinesterase inhibtiors
tacrine
donepezil
riristigmine
galantamine
anesthetic mgmt of patients with alzheimers
poor candidates for MAC because they are often scared, confused, and uncooperative
use short acting drugs
avoid pre-op sedation
cholinesterase inhibitors incrase DOA of sux (this is debatable as to if actually clinically significant or not)
can get parasympathetic symptoms for their anticholinesterase medication (bradyardia, syncope, N/V)
if you have to use anticholinergic glycopyrrolate is best because no crossing BBB
which two inhaled anesthetics increase beta-amyloid production?
halothane and isoflurane
explain pathophys of parkinsons dz
chronic neurodegeneration of basal ganglia
dopaminergic neurons in basal ganglia are destroyed
relative increase in cholinergic activity > increased GABA in thalamus > cortical motor system supressed > increased activity of extrapyramidal system
main treatment for parkinsons dz and how it works
levodopa and carbidopa
levodopa gets converted to dopamine but dopamine in the blood doesn’t enter CNS.
carbidope prevents levodopa breakdown so more levodopa can enter CNS
another medication to treat parkinsons besides levodopa/carbidopa
selegine
MAO-B inhibitor. decreases dopamine metabolism in CNS so more DA is available
should pt with parkinsons take levodopa/carbidopa DOS? What is the DOA and associted anesthetic consideration?
yes. if not risk of muscle rigidity that can impair ventilation.
lasts 2-6 hours and my need to redose through OG for long procedure
which drugs are contraindicated in parkinsons dz?
antidopaminergics:
metoclopramide
butyrophenones (Haldol, droperidol)
promethazine
is diphendyramine okay in parkinsons dz?
yes, it has anticholinergic properties which can help
how can alfentanil affect parkinsons dz?
it can disrupt central dopaminergic transmission
is ketamine okay in parkinsons dz?
contraversial becaues of potential SNS effects
are sux and NDNMB okay in parkinsons dz?
yes
anesthetic considerations for Deep brain stimulator for parkinsons dz
may want to hold levodopa/carbidopa to make symptoms worse for better lead placement
pt head in rigid frame can complicated airway mgmt
pt needs to be awake for electrode placement, okay to give precedex or opioids though
avoid GABA agonists (propofol and versed) can interfere with electrophysiologic brain monitoring in the thalamus
sitting position ^ risk of VAE. flood field with saline if VAE occurs.
keep SBP < 140
seizure can be treated with small dose of propofol, barbiturate or benzo
what is the most common peri-op opthalamic complication
corneal abrasion
how do you diagnose corneal abrasion
fluorescin stain to pt eye and then look at eye with cobalt blue pen light
when should you consult opthamologist for corneal abraison?
if severe pain present
what is the best way to prevent corneal abrasion?
eye tape.
eye lube is contraversial
how long before corneal abraision gets better?
usually self limitting and healed within 1-3 days
is ischemic optic neuropathy a nerve or vascular problem?
nerve
what is the most common cause of post-op vision loss
ION
Is Ant. ION or Post. ION associated with a swollen optic disc?
Ant. ION
when does ION usually present?
24-48hr post op and is not painful
after what procedure is ION most common?
spine surgery in prone position
what is CRAO?
central retinal artery occlusion
is CRAO nerve or vascular problem?
vascular
how does CRAO present?
sudden painless vision loss on emergene
what is most common cause of CRAO?
horseshoe head rest in prone position
what are three things that can cause CRAO
improper head position that impairs venous outflow
embolism
N20 use after intraocular gas bubble placement
