brain Flashcards
ID the 12 cranial nerves and their function
CN 1 bedside test
olfactory (sensory) smell
CN 2 bedside test
optic (sensory) vision
CN 3 bedside test
oculomotor (motor) eye movement, pupil constriction
CN 4 bedside test
trochlear (motor) eye movement
CN 5 bedside tests
trigeminal (both)
V1 ophthalmic: somatic sensation to the face
V2 maxillary: somatic sensation to anterior 2/3 of tongue
V3 mandibular: muscles of mastication
CN 6 bedside test
abducens (motor) eye movement
CN 7 bedside test
facial (both)
temporal, zygomatic, buccal, mandibular, cervical
facial movement except mastication, eyelid closing, taste to anterior 2/3 of tongue
CN 8 bedside test
vestibulocochlear (sensory) hearing and balance
CN 9 bedside test
glossopharyngeal (both) somatic sensation and taste to posterior 1/3 of tongue
CN 10 bedside test
vagus (both) swallowing
CN 11 bedside test
accessory (motor) shoulder shrug
CN 12 bedside test
hypoglossal (motor) tongue movement
mnemonic for sensory and motor
some say marry money but my brother says big boobs matter more
ID the eye muscles controlled by CN 3 and what they do
superior rectus- supraduction
medial rectus: adduction
inferior oblique: extorsion- elevation
inferior rectus- infraction
ID the eye muscles controlled by CN4 and CN 6 and what they do
superior oblique- intorsion, depression
lateral rectus- adduction
cranial nerve surrounded by dura
CN2 because its not a part of the PNS
mnemonic for 5 branches of facial nerve
the zebra bit my carrot
temporal, zygomatic, buccal, mandibular, cervical
bells palsy results from injury to which CN
7 (causes ipsilateral facial paralysis)
PSNS output carried by CN’s
3,7,9,10
what forms the grey matter and what forms the white matter on a neuron
cell bodies form grey matter while axons form white matter
ID these parts of the neuron
soma
axon hillock
dendrites
axon
myelin
nodes of ranvier
presynaptic terminal
3 types of neurons found in CNS
- multipolar (most of CNS neurons)
- pseudo unipolar (dorsal root ganglion, cranial ganglion)
- bipolar (retina, ear)
glial cells support neuronal function by
creating healthy ionic environment
modulating nerve conduction
controlling reuptake of NT’s
repairing neurons following neuronal injury
type of glial cell
function
astrocytes
most abundant type
regulation of metabolic environment
repair neuron after neuronal injury
type of glial cell
function
ependymal cells
concentrated in roof of 3rd and 4th ventricles of spinal canal
form the choroid plexus which produces CSF
type of glial cell
function
oligodendrocytes
form myelin sheath in CNS
(schwann cells form myelin sheath in PNS)
type of glial cell
function
microglia
act as macrophages and phagocytize neuronal debris
most brain tumors arise from
glial cells
4 lobes and cortex it contains
- frontal contains motor cortex
- parietal contains somatic sensory cortex
- occipital contains vision cortex
- temporal contains auditory cortex and speech centers
wernickes area versus brocas area
wernickes: understanding speech
brocas: motor control of speech (in front lobe but is connected to wernickes area via neuronal pathways)
cerebral hemispheres contain the following structures (4 and what they do)
cerebral cortex: cognition, movement, sensation
hippocampus: memory and learning
amygdala: emotion, appetite, responds to pain and stressors
basal ganglia: fine control of movement. caudate nucleus, globus pallidus
2 structures in diencephalon and what they do
thalamus: acts as a relay station that directs information to various cortical structures
hypothalamus: primary neurohumoral organ
4 structures in brain stem and what they do
midbrain: auditory and visual tracts
pons: autonomic integration
reticular activating system: controls consciousness, arousal, and sleep
medulla: autonomic integration
3 parts of cerebellum and what they do
archicerebellum: maintains equillibrium
paleocerebellum: regulates muscle tone
neocerebellum: coordinates voluntary muscle movement
CSF volume
~150mL
SG of CSF
1.002-1.009
CSF is produced by __________ at a rate of
empendymal cells of choroid plexus at a rate of 30mL/h
the choroid plexus is located in
all 4 cerebral ventricles
CSF pressure
5-15mmHg
CSF site of reabsorption
arachnoid villi at superior saggital sinus
-reabsorption is dependent on pressure gradient between CSF and venous circulation
CSF flow in the brain
lateral ventricles
Monroe (foramen)
3rd ventricle
sylvius (aqueduct)
4th ventricle
luschka
magendie
CSF is isotonic with
plasma (but is not an ultrafiltrate of the plasma)
compare CSF v plasma
osmolarity
Na (mEq/L)
K (mEq/L)
Cl- (mEq/L)
HCO3- (mEq/L)
PaCO2 (mmHg)
pH
glucose (mg/dL)
protein (mg/dL)
2 types of hydrocephalus
- obstructive hydrocephalus: obstruction to CSF flow in ventricular system (most common)
- communicating hydrocephalus: decreased CSF absorption by arachnoid villi (ex ICH) or overproduction of CSF (very rare)
ID the curves on this graph
(ICP, PaO2, CPP, PaCO2)
CPP=
and normal global value
CBF/CVR
normal global value: 45-55mL/100g tissue/min or 15% of CO
critical thresholds for global CBF include (3)
~20mL/100g tissue/min –> evidence of ischemia
~15mL/100g tissue/min –> complete cortical supprssion
<15mL/100g tissue/min –>membrane failure and cell death
normal CMRO2 and what is coupled to it
CMRO2 3-3.8mL/O2/100g brain tissue/min
CBF is coupled to it
CMRO2 decreases by what % for every 1 degree celsius drop in temperature? when does EEG suppression occur?
7% drop for every 1 degree celsius drop in temp
EEG suppression occurs 18-20c
CMRO2 is decreased by (5)
hypothermia, halogenated anesthetics, propofol, etomidate, barbiturates
describe the relationship between CBF and volatiles
uncouples CBF from CMRO2 which explains why CBF increases but cerebral metabolism decreases
how to improve patient outcomes when they suffer from anoxic brain injury
decrease CMRO2 by cooling patient between 32-24c for 12-24h after hospital admission
what increases CMRO2 (4) and what is the temp threshold where CBF starts to decrease
increased by hyperthermia, seizures, ketamine, nitrous oxide
at 42c, proteins are denatured, neurons destroyed, CBF starts to decrease
brain auto regulates CBF between CPP of what or MAP of what
CPP 50-150, MAP 60-160
CPP=
MAP-ICP (or CVP, whichever is higher)
how does chronic systemic HTN affect cerebral auto regulation curve
traditional: shift to the right
contemporary: plateau of curve narrows and CBF becomes more closely dependent on CPP
at a PaCO2 of 40mmHg, global CBF is ____________
50mL/100g brain tissue/min
for every 1mmHg increase in PaCO2, CBF will increase by
for every 1 mmHg decrease in PaCO2, CBF will decrease by
1-2mL/100g brain tissue/min
max vasodilation occurs at PaCO2
80-100mmHg
max vasoconstriction occurs at PaCO2
~25mmHg
theres a linear relationship between PaCO2 and
CBF
pH of CSF controls
cerebral vascular resistance
decreased CSF pH (aka increased PaCO2) decreases CVR and increases CBF aka resp acidosis increases CBF
does metabolic acidosis directly affect CBF
no because H+ in blood does not pass through BBB
why does the steal phenomena occur
CBV that have healthy brain tissue have vascular tone (they alter based on PaCO2). ischemic or atherosclerotic vessels are maximally dilated.
vasodilating healthy tissue “steals” BF away from ischemic areas. called cerebral steal
describe inverse steal or robin hood effect
concept of using hyperventilation to constrict the healthy BV’s that supply brain tissue. the idea is the flow will be re distributed to ischemic regions that are already maximally dilated
PaO2 below ________ causes cerebral vasodilation and increases CBF
50-60mmHg
when PaO2 is above ______, CBF is unaffected by PaO2
60mmHg
what is the consequence of increased venous pressure in the brain
reduces cerebral venous drainage and increases cerebral volume. reduces arterial/venous pressure gradient (MAP/CVP)
conditions that impair venous drainage include (4)
jugular compression due to improper head positioning (head flexion in sitting position)
increased ITP secondary to coughing or PEEP
vena cava thrombosis
vena cava syndrome
fixed and dilated pupil suggests herniation of the
temporal uncus (number 3 on the image, CN 3)
cerebral HTN occurs if ICP >
20mmHg
gold standard of ICP measurement
intraventricular catheter
ICP measurement is indicated with a GCS <
7
s/sx of intracranial HTN
HA, n/v, papilledema (swelling of optic nerve), pupil dilation and non reactivity to light, focal neurological deficit, seizures, coma
monroe kelli doctrine
brain, blood, CSF
at lower CPP’s, CSF is shunted towards
spinal cord
cushings triad
HTN (to maintain CPP)
bradycardia (baroreceptor reflex from HTN)
irregular respirations (compression of medulla)
ways to decrease CBF/CBV (6)
-hyperventilation (PaCO2 30-35mmHg)
(<30 increases the risk of cerebral ischemia d/t vasoconstriction and shifting oxyHGB curve to the left)
-avoid hypoxemia (PaO2 50-60mmHg greatly increases ICP and CBF)
-avoid cerebral vasodilators
-neo to maintain CPP
-increase venous outflow (head elevation >30 degrees helps)
-reduce ITP (dont do high PEEP)
how long do the effects of hyperventilation last
only 6-20 hours because the pH of CSF equilibrates with PaCO2
is PaCO2 response reserved in the traumatized brain
yes
how to reduce CSF
-can drain if theres an obstruction such as hydrocephalus
-acute tx: drain placed in lateral ventricles or intrathecal space improves ICP by reducing CSF volume
-chronic tx: shunt VP or VA (atrium)
-acetazolamide and furosemide decrease CSF production
how to reduce cerebral mass
tumor debunking or reducing cerebral edema with diuretics (mannitol)
how to achieve cerebral edema reduction (2 categories with subcategories)
diuretics
-loop diretics (also decrease CSF production)
-osmotic diuretics (increases osmolarity, .25-1g/kg)
-3% NaCl (not technically a diuretic)
corticosteroids
-dexamethasone and methylprednisolone reduce cerebral edema caused by mass lesions
-corticosteroids do cause hyperglycemia which is muy malo
-steroids are also used for SCI
mannitol in the setting of a disrupted BBB
mannitol will then enter the brain and increase cerebral edema
steroids should not be used for
TBI or functional pituitary adenoma
cerebrovascular artery that is not paired
basilar artery
ID anterior cerebral artery, middle cerebral artery, and posterior cerebral artery
which arteries supply anterior circulation, where do they enter the skull, and what is the path to the cerebral hemispheres
internal carotid arteries, enter skull through foramen lacerum
aorta–>carotid a–>internal carotid a–>circle of willis–> cerebral hemispheres
which arteries supply posterior circulation, where do they enter the skull, and what is the path to the cerebral hemispheres
vertebral arteries, enter skull through foramen magnum
aorta–> subclavian a–>vertebral a–> basilar a–>posterior fossa structures and cervical spinal cord
where on this image is the circle of willis
hoe, its in the circle. get your shit together
cerebral venous circulation can be divided into two separate circulations. where does blood from cerebral cortex and cerebellum drain
via superior saggital sinus and dorsal sinus
cerebral venous circulation can be divided into two separate circulations. where does blood from basal brain structures drains
via inferior saggital sinus, vein of galen, and straight sinuses
both venous pathways converge at the
confluence of sinuses
all venous blood exits brain via
paired jugular veins
all venous blood exits brain via
paired jugular veins
eye movement is controlled by which cranial nerves
3 (responsible for the rectus’ and inferior oblique)
4 (superior oblique)
6
bells palsy is which nerve
CN7
where in the brain is the BBB not present?
CTZ
hypothalamus
pineal gland
posterior pituitary gland
choroid plexus
ID most common site of herniation in this photo
3 (temporal uncus)
manifests as fixed and dilated pupil because this herniation compresses CN3
