UNIT 7 Neuro Flashcards
Name 4 types of glial cells and describe the function of each
astrocytes
- most abundant
- regulation of metabolic environment
- repair neuron after neuronal injury
ependymal cells
- concentrated in roof of 3rd/4th ventricles & SC
- form the choroid plexus, which produces CSF
oligodendrocytes
- form the myeline sheath in the CNS
- schwann cells form the myelin sheath in the PNS
microglia
- act as macrophages and phagocytize neuronal debris
list the name and function of the 4 lobes of the cerebral cortex
frontal: motor cortex
parietal: somatic sensory cortex
occipital: vision cortex
temporal: auditory and speech
- Wernicke’s area: understanding speech
- Broca’s area: motor control of speech
Name the 12 cranial nerves
I olfactory II optic III oculomotor IV trochlear V trigeminal VI abducens VII facial VIII vestibulochochlear IX glossopharyngeal X vagus XI spinal accessory XII hypoglossal
What CNs provide motor control of the eyes? How does each nerve contribute to the eye’s movement?
CN 3, 4, 6:
CN III:
- up (in, out, and straight)
- in
- down (out and straight)
CN IV
- in and down
CN VI
- out
What bedside tests are used to assess the CN?
I smell II vision III eye movement, pupil constriction IV eye movement V facial sensation (+ ant 2/3 tongue sensation) VI eye movement VII facial movement except chewing VIII hearing, balance IX posterior 1/3 tongue sensation X swallowing XI shoulder shrug XII tongue movement
Which CN resides in the CNS? What is the implication of this?
CN II is the only CN that is part of the CNS (the rest are part of the PNS). This means that CN II is the only CN that is surrounded by dura.
It is bathed in CSF. If you inject LA into the optic nerve during RA of the eye, you will have a big problem.
What is tic douloureux? What CN contributes to this problem?
trigeminal neuralgia
CN V
causes excruciating neuropathic pain in the face
What is Bell’s palsy? What CN contributes to this problem?
CN VII
causes ipsilateral facial paralysis
What is the function of CSF, and where is it located?
cushions the brain, provides buoyancy, and delivers optimal conditions for neurologic function.
It is located in the:
- ventricles (lateral, 3rd, and 4th)
- cisterns around the brain
- subarachnoid space in brain & SC
What regions of the brain are NOT protected by the BBB?
BBB separates the CSF from the plasma. It has tight junctions that restrict pass of large molecules & ions.
The BBB isn’t present at the chemoreceptor trigger zone, posterior pituitary gland, pineal gland, choroid plexus, and parts of the hypothalamus
What is the normal volume and specific gravity of CSF?
volume 150mL
spec grav 1.002-1.009
Describe the production, circulation, and absorption of CSF.
CSF production: ependymal cells of the choroid plexus (of lateral ventricles), rate of 30mL/hr
need to match to image
absorption: arachnoid villi within the superior sagittal sinus (to the venous circulation)
What is the formula for CBF? what are the normal values for global, cortical, and subcortical flow?
CBF = CPP/CVR (CVR = cerebral vascular resistance)
global 45-55mL/100g (or 15% of CO)
cortical 75-80mL/100g
subcortical 20mL/100g
What are the 5 determinants of CBF? You need to know where to label it on the graph
CMRO2 CPP venous pressure PaCO2 PaO2
What is the normal value for CMROs? What factors cause it to increase? To decrease?
CMRO2 describes how much O2 the brain consumes per minute.
3.0-3.8mL O2/100g brain tissue/min
decreased by hypothermia (7%/1C), IA, propofol, etomidate, barbs
increased by hyperthermia, ketamine, N2O
What is the formula for CPP? What is normal?
CPP = MAP - ICP (or CVP, whichever is higher)
autoregulation via vessel diameter changes to provide a constant CPP of 50-150mmHg
- i.e. MAP needs to be higher
- autoreg is influenced by products of local metabolism, myogenic mechanisms, and autonomic innervation
What are the consequences of a CPP that exceeds the limits of autoregulation (too high and too low?)
CPP <50
- vessels are maximally dilated
- CBF becomes pressure dependent
- risk of cerebral hypoperfusion
CPP >150
- vessels are maximally constricted
- CBF becomes pressure dependent
- risk of cerebral edema & hemorrhage
list 4 conditions that reduce CPP as a function of increased venous pressure.
a high venous pressure decreased cerebral venous drainage & increases cerebral volume –> backpressure is created to the brain that reduces the arterial/venous pressure gradient (MAP-CVP)
conditions that impair drainage:
- jugular compression d/t head position
- increased intrathoracic pressure d/t cough, PEEP
- vena cava thrombosis
- vena cava syndrome
What is the relationship b/n PaCO2 and CBF? What physiologic mechanism is responsible for this?
linear
- pH of the CSF around the arterioles controls the cerebral vascular resistance
- at a PaCO2 of 40mmHg, CBF is 50mL/100g tissue/min
At what PaCO2 does maximal cerebral vasodilation occur? How about maximal cerebral vasoconstriction?
for every 1mmHg change in PaCO2, CBF will change by 1-2mL/100g tissue/min
max vasodilation occurs at PaCO2 of 80-100mmhg
max vasoconstriction occurs at PaCO2 of 25mmHg
What is the relationship b/n CMRO2 and CBF?
- things that increase the amount of O2 the brain uses (CMRO2) tend to cause cerebral vasodilation (increased CBF) –> hyperthermia, ketamine
- things that decrease CMRO2 tend to cause cerebral vasoconstriction (decreased CBF) –> hypothermia, propofol
halogenated anesthetics are an exception; they decouple the relationship: reduce CMRO2, but also cause cerebral vasodilation
- this is why TIVA is a better choice w/ intracranial hypertension
How do acidosis & alkalosis affect CBF?
resp acidosis = increased CBF
resp alkalosis = decreased CBF
met acidosis/alkalosis don’t directly affect CBF. This is because H+ doesn’t pass through the BBB. A compensatory change in MV can, however, affect CBF.
How does PaO2 affect CBF?
PaO2 <50-60mmHg causes cerebral vasodilation & increases CBF
When PaO2 is >60mmHg, it doesn’t affect CBF.
What is the normal ICP? What values are considered abnormal?
ICP is the supratentorial CSF pressure
normal = 5-15mmHg
cerebral HTN > 20mmHg
When is ICP measurement indicated? What is the gold standard for measurement?
when GCS <7
intraventricular catheter is the gold standard
other ways:
- subdural bolt
- catheter placed over the convexity of the cerebral cortex
List the s/s of intracranial HTN
HA N/V papilledema (swelling of the optic nerve) focal neurologic deficit decreased LOC seizures coma
discuss the monroe-kellie hypothesis
brain lives in a rigid, bony box containing brain, blood, and CSF
- if one component increases in volume, another component must decrease in order to maintain constant pressure
- remember intracranial compliance curve
What is Cushing’s triad? What is the clinical relevance of this reflex?
indicates intracranial HTN
- HTN
- bradycardia
- irregular respirations
increased ICP –> decreased CPP w/ compensatory HTN
–> baroreceptor reflex activation
compression of medulla –> irregular respirations
name 4 areas where brain herniation can occur.
- of the cingulate gyrus under the falx
- transtenotorial
- cerebellar tonsils via the foramen magnum
- via a site of surgery or trauma
How does hyperventilation affect CBF? What is the ideal PaCO2 to achieve this effect?
CO2 dilates vessels –> decreased CVR –> increased CBF –> increased ICP
hyperventilation –> decreased ICP in this manner
lowering PaCO2 <30 increases the risk of cerebral ischemia d/t vasoconstriction & L shift of the oxyHgb dissociation curve
How do NTG & SNP affect ICP?
cerebral vasodilators –> increases CBF –> increase ICP
How does head position affect ICP?
head elevation >30 degrees facilitates venous drainage away from the brain
neck flexion or extension can compress the jugular veins, reduce venous outflow, increase CBV, and increase ICP
head down positions increase CBV & ICP
How does mannitol reduce ICP? What problems can arise when mannitol is used in this way?
0.25-1g/kg increases serum osm & “pulls” water across the BBB towards the bloodstream for excretion
problems:
- if BBB is disrupted, mannitol enters the brain & promotes cerebral edema
- mannitol transiently increases blood volume, which can increase ICP & stress the failing heart
describe anterior & posterior circulation of the brain. Where do these pathways converge?
converge at the circle of willis
anterior
ICA enter skull via foramen lacerum
aorta –> carotid –> ICA –> circle of willis –> cerebral hemispheres
posterior
vertebral a enter skull via foramen magnum
aorta –> SC –> vertebral –> basilar –> posterior fossa structures & cervical SC
Describe the anatomy of the circle of willis. Need to know how to label
primary function of the circle of willis is to provide redundancy of blood flow in the brain. If one side of the circle becomes occluded, the other side should theoretically be able to perfuse the affected areas of the brain
basilar PCA pcomm MCA ACA acomm
Which population of stroke patients should receive a thrombolytic agent?
CVA d/t thrombosis
diagnosis must be made by emergent head CT prior to administration
if tx can begin <3hrs after onset of symptoms, the pt should receive tPA
- aspirin is acceptable if tPA cannot be administered
What is the relationship b/n hyperglycemia & cerebral hypoxia?
During cerebral hypoxia, glucose is converted to lactic acid. Cerebral acidosis destroys brain tissue & is associated w/ worse outcomes
monitor serum glucose, treat hyperglycemia, be careful administering dextrose containing IVF
in the context of cerebral aneurysm, how is transmural pressure calculated?
an increased transmural pressure predisposes the aneurysm to rupture.
transmural pressure = MAP - ICP
MAP = pressure pushing outward against the aneurysmal sac
ICP = counterpressure that pushes against it.
–> creates a tamponade effect
risk of rupture is increased by HTN and/or acute reduction in ICP
What is the most common clinical finding in a patient w/ SAH? What are the other s/s?
WHOL (worst HA of life)
others
- LOC (50%)
- neurologic deficits
- N/V
- photophobia
- fever
What is the most significant source of M&M in the patient w/ SAH?
cerebral vasospasm (delayed contraction of the cerebral arteries); can lead to cerebral infarction
free Hgb that is in contact w/ the outer surface of the cerebral arteries increases the risk –> +correlation b/n amount of blood observed on CT & vasospasm incidence
What is the incidence of cerebral vasospasm? When is it most likely to occur?
25% of patients
most likely 4-9days after SAH
What is the treatment for cerebral vasospasm?
triple H therapy (hypervolemia, HTN, permissive hemodilution to Hct 27-32%)
nimodipine (CCB) reduces M&M associated w/ vasospasm –> doesn’t actual reduce the spasm, but increases the collateral blood flow
during endovascular coil placement for a cerebral aneurysm, the aneurysm ruptures. What is the best treatment at this time?
protamine 1mg/100U heparin
low/normal MAP
+/- adenosine to temporarily arrest the heart
be able to calculate the Glascow coma scale
eyes (1-4)
motor (1-6)
verbal (1-5)
How do you treat the patient w/ an ICH who is on warfarin?
FFP, prothrombin complex concentrate, and/or recombinant factor VIIa to reverse the warfarin
vitamin K isn’t the best option for acute warfarin reversal
discuss the blood flow to the SC
SC is perfused by:
1 anterior spinal artery (anterior 2/3 of SC)
2 posterior spinal arteries (posterior 1/3 of SC)
6-8 radicular arteries
Envision the anatomy of the SC & spinal nerve in cross section.
sensory neurons from the periphery via the dorsal nerve root
motor & autonomic neurons exit via the ventral nerve root
Discuss the presentation & pathophysiology of autonomic hyperreflexia.
classic presentation = HTN & bradycardia.
stimulation below the level of SCI triggers sympathetic reflex arc that creates a profound degree of vasoconstriction below the level of injury –> baroreceptor activation in carotid bodies (bradycardia) –> body attempts to reduce afterload w/ vasodilation above the level of the injury.
other s/s:
- reflex vasodilation above level of SC injury –> nasal stuffiness
- HTN –> HA/blurred vision
- malignant HTN –> CVA, sz, LV failure, dysrhythmias, pulmonary edema, and/or MI
describe the patho of myasthenia gravis
autoimmune disease
IgG Ab destroy post-junctional nAChR at the NMJ.
(ACh is present in sufficient quantity, the receptors just aren’t there)
–> skeletal m weakness.
Key feature is skeletal m weakness that becomes worse later in the day or that develops w/ exercise & can recover some w/ rest.
describe the patho of Eaton Lambert syndrome
IgG mediated destruction of the presynaptic v-gated Ca++ channel at the presynaptic nerve terminal.
When the AP depolarizes the nerve terminal, Ca++ entry into the presynaptic neuron is limited, thereby reducing the amount of ACh that is released into the synaptic cleft.
Postsynaptic nAChR is normal
describe the patho of Guillain-Barre syndrome.
characterized by an immunologic assault on the myelin in the peripheral nerves. The AP can’t be conducted –> the motor endplate never receives the incoming signal
usually persists for approx 2 weeks and ends w/ full recovery in approx 4 weeks.
What is the Cobb angle and what is its significance?
describes the magnitude of the spinal curvature
40-50degrees = indication for surgery 60 = decreased pulmonary reserve 70 = pulmonary symptoms present 100 = gas exchange significantly impaired, higher risk of post-op pulmonary complications
List 3 ways that rheumatoid arthritis affects the airway.
- TMJ: limited mouth opening
- cricoarytenoid joints: decreased diameter of glottic opening
- cervical spine: A-O subluxation w/ flexion + limited extension
describe the patho of systemic lupus erythematosus.
SLE is an autoimmune disease characterized by the proliferation of antinuclear Ab.
SLE affects nearly every organ system & most consequences are the direct result of Ab-induced vasculitis and tissue destruction
what drugs can exacerbate SLE?
occurs d/t stress or drug exposure
drug induced usually persists for several weeks-months & presents w/ mild symptoms
most common offenders (PISSED CHIMP) Pregancy Infection Surgery Stress Enalapril D-penicillamine Captopril Hydralazine Isoniazid Methyldopa Procainamide
A!
Intrathecal opioids act centrally by diffusion into the spinal cord and interact with mu receptors in the substantia gelatinosa in the dorsal horn.
Opioid receptors (mu receptors) are present in the substantia gelatinosa (A) of the dorsal horn in the spinal cord. The substantia gelatinosa comprises the cell bodies of the second-order projection neurons that ascend from the spinothalamic tract to the thalamus. These cells are densely populated with mu receptors and form the primary immediate site of action of intrathecal opioids that diffuse from the cerebrospinal fluid into the spinal cord.
