1
Q
What type of information travels up the spinal cord? Which travels down?
A
Up = input or afferent signals (tend to be sensory)
Down = output or efferent signals (tend to be motor)
2
Q
What are the 3 sub-divisions of the somatic nervous system?
A
Cranial nerves, spinal nerves and sensory/motor neurons
3
Q
What are the 2 sub-divisions of the ANS?
A
Sympathetic and parasympathetic NS
4
Q
What part of the brain is responsible for higher functions?
A
Cerebrum
5
Q
What part of the brain is responsible for balance, posture and coordination?
A
Cerebellum
6
Q
What part of the brain is responsible for automatic functions?
A
Brainstem
7
Q
What lobe of the cerebrum is responsible for: personality, speech, behavior and self awareness?
A
Frontal
8
Q
What lobe of the cerebrum is responsible for: language, words, sense of touch and spatial perception?
A
Pareital
9
Q
What lobe of the cerebrum is responsible for: interpretation of visual stimuli (light/color)?
A
Occipital
10
Q
What lobe of the cerebrum is responsible for: understanding language, memory and hearing?
A
Temporal
11
Q
Grey matter makes up what percentage of the neuron bodies? White matter?
A
Grey = 40%
White = 60%
12
Q
What type of matter in the brain has axons that travel deeper into the brain to communicate with other areas?
A
White matter
13
Q
What glial cells are found the in PNS only?
A
Schwann cells and satellite cells
14
Q
T/F: most communication between neurons are from electrical synapses
A
False: most are chemical carried out via neurotransmitters/chemical messengers
15
Q
What releases synaptic vesicles in the axon terminal?
A
The influx of Ca in response to an AP
16
Q
T/F: nerves can release more than 1 neurotransmitter in response to an AP?
A
True
17
Q
What controls what exact neurotransmitter is released?
A
The frequency of nerve stimulation controls which NT is released
18
Q
In the ANS, Ach is present as a neurotransmitter in what?
A
All preganglionic fibers, both sympathetic and parasympathetic
It is also widespread in the postganglionic parasympathetic fibers
19
Q
What are some common effects that Ach has on various body systems?
A
CV: regulates heart contraction, decreases HR and decreases BP
Bladder: affects release of urine
Endocrine: assists with glandular secretion and gastric secretion
Muscular: assists with skeletal muscle contraction
Neuro: modulates attention, memory and arousal
20
Q
Sux can cause bradycardia in infants/children by action at what receptor?
A
The M2 receptors in the heart
21
Q
What is the common DOC to treat myasthenia gravis? What is it’s drugs class?
A
Pyridostigmine and it is an Ach-esterase inhibitor
22
Q
What is the acronym for cholinergic s/e?
A
S: salivation
L: lacrimation
U: urination
D: diaphoresis
G: GI upset/diarrhea
E: emesis
Occurs from drugs like neostigmine, which is why you reverse concurrently with glyco or other anti-cholinergics
23
Q
What 3 Ach-esterase inhibitors are used to increase the availability of Ach in disease processes like Alzheimer’s and Parkinson’s?
A
Rivastigmine, Donepezil and Galantamine
24
Q
How does scopolamine help treat N/V?
A
By blocking communication between the nerves of the vestibule and the vomiting center in the brain
25
What is the primary excitatory neurotransmitter?
Glutamate
26
If you primary goal was to block the excitatory effects of glutamate during surgery, what would be a good drug to consider?
Ketamine
27
How does excessive activation of glutaminergic synapses cause damage in the brain?
Large influxes of Ca -> excitotoxicity -> cell damage/death
*So over activation of glutaminergic receptors can cause problems like Parkinson's, Huntington's, Alzheimer's and depression*
28
What is dopamine derived from?
Phenylalanine
29
Does dopamine generally have inhibitory or excitatory effects?
Inhibitory
30
Where would you find most of your dopaminergic neurons?
In the substantia nigra and caudate nucleus/putamen, in limbic system, retina, and olfactory system
31
What kind of effects does dopamine have outside the CNS?
Paracrine effects [acts as a hormone on nearby cells] – inhibits norepi release, increases sodium excretion, reduces insulin secretion
32
What is the most effective drug to treat Parkinson's?
Levodopa -> passes into the brain to be turned into dopamine (dopamine cannot cross the BBB)
*It MUST be combined with carbidopa as it protects levodopa from early conversion*
33
T/F: epi and norepi are made from dopamine
True
34
What primarily produces epi?
The adrenal glands
35
What primary produces norepi?
The Locus Coeruleus
36
Where is norepi generally released from?
Sympathetic nerve endings in peripheral nervous system
37
Which NT generally has a greater effect on the blood vessels? The heart?
BV = norepi
Heart = epi
38
Where is most of our serotonin made?
90% is made in the GI tract in the enterochromaffin cells
39
When can serotonin cause vasoconstriction? Vasodilation?
Causes vasoconstriction in pathologic states (HTN, atherosclerosis)
Causes vasodilation in physiologic states (release of NO)
40
What is serotonin synthesized from?
Tryptophan
*High in concentration in turkey, part of what makes you sleepy after thanksgiving meal, not just having to deal with all your extended family*
41
If your body lacks serotonin, what negative effects can occur?
Depression
Anxiety
Digestive problems
OCD
Panic disorders
Phobias
Schizophrenia
42
Where would you find a large amount of GABA outside of the CNS?
The pancreas in the beta cells
43
What endocrine effects does GABA have?
Inhibits glucagon secretion
44
What are some common actions of GABA?
Regulates formation of synapses, secretion of cytokines
Calming, controlling nerve cell hyperactivity
Immune responses
45
What do most of our GABA related drugs bind to on the GABA receptor?
GABA-A or GABA-B
46
Where do endorphins bind to? What do they block in relation to pain?
PNS: The MU receptors and the block the release of substance P
CNS: inhibits GABA release which increases dopamine
47
What does the internal carotid bifurcate into in the brain?
The anterior and middle cerebral arteries
48
What vessels create the posterior cerebral arteries?
The vertebral arteries ascend and combine into the basilar artery which then becomes the posterior cerebral arteries
49
Describe the progression of arteries from the circle of willis extending out to their terminal arterial branches
Arteries leave from the circle of willis -> travel up/along the brain surface becoming the pial arteries -> branch into penetrating arteries -> branch further into intracerebral arterioles which perfuse deeper brain tissue -> end in the capillary branches (carrying out standard capillary functions)
50
What EXACT part of the internal carotid branches into the ACA and MCA?
The distal end of the ICA (also known as the terminal segment)
51
What artery is technically not a part of the circle of willis?
MCA
52
What is the most prominent sinus on the surface of the cerebrum?
Superior sagittal sinus
53
What are the 3 superficial dural venous sinus?
Superior sagittal, transverse and cavernous sinuses
54
What do the deep veins in the deep brain tissue combine to form?
Join behind midbrain to form Great Cerebral Vein (Great Vein of Galen), which then drains into the inferior sagittal sinus which then becomes the straight sinus
55
The superficial and deep drainage system of the brain create what structure?
The confluence of sinuses
56
What does the confluence of sinuses drain into?
The IJ
57
How much CO does the brain consume?
10 - 15%
*This is in spite of the fact that the brain only constitutes 2% of our body weight, about 1400 grams*
58
What is the formula to calculate CBF?
50 - 60 mL of blood per 100 grams of brain tissue per minute
59
What would be the CBF if your brain weighed 1750 grams?
50 - 60 / 100 = 0.5 or 0.6
0.5 or 0.6 x 1750 = 875 - 1050 mL/minute
60
At what CBF would you expect to find cerebral impairment with slowing of the EEG?
CBF of less than 20 - 30 ml/100g/min
61
At what CBF would you expect to find a flat, isoelectric EEG?
15 - 20 ml/100g/min
62
At what CBF would irreversible brain damage begin to occur?
10 ml/100g/min
63
What is the formula to calculate CPP?
CPP = MAP - ICP
64
What are the 3 main factors that dictate CBF?
Myogenic, neurogenic and metabolic factors
*All are considered subsets of autoregulation*
65
Define/describe each of the main subsets of cerebral autoregulation
Myogenic = changes in vessel wall stretch
Neurogenic = changes in sympathetic tone
Metabolic = driven by changes in oxygen demand
66
What is the normal cerebral autoregulatory range for CBF?
50 - 150 mmHg
67
How would chronic HTN change the cerebral autoregulation curve?
A right shift - so a MAP of around 70 to 80 could actually be too low and cause a decrease in CBF
68
Smooth muscle in cerebral arterioles directly respond to changes in what?
Transmural pressure
*Reminder, transmural pressure is the pressure difference across the wall of a hollow structure*
69
Sympathetic innervation to the large cerebral arteries arises from what structure?
The superior cervical ganglia
70
Of the 3 factors modulating CBF, which tends to have the least impact?
Neurogenic
71
Why can hypoglycemia quickly lead to unconsciousness?
The brain cannot store glucose - if the total supply is disrupted dysfunction can quickly follow. So the brain is dependent on second by second delivery of O2 and glucose
72
What is the relationship of CBF and CMRO2 in a healthy state?
Proportional; if one goes up, the other should go up and vice versa
73
What is the normal CMRO2 oxygen consumption rate?
~ 3 ml O2/100g of brain tissue/minute
In a normal person, this is about 40 - 50 ml of O2 needed per minute
74
What PaO2 and SpO2 correlate with hypoxia?
PaO2 less than 60 mmHg, SpO2 less than 90
75
Does hypoxia cause vasodilation or vasoconstriction in the brain?
Vasodilation
76
What is a common cause of a decrease in CaO2 in neurosurgery?
Hemodilution
*Reminder, CaO2 is arterial oxygen content*
77
What is the relationship of temperature decrease to CMRO2?
Every one degree Celsius decrease in temperature decreases CMRO2 by 6 - 7%
78
What is the relationship of temperature increase to CMRO2?
Increases up to a point, 42 degrees C
*At that point, CMRO2 begins to decrease d/t toxic effects*
79
What BG levels will increase CBF?
BG less than 2 mmol/L or 36 mg/dL
80
T/F: seizures increase CMRO2
True
81
Describe the series of events that excess CO2 causes cerebral vasodilation
Excess arterial CO2 -> creates carbonic acid -> dissociates into H+ and HCO3- -> causes vasodilation of cerebral vessels
82
T/F: continued increases in CO2 will further increase CBF
False: there is a ceiling effect, eventually the brain will reach maximum CBF, so further increases in CO2 will not increase CBF if we have hit the ceiling effect
83
What is the relationship of H+ to CBF?
Proportional
*Common sources of H+ include lactic acid, pyruvic acid and other acidic materials formed during metabolism*
84
Which is higher; ETCO2 or PaCO2?
PaCO2 - generally the PaCO2 should be around 2 - 5 mmHg higher than the ETCO2
*Throwback to the Schmidtness - this difference is primarily due to alveolar deadspace, though there are other contributing factors*
85
What are the primary functions of the astrocyte?
Help regulate neuroinflammation
Antioxidant response
86
Glutaminergic excitatory neurons can stimulate astrocytes which causes what?
Increase in Ca2+ ion concentration in the astrocytes foot projections which causes vasodilation of nearby arterioles/capillaries
87
What 2 mechanisms do astrocytes have to modulate cerebral blood flow?
Through vasodilation by glutaminergic stimulation (Ca2+ increase -> vasodilation)
By direct release of NO
88
What is the goal MAP management in chronic HTN to preserve CBF?
Maintain MAP within 20 - 25% of baseline
89
What mechanisms disturb CBF/autoregulation in head trauma?
Impaired or absent in TBI
Decreased CPP -> Decreased CBF
Possible ischemia & secondary brain injury
90
What are common causes of brain compression?
Tumors, bleeds and edema
91
How does brain compression impact CBF?
Disruption of blood-brain barrier
Vasogenic edema -> increase in ICP
Autoregulation in peritumoral areas impaired susceptible to ischemia
92
What 2 anesthetics are associated with increases in CMRO2?
Nitrous and ketamine
93
What IV anesthetic is a known potent cerebral vasodilator?
Ketamine
94
What drug class causes the "robin hood" effect? Describe the robin hood effect
Barbiturates (decrease CMRO2)
Barbiturates cause vasoconstriction in healthy tissue to allow preferential perfusion to less healthy/ischemic areas. So robbing from the rich to feed the poor
95
What effect does etomidate, propofol and opioids have on CBF/CMRO2?
Parallel reduction in both
*Throwback to ICU days, this is part of why Dr. Oro wanted high dose propofol on his status epilepticus patients before starting a versed drip*
96
Why do most of our volatile anesthetics agents have a negligible effect on CBF?
Because most volatile anesthetics do decrease CMRO2 (which would tend to cause vasoconstriction), they also vasodilate, opposing the reduction in CMRO2. These opposing effects crease a balance between our anesthetics reducing CMRO2 but also vasodilating = minimal change to CBF
97
At what MAC does potent cerebral vasodilation occur?
Greater than 1 MAC of gas
98
How many anterior spinal arteries are there? How many posterior spinal arteries?
Anterior = 1
Posterior = 2
99
What does the anterior spinal artery perfuse?
The anterior 2/3 of the spinal cord
100
Where does the anterior spinal artery originate from?
The vertebral artery
101
Where would you find the anterior spinal artery?
Midline in the foramen magnum to the filum terminale
102
What do the posterior spinal arteries perfuse?
The posterior 1/3 of the spinal cord
103
What vessels feed into the posterior spinal arteries?
The radicular and medullary arteries at each spinal level
104
What is the largest anterior medullary segmental artery?
The Artery of Adamkiewicz (great radicular artery)
105
Where does the artery of Adamkiewicz generally emerge from?
The left side of the aorta around levels T9 - 12
106
What does the artery of Adamkiewicz perfuse?
The anterior thoracolumbar spinal cord
107
What conditions can cause ischemia or infarction to the artery of Adamkiewicz?
AAA dissection or repair
Malignancy
Vascular malformations or emboli
Spine surgery
108
In very simple terms, what kind of s/sx would you see from a patient if they experienced obstruction of the artery of Adamkiewicz?
Impaired leg motor function, but sensory intact
*More specifically, impaired motor function of the legs, paralysis, urinary/fecal incontinence but intact sensation*
109
What is tethered cord syndrome?
When the spinal cord attaches to the spinal column -> which limits the ability of the spinal cord to move and can cause a rubber band like reflex causing nerve damage
110
What is the normal ICP when horizontal?
~ 10 mmHg (normal range is 7 - 15)
111
What term describes areas where the arachnoid membrane and pia mater are furthest apart allowing for CSF to pool?
Cisterns
112
What is the highly organized tissue that lines all the ventricles?
Choroid plexus
113
Where is most of our CSF made?
In the choroid plexus
114
How much CSF do we make each day?
~ 500 - 600 ml/day
115
What are the 2 main processes involved in making/moving CSF?
Ultrafiltration and secretion by cells of choroid plexus and ependymal cells (cells that line the ventricles)
Passage of water and electrolytes across blood brain barrier
116
What tissue is involved in moving CSF into the ventricles? What tissue is involved in absorbing the CSF?
The ependymal cells excrete fluid into the ventricles (E for excrete)
The arachnoid villi absorb CSF into the cerebral veins (A for absorb)
*Arachnoid villi have one way valves to prevent back flow*
117
What structure connects the lateral and 3rd ventricles?
The foramen of Monro (intraventricular septum)
118
What structure connects the 3rd and 4th ventricles?
Aquedeuct of Sylvius
119
What structures does CSF flow through to access the cisterna magna?
The foramen of Luschka and foramen of Magendie
120
What is the Monro-Kellie Doctrine?
The pressure/volume in the head is fixed, so if one variable changes, the other change in kind (if volume goes up, pressure goes up)
121
What is the blanket term for an obstruction of CSF without an obvious tumor/reason?
Idiopathic intracranial HTN (Pseudotumor Cerebri)
122
What population is most at risk for idiopathic intracranial HTN?
Obese women of reproductive age
123
T/F: Neuraxial is contraindicated in idiopathic intracranial HTN
False: Epidural is generally safe, spinal is not contraindicated but must ensure ICP is not dangerously elevated prior to sticking the needle
124
What ICP indicates increased ICP?
Greater than 15
125
What ICP is considered pathologic/critical?
Greater than 20
126
What formula is used to calculate ICP?
CPP = MAP - ICP
127
What is a normal CPP? What is the critical ischemia threshold?
60 - 80 mmHg
Critical threshold is 30 - 40 mmHg of CPP
128
What are common s/sx of increased ICP?
Headache
N/V
Blurred vision
Somnolence
Papilledema
Midline shift on CT
Hydrocephaly
Edema
129
What is Cushings triad?
Irregular respiration, widened pulse pressure, bradycardia
130
How long can you hyperventilate to help reduce ICP?
6 - 12 hours
131
What are common drugs used to help reduce ICP?
Hyperosmotic Drugs (Mannitol)
Increase osmolarity of plasma draws water away from tissue
Careful with hypervolemia, hypovolemia
Usually given 0.5-1 grams/kg
Onset within 30min
Anticonvulsants
Seizure activity can be caused by brain irritation
Seizures increase CMRO2 -> increasing ICP by means of increased CBF
Loop diuretics
May be given to patients with hypervolemia, pulmonary edema, CHF
Corticosteroids
Lower ICP caused by local cerebral edema (tumors)
Reduce swelling around the tumor
Most effective when instituted 48 hours prior to surgery
May increase blood glucose concentration
Decreased elasticity of blood vessels cerebral ischemia
132
What is the best time to administer steroids prior to brain surgery?
48 hours before
*Common dose is 10 mg q6h*
133
What is the dose of mannitol?
0.5 - 1 gm/kg
Give in incremental doses of 12.5 gm to limit rapid hyperosmolarity or HOTN
134
What is rebound cerebral edema with mannitol administration?
Can occur if mannitol accumulates in brain tissue (especially with disrupted BBB)
This creates reverse osmotic shift, drawing water back into neurons and glia
Thought to be mediated in part by chloride-driven osmotic effects
135
How do lasix and mannitol work in reducing ICP?
Mannitol establishes an osmotic gradient, pulling water out of brain tissue
Furosemide promotes diuresis, accelerating the renal excretion of that free water
*Lasix also inhibits chloride transport which may help prevent rebound cerebral edema*
136
How does keppra prevent seizures?
Binds to synaptic vesicle protein 2A (SV2A) -> binding to this prevents vesicle release which prevents neurotransmitter release
137
What are the risk factors of ischemic optic neuropathy?
Low BP, low Hct, long surgery, large volume admin
138
What is the ideal fluid to use during brain surgery?
NS because its osmolarity is 308 mOsm/L
LR is 274 mOsm/L
139
Why should dextran be used with caution during brain surgery?
It can cause a dilutional coagulopathy and directly interfere with platelets and factors VIII
140
T/F: hypothermia is recommended in neurosurgery
False: it does reduce electrophysical activity in the brain but has not demonstrated outcome benefits
141
Why is it recommended to keep BG 150 - 200 during neurosurgery?
The brain can't store glucose, you need to make sure there is enough in the blood to reach the brain
142
What is the gold standard for ICP monitoring?
Intraventricular pressure monitoring
143
What are some examples of intraparenchymal monitoring devices (include the basics of how they work)?
Camino (fiberoptic ICP)
Codman (strain gauge ICP)
Licox (PbtO₂ + ICP + temperature)
*PbtO2 = PP of brain tissue oxygen*
144
What does cerebral oximetry measure?
Regional blood hemoglobin oxygenation saturation (rScO2)
145
What is a normal cerebral oximetry measurement?
70% +/- 20 - 30%
146
Where do SSEPs travel?
Up the dorsal columns to the cerebral sensory cortex
147
What SSEP findings indicate disruption of the neural pathway?
10% increase in latency
(time required for impulse to travel from one point to another)
50% decrease in amplitude
148
MEPs are more useful for what type of neurosurgery?
Ones that are more anterior in nature
149
T/F: MEPs are more sensitive to anesthetics than SSEPs?
True
150
Which is more reliable for injury/disruption of the neural pathway, latency or amplitude?
50% decrease in amplitude is more reliable/significant
151
How do opioids affect SSEP/MEP waveforms?
They have no effect
152
What type of stroke is most common?
Embolic
*Though hemorrhagic have 4x more likely to cause death*
153
What are 3 common treatments for embolic strokes?
tPA: Tissue Plasminogen Activator (Alteplase)
Catalyzes conversion of plasminogen to plasmin
Breaks down blood clots
Only effective if administered within ~3 hours of symptoms (FDA)
Endovascular Thrombectomy
Interventional radiology
Tiny catheter inserted under angio to break up clot/stents inserted if needed
TCAR (Trans-carotid Artery Revascularization), Carotid endarterectomy (if carotid blockage or high risk for carotid blockage)
154
What are the hemodynamic goals during embolic strokes?
Maintain or slightly elevate blood pressure
Preserve perfusion to the ischemic penumbra
Avoid hypotension → worsens infarct size
MAP goal typically ≥ 70–80 mmHg (institution dependent)
155
What are the induction goals for an embolic stroke?
Rapid, smooth induction
Often RSI (due to altered mental status, full stomach, aspiration risk)
Etomidate or propofol ± fentanyl for stable hemodynamics
Rocuronium preferred for muscle relaxation
156
What are common causes of an intracranial hemorrhage?
HTN
Arteriovenous malformation
Aneurysm rupture/leak
Trauma
Coagulopathy
157
Treatments for an ICH?
Craniotomy:
Surgical clipping of aneurysm
Interventional radiology coiling of aneurysm
Removal of AVM
Burr hole
Drain blood from brain
158
What is the primary medical management concern when choosing between clipping vs coiling?
Anti-coagulation afterwards -> Clipping does not require long term anti-coagulation, coiling does
159
Why is a gentle/slow/deep induction vital in a hemorrhagic stroke?
Rebleeding at induction is often fatal!
Poorly organized clot over the aneurysm
Escaping arterial blood is more likely to penetrate brain tissue
ICP increase more extreme due to poor compliance of space
160
What drug is a good choice if you need emergent induced hypotension?
Adenosine
161
What are some techniques during emergence to help reduce the chances coughing/straining?
Use of lidocaine, esmolol, labetalol
Good amounts of narcotic/timing of narcotic gtt cessation
Time emergence with dressing, not final suture
162
What drug class is useful to help treat/prevent vasospasm?
CCBs
163
What is triple H therapy is preventing vasospasm?
Hypertension (20-30mmHg above baseline)
Phenylephrine or dopamine gtt
Hypervolemia (really euvolemia)
Hemodilution
Hct low ~30
*Last ditch effort is intra-arterial administration of vasodilators in IR*
164
What area of the brain is targeted during a deep brain stimulator insertion?
The subthalamic region
165
What stage of a DBS insertion can be done under MAC?
Stage 1
166
What are the 2 stages of a DBS insertion?
1st Stage – Placement of electrodes under lighter sedation with stereotactic techniques, will wake patient up for intra-operative testing -> can be done under MAC
2nd Stage – GETA, ~1 week later, tunneling of leads from brain to generator (implanted under skin on chest)
167
Why is a precordial doppler used for stage 1 of a DBS insertion?
To help monitor for a VAE
168
What drugs are avoided for stereotactic ablations for focal seizures?
Avoid BZDs, ketamine, methohexital, etomidate, alfentanil, meperidine can all induce seizure activity
169
What is the most common cause of an epidural hematoma?
Skull fracture
170
What vessel is most commonly responsible for an epidural hematoma?
Tear of the middle meningeal artery -> generally leads to LOC and is life threatening
171
What vessel is generally responsible for a subdural hematoma?
Tear of the saggital veins
*Usually treated with burr hole surgery*
172
At what GCS do you intubate?
Less than 8
173
What is the triad of symptoms associated with hydrocephalus with normal ICP?
Dementia, gait changes and urinary incontinence
174
What is the other term for hydrocephalus with normal ICP?
Communicating hydrocephalus
175
What diagnostic findings indicate hydrocephalus with normal ICP? With elevated ICP?
Normal
LP: normal or low CSF pressure
CT/MRI: enlarged ventricles
Elevated
LP: high pressure
CT: enlarged ventricles
176
Common s/sx of elevated ICP r/t hydrocephalus
N/V, altered LOC, papilledema, bradycardia, hypertension, breathing pattern change
177
What is the most common form of non-communicating/obstructive hydrocephalus?
Stenosis of the aqueduct of sylvius (between the 3rd/4th ventricles)
178
Why do you need profound muscle relaxation for a VP shunt placement?
Tunneling of the catheter is very stimulating
179
What are 3 common types of primary brain tumors
Meningioma: usually benign; arising from coverings of brain
Commonly near sagittal sinus; VAE more likely
Gliomas: non-aggressive; surgical resection successful
Astrocytes, ependymal cells, oligodendrocytes
Glioblastoma: most aggressive and most common
Microinvasion, grows quickly; life expectancy weeks/months
180
What is the definition of a primary brain tumor?
A tumor arising from the brain and its coverings
181
What part of the pituitary gland do tumors generally arise from?
The anterior pituitary gland
182
What are the differences between microadenomas and macroadenomas?
Microadenomas (functional): hormone secreting;
symptoms related to hormone
Macroadenomas (non-functional): non-hormone
secreting; symptoms relate to mass
183
What are the 3 hormones the microadenomas secrete?
Prolactin, ACTH (adrenocorticotropic hormone) and growth hormone
184
What is the surgery of choice for resection of pituitary tumors?
Transsphenoidal hypophysectomy
185
What 2 surgical specialties are usually involved in a transsphenoidal hypophysectomy?
Otolaryngologist reaches sphenoid sinus
Runs along optic nerve and carotid artery
Neurosurgeon excises tumor
CSF leaks controlled with fat or muscle graft
Otolaryngologist
Sella floor reconstructed with bone; sphenoid sinus closed
186
What CN is involved with an acoustic neuroma?
A benign schwannoma of CN VIII - vestibulocochlear
187
What type of neuromonitoring is used for an acoustic neuroma?
Auditory evoked potentials
188
Where do metastatic brain tumors usually originate from?
Lungs or breast
189
Why is NO use controversial for a crani?
It increases the risk for VAE
190
Retraction of the dura over the parietal lobe can induce what reflex?
The trigeminal cardiac reflex -> sudden hypotension and bradycardia
This can also induce brain irritation/seizures
191
What are the primary effects of a VAE?
Pulmonary outflow obstruction → ↓ cardiac output
Right heart strain/failure
Bronchoconstriction (from mediator release, e.g., serotonin, histamine)
V/Q mismatch and hypoxemia
Increased dead space and ETCO₂ drop
192
What are the cardiac s/sx of a VAE?
HEMODYNAMIC INSTABILITY/Sudden drop in CO2***
A mill-wheel murmur (loud and machinery-like) ***
Tachy or bradyarrhythmias
Myocardial ischemia
193
What are the pulmonary s/sx of a VAE?
Rales, wheezing
Cyanosis
Tachypnea
Apnea
HYPOXIA
194
What issues can occur during neurosurgery if a right to left shunt exists?
Air can bypass the lungs and enter systemic circulation:
Cerebral arterial embolism → Stroke, seizures, LOC
Coronary artery embolism → Myocardial ischemia or arrest
Retinal embolism (rare)
Spinal cord ischemia (if involving vertebral arteries)
195
What steps should you take if a VAE occurs?
Discontinue N2O if using (you probably shouldn’t be…)
Operative site flooded
Surgeon should use bone wax/wet sponges
Aspiration of right heart
All sitting posterior fossa procedures must have right heart catheter
Pure oxygen administered
Supportive treatment
196
When can DI occur from neurosurgery?
If the posterior pituitary is damaged during transsphenoidal tumor excision
197
When does DI usually manifest after posterior pituitary damage?
12 - 48 hours post-op
198
What findings indicate DI?
Polyuria
Rising serum osmolality
Hypo-osmolar urine
199
Treatment of DI?
½ normal saline
Hourly maintenance fluid + 2/3 previous hour’s urine output
Desmopressin (DDAVP) if U/O > 350-400 ml/hr
200
What are some common causes of interference on an EEG?
Hypoglycemia
Body or eye movement during the test
Lights, especially bright or flashing ones (Can be used to try to induce seizure)
Benzo’s, sedatives
Caffeine
201
What changes to the EEG do seizures cause?
Creates sharp spiking waves
202
What kind of EEG changes would a tumor, stroke, anesthesia and deep sleep cause?
Slow waves, also known as Delta waves - high amplitude/low frequency waves
203
What range of Hz do delta waves fall under?
1 - 4 Hz
204
What surgery generally requires burst suppression?
Aneurysm clipping
205
What is a epoch on an BIS tracing?
A signal over 5 - 10 seconds that is analyzed to give you an BISnumber
206
What BIS number correlates to normal awake state?
85 - 100
207
What BIS number is consistent with GA?
40 - 60
208
What BIS number correlates to cortical electrical silence?
0
209
What are common causes of single seizures?
Single seizures may result from transient abnormalities such as hypoglycemia, hyponatremia, hyperthermia, brain injury, and drug toxicity
210
What factors are common to focal seizures
“Partial” seizure
Start in a particular part of brain
Feel/see/hear things that aren’t there
Can be mistaken for mental illness
211
What seizure is also known as a partial seizure?
Focal seizures
212
What factors are common to generalized seizures?
213
What kind of seizures may start as one kind and become another?
Unknown-onset seizures
214
What kind of seizure commonly displays rhythmic jerking?
Clonic seizures
215
What kind of seizure is much more common in kids than adults?
Absence or petit mal seizures
216
What seizure has the hallmark symptom of making you fall?
Atonic
217
T/F: MS is not an a contraindication to neuraxial anesthesia
True
217
What kind of s/sx would you expect to see in petit mal seizures?
Eyes rolling back and/or staring into space
218
What anti-seizure drugs works by reducing the inward voltage gated positive currents?
Lamotrigine (Lamictal)
Carbamazine (Tegretol)
219
What anti-seizure drugs works by increasing inhibitory neurotransmitter activity (GABA)?
Valproate
220
What kind of seizure activity would be classified as status epilepticus?
Two or more seizures without return of consciousness or a continuous seizure
221
What anti-seizure drugs works by decreasing excitatory neurotransmitter activity (glutamate, aspartate)?
Keppra
*Keppra binds to SV2 (synaptic vesicle protein 2A to inhibit release of NT)*
222
What is the primary concern with older generation anti-seizure drugs?
CYP-450 upregulation
222
What drugs are commonly used to manage MS relapse symptoms?
Corticosteroids: anti-inflammatory effects, help restore BBB
Interferon: limited to patients with rapidly progressing symptoms
Limited d/t: Flu-like symptoms, depression, liver tox, and rarely cardiac toxicity
Azathioprine: purine analogue
Immunosuppressant
Off-label
Methotrexate:
Immunosuppressant/anti-inflammatory
slows progression/off label
223
What anesthetic drugs/agents should be avoided if seizures are a concern?
Etomidate and demerol
224
Status epilepticus treatment?
Airway
Ventilation
Treatment of hypoglycemia
Antiepileptic anesthetics– i.e. benzos, barbs, prop
Arterial Blood gases
Muscle relaxants
225
T/F: MS can affect both the PNS and CNS
True, though MS primarily damages the CNS
226
What is a common 1st sign of MS?
Visual disturbances
226
What are the 3 primary characteristics of MS?
Inflammation
Demyelination
Axonal damage in the CNS (not PNS)
226
What disease process is described as an acute inflammatory demyelinating polyradiculoneuropathy?
Guillain Barre
226
What s/sx may indicate spinal cord dysfunction in MS?
Paresthesia , weakness, incontinence
227
What paralytic should be avoided in MS?
Sux (too many ACh receptors, they are very sensitive to sux s/e) whereas they are resistant to NDMR d/t the upregulation of ACh receptors
227
T/F: MS treatment medication regimen is focused on slowing disease progression?
False: we cannot alter/slow progression of the disease, medical treatment is focused on decreasing the duration of relapse symptoms
227
What are common anesthetic management strategies in GBS?
ETT (MAC likely not appropriate)
Could have airway reflex dysfunction
Respiratory compromise
Consider arterial line
Avoid succinylcholine, use NMDR judiciously
Prepare for postop ventilation
228
T/F: you should continue MS medical regimen the day of surgery
True
229
What is the concern in MS patients undergoing GA if they are on baclofen?
Baclofen increases their sensitivity to NDMRs
229
How is GBS commonly diagnosed?
By symptoms; sudden onset of skeletal muscle weakness or paralysis
First sign is usually “Pins and needles”/numbness
Weakness begins in legs and spreads to upper body
230
What is the most important risk factor for Parkinsons?
Increasing age
230
What are the 2 serious signs r/t Guillain Barre?
Difficulty swallowing and impaired ventilation
231
What are common risk factors for MS relapse?
Fever
Hyperthermia (Even temp increase of 1 degree can exacerbate symptoms)
Infection
Emotional stress – Versed pre-op!
232
Which catecholamine has decreased production in Parkinsons?
Norepi
232
What are the common characteristics of Parkinson's disease?
Unknown cause
Loss of dopaminergic fibers from the basal ganglia (movement)
Decreased norepinephrine production (ANS function)
Clumps of protein: alpha-synuclein (Lewy bodies)
233
What is the common pneumonic used to help remember Parkinsons symptoms?
T- tremor
R - rigidity
A - akinesia
P - posture/balance
233
When are tremors most prominent in Parkinsons?
At rest
233
What are the 2 drugs of choice to treat Parkinsons (include how they work)?
Levodopa
Crosses BBB and increases amount of dopamine
Carbidopa (decarboxylase inhibitor)
Prevents Levodopa breakdown prior to reaching BBB
233
What occurs to the muscles in GBS?
The muscles denervate, leading to upregulation of ACh receptors
234
Where does muscle rigidity first appear in Parkinsons?
Proximal muscles of the neck - creating the characteristic "loose arm swinging"
234
What kind of autonomic dysfunction s/sx are common to GBS?
BP fluctuations
HTN with laryngoscopy
HOTN with position/positive airway pressure
Resting tachycardia
Profuse diaphoresis
Orthostatic hypotension
Sudden death
235
What anesthetic plan should be considered first in Alzheimers?
TIVA - they tolerate it better than volatiles
235
What is the name for the clumps of protein in Parkinsons?
Alpha-synuclein (Lewy bodies)
236
What is the triad of symptoms in Parkinsons?
Skeletal muscle tremor
Rigidity
Akinesia
237
What surgery may help treat Parkinsons symptoms?
DBS insertion
237
What are the common s/e of Levodopa/Carbidopa therapy?
Side effects: Dyskinesias, altered myocardial contractility, orthostatic hypotension, N/V
238
What condition has a poorly understood cause, cortical atrophy, and changes in memory/mood/emotion/function?
Alzheimers
238
What is the primary treatment goal in Parkinsons?
Increase dopamine in the basal ganglia
239
What condition is a rare genetic disease, characterized by as a movement disorder, enlargement of the lateral ventricles and has mental health symptoms such as outbursts and depression?
Huntingtons
239
What condition is characterized by degeneration of motor neurons leading to progressive paralysis that is eventually fatal with no known cure?
ALS - Lou Gehrigs disease
240
At what receptors do anti-cholinergics primarily work at?
Muscarinic receptors
241
Myasthenia gravis is an autoimmune disorder that is characterized by what changes to the NMJ?
Destruction of post-synaptic nicotinic Acetylcholine receptors at NMJ
As many as 80% may be lost
242
What are common triggers for MG?
Stress, surgery and pregnancy
243
Other than anti-cholinesterase drugs, what can precipitate a cholinergic crisis?
Pesticides and nerve gas
243
What are the hallmarks symptoms of MG?
Weakness
Rapid exhaustion of voluntary muscles (skeletal) followed by partial recovery with rest
244
How is MG diagnosed?
Blood test
EMG (Electromyography)/Repetitive Nerve Stimulation test
May be caused by a tumor on the thymus gland
245
Why is edrophonium used to help diagnose MG?
It is a short acting anti-cholinesterase, so the effects are brief
*Make sure you give with atropine*
245
What changes would you expect to see if a patient who has MG received a dose of edrophonium?
Rapid improvement in symptoms
246
What s/sx would indicate a cholinergic crisis?
PROFOUND MUSCLE WEAKNESS/FLACCID PARALYSIS CAUSED BY CONTINUOUS DEPOLARIZATION OF THE POSTSYNAPTIC MEMBRANE
*Also excessive PNS effects - SLUDGE*
246
What would your treatment be for a patient in myasthenic crisis?
Give more AChE inhibitor
246
What drugs should be avoided in MG?
Avoid calcium channel blockers or magnesium
CCB inhibit ca2+ from entering cell;
blocking nerve impulse at NMJ
Mag causes muscle weakness
247
The Tensilon test can be used to diagnose what disease(s)?
MG and Lambert-Eaton
248
What are the 2 anti-cholinesterase drugs used to treat MG?
Neostigmine and Pyridostigmine
249
When is immunosuppression indicated in MG?
Indicated when skeletal weakness is not adequately treated with anticholinesterase drugs; very effective but lots of side effects
Steroids
Azathioprine
Cyclophosphamide
Cyclosporin
249
In a myasthenic patient that is deteriorating, if symptoms get worse with edrophonium what kind of crisis are they experiencing?
A cholinergic crisis - overmedication
250
What surgical procedure is intended to induce remission in MG?
Thymectomy - it is the treatment of choice for the majority of MG patients
251
What are common anesthetic management strategies in MG?
High risk for aspiration
Pharyngeal/laryngeal muscles VERY commonly affected
PPI, H2 blocker, prokinetic (Reglan)
Extubate AWAKE
Continue MG medications
Sensitive to opioid & benzo effects… use with caution!
Volatile anesthetics may be sufficient for relaxation
Resistant to depolarizers
Very sensitive to non-depolarizers
Use Sugammadex
Awake extubation
252
What is the relationship of depolarizers and non-depolarizer paralytics in MG?
Resistant to sux, sensitive to non-depolarizers
253
Lambert-Eaton and MG are similar to each other, what muscle changes help differentiate them from each other?
In Lambert-Eaton they have improved muscle strength with repeated use, decreased reflexes and the proximal muscles are more affected than in MG
254
Of the syndromes covered in this lecture series, which do have autonomic dysfunction?
MS, GBS, Parkinsons and LES
*MG is the one that does NOT have autonomic dysfunction*
255
How do MG and LES compare to each other in terms of muscle weakness
MG: weakness worsens with prolonged exercise
LES: weakness improves with prolonged exercise
256
How does nerve stimulation compare in MG and LES?
MG: repeated stimulation leads to an incrementally weaker response
LES: repeated stimulation leads to an incrementally greater response
257
How do reflexes compare in MG vs LES?
MG: DTRs are normal/intact
LES: DTRs are weak or absent
Semester 7 TxWes
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