week 1 neuroanatomy 4 of 4 Flashcards

slide 176-234 (147 cards)

1
Q
A
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2
Q

what is another term for luxury perfusion in the brain

A

cerebral steal

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3
Q

define cerebral steal

A

stealing blood from one area of the brain to another- “blood robbery”

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4
Q

blood vessels in ischemic brain regions characteristic?

A

maximally dilated with an exhausted cerebrovascular reserve

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5
Q

blood vessels in non ischemic brain regions characteristic?

A

blood vessels have tone

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6
Q

what happens to the brain blood vessels (non ischemic and ischemic) when a vasodilator such as nitroprusside is administered

A

vessel in non ischemic brain dilate. flow to nonischemic brain increase- flow to ischemic brain decreases

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7
Q

when a patient is hypoventilated -so CO2 can accumulate- what happens to the brain blood vessels (nonischemic and ischemic)

A

vessel in non ischemic brain dilate. flow to nonischemic brain increase- flow to ischemic brain decreases

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8
Q

vasodilators or hypoventilation help promote _______ in brain blood vessels

A

cerebral steal

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9
Q

what is the robin hood effect

A

inverse steal

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10
Q

how does inverse steal occur

A

when a patient with an ischemic region of brain is hyperventilated (decrease PCO2) blood vessels in non ischemic brain constrict and blood is diverted to ischemic brain.

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11
Q

defined as redistributing more cerebral blood flow from well perfused non ischemic area (rich) to ischemic area (poor)

A

inverse steal (robin hood effect)

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12
Q

the result of hyperventilation to ischemic brain

A

improves blood flow to ischemic brain

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13
Q

CEREBRAL STEAL non ischemic brain -blood flow -vessel diameter ischemic brain -blood flow -vessel diameter

A

non ischemic brain blood flow increases vessel diameter increases ischemic brain blood flow decreases NO CHANGE (maximally dilated)

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14
Q

INVERSE STEAL non ischemic brain -blood flow -vessel diameter ischemic brain -blood flow -vessel diameter

A

non ischemic brain blood flow decreases vessel diameter decreases ischemic brain blood flow increases vessel diameter NO CHANGE(maximally dilated)

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15
Q

what is the result of shivering

A

heat production

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16
Q

Thyroid Hormone (TH) increase heat production by stimulating what pump

A

na/k/atpase

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17
Q

activation of beta receptors in brown fat produces two increased responses?

A

increase sympathetic activity increase basal metabolic rate

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18
Q

who controls heat loss in the brain

A

anterior hypothalamus

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19
Q

how does the body loose heat when overheated? 4 things

A

increase sweating cutaneous vasodilation radiation convection

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20
Q

the thermostat in the hypothalamus compares core body temperature to ??

A

the set point temperature

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21
Q

what do Pyrogens do to the bodies set point temperature? what does this result in?

A

increases the set point- resulting in shivering

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22
Q

what is the role of COX inhibitors (aspirin) and steroids in the production of prostaglandin

A

COX inhibitors decrease the production of prostaglandin

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23
Q

what do pyrogens increase the production of? this leads to …

A

increases production of interleukin - 1 - increase production of prostaglandin E -increase set point temperature - more heat generated- fever

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24
Q

the most common 1 degree brain tumor with grave prognosis with less than 1 year life expectancy.

A

astrocytoma

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25
where is astrocytoma found in the brain treatment?
found in cerebral hemisphere resection, radiation and chemo
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what portion of the adult brain tumor are metastases
Half
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Neurons never give rise to cancer. WHY?
neurons dont divide- so they can't give rise to cancer
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the majority of childhood 1 degree tumors are found where
infratentorial (region of the brain is the area located below the tentorium cerebelli.)
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the majority of adult 1 degree tumors are found where
supratentorial (located above the tentorium cerebelli)
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intracranial tumors clinical presentation is due to mass effects such as...
seizures, dementia, focal lesions.
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do 1 degree brain tumors undergo metastasis
rarely
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intracranial tumors Oligodendroglioma how frequent? rate of growth?
relatively rare slow growing
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intracranial tumors ependymoma found where? can cause? prognosis?
Found in 4th ventricle Can cause hydrocephalus Poor prognosis
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intracranial tumors meningioma how common is this 1 degree brain tumor? occurs where? rate of growth? resectable?
2nd most common 1 degree brain tumor Occurs in convexities of brain and parasigittal region Arise from arachnoid cells external to brain (NOT dura) Slow growing Resectable
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intracranial tumors pituitary adenoma how common? vision effects?
Most commonly prolactinoma Bitemporal hemianopia “ tunnel vision” Hyper or hypo pituitarism are sequelae (consequence)
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Intracranial Tumors Schwannoma how common is this first degree brain tumor? is it resectable? what cranial nerve does it disrupt?
3rd most common 1 degree brain tumor. Schwann cell origin; often localize to VIII nerve - acoustic schwannoma Resectable (able to be removed with surgery)
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etiology of stroke
Atherosclerosis Small or large artery disease
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Risk factors stroke (7)
Diabetes, HTN, Smoking, A fib, Cocaine, Male gender, Advance age
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Acute onset of focal neurological deficits resulting from diminished blood flow is defined as
stroke
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ischemic stroke occurrence
87%
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hemorrhagic stroke occurrence
13%
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History/PE stroke
Aphasia Hemiparesis Loss of vision Coma Cranial nerve palsies Ataxia TIA: neurological deficit \< 24 hrs
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Differential stroke
Tumor, hematoma, abscess, MS, Metabolic (hypoglycemia) neurosyphilis
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Evaluation (tests/blood work) stroke
CT w/o contrast ( to differentiate ischemic vs. hemorrhagic) MRI CBC, glucose , coag, lipid profile EKG and echo Vascular studies
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Treatment stroke
Heparin and aspirin Monitor ICP Thrombolysis Don’t over-treat hypertension (may diminish cerebral perfusion)
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Prevention stroke
Aspirin or clopidogrel Carotid endarterectomy if stenosis is \>60% Anticoagulation Management of hypertension
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Transmissible spongiform ecephalopathies (TSEs) can occur in humans and other animals what is an example of this
mad cow disease (Creutzfeldt-Jakob Disease)
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T/F TSEs are neurologic degenerative diseases that can be transmitted within or between species
True! can be transmitted within or between species
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do TSE's abnormal prions trigger an immune response
no
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Transmissible spongiform ecephalopathies (TSEs) how does death of the host occur?
nerve cell death leading to sponge like holes in brain tissue from insoluble aggregates of abnormal prions in the brain
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symptoms of Transmissible spongiform ecephalopathies
dementia weakened muscles loss of balance
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name the human form of TSE
CJD (Creutzfeldt-Jakob disease)
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Sudden onset of brain electrical activity is defined as
seizures
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seizure presentation
loss of consciousness, sensory or motor or behavior abnormalities
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what can precede a seizure
an aura - subjective sensation / feeling
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diagnostic for seizures
EEG
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\_\_\_\_arise from discrete region, no loss of consciousness
focal (partial)
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adult causes of seizures
tumors, trauma, stroke, infection
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elderly causes of seizures
stroke, tumor, trauma, metabolic, infection
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children causes of seizures
genetic, infection (febrile), trauma, congenital, metabolic
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Todds paralysis is defined as
focal deficit after the attack
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complex seizures signs and symptoms
loss of consciousness hallucinations confusion amnesia
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simple partial seizure may involve
motor, sensory or autonomic function. NO loss of consciousness
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evaluation of seizures
Rule of systemic causes EEG CT/MRI
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treatment of seizures
Phenytoin Carbamazepine
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sustained seizure activity lasting at least 30 minutes
status epilepticus
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status epileptics is a medical emergency due to risk of
hypoxia aspiration rhabdomyolysis multiple trauma
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treatment of seizure
Establish airways “ABC” Adequate oxygenation Glucose +thyiamine Lorazepam – short term control Phenytoin or phenobarbital
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Inflammation and demyelination of PNS motor neurons Associated with viral infections e.g. HZV
Guillain-Berré syndrome
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Lower motor neuron lesions Symmetrical ASCENDING paralysis
Guillain-Berré syndrome
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Guillain-Berré syndrome dreaded complication
respiratory paralysis
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what irregularities are associated with guillain barre syndrome
Cardiac and respiratory irregularities
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Guillain-Berré syndrome diagnosis
increase CSF proteins Slow nerve conduction velocity due to DEMYELINATION
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Guillain-Berré syndrome Treatment
Monitoring vital capacity is critical Plasmapheresis IV immunoglobulin per mo- really theres no treatment- just hope it doesn't affect their diaphragm
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slide 197
slide 197
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Poliomyelitis:
LMN lesion due to destruction of anterior horn cell lead to flaccid paralysis
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Multiple sclerosis:
mostly white matter demyelination; scanning speech, intentional tremors, diplopia, remission and relapses
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Amyotrophic lateral sclerosis:
Both UMN and LMN lesion. No sensory deficit
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Occlusion of anterior spinal artery:
spares dorsal column and tract of lissauer
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Tabes dorsalis (3 degree syphilis):
degeneration of dorsal root and dorsal column tract; impaired proprioception and ataxia
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Syringomyelia:
damage to spinothalamic tract; loss of pain and temperature
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VitB12 deficiency and Friedreich’s ataxia:
demyelination of dorsal column
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EEG activity from ketamine
Ketamine produces unusual activation
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EEG activity from opioids
Opioids produce monophasic depression
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EEG activity from anesthetics
Most anesthetic produce biphasic pattern Activation followed by depression
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what are EEG useful for
assessment of cerebral perfusion
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Reticular Activating System (RAS) what does it maintain
Maintains alert/awake state
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is RAS on or off when sleeping
RAS is OFF when sleeping
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complete loss of RAS activity is
coma
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what does general anesthesia do to the RAS
GA produces sedation and hypnosis by depressing RAS
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dorsal column tract is considered what kind of route
a direct rout
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RAS is considered
INDIRECT ROUT for sensory information reaching to sensory strip
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It Test the integrity of dorsal column (cuneatus and gracilis tracts) and sensory cortex Carries fine touch, pressure, vibration and proprioception sensations
Somatosensory Evoked Potential –SSEP
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during brain and spinal cord surgeries what does the Somatosensory Evoked Potential –SSEP do examples of these surgeries (4)
detects global ischemia from HYPOXIA or ANESTHETIC OVERDOSE Aortic reconstruction Spinal cord tumors Carotid endarterectomy Instrumentation of spine
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when is SSEP altered ( i.e. reduce intensity and delayed arrival in cerebral cortex
in case of ischemic injury to brain and spinal cord
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what nerves are stimulated for SSEP to be recorded from the scalp
tibial, median, or ulnar nerves
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write down the pathway from tibial nerve to sensory cortex
...slide 206
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which somatosensory area? leg arm face
...
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which somatosensory area? thigh thorax neck hsoulder hand fingers tongue abdomen
...
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Stimulation of tibial nerve at ankle must be recorded at the
midline (over longitudinal fissure)
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Stimulation of median/ulnar nerve must be recorded at
Lateral side
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Visual evoked potential used during these 4 procedures
craniofacial procedures pituitary surgery surgery in the visual tracts occipital cortex
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Visual evoked response tracing of amplitude versus time after stimulus. The measurement of latency and amplitude for the negative peak at
70msec
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Components of SSEP early peak "direct" action potentials via
DORSAL COLUMN TRACT
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Components of SSEP Late peak “indirect” Larger Action potentials via
RETICULAR ACTIVATING SYSTEM (RAS)
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Amplitude of SSEP refers to
Magnitude or size of evoked potential
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Latency of SSEP refers to
Time taken by action potential to travel from peripheral nerve -spinal cord - inner brain - cerebral cortex
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decreasing amplitude or increasing latency indicates what about the neural pathway being monitored
indicates damage
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An amplitude reduction of \_\_% or latency increase of \_\_% of an evoked potential is considered significant
50% 10%
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in evoked potential what can smaller changes in amplitude and latency indicate
impending compromise
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in evoked potential management how important is anesthetic management?
Anesthetic management often plays a critical role in the intervention.
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Applications of SSEP
Spinal surgeries Aortic reconstruction Carotid endarterectomy
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Factors affecting SSEP
Hypo or hyperthermia Hypotension PCO2 PO2
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during brain surgery is a noninvasive technique for measuring neural functions, e.g. during acoustic neuroma resection where the vestibulocochlear nerve ( CN VIII) at risk
Brainstem Auditory Evoked Potential (BAEP)
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how is Brainstem Auditory Evoked Potential (BAEP) elicited
by auditory click, tones
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what can Brainstem Auditory Evoked Potential (BAEP) detect
Detects global ischemia or anesthetic overdose
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can be used to monitor the optic nerve (CN II), anterior visual pathways during craniofacial procedures, pituitary surgery, and surgery in the visual tracts and occipital cortex
Visual evoked potential (VEP's)
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how are Visual evoked potential elicited
by flashes of light
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method of delivering stimulus for Brainstem Auditory Evoked Potential (BAEP)
ear transducer
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I/ V anesthetics effects on evoked potential
fewer effects
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GA and volatile anesthetics have what effect on evoke potentials
have the greatest effect on evoke potentials causing dose dependent decrease amplitude and increase latencies
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how much (compared to other paralytics) does vecuronium have an effect on evoked potential
least effect
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evoked potentials monitoring order for sensitivity to anesthetic agents
VEP \> SSEP \> BAEP [Very ; Somewhat ; Barely]
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XII hypoglossal
Genioglossus muscle (tongue)
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Monitoring Site or Method XI spinal accessory
Sternocleidomastoid and/or trapezius muscles
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Monitoring Site or Method X vagus
Vocal folds, cricothyroid muscle
127
monitoring site or method IX glossopharyngeal
Stylopharyngeus muscle (posterior soft palate)
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Monitoring Site or Method VIII auditory
Auditory brainstem responses
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Monitoring Site or Method VII facial
Orbicularis oculi and/or orbicularis oris muscles
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Monitoring Site or Method VI abducens
Lateral rectus muscle
131
Monitoring Site or Method V trigeminal
Masseter muscle and/or temporalis muscle [sensory responses can also be monitored]
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Monitoring Site or Method IV trochlear
Superior oblique muscle
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monitoring site or method III oculomotor
Inferior rectus muscle
134
monitoring site or method II optic
Visual evoked potentials
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monitoring site or method I olfactory
No monitoring technique
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Neurocranium consists of 8 bones
Frontal Ethmoid Sphenoid Occipital Temporal (pair) Parietal (pair)
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Viscerocranium consists of 15 irregular bones
Mandible Ethmoid Vomer Maxilla (pair) Inferior nasal choncha (pair) Zygomatic (pair) Palantine (pair) Nasal (pair) Lacrimal (pair)
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Neurophysiologic monitoring with EMG and evoked sensory and motor responses has become an important tool - these methods have demonstrated
reduce morbidity and have become a standard of care provide greater assistance to the surgeon indispensable intraoperative diagnostic tool
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what type of anesthesia is preferred during motor evoke potential
IV anesthetics as it suppresses MEP less than inhaled agents
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motor evoke potential is monitor in patients with what
neurologic disease
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with use of total IV anesthesia. MEP's are successfully obtained in more than what percent of patients
90%
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failures with MEP are associated with what two things
preexisting neurotic disorders or equipment failure
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The pathway synapses in the anterior horn of the spinal cord and the response travels to the muscle via the neuromuscular junction (NMJ). The response is typically recorded near the muscle as a compound muscle action potential (CMAP). what evoked potential is this
motor evoked potential
144
Motor evoked potentials
are produced by stimulation of the motor cortex (hollow arrow). The response can be recorded epidurally over the spinal column as a D wave followed by a series of I waves.
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slide 222
slide 222
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