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SUM'20 - Anatomy & Physiology > week 1 neuroanatomy 4 of 4 > Flashcards

week 1 neuroanatomy 4 of 4 Flashcards

slide 176-234

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
Q

where is astrocytoma found in the brain

treatment?

A

found in cerebral hemisphere

resection, radiation and chemo

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26
Q

what portion of the adult brain tumor are metastases

A

Half

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27
Q

Neurons never give rise to cancer. WHY?

A

neurons dont divide- so they can’t give rise to cancer

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28
Q

the majority of childhood 1 degree tumors are found where

A

infratentorial (region of the brain is the area located below the tentorium cerebelli.)

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29
Q

the majority of adult 1 degree tumors are found where

A

supratentorial (located above the tentorium cerebelli)

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30
Q

intracranial tumors clinical presentation is due to mass effects such as…

A

seizures, dementia, focal lesions.

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31
Q

do 1 degree brain tumors undergo metastasis

A

rarely

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32
Q

intracranial tumors Oligodendroglioma how frequent? rate of growth?

A

relatively rare slow growing

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33
Q

intracranial tumors ependymoma found where?

can cause?

prognosis?

A

Found in 4th ventricle Can cause hydrocephalus Poor prognosis

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34
Q

intracranial tumors meningioma how common is this 1 degree brain tumor?

occurs where?

rate of growth?

resectable?

A

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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35
Q

intracranial tumors

pituitary adenoma

how common?

vision effects?

A

Most commonly prolactinoma Bitemporal hemianopia “ tunnel vision” Hyper or hypo pituitarism are sequelae (consequence)

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36
Q

Intracranial Tumors

Schwannoma how common is this first degree brain tumor?

is it resectable?

what cranial nerve does it disrupt?

A

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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37
Q

etiology of stroke

A

Atherosclerosis Small or large artery disease

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38
Q

Risk factors stroke (7)

A

Diabetes, HTN, Smoking, A fib, Cocaine, Male gender, Advance age

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39
Q

Acute onset of focal neurological deficits resulting from diminished blood flow is defined as

A

stroke

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40
Q

ischemic stroke occurrence

A

87%

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41
Q

hemorrhagic stroke occurrence

A

13%

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42
Q

History/PE stroke

A

Aphasia

Hemiparesis

Loss of vision

Coma

Cranial nerve palsies

Ataxia

TIA: neurological deficit < 24 hrs

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43
Q

Differential stroke

A

Tumor, hematoma, abscess, MS, Metabolic (hypoglycemia) neurosyphilis

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44
Q

Evaluation (tests/blood work) stroke

A

CT w/o contrast ( to differentiate ischemic vs. hemorrhagic) MRI CBC, glucose , coag, lipid profile EKG and echo Vascular studies

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45
Q

Treatment stroke

A

Heparin and aspirin

Monitor ICP

Thrombolysis

Don’t over-treat hypertension (may diminish cerebral perfusion)

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46
Q

Prevention stroke

A

Aspirin or clopidogrel

Carotid endarterectomy if stenosis is >60%

Anticoagulation

Management of hypertension

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47
Q

Transmissible spongiform ecephalopathies (TSEs) can occur in humans and other animals what is an example of this

A

mad cow disease (Creutzfeldt-Jakob Disease)

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48
Q

T/F TSEs are neurologic degenerative diseases that can be transmitted within or between species

A

True! can be transmitted within or between species

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49
Q

do TSE’s abnormal prions trigger an immune response

A

no

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50
Q

Transmissible spongiform ecephalopathies (TSEs) how does death of the host occur?

A

nerve cell death leading to sponge like holes in brain tissue from insoluble aggregates of abnormal prions in the brain

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51
Q

symptoms of Transmissible spongiform ecephalopathies

A

dementia

weakened muscles

loss of balance

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52
Q

name the human form of TSE

A

CJD (Creutzfeldt-Jakob disease)

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53
Q

Sudden onset of brain electrical activity is defined as

A

seizures

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54
Q

seizure presentation

A

loss of consciousness, sensory or motor or behavior abnormalities

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55
Q

what can precede a seizure

A

an aura - subjective sensation / feeling

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56
Q

diagnostic for seizures

A

EEG

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57
Q

____arise from discrete region, no loss of consciousness

A

focal (partial)

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58
Q

adult causes of seizures

A

tumors, trauma, stroke, infection

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59
Q

elderly causes of seizures

A

stroke, tumor, trauma, metabolic, infection

60
Q

children causes of seizures

A

genetic, infection (febrile), trauma, congenital, metabolic

61
Q

Todds paralysis is defined as

A

focal deficit after the attack

62
Q

complex seizures signs and symptoms

A

loss of consciousness hallucinations confusion amnesia

63
Q

simple partial seizure may involve

A

motor, sensory or autonomic function. NO loss of consciousness

64
Q

evaluation of seizures

A

Rule of systemic causes EEG CT/MRI

65
Q

treatment of seizures

A

Phenytoin Carbamazepine

66
Q

sustained seizure activity lasting at least 30 minutes

A

status epilepticus

67
Q

status epileptics is a medical emergency due to risk of

A

hypoxia

aspiration

rhabdomyolysis

multiple trauma

68
Q

treatment of seizure

A

Establish airways “ABC”

Adequate oxygenation

Glucose +thyiamine

Lorazepam – short term control

Phenytoin or phenobarbital

69
Q

Inflammation and demyelination of PNS motor neurons Associated with viral infections e.g. HZV

A

Guillain-Berré syndrome

70
Q

Lower motor neuron lesions Symmetrical ASCENDING paralysis

A

Guillain-Berré syndrome

71
Q

Guillain-Berré syndrome dreaded complication

A

respiratory paralysis

72
Q

what irregularities are associated with guillain barre syndrome

A

Cardiac and respiratory irregularities

73
Q

Guillain-Berré syndrome diagnosis

A

increase CSF proteins Slow nerve conduction velocity due to DEMYELINATION

74
Q

Guillain-Berré syndrome Treatment

A

Monitoring vital capacity is critical

Plasmapheresis

IV immunoglobulin

per mo- really theres no treatment- just hope it doesn’t affect their diaphragm

75
Q

slide 197

A

slide 197

76
Q

Poliomyelitis:

A

LMN lesion due to destruction of anterior horn cell lead to flaccid paralysis

77
Q

Multiple sclerosis:

A

mostly white matter demyelination; scanning speech, intentional tremors, diplopia, remission and relapses

78
Q

Amyotrophic lateral sclerosis:

A

Both UMN and LMN lesion. No sensory deficit

79
Q

Occlusion of anterior spinal artery:

A

spares dorsal column and tract of lissauer

80
Q

Tabes dorsalis (3 degree syphilis):

A

degeneration of dorsal root and dorsal column tract; impaired proprioception and ataxia

81
Q

Syringomyelia:

A

damage to spinothalamic tract; loss of pain and temperature

82
Q

VitB12 deficiency and Friedreich’s ataxia:

A

demyelination of dorsal column

83
Q

EEG activity from ketamine

A

Ketamine produces unusual activation

84
Q

EEG activity from opioids

A

Opioids produce monophasic depression

85
Q

EEG activity from anesthetics

A

Most anesthetic produce biphasic pattern Activation followed by depression

86
Q

what are EEG useful for

A

assessment of cerebral perfusion

87
Q

Reticular Activating System (RAS) what does it maintain

A

Maintains alert/awake state

88
Q

is RAS on or off when sleeping

A

RAS is OFF when sleeping

89
Q

complete loss of RAS activity is

A

coma

90
Q

what does general anesthesia do to the RAS

A

GA produces sedation and hypnosis by depressing RAS

91
Q

dorsal column tract is considered what kind of route

A

a direct rout

92
Q

RAS is considered

A

INDIRECT ROUT for sensory information reaching to sensory strip

93
Q

It Test the integrity of dorsal column (cuneatus and gracilis tracts) and sensory cortex Carries fine touch, pressure, vibration and proprioception sensations

A

Somatosensory Evoked Potential –SSEP

94
Q

during brain and spinal cord surgeries what does the Somatosensory Evoked Potential –SSEP do examples of these surgeries (4)

A

detects global ischemia from HYPOXIA or ANESTHETIC OVERDOSE

Aortic reconstruction

Spinal cord tumors

Carotid endarterectomy

Instrumentation of spine

95
Q

when is SSEP altered ( i.e. reduce intensity and delayed arrival in cerebral cortex

A

in case of ischemic injury to brain and spinal cord

96
Q

what nerves are stimulated for SSEP to be recorded from the scalp

A

tibial, median, or ulnar nerves

97
Q

write down the pathway from tibial nerve to sensory cortex

A

…slide 206

98
Q

which somatosensory area? leg arm face

A

…

99
Q

which somatosensory area? thigh thorax neck hsoulder hand fingers tongue abdomen

A

…

100
Q

Stimulation of tibial nerve at ankle must be recorded at the

A

midline (over longitudinal fissure)

101
Q

Stimulation of median/ulnar nerve must be recorded at

A

Lateral side

102
Q

Visual evoked potential used during these 4 procedures

A

craniofacial procedures pituitary surgery surgery in the visual tracts occipital cortex

103
Q

Visual evoked response tracing of amplitude versus time after stimulus. The measurement of latency and amplitude for the negative peak at

A

70msec

104
Q

Components of SSEP early peak “direct” action potentials via

A

DORSAL COLUMN TRACT

105
Q

Components of SSEP

Late peak

“indirect” Larger Action potentials via

A

RETICULAR ACTIVATING SYSTEM (RAS)

106
Q

Amplitude of SSEP refers to

A

Magnitude or size of evoked potential

107
Q

Latency of SSEP refers to

A

Time taken by action potential to travel from peripheral nerve -spinal cord - inner brain - cerebral cortex

108
Q

decreasing amplitude or increasing latency indicates what about the neural pathway being monitored

A

indicates damage

109
Q

An amplitude reduction of __% or latency increase of __% of an evoked potential is considered significant

A

50% 10%

110
Q

in evoked potential what can smaller changes in amplitude and latency indicate

A

impending compromise

111
Q

in evoked potential management how important is anesthetic management?

A

Anesthetic management often plays a critical role in the intervention.

112
Q

Applications of SSEP

A

Spinal surgeries Aortic reconstruction Carotid endarterectomy

113
Q

Factors affecting SSEP

A

Hypo or hyperthermia Hypotension PCO2 PO2

114
Q

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

A

Brainstem Auditory Evoked Potential (BAEP)

115
Q

how is Brainstem Auditory Evoked Potential (BAEP) elicited

A

by auditory click, tones

116
Q

what can Brainstem Auditory Evoked Potential (BAEP) detect

A

Detects global ischemia or anesthetic overdose

117
Q

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

A

Visual evoked potential (VEP’s)

118
Q

how are Visual evoked potential elicited

A

by flashes of light

119
Q

method of delivering stimulus for Brainstem Auditory Evoked Potential (BAEP)

A

ear transducer

120
Q

I/ V anesthetics effects on evoked potential

A

fewer effects

121
Q

GA and volatile anesthetics have what effect on evoke potentials

A

have the greatest effect on evoke potentials causing dose dependent decrease amplitude and increase latencies

122
Q

how much (compared to other paralytics) does vecuronium have an effect on evoked potential

A

least effect

123
Q

evoked potentials monitoring order for sensitivity to anesthetic agents

A

VEP > SSEP > BAEP [Very ; Somewhat ; Barely]

124
Q

XII hypoglossal

A

Genioglossus muscle (tongue)

125
Q

Monitoring Site or Method XI spinal accessory

A

Sternocleidomastoid and/or trapezius muscles

126
Q

Monitoring Site or Method X vagus

A

Vocal folds, cricothyroid muscle

127
Q

monitoring site or method IX glossopharyngeal

A

Stylopharyngeus muscle (posterior soft palate)

128
Q

Monitoring Site or Method VIII auditory

A

Auditory brainstem responses

129
Q

Monitoring Site or Method VII facial

A

Orbicularis oculi and/or orbicularis oris muscles

130
Q

Monitoring Site or Method VI abducens

A

Lateral rectus muscle

131
Q

Monitoring Site or Method V trigeminal

A

Masseter muscle and/or temporalis muscle [sensory responses can also be monitored]

132
Q

Monitoring Site or Method IV trochlear

A

Superior oblique muscle

133
Q

monitoring site or method III oculomotor

A

Inferior rectus muscle

134
Q

monitoring site or method II optic

A

Visual evoked potentials

135
Q

monitoring site or method I olfactory

A

No monitoring technique

136
Q

Neurocranium consists of 8 bones

A

Frontal Ethmoid Sphenoid Occipital Temporal (pair) Parietal (pair)

137
Q

Viscerocranium consists of 15 irregular bones

A

Mandible Ethmoid Vomer Maxilla (pair) Inferior nasal choncha (pair) Zygomatic (pair) Palantine (pair) Nasal (pair) Lacrimal (pair)

138
Q

Neurophysiologic monitoring with EMG and evoked sensory and motor responses has become an important tool - these methods have demonstrated

A

reduce morbidity and have become a standard of care provide greater assistance to the surgeon indispensable intraoperative diagnostic tool

139
Q

what type of anesthesia is preferred during motor evoke potential

A

IV anesthetics as it suppresses MEP less than inhaled agents

140
Q

motor evoke potential is monitor in patients with what

A

neurologic disease

141
Q

with use of total IV anesthesia. MEP’s are successfully obtained in more than what percent of patients

A

90%

142
Q

failures with MEP are associated with what two things

A

preexisting neurotic disorders or equipment failure

143
Q

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

A

motor evoked potential

144
Q

Motor evoked potentials

A

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.

145
Q

slide 222

A

slide 222

146
Q
A
147
Q
A

SUM'20 - Anatomy & Physiology (11 decks)

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