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Neurology - step > anatomy and phyisology part 2 > Flashcards

anatomy and phyisology part 2 Flashcards

1
Q

watershed areas of the brain

A

ACA and MCA - upper leg and upper arm weakness

PCA/MCA - higher order visual processing

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2
Q

ACA supplies

A

along olfactory bulbs on inferior surface of brain and medial parietsla dn fromtal lobes and then just arms on the medial surface

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3
Q

MCA supplies

A

inferior frontal poles and then superior temporal on the medial side and medial surface fo frontal and parietal lobes

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4
Q

PCA supplies

A

infetiot temporal and occipital and then interior temporal on medial border

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5
Q

what is most common site of aneurysm in the circle of willic

A

anterior communicationt

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6
Q

occlusion to the anterior cerebra; =

A

lower limb affected

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7
Q

occlusion of the middle cerebral

A

upper limb and face weakness and werknickes (fluent, impaired comphrehension and cannto repeat)

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8
Q

sxs of aneurysm in the posterior communicating

A

can affect CN III - down and out, ptosis, pupillary light reflex and vasodilation

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9
Q

occlusion of the posterior cerebral

A

hemanopia with macular sparing

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10
Q

two vessels that sandwich cranial nerve III

A

posterior cerebral and superior cerebellar

** also near CN VI

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11
Q

branches of the internal carotid please

A

middle cerebral – ophthalmic and the lenticulstriacte

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12
Q

what events can occur in the middle cerebral

A

thrombotic iscahemic strokes

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13
Q

what events typicaly occur at the lenticulostriate vesesl

A

hypertension

hemorrhagic stroke

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14
Q

symptoms of issues with lenticulostriate blood supply loss

A

hemiparesis
hemiplegia
(striatum and internal capsule)

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15
Q

anterior inferior cerebellar acrtery occlusion

A

lateral pontine CNVII

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16
Q

posterior inferior cerebellar artery occlusion

A

lateral medullary CNX

WALLENBERG SYNDROME

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17
Q

what is wallenbuerg syndrome

A

lateral medullary with CN X

PICA occlusion

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18
Q

anterior spinal artery occlusion

A

medial medullary syndrome
at spc - all but the dorsla colomns
CN XII

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19
Q

what is the homunculus

A

topgraphic representation of motor and sensory areas in the cerebral cortex. distorted appearance bc certain body regions are more richly innervated and thus have increased cortical represertnation.

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20
Q

describe the layout of the homunculus

A

feet dangle over the medial border with the kneea t the top. then roso and shoulders and elbow and arms. hands are at about 1-2 oclock and eyes thake over till reach chin at about 3 oclock then have toge at foru oclock lateral side

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21
Q

how is cerebral perfusion regulation

A

on tight autoregulation between 60- 150 mmHg

primarily driven by PCO2 with influence of PO2 in severe hypoxemia (less than PO2=50)

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22
Q

describe PO2 effect on cerebral blood flow

A

when PO2 reaches levels below 50 mmHg, will cause vasodilation to increased blood flow
above PO2 fo 50 mmHg, see no effect on cerebral blood flow

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23
Q

describe PCO2 effects on cerebral blood flow

A

at PCO2 of 0 to PCO2 of 90 see an increased in cerebral perfusion - then levels off
PCO2 causes vasodilation at increasing levls

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24
Q

how can you use the autoregulation of cerebral blood flow therapeutically

A

if person has increased ICP - hyperventilate to decrease bc lower levels of PCO2 cause vasoconstriction

ie in cases of cerebral oedema - want to hyperventilate to decrease PCO2 and have less blod flow

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25
Q

pathophys of fainting in a panic attack please

A

hyperventilation in panic attack leads to dereased PCO - less vasodlation - less cerebral blood flow - fainting.

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26
Q

what does cerebral perfusion depend on

A

a gradient between system blood flow and icp

CPP = MAP-ICP

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27
Q

what is the influence of MAP and ICP on CPP?

A

MAP decreases = decreased CPP
ICP increases = decreased CPP
CPP = MAP - ICP

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28
Q

what happens if CPP is zero

A

no cerebral perfusion - brain death

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29
Q

what is an aneurysm

A

an abnormal dilation of artery due to weakening of the vessel wall

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30
Q

what is a saccular/berry anuerysm

A

occurs at the birucrations in the circle of willis

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31
Q

most common site of berry anuerysm

A

anterior communicating and anterior cerebral artery junction

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32
Q

what is the most common compliation of berry aneurysms and the consequences

A

most common complication of berry aneurysm is RUPTURE – subarachnoid hemorrhage ‘‘worst headache of my life’’ or hemorrhagic stroke

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33
Q

if presents wit bitemporal heminanopia look for

A

prolactinoma/craniopharyngioma/aneurysm in AComm/ACA

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34
Q

what are risk factors for berry aneurysms

A 
Ehlers Danlos
ADPKD
advanced age
hypertension
smoking
increased incidence in blacks
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35
Q

what is a charcto-bouchard microaneurysm

A

affects small vessels ie lenticulostriates
associated with chronic hypertension
basal ganglia and thalamus (internal capsule)

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36
Q

describe central post stroke pain syndrome

A

neuropathic pain due to thalamic lesions
intintall:paresthesias –> week to month slater allogynia (ordinary non painful stimuli cause severe pain) and dysestheisa (imparment of sensation sp touch)
10% of stroke pateitns

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37
Q

pt presentation: paresthesias then weeks/months later have allodynia and dyesthesias

A

thalamic lesions
central post stroke pain syndrome
**think of like UMN and LMN lesions in spinal cord injury)

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38
Q

epidural hematoma pathogenesis

A

rupture of middle meningeal artery (maxillary artery branch - Dr Curry KBT) - secondary to temporal bone

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39
Q

epideurla hemoatome presetnation

A

lucid invtercail
rapid expansion - systemic arterial pressure
biconvex/lentiform with hyperdense blood collection

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40
Q

epidural hematoma local

A

no cross suture lines

yes croos falx and tentorium

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41
Q

pathogenesis of subdural hematoma

A

rupture of bridging veins

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42
Q

presentation of subdural hematoma

A

@ risk groups: elderly, OHics, infants, blunt trauma ie brain atrophy, shaking, whiplash

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43
Q

clinical findings in subdural hematoma

A

crescent shaped hemorrhaces
crosses suture lines
cannot corss falx or tentorium
can present with acute ( lighter on imaging) and chronic (darker on imaging)

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44
Q

pathogenesis of subarachnoid hemorrhage

A

rupture of an aneurysm (berr in ED or ADPKD) or arteriovenous malformation

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45
Q

presentation of subarachnoid hemorrhage

A

rapid time course
worst headache of my life
blood or xanthochromic/yellow spinal tap
2-3 days later have risk of vasospasm due to blood break down and rebleed

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46
Q

how to treat vasospasm post subarachnoid hemorrhage

A

NIMODIPINE CCB

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47
Q

nimodipine

A

CCB used to treat vasospasm post subarachnoid hemorrahace

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48
Q

what is an intraparenchymal hemorrhage

A

most commonly cause by systemic hypertension

also see with amyloid angiopathy, vasculitis, neoplasm

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49
Q

where do intraparenchymal hemorrhages typical occur

A

int he basal cganglia and internal capsule - charcot bouchard aneurysms of lenticulostriate cessels
can be lobar

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50
Q

who is at risk of itnraparenchymal hemorrages

A

pts with hypertension
amyloid angiopathy in elderly
vasculitis
neoplams

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51
Q

what is recurrent lobar hemorrhagic stroke

A

in elder with amyloid angiopathy

a intraparenchymal hemorrhage

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52
Q

compare how subarachoid vrs intraparenchymal strokes show up on imaging

A

subarachoind - along folds of brain surface

intraparenchymal - blob

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53
Q

how long does it take to get irrevesribel damage in ischaemic brain disease

A

within 5 minutes

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54
Q

which areas of the brain are most vulnerable to ischemic brain disease

A

hippocampus
neocortex
cerebellum
watershed

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55
Q

what do hippocampus, neocortex, cerebellum and watershed areas have in common

A

most vulnerable to iscahemic brain trauma

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56
Q

what must do before can give tPa for strokes

A

noncontrast CT to exclude hemorrhage

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57
Q

when will CT detect ischemic changes

A

6-24 hours after event

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58
Q

when will diffusion weighter MRI detect iscahemic changes

A

3-30 mins post event

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59
Q

histologic feature of icahemic damage and time course pelase

A 
12-48 hours - red neurons
24-72 hours - necrosis and PMN
3-5 days - macrophages/microglia
1-2 weeks - reactive gliosis and vascular proligeration
>2 weeks - glial scar
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60
Q

histo feature of ischaemic changes @ 12-48 hours

A

red neurons

61
Q

histo feature of ischaemic changes @ 24-72 hours

A

PMN and necrosis

62
Q

histo feature of ischaemic changes @ 3-5 days

A

microglia/macrophages

63
Q

histo feature of ischaemic changes @ 1-2 weeks

A

reactive gliosis and vascular proliferation

64
Q

histo feature of ischaemic changes @ > 2 weeks

A

glial scar

65
Q

when do you see red neurmos

A

post iscahemic trauma 12-48 hours

66
Q

when do you see necrosis and PMNs

A

24-72 hours post iscahemic trauma

67
Q

when do you see microglia

A

3-5 days post iscahemic trauma

68
Q

when do you see reactive gliosis and vascular proliferation

A

1-2 weeks post ischaemic trauma

69
Q

when do you see glial scar

A

> 2 weeks post iscahemic trauma

70
Q

what is a hemorrhagic stroke

A

intracerebral bleeding

71
Q

what causes hemorrhagic stroke

A

hypertension
anticoagulation
cancer - abnormal cessels
secondary to ischemic stroke followed by reperfusion - increased vessel fragility

72
Q

where is the most common site for intracerebral hemorrhage

A

the basal ganglia (hypertension, anticoagulation, caner)

73
Q

what is an iscahemic stroke

A

acute blockage of vessels - disruption of blood flow and subsequent ischemia = LIQUEFACTIVE NECROSIS

74
Q

what are the three types of iscahemic stroke

A

thrombotic
embolic
hypoxic

75
Q

describe a thrombotic iscahemic stroke

A

due to clot forming directly at side of infarction usually over an atherosclerotic plaque

76
Q

where is most common site of thrombotic iscahemic stroke

A

MCA

77
Q

describe an embolic iscahemic stroke

A

embolus from another part of the body obstructs vessels. can affect MULTIPLE VASCULAR territories

78
Q

what are risk factors for embolic ischaemic strokes

A

atrial fibrillation

DVT with patent foreamen ovale (paradoxical)

79
Q

describe hypoxic iscahemic stroke please

A

due to hypoperfusion or hypoxemia

common during cardiovascular surgeries @ water shed areas

80
Q

where do hypoxic ischameic strokes tend to occur

A

during cardiovascular surgeries @ water shed areas

81
Q

how to treat ischaemic strokes

A

with tPA if within 3-4.5 hours of onste and no righ of hemorrahge

82
Q

how do you reduce risk of stroke

A

medical therapy - aspirin and clopidogrel
contrl bp, sugars, lipids
treat conditions with increase risk ie atrial fibrillation

83
Q

what is a transient iscahemic attack

A

brief, reversible episode of focal neurologic dysfunction without acute infarction - show on MRI (3-30 mins; diffusion weighted)
majority resolve in 15 mins
deficits - due to focal iscahemia

84
Q

what are dural venous sinuses

A

large cenous channels that run through the dura. drain blood from cerebral veisn and received CSF from arachnoid granulations – empty into internal ugular vein

85
Q

pathway from superior sagittal to internal jugular vein pelase

A

superior sagittal - confluence of sinuses (meets up with straight sinus collecting from intferior sagittal sinus and the gret cerebral vein of galen AND the occipital sinus) - transveres - sigmoid - intrenal jugular

86
Q

what two veins drain into the cavernous sinus

A

superior opthlamic vein
sphenoparietal sinus
TRIANGLE OF DOOM or something like that on face

87
Q

describe the pathway of CSF drainage through the ventricular system

A

arachnoid villi – lateral ventricles – foramen of monro – third ventricles – cerebral aqueduct of slyvius - foruth ventricle - subarachonoid space via foramina of luschka and framen of magendie

88
Q

describe pseudotumor cerebri

A

idiopathic intracranial hypertension - increased ICP with no apparent cause on imaging (ie no hypdrocephalus or obstruction fot CSF flow)

89
Q

headache
diplopia
no metnal stauts alteration
papillemdema

A

psuedotumor cerebri/idiopathic intracranial hypertension

90
Q

what are risk factors for pseudotumor cerebri

A

women of childbearing age
vitamin A excess
danazol

91
Q

how to treat psuedotumor cerebri

A

LPs will have high opening pressure and procide headache relief
weight loss and acetazolamide, and topiramtae,

92
Q

what if initital treatment for pseudotumor cerebri don’t work

A

invasive for refractory cases - repeated LPs, CSF shunt placemnt, optic nerve fenestration surger

93
Q

what Cn usually causes diplopia in pseudotumor cerebri

A

CNVI palsy

94
Q

what is communicating hydrocephalus

A

decreased CSF absorption by arachnoid granulations - increased ICP, papilloedema, hernation

95
Q

what causes communicating hydrocephalu

A

arachnoid scarring post meningitis

96
Q

what is normal pressure hydrocephalus

A

often in elderly, idiopathyic
CSP pressure elecated ony episodically
no increase in subarachoind spave colume

97
Q

describe symptoms of normal pressure hydrocephalus

A

ventricles expand and distort the fibres of the corona radiate – wobbly wet and wacky/weird.
urinary incontinence
ataxia
congintive dysfunction

98
Q

what is non communicating hydrocephalus

A

structural blockage of CSF circulation in the ventricular system
ie stenosis of aqueduct of sylvious, colloid cyst blocking foramen of monro

99
Q

what is e vacuo ventriculomegaly

A

appearance of icnreaesd CSF of imagine but is actually due to derease brain tissue ie neural atrophy
ICP is normal
no triad

100
Q

patients to suspect ex vacuo ventriculomegaly

A

hydrocephalus mimicry

@ neuronal atrophy in Alzheimer disease, advanced HIV, and Pick disease

101
Q

how many spinal nerve pairs are there

A

31 - 8 c, 12 t, 5 l, 5 s and 1 coccygeal

102
Q

describe a vertebral disc herniation

A

nucleus pulposus the soft cenral disc remnant of the notochord - herniates through the annulus fiboruss

usually postero laterally at L4/5 ro L5/S1

103
Q

where does the spinal cord ened in adults

A

L1/2`

104
Q

where does the subarachnoid space extend to in adults

A

s2

105
Q

where should you poke for the LP

A

L3-5 at the level of the cauda equina

106
Q

to keep the cord alive keep the spinal needle between L 3 and L5

A

thanks fa

107
Q

whats in the fasciculus gracilis?

A

lower bod and legs pvtp

108
Q

whats in the fasciculus cuneatus

A

upper body and arm pvtp

109
Q

whats in the anterior corticospinal tract

A

voluntary motor

110
Q

describe where the cervical region is represented for each tract in the spc

A

cervical for lateral corticospinal tract @ closest to gray matter/medial
cervical for dorsal colomn/medial lemniscus @ closest to gray matter/lateral
cervical for lateral spinothalamic tract @ closest to grey matter/medial

111
Q

describe the pathway of the dorscal colomn

A

ascending pressure, vibration, fine touch, proprioception –> first order neron from sensory nerve ending to cell body in the dorsal root ganglion to the spinal cord and ascends ipsilaterally in the dorsal colomn –> synapse 1 at the nucleus cuneatus or gracilis in the medulla –> DECUSSATES int he medulla and ascends contralaterally in the medial lemniscus – synapse 2 in the VPL of the thalamus - third order neuron to the sensory cortex

112
Q

whats in the anteriorspinothalamic tract

A

crude touch and pressure

113
Q

describe the spinothalamic tract

A

ascending: pain and temp from lateral and crude touch and pressure from anterior – sensory nerve endinds Adelta and C with cell body in dorsal root ganglion - enters spinal core - synapse 1 in the ipsilateral gray matter of spinal cord – second order decussates and anterior white commissure and ascends contralaterally - to the vpl in the thalamus synapnses - third order to the sensory cortex

114
Q

describe the lateral corticospinal tract

A

descending - volumtanr movement of contralateral limns
umn with cell body in the primar motor cortex - descends ipsilatreally thorugh the internal capsule - most fibres decussate at cauda medullat - pyramidal decussaiton - descends contralaterally – synapse one in the cell body of the anterior/ventral/basal horn of the spc - and lower motor neuron leaves the spinal cord to synapse at the NMJ

115
Q

UMN or LMN: clasp knife spasicity

A

UMN

116
Q

UMN or LMN: everything increased, increased reflexes, increased tone, positive babinsk spasy paralysis

A

UMN

117
Q

UMN or LMN: everything decrease, decrease reflexes, decreased atone, bo Babinski and flaccid paralysis

A

LMN

118
Q

UMN or LMN: weakness

A

both

119
Q

UMN or LMN: atrophy

A

LMN

120
Q

UMN or LMN: fasciulations

A

LMN: muscle is freakign out cause its scared and alone with out its neuron

121
Q

c2 dermatome

A

posterior half of skull cap

122
Q

c3 dermatome

A

turtle neck region

123
Q

c4

A

low collar shirt

124
Q

t4 dermatome

A

nipples

125
Q

t7 dermatome

A

xiphiod process

126
Q

t10

A

umbilicus

127
Q

l1

A

inguinal ligament

128
Q

l4

A

keecaps

129
Q

s234 dermatome

A

erection and sensation of penile and anal zones

130
Q

where does referred pain from the diaphragm and gall bladder go

A

shoulder via phrenic nerves c345

131
Q

biceps reflex pelase

A

c56

132
Q

triceps reflex please

A

c78

133
Q

quadriceps reflex please

A

L34

134
Q

Achilles relfec pelase

A

S1S2

135
Q

cremaster reflex pelase

A

L1L2

136
Q

anal wink please

A

S34

137
Q

what is the nerve root of the biceps reflex

A

c5

138
Q

what is the nerve root of triceps reflex

A

c7

139
Q

what is the nerve root of quadriceps refles

A

l4

140
Q

what is the nerve root of Achilles reflex

A

S1

141
Q

what are primitive reflexes

A

present in a healthy infact but are absent in neur intact adult. normally disappear within first year of live. inhibited by develipign frontal lobe

142
Q

what to think about if see primitive reflexes in an adult

A

frontal lobe damage

143
Q

what is the moro reflex

A

abduct/extend arms when startled and then draw together

gone at three mothsn

144
Q

rooting reflex

A

movement of head towards one side if cheek or mouth is strokes - nipple seeking
gone at four months

145
Q

sucking reflex

A

sucking response when roof of moth is touched

146
Q

palmar reflex

A

curling of fingers if plam is stroked

6 months

147
Q

plantar reflex

A

dorsiflexion of large toe and fanning of toehr toes with plantar stimulation
gone at 12 motnhs
if present think UMN lesions

148
Q

gallant reflex

A

remember Grenadian hospital
stroke alogn one side of spine whil enewborn is in ventral suspension ie face down and will cause lateral flexion fo lower body toward stimulated side

Neurology - step (10 decks)

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