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Neurology - step > anatomy and physiology > Flashcards

anatomy and physiology Flashcards

1
Q

signal transmitting cells fo the nervous system

A

neurons

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2
Q

permanent cells in the brain

A

nuerons

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3
Q

dendrites?

A

receive info

have nissl bodies

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4
Q

axons?

A

give away info

no nissle bodies

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5
Q

what happens when an axon is injured

A

wallerian degeneration
degeneration distal to injuery and axonal retraction proximally
allows for potential regeneration of the axon !@ the pNS (Schwann cells)

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6
Q

what happens to the astrocytes in neuronal injury

A

reactive gliosis

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7
Q

GFAP?

A

astrocytes

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8
Q

function fo astrocytes

A 
physical support
repair
K metabolis
removal of excess neurotransmitter
glycogen fue reserve buffer
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9
Q

where astrocytes come from

A

neuroectoderm

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10
Q

what is the role fo microglia

A

phagocytic scavenger cells fo the CNS

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11
Q

what happens to microglia in response to tissue damage

A

microglia

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12
Q

does nissl stain the microglia

A

noppers

rer - not really a protein maker, the microglia

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13
Q

how does HIV affect the microglia

A

HIV infected microglia fuse to form multinucleated giant cells in the CNS

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14
Q

who cares about myelin

A

increases conduction velocity of signals transmitted down axons

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15
Q

what happes at the nodes fo ranvier

A

salutatory conduction fo the ap - high concentration of Na - inward current

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16
Q

what makes myelin in the CNS and the PNS

A

CNS - oligodendrocytes

PNS - shcwann cells

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17
Q

how does myelin increase rate of conduction

A

by wrapping and insulating the axon, myelin increase the space constant (distance before ap dissipates), and increase conduction velocity

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18
Q

how many axons does the schwann cell myelinate

A

only 1

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19
Q

role fo schwann cell please

A

myeliante sPNS axon and promotes axonal regeneration

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20
Q

what disease hurts schwann cells

A

guillina barrer

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21
Q

what is an acoustic neuroma

A

type of schwanooma in the internal acoustic meatus = affects CNVIII

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22
Q

bilateral schwanommas you think

A

neurofibromatous II

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23
Q

hows an oligodendrocyte diff from schwann cells

A

oligos - mor ethan one axon, from neuroectoderm and no regenerative properties

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24
Q

you see a fried egg on histology you think of

A

oligodendrocytes

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25
Q

what hurts oligodendrocytes

A

multiple sclerosis
progressive multifocal luekoencephathy
leukodystrophies

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26
Q

what is the predominant glial cell type in white matter

A

oligos

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27
Q

describe the fibres of: free nerve endings

A

c - slow unmyelinated

A delta - fast myelinated

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28
Q

describe the fibres of: miessner corpuscles

A

large meylinated fibres

adapt quickly

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29
Q

describe the fibres of: pacinian corpusles

A

large myelinated fibres

adapt quicly

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30
Q

describe the fibres of: merkel discs

A

larege myelinated fibres

adapt sloqly

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31
Q

describe the fibres of: ruffini corpuscles

A

dendritic endings with capsul

adapt slolwy

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32
Q

which sensory receptors adapt quickly

A

meissnuer and pacinain

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33
Q

which sensory receptors adapt slowly

A

merkel discs and ruffini corpuscles

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34
Q

location of: free nerve endings

A

all skin
epidermis
some viscera

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35
Q

location of: meissner corpuscles

A

glabrous/hairless skin

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36
Q

location of: pacinain cortpscules

A

deep skin layers
ligaments
joints

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37
Q

location of: merkel discs

A

finger tipes

superficial skin

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38
Q

location of: ruffini corpuscles

A

finger tips

joints

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39
Q

sensory receptors in joints please

A

pacinian and ruffini

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40
Q

superficial sensory receptors in skin pelase

A

free nerve endings
meissner corpuscles
meckel discs

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41
Q

receptors for: pain and temperature

A

free nerve endings

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42
Q

receptors for: dynamic, dine/light toucn/position sense

A

meissners

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43
Q

receptors for: pressure, deep static touch (shapes and edges), position sense

A

mekels discs

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44
Q

receptors for: vibration and pressure

A

pacinian

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45
Q

receptors for: pressure, dlippage of objects along surface of skin and joing angle change

A

ruffinin corpuscles

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46
Q

what do the messiner copruscles sense

A

light tough
dynamic
position sense

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47
Q

what do the meckels disc sense

A

pressure
deep static touch
position sense
shapes/edges

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48
Q

what do ruffini corpuscles sense

A

pressure
slippage of objects
joint position sense

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49
Q

what do pacinian corpuscles sense

A

vibration

poressure

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50
Q

list the layers of a peripheral nerve

A

nerve - endoneurium - perineurm - ectoneurium

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51
Q

which layer of a peripheral nerve needs to be connected in microsergry for limb reattachment

A

peripneurium

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52
Q

what part of nerve affected at guilliarn barre

A

endoneurium - inflammatory infiltrate

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53
Q

synthesis of Ne occurs at?

A

locus coreuleus at the ponts

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54
Q

where is DA made?

A

substnatia nigra pars compacta in midbrain

ventral tegmentum

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55
Q

where is 5-HT made

A

raphe nuclei @ pons, midbrain and medulla

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56
Q

where is ACh made

A

basal nucles of meynert

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57
Q

what is GABA made

A

nucleus accumbens

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58
Q

what is the locus ceruleus responsible for

A

stress and panic

NE

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59
Q

what is the nucleus accumbens and septal nucles responsible for?

A

GABA

reward centre, pleasure, addiction, fear

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60
Q

list the changes in NE seen in different pathos

A

NE increased in anxiety

NE decreased in depression

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61
Q

list the changes in DA seen in different pathos

A

DA decreased in Parkinson
DA increased in Huntington
DA decreased in depression

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62
Q

list the changes in 5-HT in different pathos

A

decreased in depression

increasedin depression

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63
Q

list the changes in Ach in different pathos

A

increased in Parkinson
decreased in Alzheimer
decreased in huntington

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64
Q

list the changes seen in GABA

A

decreased in anxiety

increasedin huntington

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65
Q

neurotransmitter changes: anxiety

A

anxiety - increased Ne, decreased 5HT, decreased DA

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66
Q

neurotransmitter changes: depression

A

depression - decreased Ne, decreased 5HT, decreased DA

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67
Q

neurotransmitter changes: huntington

A

Huntington- increased DA, decreased GABA, decreased ACh

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68
Q

neurotransmitter changes: parkinson

A

Parkinson - decreased DA, increased Ach

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69
Q

neurotransmitter changes: alzheimer

A

decreased Ach )Ach decreased in elderly brains natural course too)

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70
Q

what are the three strucutres that form the BBB

A

tight junctions between nonfenestrated capillary endotheial cells
basement membrane
astrocyte foot processes

vrs GFR ;)

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71
Q

how are glucose and amino acids transported across the BBB

A

carrier mediated transport

SLOW

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72
Q

how are lipid molecules transported across the BBB

A

diffusion

FASTER

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73
Q

whats the point of having no BBB in certain areas in the brain

A

molecules in blood can affect brain function and neurosecretory products enter circulation

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74
Q

list some locations where there is no BBB and what the point of them is pelase

A

OVLT: senses osmotic stuffs
area postrema: vomit needed
neurohypohysis: Secretion of hypothalamix to circulation

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75
Q

what can cause damage to the endothelial cells of the BBB

A

infarction and or neoplasm detrosy endothelila cell tight junctions

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76
Q

whats the result of infarction or neoplasm on the endothelial cells of the BBB

A

disrupts tight junctions – VASOGENIC OEDEMA

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77
Q

where are other notable barriers besides the BBB located in the body

A

blood-testis barrier

maternal-fetal blood barrier of the placenta

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78
Q

what is the hypothalamus responsible for

A 
TAN HATS
thermoregulation 
adenohypophysis
neurohypophysis
hunger
autonomic regulation
thirst and water balance
sexy urges
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79
Q

what are the inputs to the hypothalamus

A

no BBB = OVLT for osmolarity monitoring and the area postrema for response to emetics as well as the supraoptic nucleus for ADh and the paraventricular nucleus for oxytocin.

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80
Q

where are ADh and oxytocin sotred

A

the posterioir pituitary

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81
Q

what part of the hypothalamus drives hunger

A

lateral

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82
Q

what part of the hypothalamus drives satiety

A

ventromedial

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83
Q

what happens if knock out lateral hypothalmaus

A

responsible for eating - so get skinny

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84
Q

what happens if you knock out the ventromedial hypothalamus

A

tells you that you are full - so get bigger

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85
Q

what is the role of leptin on the lateral hypothalamus

A

leoin from fat cells wants to make you not eat

so will inhibit the lateral hypothalamus that is telling you to get lat/fat

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86
Q

what is the role of leptin on the ventromedial hypothapamus

A

leptin from adipose wants to make you not eat

so will stimulate the ventromedial hypothalmaust that is telling you already that you are satieated

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87
Q

whats the rold of the anterior hypothalamsu

A

cools you down like A/C (anterior/cools)

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88
Q

whats the role of the posterior hypothalamus

A

heast you up

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89
Q

what happens if you lesion out the anterior hypothalamus

A

cant cool down

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90
Q

what happens if you lesion out the posterior hypothalamus

A

cant heat up

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91
Q

whats the role of the suprachiasmatic nucleus

A

circadian rhythm

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92
Q

what regulates sleep

A

the suprachiastmatic nucleus via circadian rhythm

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93
Q

describe the molecular regulation of sleep

A

circadian thrythm - nortuncl relase of ACTH, prolactin, melatonin, NE

the SCN –> norepinephrine release - pineal gland - melatonin

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94
Q

what regulates the SCN

A

light :) always thought this was romantic

light controls our dreams

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95
Q

what hormones are under circadian ctonrol

A

ATCH
prolactin
melatonin
NE

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96
Q

what do ATCH, prolaction, melatonin and NE have in common

A

circadian control

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97
Q

what stage of sleep has EOM movements

A

REM

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98
Q

what causes the rapid eye movemenst in rem

A

PPRF activity
paramedian pontine reticular formation
ie the conjugate gaze centre

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99
Q

how often does REM occur

A

every 90 minutes

increases in duration through the nigth

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100
Q

what causes decreased REM sleep

A

alcohol
benzodiazepines
barbiturates
NE

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101
Q

what causes decreased delta sleep

A

NE

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102
Q

effect of OH, benzos, barbituates on sleep

A

decreased REM sleep

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103
Q

effect of NE on sleep

A

decreased REM sleep and decreased delta waves

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104
Q

how do you treat sleep enuresis

A

oral desmopression
an ADH analogue
(also vWF and Hemophilia VIII)

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105
Q

how else can you treat bedwetting?

A

desmopression > imipramine

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106
Q

how do you treat night terros and sleepwalking

A

benzodiazepines

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107
Q

when do night terrors occur

A

nonREM

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108
Q

describe brain activity when awake with eyes open

A

beta waves - highest frequency and lowest amplitude

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109
Q

describebrain activity when awak with eyes closed

A

alpha waves

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110
Q

describe brain activity in nonREM I

A

theta waves

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111
Q

describe brain acitivty in nonREM II

A

K complexes

sleep spindles

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112
Q

describe brain activity in nonREM III

A

delta waves

lowest frequency, highest amplitude

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113
Q

describe REM brain activity

A

beta waves
highest frequency
lowest amplitude

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114
Q

when does bruxism?

A

during deepr sleep with sleep spindles and K complexes

nonREM II

115
Q

what is bruxism?

A

teeth grinding

116
Q

what is the deepest non REM sleep?

A

stage nonREM III
delta waves
lowest frequency and highest amplitude

117
Q

what happens in N3 sleep?

A

delta waves
sleep walking
night terrors
bedwetting

118
Q

when does sleepwalking, night terrors, and bedwetting occur?

A

nonREM III

delta waves

119
Q

brain activity in light sleep

A

theta

120
Q

brain activity in deep sleep

A

delta waves

121
Q

describe what happens in REM sleep

A 
loss of motoro tone
increased brain O 2 use
increased and variable puls and blood pressure
dreaming
penile clitoral tumescence
memory processing function
BETA WAVES
122
Q

name sleep state: night terrors

A

N3 with delta waves

123
Q

name sleep state: bruxism

A

N2 with k complexes and sleep spindles

124
Q

name sleep state: memory consolidation

A

REM with beta waves

125
Q

name sleep state: dreaming

A

REM with beta waves

126
Q

name sleep state: sleep walking

A

N3 with delta waves

127
Q

name sleep sate: bed wetting

A

N3 with delta waves

128
Q

name sleep state: penile/clitoral stuffs

A

same as dreaming

REM

129
Q

alpha waves

A

awake with eyes close

130
Q

delta waves

A

N3

131
Q

theta waves

A

N1

132
Q

K spikes

sleep spindles

A

N2 - teeth grnding

133
Q

what stage of sleep si most time spent in

A

45% N2 - k spikes and sleep spindles

134
Q

what is second most common stage ot sleep

A

REM (memory, dreams, night mares bp and pulse, motor O2 use e, beta) and N3 (delta waves, sleep walking, bed wetting, night terrors) are tied with 25%

135
Q

what is the least amount of time spent in sleep

A

n1 - tehta waves - 5%

136
Q

rank time for each stage of sleep from most to least

A

N2 > N3=REM > N1

137
Q

whats the point of the thalamus

A

major relay for all ascending sensory information except olfaction

138
Q

what is the only ascending sensory pathway that bypasses the thalamus

A

olfactory

139
Q

what is the input for the VPL

A

spinothalamic and dorsal colomns/medial lemniscus

140
Q

what info does the VPL receive

A

spinothalamic - pain and temp

dorsal colomns/medial lemniscus - vibration, proprioception, touch, pressure

141
Q

where does the VPL send information

A

primary somatosensory cortex

142
Q

what is the input to the VPM

A

ma face!

trigeminal and gustatory pathway

143
Q

what info does the VPM receive

A

face sensation and taste

144
Q

what part of thalamus does taste go through?

A

VPM with face sensation

145
Q

where does VPM send information

A

primary somatosensory cortex

146
Q

Makeup goes on the face

A

face and taste to VPM

147
Q

what info goes to the LGN

A

vision

L is for Light and LGN

148
Q

what is the input to the LGN

A

CN II

149
Q

where does the LGN send information

A

visual information to the calcarine sulcus

150
Q

what is the input to the MGN

A

superior olive and inferior colliculus of tectum

Music at the MGN

151
Q

what information goes to the MGN

A

auditory

152
Q

where does the MGN send information

A

to the auditory cortex of the temporal lobe

153
Q

what input goes to the VL

A

basal ganglia and the cerebellum

154
Q

what info goes to the VL

A

motor

155
Q

where does the VL send its info

A

motor cortex

156
Q

describe the thalamus and pain, temp, pressure, touch, vibration and proprioception

A

input via the spinothalamic and dorsal colomns/medial lemniscus to the VPL to the primary somatosensory cortex

157
Q

describe the thalamus and facial sensation and taste

A

input via the trigeminal and gustatory pathway to the VPM to the primary somatosensory cortex

158
Q

describe the thalamus and vision

A

input via CN II to the LGN to the occipital cortex

159
Q

describe the thalamus and auditory

A

superior olive and inferior colliculus to the MGN to the auditory cortex in the temporal lobe

160
Q

describe the thamalus and motor

A

input via the basal ganglia and cerebellum to the VL to the motor cortex

161
Q

what is the limbic system

A

a collection of neural structures involved in emotion, long term memory olfaction and behaviour modulation

162
Q

olfactory doesn’t go through the thalamus, it goes through

A

the limbic system

163
Q

function of the limbic ystem

A 
emotion
long term memory
olfaction
behavioural modulation
ANS function
feed, feel, flee, fight, sex
164
Q

what structures make up the limbic system

A 
acfm
amygdala
cingulate gyrus
fornix
mammillary bodies
ACFM
165
Q 
acute paralysis - cant move
dysarthria - cant speak
dysphagia - cant swallow
diplopia - cant see
loss of consciousness
A

osmotic demyelination syndrome

central pontine myelinolysis

166
Q

symptoms of osmotic demyelination syndrome/central pontine myelinolysis

A 
acute paralysis
loss of consciousness
diplopia
dysphagia
dysarthria
167
Q

what is the pathophys of osmotic demyelination syndrome/central pontine myelinolysis

A

massive asocan ldemyelination in pontine white matter secondary to osmotic changes

168
Q

what causes osmotic demyelination syndrome/central pontine myelinolysis

A

rapid correction of hyponatremia

169
Q

what happens when hyponatremia is rapidly corrected

A

osmotic demyelination syndrome/central pontine myelinolysis: loss fo consciousness, acute paralysis, diplopia, dysphagia, dysparhtira

170
Q

what happens hypernatremia is rapidly corrected?

A

cerebral edema/herniation

171
Q

from low to high?

A

your pons will die: acute paralysis, loss of consciousness, diplopia, dysarthria, dysphagia

172
Q

from high to low?

A

your brain will blow - cerebral edema, and herniation

173
Q

what is the function of the cerebellum

A

modulates movement

aids in coordination and balance

174
Q

what is the input to the cerebellum

A

contralateral cortex ia middle cerebellar peduncle

inpsilateral proprioceptive information via inferior cerebellar peduncle from spinal cord

175
Q

inferior cerebellar peduncle

A

ipsilateral proprioceptive information from spinal cord

176
Q

middle cerebellar peduncle

A

contralateral input form cortex

177
Q

what is output of the cerebellum

A

info to the contralateral cortex to mosulate movement.

178
Q

desribce the output nerves of the cerebellum

A

purkinje cells - deep nuclei of cerebellum - contralateral cortex via superior cerebellar peduncle

179
Q

superior cerebellar peduncle

A

purkinje cells - deep nuclei of cerebellum - contralateral cortex out via superior cerebellar peduncle

180
Q

what are the deep nuclei of the cerebellum

A

dentate - emboliform - globose - fastigial

181
Q

DONT EAT GREASY FOODS

A

dentate - emboliform - globose - fatigial

lateral to medial deep nuclei of the cerebellum

182
Q

lateral lesions present as

A

propensity to fall to ispilatera sides as lesions

183
Q

what is lateral cerebellum responsible for

A

voluntary movements of extremities

184
Q

what are the midline structures

A

fastigial nucles and verma cortex and of the flocculonodular lobe

185
Q

what happens when the fastigial nucleus/veris cortex and or the flocculonodular lobe

A

trnucal ataxia - wide based cerebellar gait
nystagmus
head tilting

186
Q

wide based cerebellar gait
nystagmus
head tiliting

A

midline cerebellar lesion
gastigial nucleus
vermis
flocculonodular lobe

187
Q

midline lesions of cerebellum usually result in?

A

bilateral motor deficits affecting axial and procimal limb musculature
wide based cereberllar gait - truncal ataia
nystagmus and head tilting

188
Q

what are the basal ganglia good for

A

important I voluntary movements and making postural adjustments

189
Q

where does the basal ganglia receive its input from

A

cortical input

190
Q

what is putput of the basla ganglia

A

negative feedback to the cortex via the VL of the thalamus

191
Q

what is the striatum

A

putamen (motor) and caudate (cognitive)

192
Q

what is the lentiform

A

putamen and globus pallidus

193
Q

describe the direct pathway in the basal ganglia

A

substantia nigra pars compacta receives stimulatory input from the motor cortex - sends out DA to the putamen - inhibits the globus pallidus interna – inhibits the thalamus – stimulates the cortex –. when activated results in increased motion

194
Q

describe the indirect pathway in the basal ganglia

A

cortex stimulates the substanstia nigra pars compacta - DA sent out to putamen and inhibits it - sends out inhibitor to globus pallidus externa - inhibits the subthalamic nucleus - stimulates the thalamus - inhibits the cortex - results in decreased motion

195
Q

what is the inhibitor neurotransmitter used in the direct pathway

A

GABA

196
Q

what is the pedunculopontine nucleus?

A

from cortex to the spinal cord

197
Q

athetosis

A

slow writhing movements especially in fingers

198
Q

writhing, snake like movement

A

athetosis

199
Q

where is athetosis seen?

A

huntington

200
Q

damage to the ? causes athetosis

A

basal ganglia

201
Q

what is chorea

A

sudden, jerky, purposeless movements

202
Q

'’dancing’’

A

chorea - sudden jerky purposeless movements

203
Q

damage to the ? causes chorea

A

basal gangial

204
Q

huntingotn movement disorders observed

A

athetosis: slow, writhing movements esp in fingers AND
chorea: sudden jjerky purposeless movements
both due to damage at the basal ganglia

205
Q

what is dystonia

A

sustained, involuntary muscle contractions

206
Q

sustained, involuntary muscle contractions

A

dystonia

207
Q

what type of movement disorder is writers cramp

A

dystonia - sustained involuntary muscle contractions

208
Q

what type of movement disorder is blepharospams

A

dystonia - involuntary muscle contractions - sustained eylid twtiches

209
Q

exampls of dystonia

A

writers cramp and blepharospasm

210
Q

what is an essential tremor

A

high frequency remor with sustained posture

worse with movement or when anxious

211
Q

tremor self medicated with EtOH = ?

A

essential tremor

decreases tremor amplitude

212
Q

how do you treat essential tremors

A

beta blockers and PRIMIDONE

213
Q

beta blockers and primidone treatment for

A

essential tremor - high frequency tremor with sustained postire, worse with movement or when anxious - why can treat with beta blocker

214
Q

what is hemiballismus

A

sudden wild flailing fo one arm with or wtihotu ipsilateral leg

215
Q

where is the lesion with sudden wild flailing of one arm with or without ipsilateral leg

A

contralateral subthalamic nucleus

216
Q

lesion in subthalamic nucleus

A

hemiballisumus ie sudden wild flailing of one arm with or without ipsilateral leg

217
Q

what type of stroke can cause hemiballismus

A

lacunar stroke

218
Q

movement disorder associated with lacunar stroke

A

subthalamic nucleus infarction - contralateral subthalamic nucleus

219
Q

what is an intention tremor

A

slow sizsax motion with pointing ot extending towars a target

220
Q

what causes an intention tremor

A

cerebellar lesion

221
Q

what is myoclonus

A

sudden, brief, uncontrolled muscle contraction

222
Q

examples of myoclonus

A

jerks
hiccups
common in metabolic abnormalities such as renal and liver dailure

223
Q

sudden brief, uncontrolled muscle contractions you suspect

A

metabolic abnormalities ie RENAL and LVIER failure

224
Q

what is a resting tremor

A

uncontrolled movement of DISTAL appendages - mostly in hands

tremor alleviated by intestinal movement (vrs essential that is worse with movement)

225
Q

where do you see a resting tremor

A

Parkinson

occurs at rest

226
Q

pill rolling tremor

A

uncontrolled movement of distal appendanges mostly inhands that is alleviated by intestinal movement

227
Q

uncontrolled movement of distal appendanges mostly in hands that is alleviated by intentional movement

A

pill rolling tremor

228
Q

lewy bodies

A

Parkinson disease

composed of alpha synucleni - intracellular eosinophilc inculsions

229
Q 
pill rolling remor at rest
cogwheel rigidity
akinesia
postural instability
shuffling gait
A 
Parkinson disease
lewy bodies
alpha synuclein
loss of da ercig nerus in substantia nigra pars compacta
increased Ach and decreased DA
230
Q

describe Huntington disease

A

AD
trinucleotide of CAG
chromosome 4

231
Q

wen do symptoms manifest in hunting ton

A

between twenty and fity

232
Q

choreiform movements
aggression
depression
dementia

A

hntington disease

233
Q

presentation of Huntington please

A 
choreiform movements
aggression
depression
dementia 
sometimes initially mistaken for substance abuse
234
Q

neurotransmitter changes in huntingotn disease

A

decreased Ach
increased DA
decreased GABA

235
Q

what causes the neuronal death in Huntington disease

A

cia NMDA receptor bidngin an dGLUTAMATE TOXICTY

236
Q

MRI of huntingotn disease

A

atrophy of caudate nuclei with ex vacuo dilatation of frontal horns

237
Q

atrophy of caudate nuclei with ex vacuo dilatation of fronal horns

A 
Huntington
depression
aggression
dementia
choreiform
238
Q

CAG - caudate loses Ach and GABA

A

glutamate toxo and NMDA receptor binding

239
Q

define aphasia please

A

higher order inability to speak

240
Q

what is dysarthria

A

motor inability to speak via movement deficit

241
Q

what is a non fluent aphasia

A

cant speak

242
Q

fluent aphasia

A

speak

243
Q

where is brocas area

A

inferior frontal gyrus of frontal lobe

244
Q

inferior frontal gyrus of frontal lobe damage

A

brocas aphasia

245
Q

what are symptoms of brocas aphasia

A

nonfluent aphasia
inctact comphrehension
inability to repeat

246
Q

where is wernickes area

A

superior temporal gyrus of temporal lobe

247
Q

superior temporal gyrus of temporal lobe damage

A

wernickes aphasia

248
Q

fluent aphasia, impaired concentration, impaired repitition

A

wernickes aphasia

249
Q

describe sxs of wernickes aphasia

A

fluent apadia
imapried comprehension
impaired repetition

250
Q

whats the purpose do the arcuate fasciculus

A

connets brocas to wernickes

251
Q

conduction aphasia

A

damage to the arcuate fasciculus

252
Q

fluent speech
intact comphrehension
impaired repetition

A

conduction aphasia

impaired arcuate fasciculus

253
Q

sxs of conduction aphasia

A

fluent speech
intact comprehension
imapreid repetition

254
Q

nonfluent aphasia
intact comprehension
intact repetition

A

transcortical motor aphasia

255
Q

sxs of transcortical motor aphasia

A 
nonfluent aphasia
intact comprehension
intact repetition (brocas except with repetition is good)
256
Q

fluent aphasia
impaired comprehension
intact repetition

A

transcortical sensory aphasia

257
Q

sxs of transcortical sensory aphasia

A

fluent aphasia
impaired comprehension
intact repetition
wernickes only with godo repeittion

258
Q

nonfluent speech
impaired comprehension
intact repetition

A

mixed transcortical aphasia

259
Q

sxs of mixed transcortical aphasia

A

nonfluent speech
impaired comprehension
intact repetition

260
Q

what areas are damage in mixed transcortical aphasia

A

brocas and wernicks

arcuate fasciculs not involved (or else would lose repetition)

261
Q

what is damaged in global aphasia

A

broas, wernickes, arcuate fasciculs

262
Q

nonfluent aphasia
impaired comprehension
impaired repetition

A

global aphasia

263
Q

where is the extrapyramidal circuit

A

premotor areas in the frontal cortex

264
Q

disinhibited behaviour
hyperphagia
hypersexuality
hyperorality

A

amygdala damage

KLUVER BUCY SYNDROME

265
Q

sxs of kluver bucy syndrome

A

amygdala damage
hyperphagia
hyperoralitiy
hypersexuailtiy

266
Q

what virus is associated with kluver bucy syndrome

A

HSV-1

bad news for its spread

267
Q

disinhibtion and deficits in concentration, orientation, judgement,

A

frontal lobe

268
Q

brain lesion associated with re-emergence of primitive reflexes

A

frontal lobe

deficits in concentration, orientation ,judgement

269
Q

nondominant parietal temporal cortex

A

hemispatial neglect syndrome

agnosia of the contralateral side fo the world

270
Q

dominant parietal temporal cortex

A

agraphia
acalculi
finger agnosia
left right disorientation

271
Q

what is gerstmann syndrome

A 
dominant parietal temporal lobe lesion
agraphia
acalculi
finger agnosia
left right disorientation
272
Q

lesion of reticular activating system/midbrain

A

reduce levesl or arousal and wakefulness

273
Q

bilateral mammillary bodies damage

A

Wernicke: confusion, ataxia, ophthalmoplegia
Korsakoff: personality changes, confabulation, memory loss (antero and retrograde)

274
Q

what is mamilliary bodies bilateral lesions associated with

A

B1 deficiency

excessive EtOH

275
Q

what can worsen a) confusion, ataxia, opthalmoplegia and b) confabulation, personality changes and memory loss

A

glucose infusion without B1

276
Q

lesion of basal ganglia

A

tremor at rest
chorea
athethosis

277
Q

what disease are associated with basal ganglia lesion

A

Parkinson disease

Huntington disease

278
Q

lesions to the cerebellar hemispheres

A 
LATERAL
intention tremor
limb ataxia
loss of balance
IPSILATERAL DEFICINTS
fall to same side
279
Q

lesion to the cerebellar vermis

A

MEDIAL
truncal ataxia and dysarthria
nystagmus
head tilting

280
Q

damage to subthalamic nucleus

A

hemiballsimus on contral ateral side

lacunar infarcts

281
Q

hippocampus bilateral lesion

A

anterograde amnesia

282
Q

paramedian pontine reticular formation

A

eyes look away from side of lesion

283
Q

frontal eye field lesion

A

eyes look toward the lesion

Neurology - step (10 decks)

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