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Neurology > Neuro Exam (Lectures) > Flashcards

Neuro Exam (Lectures) Flashcards

1
Q

ependyma

A

thin epithelium-like lining of the ventricular system and central canal

some develop into the choroid plexus

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2
Q

oligodendrocytes

A

surround and insulate some CNS nerve processes

can simultaneously myelinate MANY axons

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3
Q

astrocytes

A

wrap around capillaries and neurons to provide structural support, repair processes, facilitate metabolic exchange between blood and neurons, and help form the BBB

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4
Q

microglia

A

resident immune cells of the nervous system

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5
Q

resting membrane potential

what does it result from?

A

1) selective permeability
2) differential ionic concentrations across the plasma membrane

maintained by active ion transport Na/K pump

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6
Q

signal transduction

A

chemical, temperature, pH, mechanical > electrical > chemical (NTs/peptides)

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7
Q

shape of an action potential

A

1) Na+ channels open, Na+ enters cell
K+ channels open, K+ begins to leave cell

2) Na+ channels close
K+ leaves cell

3) K+ channels close
Excess K+ outside diffuses away

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8
Q

action potential properties

A

1) All or none
2) AP amplitudes can differ across neurons and neuron types but are a FIXED property of a given neuron
3) frequency of firing encoding information

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9
Q

Where are Na+ and K+ channels concentrated on an axon?

A

Nodes of Ranvier

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10
Q

benefits of myelin

A

1) decrease capacitance
2) increase membrane resistance

together this increases conduction velocity

3) less biological demand on the neuron
> less channels/pumps expressed
> less energy demand to maintain membrane potential

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11
Q

Proteins involved in vesicular release?

A

v-SNAREs and t-SNAREs

botulinum and tetanus toxins are zinc-dependent proteases that cleave VAMP

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12
Q

mechanisms for removing neurotransmitter from synaptic cleft

A

1) degradation
2) reuptake
2) diffusion

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13
Q

degradation example

A

acetylcholinesterase cleaves ACh into choline and acetate

note: edrophonium short-acting AChE inhibitor used to distinguish clinical btwn MG and Lambert-Eaton syndrome

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14
Q

reuptake example

A

monoamines (serotonin, dopamine, glutamine)

note: SSRIs work by inhibiting this mechanism!

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15
Q

postsynaptic response

A

1) receptors
2) synaptic integration
3) modulation

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16
Q

ionotropic receptors

A

RAPID/TRANSIENT

Nicotinic ACh
NMDA
AMPA
GABAa

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17
Q

metabotropic receptors

A

SLOW/SUSTAINED
G-protein coupled

mGlu
GABAb
Muscarinic ACh
B-adrenergic

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18
Q

AMPA

A

major mediator of EXCITATORY synaptic transmission

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19
Q

NMDA

A

conducts Na+ and Ca2+

Mg2+ blocks the channel and cannot pass current even when NT bound to the receptor

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20
Q

what factors influence summation?

A

1) spatial distribution of inputs

2) temporal nature of the inputs

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21
Q

endocannabinoid modulation

A

endocannabinoid allows for communication from the post-synaptic cell to the pre-synaptic cell

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22
Q

NMJ vs. CNS

INPUTS

A

NMJ: one
CNS: many

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23
Q

NMJ vs. CNS

NT

A

NMJ: ACh
CNS: many

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24
Q

NMJ vs. CNS

TRANSMITTER REMOVAL

A

NMJ: AChE
CNS: high affinity transporters

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25
Q

NMJ vs. CNS

POST-SYNAPTIC RECEPTOR

A

NMJ: nicotinic ACh receptor
CNS: metabotropic and ionotropic receptors

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26
Q

NMJ vs. CNS

SAFETY FACTOR

A

NMJ: very high
CNS: relatively low

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27
Q

NMJ vs. CNS

SYNAPTIC EFFICACY

A

NMJ: high
CNS: low

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28
Q

NMJ vs. CNS

excitatory vs. inhibitory

A

NMJ: excitatory only
CNS: both

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29
Q

10 Functional Components of Nervous System

A
  1. lateral corticospinal
  2. DCML
  3. anterolateral
  4. basal ganglia
  5. cerebellar
  6. visual
  7. cranial nerves
  8. limbic
  9. diffuse
  10. cerebral cortex
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30
Q

specific afferent fibers for sensory detection of fast, well-localized pain

A

A-delta fibers

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31
Q

specific afferent fibers for sensory detection of slow, diffuse pain

A

C-fibers

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32
Q

specific afferent fibers for sensory detection pleasurable touch

A

A-beta fibers

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33
Q

allodynia

A

pain from a stimulus that does not normally evoke pain

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34
Q

hyperalgesia

A

exaggerated response to a normally painful stimulus

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35
Q

taxonomy of pain

A

nociceptive
inflammatory
neuropathic
dysfunctional

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36
Q

nociceptive

A

no pathology
requires ongoing noxious stimulus
evoked by HIGH-intensity stimuli

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37
Q

inflammatory

A

tissue injury w/inflammation
allodynia, hyperalgesia and spontaneous pain
evoked by LOW and HIGH-intensity stimuli

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38
Q

neuropathic

A

PNS or CNS lesions
allodynia, hyperalgesia, spontaneous pain
sensory amplification
evoked by LOW and HIGH-intensity stimuli

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39
Q

dysfunctional (centralized)

A

altered CNS function (no known lesion/no peripheral pathology)
allodynia, hyperalgesia, spontaneous pain

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40
Q

Somatosensory

specialized receptors

A

pacinian corpuscles
meissner’s corpuscles
c fibers

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41
Q

visual

specialized receptors

A

photosensitive molecules (e.g., rhodopsin) in photoreceptor cells

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42
Q

auditory

specialized receptors

A

sterocilia on hair cells

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43
Q

Somatosensory

receptive field of first order sensory neurons

A 
a discrete spot on the skin 
discrete temperature 
pH 
taste 
odor
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44
Q

visual

receptive field of first order sensory neurons

A

a discrete spot in the visual field (center-surround)

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45
Q

auditory

receptive field of first order sensory neurons

A

a pure tone (single frequency)

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46
Q

Somatosensory

mechanism of potential change in neurons

A

physical properties
compression of skin opens FORCE-GATED ion channels
temperature opens THERMAL SENSITIVE channels

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47
Q

visual

mechanism of potential change in neurons

A

light-activated rhodopsin G-protein mediated effect

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48
Q

auditory

mechanism of potential change in neurons

A

mechanical displacement of hair cell cilia from sound waves opens FORCE-GATED ion channels

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49
Q 
visual 
adaptation (physical changes in receptors)
A

tuned for change, ignore “white space”, sense motion

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50
Q 
auditory 
adaptation (physical changes in receptors
A

accommodate to loud noises, hear a voice over a drone

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51
Q

somatosensory

location of first order neuron

A

DRG

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52
Q

visual

location of first order neuron

A

ganglion cells of the retina synapsing with photoreceptors (rods and cones) in retina

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53
Q

auditory

location of first order neuron

A

spiral ganglion synapsing with hair cells

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54
Q

somatosensory

higher processing in second-order neurons

A

shapes, edges of objects being touched

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55
Q

visual

higher processing in second-order neurons

A

orientation/edges of visual stimuli

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56
Q

auditory

higher processing in second-order neurons

A

localization of stimulus _ tone; focus on individual speakers over a crowd

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57
Q

right-left auditory discrimination

A
  1. right-left ear discrimination of TIME LAG

2. right-left ear discrimination of SOUND INTENSITY

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58
Q

up-down auditory discrimination

A

angle sound hits pinna

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59
Q

common causes of otitis media

A

H. influenzae
S. pneumo
Moraxella catarrhalis

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60
Q

motor system function: cortex

A

planning and initiation of voluntary movements and integration of inputs from other brain areas

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61
Q

motor system function: basal ganglia

A

enforcement of desired movements and suppression of undesired movements

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62
Q

motor system function: cerebellum

A

timing and precision of fine movements, adjusting ongoing movements, motor learning of skilled tasks

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63
Q

motor system function: brainstem

A

control of balance and posture, coordination of head, neck and eye movements, motor outflow to cranial nerves

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64
Q

motor system function: spinal cord

A

spontaneous reflexes, rhythmic movements, motor outflow to the body

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65
Q

motor system function: muscles

A

movement of body, sensory organs-muscle spindle and golgi tendon organs

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66
Q

motor unit

A

a single neuron and all the muscle fibers it innervates

smallest division that the system can control individually

either SLOW or FAST

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67
Q

innervation ratio

A

number of muscle fibers per neuron (variable)

eye (low ratio)
quad (high ratio)

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68
Q

slow twitch, type 1

A

darker
aerobic metabolism
contract more slowly
generates less force

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69
Q

fast twitch, type 2

A

paler
anaerobic metabolism
contract quicker
generates more force

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70
Q

fast fatigue-resistant

A

properties that are intermediates between the other two types

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71
Q

what does the muscle spindle sense?

A

length or stretch

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72
Q

what does the golgi tendon sense?

A

tension

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73
Q

encapsulated structures mechanically connected in parallel with muscle fibers?

A

muscle spindles

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74
Q

encapsulated structures mechanically connected in series with muscle fibers?

A

golgi tendon

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75
Q

three main components of muscle spindle

A
  1. intrafusal fibers
  2. afferent sensory neurons
  3. efferent motor neurons (gamma neurons)
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76
Q

dynamic bag fibers

A

respond primarily during CHANGES in the length of the muscle

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77
Q

static bag and nuclear chain fibers

A

primarily signal the length if the muscle without the phasic changes

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78
Q

types of infrafusal fibers

A

dynamic bag
static bag
nuclear chain

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79
Q

type of sensory fibers

A

primary (Type Ia) -terminate on all three types of intrafusal fibers

secondary (Type II)-terminate only on static bag and nuclear chain fibers

Note: cell bodies of sensory afferents in the DRG

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80
Q

function of the gamma motor neurons

A

cause the polar ends of the intrafusal fibers to contract …maintains the sensitivity of the spindle even when the muscle is shortening

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81
Q

UMN Clinical Correlates

A

lesion above alpha motor neuron

Weakness
No atrophy
Exaggerated reflexes, Positive Babinski
Spasticity

82
Q

LMN Clinical Correlates

A

lesion of the alpha motor neurons

Weakness
Atrophy
Diminished reflexes, Negative Babinski
No spasticity

83
Q

Examples of Neurogenic Diseases

A

ALS
Polio
Guillian-Barre Syndrome

84
Q

Example of Myopathic Diseases

A

Muscular Dystrophy

Polymyositis

85
Q

Etiology of Neurogenic vs. Myopathic Diseases

A

Neurogenic-damage to motor neurons

Myopathic-degenerations of muscle

86
Q

Atrophy?

Neurogenic vs. Myopathic Diseases

A

YES BOTH!

87
Q

Fasciculations?

Neurogenic vs. Myopathic Diseases

A

Neurogenic -YES

Myopathic-NO

88
Q

Loss of Reflexes?

Neurogenic vs. Myopathic Diseases

A

YES BOTH!

89
Q

Creatine Kinase?

Neurogenic vs. Myopathic Diseases

A

Neurogenic-Normal

Myopathic-Elevated

90
Q

Group 1a Interneuron function

A

mediate muscle-spindle inhibition of ANTAGONIST muscles in the stretch reflex

receive input from descending tracts

allow for coordination of agonist-antagonist muscles

91
Q

Group 1b Interneuron function

A

mediate golgi-tendon inhibition of AGONIST muscle

prevent excessive tension

receive multiple muscle, cutaneous, proprioceptive and descending inputs

92
Q

C3, C4, C5

A

keep the diaphragm alive

93
Q

C5

A

deltoid

94
Q

C6

A

biceps

95
Q

C7

A

triceps

96
Q

C8-T2

A

Fingers

97
Q

L4

A

Quads

98
Q

L5

A

Foot Dorsiflexion

99
Q

S1

A

Plantar Flexion

100
Q

S2-S5

A

Sphincter Control

101
Q

UMN + LMN Disease

A

ALS
amyotrophy-muscle atrophy
sclerosis-scarring

102
Q

nerve typically affected first in ALS

A

hypoglossal nerve

103
Q

what can cause BG dysfunction?

A

stroke-lacunar infarcts (GPi/Putamen)
multiple sclerosis
tumor
idiopathic and/or familial

104
Q

Classic Parkinsonian Signs

A 
TRAP 
Tremor 
Rigidity 
Akinesia, Bradykinesia 
Postural instability (ataxia)
105
Q

Basic Life Functions Coordinated by Hypothalamus

A 
Energy metabolism 
Fluid and electrolyte balance 
Thermoregulation 
Reproduction 
Arousal and Stress Responses
106
Q

Hypothalamus gathers information from

A 
1. Exteroceptive 
visual 
somatosensory 
visceral (gustatory) 
olfactory 
multimodal-limbic
  1. Interoceptive
    local: temp, Na, osm, glc
    circumventricular organs
107
Q

circumventricular organs

A

lack a normal BBB

ex. median eminence, pineal gland

108
Q

flip flop switch

A

mutual inhibition between VLPO and the ascending monoamine systems (no intermediate states!)

VLPO inhibits LC, TMN, Raphe
LC, TMN, Raphe inhibits VLPO

109
Q

reinforces the waking state

A

orexins (hypocretins)

Orexin activates LC, TMN, Raphe
VLPO inhibits orexin

110
Q

what drives the homeostatic sleep drive?

when is it at its peak?

A

adenosine

right before sleeping

111
Q

when is the circadian sleep drive at its peak?

A

upon waking

112
Q

hypothalamic output

A

autonomic: PNS, SNS
endocrine: pituitary
behavior: motor automatisms, arousal, autonomic influences

113
Q

diffuse projecting systems key principles

A
  1. cell bodies occupy very small space
  2. projections spread wide
  3. branch diffusely
  4. secrete NTs and communicate by volume transmission
  5. modulate behavioral states
  6. evolutionarily conserved
114
Q

synthesis, biogenic amines

A

amino acid precursor actively transported across BBB
modifying enzymes convert AA to NT

NT

  • serotonin
  • dopamine
  • norepinephrine
  • histamine
115
Q

storage, biogenic amines

A

VMAT2 integral membrane protein transports monoamines into vesicle where they accumulate

116
Q

release, biogenic amines

A

voltage-dependent calcium channels
calcium influx
vesicle release

117
Q

modulation, biogenic amines

A
  1. high affinity reuptake transporter
  2. autoreceptors (can decrease firing and decrease synthesis)
  3. degradation/inactivation (oxidation, methylation etc)
118
Q

METH

A

lipophilic weak base, MAOi

can readily cross BBB 
looks like dopamine and can be taken up by DAT and transported into synaptic vesicles by VMAT2 
alkalinizes vesicle 
DA goes back into cytosol, builds up 
DAT reverses direction

massive DA action and then crash (bc autoregulators)

119
Q

Cocaine

A

dopamine reuptake inhibitor thus blocking action of DAT
increase of DA in synaptic cleft

autoregulators shut down production of DA

massive DA action and then crash

120
Q

coma

A

occurs with lesions of the ascending system or with diffuse, bihemispheric dysfunction

121
Q

what determines level of consciousness

A

ascending system of connections from brainstem and hypothalamus

122
Q

what is wakefulness?

A

awareness of self and one’s environment

123
Q

REM Sleep is?

A

unconscious but cortex active
dreaming
paralysis
saccadic eye movements

124
Q

NREM Sleep is?

A

unconscious with little cortical activity

125
Q

somnogens

A

adenosine

increased during inflammation…more relevant in times of illness
prostaglandin D2
TNF-alpha

126
Q

activity of state-regulatory nuclei

WAKE

A

Monoamines
Acetylcholine
Orexin

127
Q

activity of state-regulatory nuclei

NREM

A

Monoamines

GABA

128
Q

activity of state-regulatory nuclei

REM

A

Acetylcholine

GABA

129
Q

what kind of memory does sleep improve

A

declarative (facts)
procedural (skills)

also helps with consolidation

130
Q

cataplexy

A

sudden, brief episodes of muscle weakness triggered by strong emotions

131
Q

dysfunction in visual unimodal association area

A
  1. visual object agnosia
  2. prosopagnosia
  3. simultanagnosia
132
Q

visual object agnosia

A

cannot recognize visually presented object

a) appreceptive form
impaired ability to perceive the elementary shape of the object

b) associative form
intact ability to perceive the elementary shape of the object

133
Q

prosopagnosia

A

associated with fusiform gyrus

inability to recognize faces

134
Q

simultanagnosia

A

inability to perceive more than one object simultaneously

135
Q

Ballints syndrome

A 
simultanagnosia 
ocular apraxia (trouble directing eyes) 
optic ataxia (impairment in making visually guided arm movements)
136
Q

what visual pathway

A

temporal

137
Q

where visual pathway

A

parietal

138
Q

lesion in unimodal somatosensory association cortex

A

tactile agnosia

139
Q

lesion in unimodal auditory association cortex

A

1) nonverbal auditory agnosia (impaired auditory recognition)
2) pure word deafness (isolates primary auditory cortex from language centers)

140
Q

dysfunction in unimodal motor association cortex

A

1) low-level apraxia: finely graded finger movement
2) middle-level apraxia: learned skilled movements
2) high-level apraxia: series of acts or sequence

141
Q

Gerstmann’s syndrome

A

lesion in left angular gyrus (junction btwn parietal and temporal)

AGRAPHIA
ACALCULIA
FINGER AGNOSIA
RIGHT-LEFT DISORIENTATION

142
Q

key early events in cerebral cortex development

A

neural tube closure

specification/regionalization of neural tube

143
Q

stages of cerebral cortex development

…and broad type malformations

A
  1. proliferation
    • > too much
    • > too little
  2. migration
    • > premature termination
    • > overmigration
  3. neuritic outgrowth/axon guidance
    • > incorrect projections/connections
  4. synapse formation and pruning/neurotransmission
    • > too much
    • > too little
  5. behavior
144
Q

malformations of cortical development lead to a range of phenotypes but severe malformations often result in varying degrees of with TRIAD OF SYMPTOMS?

A

Intellectual Disability
Developmental Delay
Seizures

145
Q

ethanol affects which stage of brain development

A

ALL

146
Q

extracellular cues binds to receptors at the growth cone guide what?

A

axonal growth

note: growth cone only transiently present

147
Q

many more synapses are produced than are necessary. what glial cell types is responsible for tagging synapses for deletion?

A

astrocytes

148
Q

cerebral cortex progenitor cells line what structures?

list zones starting from this structure …

A

lateral ventricles

ventricular zone 
subventricular zone 
intermediate zone 
cortical plate 
marginal zone
149
Q

cortical plate formation

name order of layer formation

A

1 > 6> 5> 4> 3> 2

migrates to final location via radial (excitatory neurons) and tangential (inhibitory neurons) migration

150
Q

three frontal regions

A
  1. lateral prefrontal cortex
  2. orbital frontal cortex
  3. medial prefrontal cortex
151
Q

lateral prefrontal cortex

A

involved in working memory
executive function

mental status exam: verbal fluency

cognitive neurosci. task: categorizing, wisconsin card sort test

152
Q

orbital frontal cortex

A

emotional judgments and regulation

cognitive neurosci. task: iowa gambling task

153
Q

medial prefrontal cortex

A

initiation, error detection and monitoring of behavior

cognitive neurosci. task: serial reaction time task

154
Q

working memory

A

the ability to maintain information online and manipulate it to guide behavior

dopamine is critical for function

155
Q

LPFC Circuit

A

LPFC
medial dorsal nucleus thalamus
lateral GPi/SNr
Caudate Nucleus

input: sensory what and where pathways at LPFC

156
Q

what is verbal fluency? what does it test?

A

list all the words they can that begin with a specific letter in a minute

normal scores dependent on age and education (12-16/minute)

working memory, LPFC

157
Q

OFC Circuit

A 
OFC 
medial dorsal nucleus thalamus 
ventral GPi 
nucleus accumbens 
OFC

inputs: olfactory, taste, internal body, amygdala @ OFC

outputs: hypothalamus and periaquaductal gray
- cardio
- gastric
- respiratory
- sexual

158
Q

medial frontal regions

A 
frontal pole (unknown function) anterior cingulate (monitoring) 
supplementary motor (initiate/sequencing) 
subgenual cortex (depression)
159
Q

causes of aphasia…

A

stroke (most common cause)
dementia
trauma
brain tumors

160
Q

how are aphasias classified

A

1) fluency
- ease of speech production
- long phrase length (at least 7 normal)
- small connector words (is, and, the) present
2) comprehension
3) repetition

161
Q

broca’s aphasia

A

comprehension intact
non-fluent speech
poor repetition

associated signs

  • right hemiparesis
  • apraxia

sometimes called “expressive aphasia”

162
Q

wernicke’s aphasia

A

poor comprehension
fluent speech, non-sensical
poor repetition

poor insight/angry at listener

associated signs
-right homonymous hemianopia

163
Q

conduction aphasia

A

good comprehension
fluent speech w/phonemic paraphasias
poor repetition

164
Q

role of right hemisphere in language

A

prosody (non-verbal cues)
humor
theory of mind (ability to attribute mental states to oneself)

165
Q

goal of image-guided neurosurgery

A

complete resection
no neurological injury

want to see:

  • lesion and define margins
  • critical structures
  • relationship btwn lesion and eloquent areas

accomplish:
- preop planning
- surgical decision making

166
Q

diffusion tensor imaging is a way of mapping what in vivo?

A

white matter tracts

167
Q

usual localization of tumor in adults vs. children

A

adults: supratentorial
children: infratentorial

168
Q

what is the only firmly established environmental risk factor for brain tumors?

A

ionizing radiation

169
Q

parinaud’s syndrome

A

failure of upgaze
pupillary dilation
poor reactiveness to light
retraction nystagmus

assoc. with pineal gland tumor

170
Q

brain tumor diffuse symptoms

A 
Headache 
Vomiting 
Lethargy 
Irritability 
Behavior change 
Increased head circumference 
Seizure
171
Q

when does a headache become concerning?

A 
change in prior headache pattern 
unresponsive to prev. effective therapy 
focal symptom or sign 
worse at night, bending, sneeze, valsalva 
vomiting 
awakens child from sleep 
papilledema
172
Q

signs of hydrocephalus

A

bulging fontanelle
sundowning
increased head circumference

173
Q

brain tumor differential diagnosis

A 
stroke/cerebral hemorrhage 
abscess/parasitic cyst 
demyelinating disease (MS) 
metastatic tumors 
primary CNS lymphome
174
Q

differential of late-life dementia

A 
alzheimer's disease
vascular dementia 
parkinson's disease with dementia 
dementia with lewy bodies 
frontotemporal dementias (incl. Picks) 
CJD and related prion dementias
175
Q

alzheimer’s disease defining characteristics

A 
amyloid plaques 
neurofibrillary tangles 
inflammation (microgliosis and astrocytosis) 
selective neuronal degeneration 
synaptic loss 
multiple NT deficits
176
Q

neurofibrillary tangles

A

intraneuronal

composed of highly phosphorylated forms of the microtubule-associated protein, tau

177
Q

amyloid plaques

A

extracellular

composed of 40- and 42-residue amyloid beta-proteins

178
Q

mechanisms of disease in proteinopathies

A
  1. excessive production
  2. decreased clearance
  3. mutations (missense; expansion)
  4. certain biochemical conditions (e.g., extreme pH)
  5. failure of chaperone systems
  6. prolonged time (age)
179
Q

genetic factors predisposing to AD

A

APP mutations (ch21)
ApoE4 polymorphism (ch19)
Presenilin 1 mutations (ch14)
Presenilin 2 mutations (ch1)

180
Q

simple, partial seizure

A

focal, consciousness intact

181
Q

complex, partial seizure

A

focal, unconscious

182
Q

generalized, absence

A

motionless starring
loss of awareness
no postictal confusion/immediately resume back to normal behavior

Rx: ethosuximide

183
Q

generalized, tonic-clonic

A

tonic-stiffening

clonic-rhythmic jerking

184
Q

generalized, atonic

A

drop seizure, loss of muscle tone

185
Q

can focal-onset seizures become secondarily generalized tonic-clonic?

A

YES

186
Q

what is the most common site of focal-onset seizures in adults?

A

medial temporal lobe

  • deja vu
  • olfactory and gustatory hallucinations
  • fear, anxiety
  • nausea
187
Q

epilepsy

A

tendency towards recurrent, unprovoked seizures

diagnosed after two unprovoked seizures

188
Q

what factors can affect CNS excitability?

A

1) intrinsic neuronal factors
(problem with neuron)

2) synaptic or extrinsic/extraneuronal factors
(ex. toxins)

3) neuronal circuit or network factors
(abberant circuits lead to hyperexcitability)

189
Q

Factors important related to recurrence

A

type
etiology
EEG

190
Q

categories of treatment for epilepsy

A 
vagus nerve stimulation 
brain surgery 
hormonal therapies 
ketogenic diet 
deep brain stimulation
191
Q

stroke ischemic vs. hemorrhagic

A

85% ischemic

15% hemorrhagic

192
Q

T1

A

CSF dark

good for

  • atrophy
  • cortical dysplasias
  • subacute hemorrhage
193
Q

T2

A

CSF white

good for

  • chronic infarctions
  • demyelination
  • white matter lesions
  • edema/inflammation
194
Q

Flair

A

T2 with CSF brightness removed

good for edema

195
Q

Types of Declarative Memory

A

1) Episodic: ability to re-experience past events
2) Semantic: system for receiving, retaining, transmitting information about meaning of words, concepts and classification of concepts
3) Working: ex. remembering a new phone number while dialing it

196
Q

Types of Non-declarative memory

A

Procedural (skills)

197
Q

disorders of semantic memory

Is this normal in aging? What diseases are associated?

A

Spared in normal aging
rare

Viral brain infections
Unusual types of strokes
Semantic dementia
Alzheimers

198
Q

disorders of working memory

Is this normal in aging? What diseases are associated?

A

Commonly declines in normal aging
commonly affected in neuropsych disorders

CVD 
MS 
TBI 
PD 
Depression 
Schizophrenia
199
Q

encoding

what is needed?

A

the learning of new info

basic attention and working memory are necessary

200
Q

storage

when does storage happen?

A

“consolidation”
as time passes, information is less dependent on medial temporal lobe

this happens during sleep

201
Q

retrieval

names two types

A

recall (fill info recovered)
vs.
recognition (multi-choice)

202
Q

processes involved in episodic memory

A

encoding
storage
retrieval

Neurology (4 decks)

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