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Brain and Behavior > Week 3/4 Lectures > Flashcards

Week 3/4 Lectures Flashcards

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1
Q

Conductive disorders are principally found in ____.

A

middle ear –> treatable and reversibl (blockage of sound conducting path from source to cochlea)

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2
Q

Sensorineural hearing loss arises principally in _____.

A

cochlea –> damage or loss of hair cells + auditory nerve connections, damage to central auditory pathway –> irreversable

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3
Q

T/F Complete deafness can be overcome.

A

T –>cochlear implant

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4
Q

Natural hearing loss with age is called _____.

A

Presbycusis

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5
Q

T/F Hearing loss is a predictor of dementia.

A

T

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6
Q

The amount of condensation in sound translates to a perception of _____.

A

loudness

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7
Q

The time it takes a sound to go from maximum condensation to the next maximum condensation (or rarefaction) translates to a perception of _____.

A

pitch

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8
Q

Components of the labyrinth

A

vestibular (dorsal) and cochlear (ventral segments + outer bony perimeter and membranouse labyrinth soft tissue chamber–> set of channels carved into temporal bone during development

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9
Q

Chambers of the cochlea

A

upper (Scala vestibuli), meiddle (Scala media), and lower (Scala tympani)

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10
Q

Which cochlear chambers are filled with endolymph?

A

middle (upper and lower have perilymph)

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11
Q

The vibrational input from the stapes is into the scala ______ and the pressure release of these vibrations is via the round window at the end of scala _____.

A

vestibuli and tympani

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12
Q

Endolymph is a filtrate of _____ and enters the inner ear via the ________.

A

CSF and endolymphatic duct

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13
Q

Endolymphatic potential

A

+80mV in scala media

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14
Q

Two organ of Corti sensory cells

A

1 row of inner hair cells (afferent to brain) and three rows of outer hair cells (hearing sensitivity)

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15
Q

The tallest row of the sensory hairs on the hair cells are in contact with an acellular overlying membrane, the _________.

A

tectorial membrane –> Up
and down movements of the organ of Corti during sound stimulation will cause a deflection of the sensory hairs (stereocilia).

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16
Q

What happens when tiplinks are open?

A

Inner hair cells: Influx of K+ into hair cell –>depolarization –> synaptic release –> glutamate AP /// Outer hair cells –> prestin contraction

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17
Q

What happens when tiplinks are closed

A

hyperpolarization

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18
Q

High frequency sounds elicit vibrations at the _____ of the basilar membrane.

A

Base

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19
Q

Low frequency sounds elicit vibrations at the ____ of the basilar membrane

A

apex

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20
Q

Tonotopic organization

A

frequency to place translation along hte basilar membrane –> high to low from base to apex

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21
Q

Phasic depolarizations of hair cells occur at high/low frequencies.

A

low (steady state depolarization with high frequency)

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22
Q

T/F Outer hair cells have efferent feedback from the brain

A

T

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23
Q

T/F Axons themselves, by virtue of its position of origin, “tells” the CNS the frequency carried in that “wire” independent of any discharge code itself.

A

T –> labeled line scheme of sensory coding

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24
Q

T/F Mechanical tuning of the basilar membrane and neural tuning of auditory nerve discharges are the same for the same cochlear location.

A

T –> tuning properties of basilar membrane require sound intensity to achieve displacement at a given frequency; same for nerve –> direct transfer

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25
Q

Prestin

A

outer hair cells are sensory and motor effectors –> feedbacks energy into the basilar membrane to boost inner hair cell stimulus –> selective attention

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26
Q

T/F Destruction of outer hair cells and the sharpness of type 1 afferent tuning curves from inner hair cells are greatly blunted.

A

T –> less sharp/exhibit poorer frequency selectivity

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27
Q

T/F There are more unmyelinated auditory nerve axons than myelinated.

A

F –> more type 1 myelinated afferents per IHC//fewer type ii afferents per OHC

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28
Q

Auditory pathway

A

hair cell –> cochlear nuclei (3)–> trapezoid body –> superior olivary nuclei –> lateral lemniscus –> inferior colliculus –> medial geniculate- ->auditory cortex

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29
Q

First binaural input in the auditory system

A

superior olivary nuclei

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30
Q

Interaural time difference

A

CNS detects sound delay between two ears –> superior olivary nucleus

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31
Q

MSO

A

measures interaural time differences (medial superior olive) –> if excitatory input from the two ears (contralateral and ipsilateral) arrive at a cell in the MSO at the same time noncoincidentally –> MSO acitvated –>temporal map in the MSO for specific time differences

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32
Q

LSO

A

measures interaural volume differences

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33
Q

The ipsilateral ear provides ______ input to the LSO cell while the contralateral ear provides _____ input.

A

excitatory vs inhibitory

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34
Q

T/F detection of sound in the vertical plane requires only one ear.

A

T –> ear can calculate differences in combined sounds from direct and reflected pathway

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35
Q

The output axons from the MG form the __________ and project to the auditory cortex.

A

auditory cortical radiations

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36
Q

3 main levels of auditory cortex processing

A

core (tonotopic + simple sounds), belt and parabelt (no tonotopicness +complex sounds)

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37
Q

3 primary auditory cortices

A

A1, Rostral, Rostrotemporal

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38
Q

Arcuate fasciculus deficit

A

can understand speech, can encode speech, but can’t respond appropriately –> connects frontal, parietal, temporal

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39
Q

T/F there are clear frequency gradients in the core auditory cortex [R and A1] and that these gradients become less clear outside of the core.

A

T

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40
Q

T/F selectivity for certain types of sounds increases between the primary and non-primary auditory cortices

A

T

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41
Q

What problem do older folks and people with hearing aids have with auditory processing?

A

cannot distinguish sources of different sounds//disentagle single waveforms to distinct sounds

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42
Q

How the brain distinguishes sounds

A

detect regularities–> form auditory objects (e.g. location, similarity in timbre/pitch, proximity in space/time, continuity in direction, common fate)

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43
Q

Proximity

A

a stimulus with similar frequencies tend be heard as a single sound –> frequency proximity; with disparate frequencies –> two sounds

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44
Q

Perceptual categories

A

forming representations of stimulus-invariant representations of auditory objects

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45
Q

Abstract categories

A

based on higher order or semantic information;; not based wholly on perceptual similarity

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46
Q

Ventral auditory streams code what features of a sound?

A

identity

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47
Q

Dorsal auditory streams code what features of a sound?

A

where a sound is

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48
Q

The primary olfactory sensory neurons (olfactory receptor neurons) are located in the______.

A

neuroepithelium in the nose

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49
Q

Axons of olfactory receptors are myelinated/unmyelinated

A

unmyelinated

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50
Q

Second order neurons for smell are where?

A

olfactory bulb

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51
Q

Smell pathway

A

olfactory receptors –> olfactory bulb –> olfactory tract –>pyriform cortex (smell perception), amygdala (odor emotions) –> frontal cortex, hippocampus (memory), and hypothalamus (hormone/autonomic response)

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52
Q

T/F humans have a functional vomeronasal organ for pheremone sense.

A

F

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53
Q

Smell is ipsilateral/contralateral

A

ipisilateral

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54
Q

T/F OSN or receptor cells regenerate throughout life

A

T –> cilitated bipolar neurons, supported by glia-like cells, regnerated by basal stemcell-like cells

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55
Q

Odor g-protein

A

odor –> Golf –> adneylyl cyclase- ->cAMP –> CNG channels –> Cl- channel –> depolarization (Na/Ca in, Cl out) –> AP

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56
Q

T/F odor quality and intensity are encoded by combinations of receptors/neurons.

A

T –> population coding at epithelial level

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57
Q

Olfactory glomeruli

A

axons of sensory neurons synapse with bulb neurons forming neuropils (dense axonal network) –> glomeruli // a few glomeruli receive axons of OSNs with the same receptor

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58
Q

3 cell types in olfactory bulb

A

mitral/tufted (inputs from OSNs), periglomerular (modulate/temper inputs to mitral/tufted cells), granule (modulate output from tufted cells to cortex)

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59
Q

Piriform Cortical Nuerons

A

two synapses away from sensory input –> mitral cells project diffusely to the cortex, enabling individual cortical neurons to assemble convergent input from mitral cells from different glomeruli

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60
Q

T/F Odor representation is distributed without apparent spatial preference.

A

T

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61
Q

Anosmia

A

absence of smell

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62
Q

Hyposmia/hyperosmia

A

decreased/increased smell sensation

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63
Q

dysosmia

A

distortion of smell

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64
Q

phantosmia

A

dysosmia in the absence of appropriate stimulus

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65
Q

Olfactory agnosia

A

inability to recognize odor sensation

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66
Q

5 modalities of taste

A

salty, sour, bitter, sweet, umami (AA)

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67
Q

Taste pathway

A

taste buds (cirumvallate, foliate, fungiform) –> sensory neurons –>facial, glossopharyngeal, vagus –> solitary tract –> VPM –> ipsilateral, primary gustatory cortex in insula

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68
Q

Gustatory coding

A

different taste modalities by different taste mechanisms –> salty = ENaC; sour = H+ ions through transient receptor potential channel; sweet = T1R2+T1R3, Umami = T1R1+T1R3, Bitter = T2R

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69
Q

Labeled-line coding

A

each modality of taste is detected by distinct, non-overlapping receptor cells

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70
Q

Anosmia

A

absence of smell

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71
Q

Hyposmia/hyperosmia

A

decreased/increased smell sensation

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72
Q

Hyposmia/hyperosmia

A

decreased/increased smell sensation

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73
Q

dysosmia

A

distortion of smell

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74
Q

dysosmia

A

distortion of smell

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75
Q

phantosmia

A

dysosmia in the absence of appropriate stimulus

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76
Q

phantosmia

A

dysosmia in the absence of appropriate stimulus

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77
Q

Olfactory agnosia

A

inability to recognize odor sensation

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78
Q

Olfactory agnosia

A

inability to recognize odor sensation

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79
Q

5 modalities of taste

A

salty, sour, bitter, sweet, umami (AA)

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80
Q

5 modalities of taste

A

salty, sour, bitter, sweet, umami (AA)

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81
Q

Taste pathway

A

taste buds (cirumvallate, foliate, fungiform) –> sensory neurons –>facial, glossopharyngeal, vagus –> solitary tract –> VPM –> ipsilateral, primary gustatory cortex in insula

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82
Q

Gustatory coding

A

different taste modalities by different taste mechanisms –> salty = ENaC; sour = H+ ions through transient receptor potential channel; sweet = T1R2+T1R3, Umami = T1R1+T1R3, Bitter = T2R

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83
Q

Labeled-line coding

A

each modality of taste is detected by distinct, non-overlapping receptor cells

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84
Q

T/F the sense of flavor results from integration of olfactory, gustatory, and somatosensory inputs.

A

T –> 70/80% = ofactory, gustatory/somatosensory = everything else

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85
Q

T/F Interocular muscles have no stretch receptors.

A

T

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86
Q

T/F interocular muscles have a medium twitch time.

A

F –> fast

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87
Q

T/F While different neural subsystems provide for the various types of eye movements, the final executor of all eye movements are
the motorneurons

A

T

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88
Q

Which muscle does a given oculomotor nucleus innervate contralaterally?

A

superior rectus

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89
Q

Pulse and step system

A

the firing rate must consist of a large, high frequency pulse (burst) followed by a much smaller step (the burst to overcome the inertia/viscous resistance followed by a step to overcome the elastic restoring forces and hold the eye in its new position)

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90
Q

The pulse generator for horizontal eye movements is in the

A

Paramedian pontine reticular formation

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91
Q

Horizontal saccade pathway

A

FEF + Superior colliculus –> PPRF –> integrator –> Nucleus of 6 –> lateral rectus

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92
Q

The neural integrator for horizontal eye movements is in the __________

A

nucleus prepositus hypoglossi –> ensures appropriate step for nuc 6

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93
Q

vertical saccades with the pulse generator in the _________________

A

rostral interstitial nucleus of the MLF

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94
Q

The superior colliculus mediates ________

A

“express saccades”, very short latency (~100 msecs) saccadic eye movements in response to the sudden appearance of a visual or auditory stimulus

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95
Q

T/F about half the neurons in the abducens nucleus do not innervate the lateral rectus but instead, they innervate the medial rectus subdivision of the oculomotor complex on the other side

A

T –> innervation of the medial rectus of one eye and the lateral rectus of the other are always equal. This is the ‘neural yoke’ that provides for the conjugacy of eye movements under normal circumstances

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96
Q

The outputs of semicircular canals, utricles, and sacculus are carried by axons in 8 vestibular whose cell bodies are in ______.

A

scarpa’s ganglion

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97
Q

In the utricle and saccule, the cilia protrude through a gelatinous layer in which are suspended large numbers of calcium carbonate crystals called _________

A

otoconia

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98
Q

In the semicircular canals, the kinocillia are embedded in a gelatinous mass called the _____

A

cupula –> barrier blocking the circulation of endolymphatic fluid. When the head turns in the plane of a canal, the inertia of the fluid distorts the cupula in the direction opposite to the head movement which bends the cilia and produces increased or decreased firing in the 8th nerve terminals at the base of the cupula

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99
Q

T/F linear acceleration of the head produces equal forces on the two sides of the canal and no net signal

A

T

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100
Q

In angular acceleration, which canal increases its discharge rate

A

on the side toward which the head is rotating

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101
Q

The afferents from the SSCs carry a signal proportional to head velocity but only
when ______

A

when head acceleration is not zero

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102
Q

The purpose of the ___ is to provide stability of gaze in spite of head movements

A

VOR

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103
Q

Nystagmus is named for which phase?

A

fast –> eg moving head to left produces a left beating nystagmus

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104
Q

The fast phase of nystagmus is directed _____ to the lesioned side.

A

opposite

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105
Q

COWS

A

cold water opposite, warm water same, i.e., irrigation of the left horizontal canal with cold water produces a nystagmus with the fast phase towards the right,

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106
Q

______ is defined as the ratio of the output magnitude to the input magnitude of VOR.

A

gain–> eye movement divided by the head

movement

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107
Q

vestibular pathway

A

vestibular nuclei –> cross midline –> medial lemniscus –> ascend to vpm –> parietal/vestibular cortex and vestibulospinal tract –> balance and posture

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108
Q

A nearly flat lens has a ____ focal length and will be_____.

A

long and weak –> power = only a few diopters (diopters = 1/focal length = power | focal length ~ image distance ~ diameter of the eye = 17mm) –> refractive power of the eye is approximately 58D

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109
Q

During accommodation, the ciliary muscle contracts, making the lens _____.

A

more spherical –> increasing the refractive power of the eye –> near objects

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110
Q

3 layers of retinal cells

A

ganglion cells, inner nuclear layer (bipolar, horizontal, amacrine) , outer nuclear layer (photoreceptors) + 2 plexiform layers

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111
Q

function of choroid

A

capture extra light and reduce scatter by reflection –> increase acuity

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112
Q

fovea contains _____

A

cones

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113
Q

T/F there are multiple rod pigments.

A

F –> only one rod pigment –> scotopic/dark vision

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114
Q

T/F rods are key structures in lit environments.

A

F –> don’t do anything; cones do all color processing

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115
Q

The switching between domination of the ganglion cells by either rods or cones takes place at the level of ____________ in the inner plexiform layer.

A

amacrine cells

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116
Q

Rhodopsin pathway

A

photoactivation –> G protein –> cGMP 5’ –> gated Na+ channel kept open by high concentrations of cGMP in dark/opposite in light

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117
Q

In the dark, the outer segment of the rod has _____ permeabilities for Na/K so the photoreceptors are _______

A

equal; depoloarized and releaseing glutamate

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118
Q

light _______ photorecepotrs to ______ the action of gluatmate on next cells in pathway.

A

hyperpolarize and decrease

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119
Q

On bipolars, glutamate is _______

A

inhibitory –> cells are hyperpolarized in the dark and become depolarized as light level increase

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120
Q

Off bipolars, glutame is _______

A

excitatory –> cells are depolarized in dark and become less depolarized as light increases

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121
Q

_________ carry information about light increments and ______ constitute a channel that carries information about light decrements.

A

On vs Off bipolars

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122
Q

_________ in the retina generate APs

A

ganglion cells –> all other cells communicate with graded synaptic release

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123
Q

H cells

A

lateral pathway in retina –> outer plexiform layer–> collect output of many photoreceptors and presynaptic to bipolar cells –> GABAergic and is opposite to the photoreceptor input –> contrast/receptive field differences

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124
Q

______cells receive from single cone bipolars (small RFs) and convert the input to firing rates

A

P ganglion

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125
Q

_______ cells receive from many bipolars (large RFs) and are especially responsive to motion.

A

M ganglion

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126
Q

Which part of the visual field is smallest?

A

the nasal visual fields

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127
Q

Cortical magnification factor

A

Want to focus brain on center of vision/macular vision –> 1/3-1/2 of the occipital lobe (posterior of lobe)

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128
Q

Visual field deficit: Lesion of right meyer’s loop

A

upper left quadrant of each eye’s visual field –>left homonymous quadrantanopsia

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129
Q

Visual field deficit: Lesion of right optic nerve

A

right eye visual field but normal left eye visual field

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130
Q

Visual field deficit: Lesion of optic chiasm

A

no temporal vision –> bitemporal hemianopia

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131
Q

Visual field deficit: lesion of right optic tract/radiation

A

(after chiasm) –> no left side field in either eye –> left homonymous hemianopia

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132
Q

Visual field deficit: lesion of right striate

A

no left field in either eye

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133
Q

The most common etiology of chiasmal deficit in adults

A

pituitary tumor

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134
Q

Dorsal visual pathway

A

M retinal ganglion cells –> magnocell layers of LGN 1 and 2 –> V1 striate cortex (IVB) –> thick CO stripes in V2–> V5 parietal and MT –> Parietal lobe –>where pathway

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135
Q

Ventral visual pathway

A

P retinal ganglion cells –> Parvocell layers of LGN 3-6 –> V1, II-III –> pale stripes in V2 –> V4 –> Inf. temporal lobe –>what pathway

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136
Q

“What” pathway disorders

A

alexia without agraphia; visual agnosias and prosopagnosia, cerebral hemi-acrhomatopsia

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137
Q

“Where” pathway disorders

A

hemi-neglect, balint’s syndrome/simultanagnosia, akinetopsia

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138
Q

Alexia without agraphia

A

unable to read, able to write + right homonymous hemianopsia –> left occipital lobe + left splenium of corpus callosum

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139
Q

Visual agnosia and prosopagnosia

A

inability to recognize objects (appercetive and associative); prosopagnosia = unable to recognize faces –> oocipito-temporal (often bilateral –> fusiform face area in medial temporal lobe)

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140
Q

cerebral hemiacromatopsia

A

lack of color vision in homonymous hemifield, upper quandrantanopsia –> fusiform and lingual gyri in inferior occipital lobe (V4)

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141
Q

Hemi-neglect

A

ignore or unaware of objects in left hemispace –> right parietal lobe

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142
Q

Balint’s syndrome

A

simultangosia (can’t put together a scene from parts), ocular apraxia (inability to move eyes under guidance), optic ataxia (inability to reach under guidance) –> bilateral parieto-occipital

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143
Q

akinetopsia

A

inability to perceive motion –> v5 of lateral occipital parietal temporal lobe

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144
Q

superior colliculus

A

midbrain structure; orients head and eye movements –> inputs = mostly m cells from retina

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145
Q

pretectal nuclei

A

receives inputs from RGCs and sends efferents are to the EW nuclei on both sides (via post. commissure) –> preganglionic parasympathetics to ciliary ganglion

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146
Q

accessory optic nuclei

A

reflex following movements

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147
Q

suprachiasmatic nuclei

A

optic nerve input synchronizes circadian rhythm to light/dark cycle –> about 1% of “other” RGCs project here

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148
Q

lateral geniculate nucleus

A

thalamic relay nucleus for primary visual cortex –> input from M and P cells

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149
Q

In the LGN, On/Off cells are separated in ____ layers.

A

P

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150
Q

Layer organization of LGN

A

1/2 = magnocellular; 3-6 = parvocellular; 1,4, 6 contralateral; 2,3,5 ipsilateral

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151
Q

T./F the LGN has binocular cells.

A

F

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152
Q

T/F midget and parasol cells are kept separate in the LGN.

A

T

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153
Q

T/F djacent points on the retina are represented by adjacent points in the LGN.

A

T –> produces a map of the contralateral hemifield in each LGN

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154
Q

T/F loss of an eye can cause anterograde transsynaptic degeneration in the LGNs

A

true

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155
Q

LGN gating

A

when animal is awake, there are active inputs in the brainstem that keep thalamic cells depolarized, Ca channels are inactivated, gate is open, and RGC activity relayed to cortex vs. at sleep, Ca channels are active, LGN cells are bursty and unpatterned

156
Q

T/F striate cortex/ V1 is retinotopically organized.

A

T –> upper/lower banks with fovea as occipital pole

157
Q

M pathway

A

M cell –> magnocellular LGN –> IVCbeta–> IVB –> thickstriped V2 and MT –>PPA

158
Q

P pathway

A

P cells –> parvocellular LGN –> IVCbeta –> blobs –> thinstripes and innerstripes of V2 and V4–>ITC

159
Q

Both M and P cortical pathways send axons into layers V and VI which are the originas of major pathways to ________ anda major feedback to the _____.

A

pontine nuclei + superior colliculus and LGN

160
Q

Cells in layer ______ encode the presence of features in the visual scene and their distance from the observer and their motion

A

IVB

161
Q

____ are the first neurons in the visual system with binocular RFs

A

cells in IVB

162
Q

Lateral connectivity of visual cortex

A

excitatory, for cells with like orientations, between columns with nonoverlapping RFs

163
Q

Striate organization

A

Retinotopically organized; LGN axons terminate in layer IVC with M and P inputs and LE/RE inputs separate; Modular: orientation, ocular dominance, color; Binocular cells (stereopsis)–layer IVb; Diverse outputs: superior colliculus, pontine nuclei, LGN, other cortical areas;M and P largely separate all the way through; Long range connections modify responses elicited from the receptive field

164
Q

like orientation rule

A

two cells fire synchronously when their RFs have the same orientation even when their RFs are widely separated in the visual field

165
Q

Any visual cortex outside of V1 is called _______ and receives input from _________.

A

extrastriate and V1 and pulvinar

166
Q

T/F V1 and V2 have similar modular structure.

A

F. Both are modular. V1 has blobs while V2 has thick, thin, and interstripes

167
Q

MT (V5) is the homunculus for ____

A

motion –> direction but not orientation selective

168
Q

columns of cells in MT respond best to what element of motion?

A

same direction of motion

169
Q

Aperture problem

A

if the RF is smaller than the object moving across the field, can’t tell the direction of the object –> multiple RFs allow you to determine motion of object

170
Q

V4

A

no special motion processing, mostly color coded, orientation selective –> lesions produce achromatopsia

171
Q

Color constancy

A

correction for spectral properties of the illuminant (kind of like white balance)

172
Q

Speech is usually lateralized in the _____ hemisphere of right handed adults.

A

left

173
Q

The left Sylvian fissure is _________ than right Sylvian fissure in right handers

A

longer and more horizontal

174
Q

3 relevant areas for language disorders

A

Broca’s, Wernicke’s, and Arcuate fasiculus

175
Q

In right handers, Broca’s and Wernicke’s are larger in _____ hemisphere.

A

left

176
Q

Speech is lateralized to ____ hemisphere in left handers.

A

Both or one or the other but both hemispheres are activated in fMRI

177
Q

_______ more likely to be aphasic following left or right hemisphere insult.

A

Lefthanders –> but milder and briefer

178
Q

T/F speech lateralization is affected by experience.

A

T

179
Q

Right handed illiterates and partial illiterates are ____ likely to have strongly lateralized speech.

A

less

180
Q

4 clinical features of speech

A

fluency, comprehension, repetition, naming

181
Q

Fluency

A

Non-fluent = effortful, agrammatic, telegraphic; fluent = melodic but with empty content/circumlocution

182
Q

Broca’s Aphasia

A

non fluent speech (effortful, telegraphic, agrammatic), intact single-word comprehension, impaired repetition, impaired/mild naming

183
Q

Wernicke’s Aphasia

A

fluent speech (empty, circumlocutory), poor single word comprehension, impaired repeittion, poor naming –> involvement of auditory association cortex

184
Q

Conduction Aphasia

A

fluent speech with intact comprehension and naming but poor repetition –> interruption of arcuate fasiculus (often by embolus)

185
Q

Global Aphasia

A

everything is poor–> often due to carotid occlusion resulting in damage to entire Sylvian area

186
Q

Right hemisphere language disorders

A

impaired prosody, poor comprehension of metaphor and humor, limited grasp of extended discourse

187
Q

Striatal aphasia

A

non-fluent speech with preserved repetition

188
Q

Thalamic aphasia

A

–> lacunar strokes/parkinson

189
Q

_______ aphasics have difficulty with grammatical expression and grammatical comprehension

A

Broca’s

190
Q

Progressive aphasia

A

neurodegeneration –> language compromised but preserved memory –> frontotemporal dementia (tauopathy)

191
Q

Semantic dementia

A

fluent, empty speech with poor single word comprehension and object comprehension –> cortical atrophy in anterior and ventral temporal lobe

192
Q

Alexias

A
  1. peripheral component (letter by letter reading) and 2. central component (pronouncing sight vocabulary and novel words)
193
Q

Agraphias

A
  1. Peripheral (apractic) and 2. Central (spelling sight vocabulary and novel words)
194
Q

____ hemisphere is responsible for language and praxis.

A

Left

195
Q

_____ hemisphere is responsible for prosody, spatial representation, attention

A

Right

196
Q

Hetero-modal association cortex

A

area with multi-modality information –> radar representation of the environment

197
Q

Praxis

A

knowledge of manipulation –> hand use, tool use –> 1. premotor cortex for implementation of motor code and 2. inferior parietal lobule for spatial kinesthetic and understanding of physics/tools

198
Q

Apraxia

A

deficit in learned or skilled movements in presence of intact strength/sensation (focal lesions, particularly cortico-basilar ganglionic degeneration, and alzheimers)

199
Q

Damage to premotor cortex will result in ______ apraxia.

A

contralateral but will be able to understand movements

200
Q

Numerosity

A

parietal lobe function b/c of role of 10 digits in hands

201
Q

Subitizing and estimating are ____ parietal lobe functions

A

Right –> rapid, confident apprehension of small quantities and estimating ratios

202
Q

counting and arithmetic have to do with _____ parietal hemisphere.

A

left

203
Q

Gerstmann’s syndrome

A

left parietal lesion/angular gyrus –> agraphia, acalculia, finger agnosia, R/L confusion –> more general body schemadisturbance aka autopagnosia

204
Q

the ______ parietal lobe is responsible for visual attention

A

right –> neglect (MCA stroke)

205
Q

Anosognosia

A

unilateral unawareness or denial of defects on one side of body –> neglect

206
Q

Somatophrenia

A

patient claims contralateral limbs don’t belong to him/her –> neglect

207
Q

T/F different lesions result in different neglects.

A

T –> object (ventral) vs space neglect (dorsal/where)

208
Q

T/F neurons in the parietal lobe reflect all frames of reference (eyes, body, head)

A

T

209
Q

T/F Weaker stimuli are easier to neglect.

A

T

210
Q

T/F People with neglect are faster to verify words semantically primed by a picture in their neglected field.

A

T

211
Q

Balint’s syndrome

A

bilateral parietal (advanced tauopathy, prion, PML) –> optic ataxia (can’t reach for targets), ocular apraxia (gaze), simultagnosia (can see one object at a time) –>disorder of reaching and looking

212
Q

Episodic memory

A

memory for prior experiences and events –> mental time travel/self related/time/place related–> hippocampal

213
Q

Anterograde vs. retrogade amnesi

A

inability to acquire new info vs loss of old info

214
Q

Item vs associative memory

A

pictures vs pictures with context

215
Q

Medial temporal lobe

A

hippocampus (subiculum, dentate, subfields) and extrahippocampal medial temporal structors (entorhinal, parahippocampal, perirhinal)

216
Q

_____ receive inputs from both unimodal and multimodal association cortices and provide the major input into the entorhinal cortex

A

Perirhinal and parahippocampal cortices

217
Q

the ______ serves as the convergence zone for multipmodal information and is critical for associative memory formation.

A

hippocampus

218
Q

Perirhinal cortex

A

represents elements of an event –> what pathway at an item level –>familiarity

219
Q

Parahippocampus

A

serves spatial contextual memory (dorsal visual pathway)

220
Q

Capras disease

A

“delusional misidentification syndrome” in which an individual thinks that someone they know well has been replaced by an identical imposter. As the person recollects the details of the visual appearance and other characteristics of the person, this is thought to represent an example of recollection without familiarity.

221
Q

Fregoli syndrome

A

involves thinking people that you don’t know are embodied by someone that you do (familiarity without recollection). Probably the best example of hyperfamiliarity is that of the aura of déjà vu experienced by patients with temporal lobe epilepsy (TLE). Imaging has revealed that these patients have specific involvement of anterior MTL (including perirhinal cortex).

222
Q

Papez circuit

A

fornix, mamillary bodies, anterior thalamic nucleus, posterior cingulate/retrosplenial cortex –> lesions = amnesia similar to isolated hippocampal lesion

223
Q

Wernicke Korsakoff syndrome

A

petchial hemorrhage of the mamillary bodies due to alcohol –> amnesia

224
Q

Ribot’s law

A

distant memories are safer than recent memories in retrograde amnesia as in MTL injury –: standard consolidation modelßß:as memories are formed, teh MTL-hippocampus binds neocortically represented features of an event ßß: over time, neocortical representations form their own associations and isolate from the MTL

225
Q

Impact of MTL lesions on semantic memory

A

episodic system is important for formation of new semantic memories

226
Q

patients with frontal lobe damage frequently exhibit _______ impairment

A

episodic memory–> patients tend to have false memories, difficulty with event order, immediate recall, free recall. However, performance is often normal on tests of cued recall or item memory or familiarity vs. MTL lesions.

227
Q

Important bit of frontal cortex for memory

A

ventrolateral frontal cortex

228
Q

Parietal lobe on episodic memory

A

patients appear to retrieve contextual details of a prior episodes to a similar extent as controls, they seem to have greater difficulty doing so spontaneously and their memories may be associated with less confidence or vividness. midline and lateral parietal activations associated with successful retrieval of memories

229
Q

______ is the most common form of dementia and most common condition associated with acquired amnesia.

A

alzheimers

229
Q

Biggest risk factor for alzheimers

A

age

230
Q

pathologic features of alzheimers

A

amyloid plaques- extracellular accumulation of aß protein, neurofibrillary tangles-intracellular, helical structures composed of hyperphosphorylated tau

231
Q

T/F 95% of Alzheimer’s cases are sporadic.

A

T

232
Q

The major genetic risk factor for Alzheimer’s is ____

A

apolipoprotein E4

233
Q

amyloid processing mutations

A

trisomy 21, presenelin 1 on chromosome 1, presenilin 2 on chromosome 1

234
Q

Alzheimers

A

syndrome involving insidiously progressive episodic memory deficits accompanied by progressive impairment in several other cognitive domains, including executive functioning, language, visuospatial function and praxis.

235
Q

Difference between Alzheimer’s and memory loss from aging

A

age-associated memory loss is marked by a greater impairment on tasks requiring the retrieval of associative information or the need to spontaneously instantiate appropriate encoding or retrieval strategies. Performance on tasks that provide environmental support or do not require associative details to be retrieved (e.g. item recognition memory) are generally spared. In contrast, patients with AD do not demonstrate significant sparing on the latter types of tasks.

236
Q

Cholinergic input effect on Alzheimer’s

A

pathology of the basal forebrain, greatly diminishing cholinergic input to the neocortex and hippocampus. While the specific role of acetylcholine in learning and memory still remains incomplete, it has been known for years that cholinergic blockers reduce memory performance in healthy subjects. Further, lesions of the basal forebrain, often associated with Anterior Cerebral Artery aneurysms, are frequently associated with memory loss. As seen above, patients with AD are particularly vulnerable to the effects of cholinergic blocking drugs, such as scopolamine. It is, in fact, the relationship of cholinergic dysfunction to AD and memory loss that was the logic behind the development of cholinesterase inhibitors as the major current therapy for AD

237
Q

Temporal nature of memory

A

Short term (attention) –> Long-term (rehearsal) –> Remote memory (consolidation)

238
Q

Phonological working memory deficits tend to localize to the left/right.

A

left

239
Q

Visuospatial working memory deficits tend to localize to the right/left

A

right parieto occipital cortex

240
Q

the _______ is implicated in almost all working memory tasks.

A

dorsolateral prefrontal cortex

241
Q

Symptoms and causes of working memory deficits

A

multitasking, forgetting rules, inefficient learning, reduced contextual memory, impaired verbal fluency –> infarcts, tumors, ms, alzheimers, parkinsons, huntingtons, lew bodies, schizo, depression, adhd

242
Q

_____ involves gradual transfer of informaiton from hippocampal circuits to neocortical ones.

A

consolidation

243
Q

_________ memory involves conscious recall of events or information

A

declarative/explicit –>encompass information that can be consciously recalled, and includes episodic and semantic memory.

244
Q

__________are unconscious memories that affect current behavior

A

non declarative –> nonassociative learning, classical, operant, and emotional conditioning, procedural memory, and priming (non hippocampal/MTL)

245
Q

nonassociative learning

A

habituation - decrease in response to benighn stimulus that is presented repeatedly; sensitization- enhanced response to stimuli after presentation with noxious/painful stimulus

246
Q

Where does habituation and sensitization take place in mammals?

A

spinal reflexes –> preattentive/do not require conscious awareness

247
Q

________learning a relationship between an organism’s behavior and the consequences of that behavior

A

operant conditioning

248
Q

______involves the learned association between a stimulus and an emotional response

A

emotional conditioning

249
Q

What portion of the brain is implicated in classical conditioning?

A

vermis or nucleus interpositus of cerebellum –> Thus when climbing fiber and mossy fiber stimulation are paired, mossy fiber stimulation comes to evoke an eyeblink, in the same way that a behavioral CS would eventually elicit a conditioned response.

250
Q

What portion of the brain is implicated in emotional conditioning?

A

amygdala –> lesion = kluver bucy –> blunted emotionality, lack of fear, altered sexual behavior, hyperorality, visual agnosia

251
Q

Operant conditioning

A

formation of predictive relationships between actions and consequences –>decision making and planning via the law of effect

252
Q

Operant conditioning pathway

A

ventral tegmental area of midbrain –> dopamine –> nucleus accumbens –> dorsomedial frontal cortex implicated in reward related behavior

253
Q

Procedural learning

A

unconscious acquisition of perceptual, motor, or cognitive behaviors –>distinct from the episodic and semantic memory systems –>

254
Q

The ______ demonstrates learning is separate from awareness in procedural learning

A

serial reaction time task

255
Q

Areas of the brain implicated in procedural learning

A

supplementary motor area, basal ganglia, cerebellum–> parkinson’s, movement disorders, tumors, strokes, depression

256
Q

Priming

A

improvement in the ability to detect or identify words or objects after recent experience with them –> unconcious –> have to do with cortex related to the stimulus/modality specific (eg. visual - visual cortex)

257
Q

In Aplysia sensitization, _____ modulates the synapse and ______ is the NT at the synapse.

A

serotonin –> Gs –> cAMP –>PKA –> close K channels –> and glutamate

258
Q

mammals the equivalent of short term synaptic plasticity is ____ while the equivalent of long term plasticity is _____

A

E ltp and L ltp

259
Q

4 key properties of ltps

A

rapid onset, long lasting, pathway specificity, associativity

260
Q

The ____ receptor mediates LTP.

A

NMDA glutamate –>NMDA receptors have a special property in which both glutamate and depolarization are required for the permeation of ions through the channel; During high-frequency synaptic activation, or when synaptic activity occurs concomitantly in many synapses onto the postsynaptic neuron, the cell depolarizes and NMDA receptors can open.

261
Q

T/F after induction, the maintenance of LTP does not require NMDA receptor activity

A

T

262
Q

NMDA receptor antagonist

A

AP5

263
Q

Calcium influx during NMDA receptor activation induces activity of ____

A

Calmodulin kinase II –> inserts more AMPA receptors into the membrane + other effects

264
Q

Long-lasting LTP requires translation and transcription, and is mediated, at least in part through the action of _____.

A

CREB

265
Q

Low frequency transmission and activation of NMDA receptors results in _______

A

long term depression via phosphatase activity that degrades AMPA receptors

266
Q

3 most common Non-alzheimer’s dementias

A

lewy body, vascular, frontotemporal

267
Q

Frontal lobe hypothesis of aging

A

problems attributable to a deficit in executive control mediated by prefrontal cortex –> slowed information processing, multitasking, reduction in working memory, attention, switching attention, forgetfullness, contextual/source memory but not semantic memory

268
Q

______ is an intermediate stage between cognitive decline in normal againg and more pronounced dementia impairments

A

MCI –> normal daily living but subjective and objective impairment in cognitive function not caused by other causes like b12 deficiency

269
Q

Amnestic MCI

A

memory impairment dominates –> single domain, multiple domain

270
Q

Non-amnestic MCI

A

deficits in executive, language, or visuospatial domains with relative preservation of memory function

271
Q

Pathological changes seen in most patients with MCI

A

atrophy, lewy bodies, plaque, vascular changes

272
Q

Amnesic MCI tends to result in _____

A

Alzheimers

273
Q

Non-amnestic MCI tends to result in______

A

non-AD dementia

274
Q

Frontotemporal dementia

A

onset typically between 45-65; relative sparing of memory; focal degeneration of the frontal and temporal lobes corresponding to cognitive and behavioral disturbances

275
Q

The _______ cortex is connected to limbic centers and contributes critically to emotional valence and to the ability to control behavior (including the ability to inhibit inappropriate behaviors).

A

orbitofrontal

276
Q

The ______ prefrontal cortex plays an especially important role in the ability to organization thoughts and actions (organization, executive function).

A

dorsolateral

277
Q

______ cortex is critical for language production in most individuals.

A

left frontal lobe

278
Q

_____ are theorized to play an important role in semantic knowledge.

A

anterior and inferior temporal lobes

279
Q

The behavioral variant of FTD (bv-FTD) preferentially affects the prefrontal cortex, with a right/left-sided predominance

A

right

280
Q

Progressive nonfluent aphasia

A

includes broca’s area; reduced words/minute, effortful, nonfluent speech, insight into impairment, sound-related errors, agrammatism, speech apraxia

281
Q

Semantic dementia

A

difficulty with contextual memory –> problems with word finding, anomia, poor comprehension, poor object recognition, surface dyslexia

282
Q

right/left temporal semantic dementias are associated with deficits in knowledge about emotions and the ability to recognize emotions in others

A

right

283
Q

Pathology of FTD

A

either tauopathy (usually pnfa) or TDP43 proteinopathy (usually semantic dementia)

284
Q

Dementia with Lewy Bodies

A

overlap with parkinson’s but second most common after AD; progressive dementia with deficits in attention and executive function –> recurrent complex hallucinations, fluctuation cognition with attention and alertness, Parkinsonisms; (occasionally sensitivity to neuroleptic and anitemetics) –> levodopa, ache inhibitor

285
Q

Lewy body

A

ubiquitin and alpha synuclein –> cortex + brainstem + substantia nigra (vs. parkisons with just substantia nigra)

286
Q

Vascular dementia

A

usually a gradual decline but in CVD more stepwise

287
Q

3 main types of vascular dementia

A

multi-infarct (large vessel stroke) vs small infarcts in white/grey matter structures –> subcortical, strategic infarct

288
Q

Multi-infarct dementia

A

ACA, MCA, PCA –> stepwise decline

289
Q

____ cerebral artery strokes are associated with aphasia on left and and neglect on right.

A

MCA

290
Q

____ cerebral artery strokes are associated with apathy, abulia, akinetic mutism.

A

ACA

291
Q

____ cerebral artery strokes are associated with amnesia, agnosia, anomia.

A

PCA

292
Q

Subcortical Vascular dementia

A

small vessel lesions of white matter –> psychomotor slowing, impaired concentration, forgetfulness, apathy and depression (absence of focal cortical deficits like aphasia and agnosia)

293
Q

Strategic infarct dementia

A

a single strategically placed infarct (e.g. in the anterior or dorsomedial thalamus or the genu of the internal capsule) lead to cognitive impairment by interrupting critical frontal-subcortical connections –> e.g. lesion of dorsomedial nucleus of thalamus with stroke of paramedian PCA or thiamine deficiency; lesion of anterior thalamus causing amnesia with apathy and reduced emotional expression via infarct of PCOM

294
Q

T/F The treatment of vascular dementia (VaD) is aimed at preventing or minimizing cerebrovascular disease

A

T

295
Q

3 types of primary headache

A

cluster, migraine, tension

296
Q

Migraine

A

constellation of symptoms: headache + pulsing, severity, movement aggravated + nausea or photo/phonophobia + 20% get an aura of visual, sensory, speech disturbances

297
Q

Tension headache

A

No associated features of migraines

298
Q

Why can migraine be felt in the back of the head?

A

C2 innervates occipital area and communicates with trigeminal ganglion which can also use V1 to get pain in the forehead/eyes

299
Q

the _________, is involved in the parasympathetic system, and it plays a role in blood vessel dilatation as well as autonomic symptoms that can accompany headache.

A

superior salivatory nucleus

300
Q

the _____ makes ascending connections with the hypothalamus, which explains why there are changes in appetite and sleep during the headache.

A

spinal nucleus of v

301
Q

the ______ projects to the posterior nucleus of the thalamus, which in turn projects to multiple association areas of the cortex. These contribute to disturbances in neurological functions involved in vision, hearing, memory, motor, and cognitive performance during the headache.

A

spinal nucleus of v

302
Q

Mutations in familial hemiplegic migraines results in ion channel changes that cause increased release or decreased uptake of the nt ______.

A

glutamate

303
Q

migraine pathway

A

hyperexcitability –> cortical spreading depression –>activation of trigememinovascular system (CSD is accompanied by large increase in the concentration of extracellular potassium ions and protons as well as neuropeptides –> vasodilation and inflammatory soup –> hypersentization of meningeal nociceptors –> normal pulsation of blood vessels are perceived as painful)

304
Q

T/F Central sensitization causes allodynia

A

T –> pain from non-painful touch in migraines

306
Q

Working definition of coma

A

no response to external stimuli other than reflexes, eyes closed without sleep wake cycles, prolonged

307
Q

2 systems required for consciousness maintenance

A

cerebral cortices and ascending reticular activating system/thalami

308
Q

ARAS

A

diffuse network of neurons that lies in the paramedian portion of the posterior (dorsal) pons and midbrain; extends from superior pons through midbrain to posterior portion of hypothalamus

309
Q

T/F Unilateral hemispheric lesions should not produce abnormal consciousness unless they are large enough to compress the
brainstem or raise ICP

A

T

310
Q

4 coma mimics

A
  1. locked in syndrome (ventral pons), 2. severe neuromuscular disease (e.g. Guillaine Barre), 3. Psychiatric disease (e.g. catatonia), 4. Akinetic mutism (injury to medial frontal lobes)
311
Q

If the coma exam localizes to the ______, think

structural lesion

A

brainstem

312
Q

If the coma exam localizes to the _______,

think systemic abnormality

A

hemispheres

313
Q

4 elements of classical neurologcal coma exam

A

pupillary response, eye movements, position/movement of limbs, breathing patterns

314
Q

T/F the nuclei of 3 and 4 and MLF are amid neurons of the ARAS

A

T

315
Q

Parasympathetic fibers in 3 are the ______ limb of the pupillary light reflex

A

efferent

316
Q

Abnormalities of the pupillary light reflex generally imply structural injury to the
__________.

A

midbrain or oculomotor nerve

317
Q

Small pupils in comatose patients are typically with injury to the _________ due to loss of descending _________
innervation

A

pontine tegmentum due to loss of descending sympathetics

318
Q

Sympathetic eye pathway

A

1st order neurons synapse in intermediolateral column –> 2nd order exit at C8, T1, T2 –> arch over apex of lung and synapse in superior cervical ganglion –> sweat fibers travel with external carotid, remaining fibers ascend with internal carotid –> enter cavernous sinus –> follow abducens nerve –> switch to V1 –> join nasociliary branch of trigeminal –> ciliary ganglion –> eye

319
Q

With ______ injury, pupils are large and non-reactive due to ______.

A

bilateral midbrain due to to bilateral oculomotor nerve injury

320
Q

With left midbrain dysfunction the _____ pupil is _______ due to unilateral nerve dysfunction. The difference between pupils is accentuated in the light/dark.

A

left midbrain dysfunction, dilated and non-reactive; enhanced in light

321
Q

With L pons dysfunction, the left pupil is ________ due to interruption of _____ fibers. The difference is accentuated in light/dark.

A

small and non-reactive due to interruption of sympathetic; in dark

322
Q

With ___________ both pupils are small and minimally response b/c of interruption of _____ fibers.

A

diffuse pontine injury due to interruption of sympathetic fibers

323
Q

T/F Comatose patients make voluntar eye movements as well as reflex eye movements.

A

F only reflex eye movements

324
Q

If an eye field is damaged on one side, the eyes will look toward which side due to unopposed activity of the contralateral eye fields?

A

the side of the damage

325
Q

Each eye field connects to the contra/ipsilateral PPRF.

A

contralateral PPRF (voluntary = FEF, involuntary = parietal eye fieldsl/7)

326
Q

Conjugate horizontal gaze

A

PPRF innervates ipsilateral abducens and via hte MLF, the contralateral oculuomotor nucleus

327
Q

Roving eye movments

A

normally, eye fields exert tonic inhibition on the brainstem to prevent roving eye movements; if cortex is damaged but brainstem intact, eyes move side to side slowly/rove

328
Q

Doll’s head, oculocephalic reflex

A

turn head –> ipsilateral horizontal semicircular canal sends impulse to ipsilateral vestibular nucleus –> synapses on contralateral abducens and via MLF to ipsilateral oculomotor –> conjugate eye deviation in opposite direction of head turn

329
Q

Oculovestibular reflexes

A

instillation of cold water into the external auditory canal decreases firing rate of the ipsilateral vestibular nucles and is analogous to a head turn toward the opposite side (eyes turn towards cold ear)

330
Q

COWS in coma

A

normal pt: eyes deviate slowly toward cold water and then have fast phase away back to midline; coma pt: absence of slow phase = brainstem, absence of fast phase = cortical dysfunction

331
Q

T/F the presence of spontaneous venous pulsations implies normal cranial pressure.

A

T

332
Q

T/F The presence of purposeful behavior implies some degree of higher cortical function.

A

T

333
Q

Decerebrate posturing implies injury below the level of _____

A

red nucleus –> extensor posturing

334
Q

Decorticate posturing implies injury above level of ______

A

red nucleus –> flexor posturing

335
Q

Cheyne Stokes respiration

A

may follow diffuse cortical injury but more often reflects bilateral thalamic injury

336
Q

Central neurogenic hyperventilation

A

reflects pontomesencephalic injury

337
Q

Apneustic respirations

A

implies lateral tegmentum of lower half of pons

338
Q

Ataxic/biot respirations

A

suggest lower dorsomedial medulla

339
Q

herniation of one hemisphere into the other across midline

A

subfalcine herniation

340
Q

herniation of central brain down onto interpeduncular space

A

central/diencephalic herniation

341
Q

Subfalcine herniation

A

herniation of cingulate cortex under falx; compression of contralateral ACA and ischemia of contralateral medial frontal lobe; ipsilateral lower extremity weakness –> usually no coma

342
Q

Uncal herniation

A

Midbrain compression, ipisilateral 3 palsy, contralateral hemiparesis, (sometimes also ipsilateral hemiparesis due to compression of peduncle against tentorial notch) –> usually coma

343
Q

Diencephalic hernation

A

early: small pupils, somnolence, Cheyne Stokes, decorticate ; intermediate: midsize pupils non reactive, breathing hyperventilation and then apneustic decerebrate posturing; late: oculovestibular and oculocephalic rostrocaudal progression of edema down brainstem –> reflexes absent, ataxic breathing –> arrest

344
Q

Tonsillar herniation

A

sudden respiratory arrest

345
Q

What is the most important recovery mechanism for peripheral nerve injury

A

sprouting of axons from adjacent motor pools

346
Q

What genes do denervated Schwann cells turn on to promote axonal generation?

A

N-cadherin, L1, NCAM, neurotrophins, cytokines

347
Q

Cajal’s neurotropic theory

A

regenerating axons are drawn to denervated Schwann cells at the distal nerve stump

348
Q

T/F severing a nerve makes regeneration more difficult

A

T –> scarring interrupts regeneration process and large gaps are difficult to cross –> basal lamina are discontinuous so axons may grow into the wrong targets

349
Q

T/F Central neurons tend to die when their axons are severed

A

T

350
Q

___________ appears to be an important inhibitory component of the glial scar; removing it with chondroitinase promotes axonal regeneration

A

Chondroitin sulfate proteoglycan

351
Q

NOGO, MAG, Split, and OMGP receptors activate _____, a key signaling component, inhibiting axonal growth.

A

Rho

352
Q

The modification of what intrinsic element promotes CNS regeneration of axons?

A

Local application of cAMP enhances axonal regeneration, but keeping injured cells alive does not help

353
Q

The modification of what extrinsic element promotes CNS regeneration of axons?

A

adding chondroitinase and trophic factors lochttp://www.cu2000.med.upenn.edu/home/bnb/2013/Week4/Lectures/Slides/bb_030613_kasner_vascular_neurology_2_stroke.pdfally

354
Q

T/F sensory neurons in olfactory epithelium are continually renewed.

A

T

355
Q

Pulse labeling reveals that cells in a few specialized regions, especially the __________, of the adult mammalian brain give rise to neurons, astrocytes, and especially oligodendrocytes

A

subventricular zone

356
Q

Most of the neuroblasts from the _____ of the adult mammalian brain migrate to the olfactory bulb, where they form interneurons. In the hippocampus, stem cells also give give to ___________cells.

A

subventricular zone and pyramidal

357
Q

T/F enriched environments can increase neuronal generation in mice.

A

T

358
Q

T/F stress can reduce the number of new neurons in mice.

A

T

359
Q

T/F Implantation of fetal nigral cells can lead to parkinson improvements

A

T –> some benefit but immunosuppression needed and inflammation marked

360
Q

T/F Exogenous stem cells can remylinate the CNS

A

to a degree–> ex. Pelizaeus-Merzbacher

361
Q

stroke

A

sudden focal neurological deficit due to vascular cause (ischemia = 80, hemorrhage = 20%)

362
Q

TIA

A

sudden focal neurological deficit due to ischemia of less than 24 hours in duration without permanent damage

363
Q

7 P’s of ischemic stroke

A

pumps, pipes, perfusion, platelets, pressure, penumbra, prevention

364
Q

________ is most commonly associated with atrial fibrillation, mural thrombus, post-MI akinetic ventricular segment, dilated cardiomyopathy, and valvular disease.

A

cardioembolic stroke –> thrombus breaks off from heart and blocks cerebral vessel –> cortical and wedge-shaped

365
Q

Most “hemorrhagic conversion of an ischemic stroke” occurs in patients with __________ infarctions.

A

cardioembolic

366
Q

__________ is usually a result of carotid artery stenosis (narrowing).

A

Large vessel atherothromboembolism –> at bifurcations like carotid

367
Q

The classic syndrome of bilateral watersheds in the _________territory causes weakness of both arms, sometimes referred to as “man in a barrel syndrome.”

A

ACA-MCA

368
Q

Small vessel occlusive disease is often synonymous with__________

A

“lacunar infarction” –> lipohyalinosis –>small infarct in deep hemispheric white matter, basal ganglia, or pons–> e.g. internal capsule: pure motor hemiparesis, pure sensory stroke, clumsy hand-dysarthria syndrome, and ataxic hemiparesis. –> absence of visual effect and cortical signs

369
Q

Cryptogenic (idiopathic) stroke is diagnosed when:

A

all other studies fail to identify any likely stroke mechanism

370
Q

What is the target of acute stroke therapy—

A

to save the penumbra –> brain tissue that can be saved –> on border of infarct –>t-PA

371
Q

The three major medical causes of death in stroke patients are _______________ all of which may be preventable with close observation and good medical care

A

infections (aspiration pneumonia and urinary tract infection), deep vein thrombosis and pulmonary embolus, and myocardial infarction

372
Q

The higher the ABCD2 score, the lower/greater the risk of subsequent stroke.

A

greater

373
Q

In the brain, heparin is a good treatment for:

A

cerebral vein thrombosis (but not arterial)

374
Q

_______ events involve the very early formation of neuronal connections, for example axons finding their initial targets and the formation of dendrites and synapses in those targets.

A

prenatal

375
Q

______ events involve the proliferation of axonal projections and a dramatic formation of synapses

A

perinatal

376
Q

_____ period is when the brain is highly plastic and sensitive to external stimuli (known as ‘critical periods’). This stage, thus, is dependent upon evoked activity—or experience

A

postnatal

377
Q

In layer ____ of the visual cortex, the units will be driven by either one eye or the other, and they will cluster into alternating ipsi- and contra-lateral columns.

A

IV

378
Q

T/F Outside layer IV, some units will be dominated by one eye, others by the other eye, and some will receive equal inputs.

A

T

379
Q

ocular dominance plasticity

A

visual cortex was incredibly plastic shortly after the eyes open. This was only true for a period of about a month; after this ‘critical period’ , the system was no longer as plastic.

380
Q

The critical period for the formation of ocular dominance columns are about _______ in humans, consistent with the relatively leisurely pace of our maturation.

A

3-5 years

381
Q

T/F If MD occurs within the critical period, the effect on ODs is permanent and largely irreversible.

A

T

382
Q

T/F If MD occurs within the most sensitive part of the critical period (e.g., first 6 wks in monkeys), just a few days of MD results in a complete loss of vision in the sutured eye.

A

T

383
Q

Critical Period

A

Postnatal period during which nerve connections are shaped by activity (experience) and are sensitive to perturbation.

384
Q

Hebb’s Postulate for Learning

A

cells that fire together wire together (LTP) and neurons out of synch lose their link (LTD)

385
Q

T/F That is, there has to be a certain level of GABAergic (inhibitory) tone in the cortex to ‘open’ the critical period.

A

T –> without inhibitory circuits, critical period plasticity does not occur

Brain and Behavior (5 decks)

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