Neuro Block 3 - Q And A

Front 1

How do simple sound waves oscillate

Back 1

in a sinusoidal motion

Front 2

What is the wave called that goes through two oscillations while the fundamental wave goes through one?

Back 2

second harmonic

(vs. third harmonic going through three, etc....)

Front 3

When sound is increased by an octave, by how much does the frequency increase?

Back 3

by a factor of 2

Front 4

What type of wave is a sound wave?

Back 4

longitudinal wave (particle displacement is parallel to direction of wave propagation)

Front 5

What happens to the speed of sound and wavelength, respectively, as frequency increases?

Back 5

speed of sound: remains constant

wavelength: decreases (inverse relationship)

Front 6

What is the wavelength at a frequency of 1 kHz?

Back 6

1 foot (.34 meters)

Front 7

What happens to beat frequency when the frequency difference between two sounds decreases?

Back 7

decreases as well (i.e. the closer two frequencies are to each other, the slower their beat frequency will appear)

Front 8

In a speech spectrum, what are the frequencies with the highest intensity called?

Back 8

formants

Front 9

How many bands in noise-vocoded speech are necessary to approximate clear speech?

Back 9

~200

Front 10

After modification of the pinnae, how does sound localization change?

Back 10

unable to locate changes in elevation (vertical location of sound), subjects regain ability over time

Front 11

What is the purpose of the round window?

Back 11

acts as a pressure release, allowing movement of the fluid inside the inner ear; without it this movement would not be possible since fluids are incompressible

Front 12

What is a myringotomy and when is it used?

Back 12

incision into the tympanic membrane with placement of ear tubes

used to relieve pressure caused by middle ear infection

Front 13

As described by von Bekesy, where in the cochlea would a low frequency (50Hz) sound produce the largest vibration?

Back 13

in the apex (furthest inward - whereas a high frequency sound does not travel far and has its highest vibration at the base of the cochlea)

Front 14

What is the typical range of frequencies a human can perceive and at what range is the threshold for hearing lowest (i.e. least amount of dB needed to hear sound)?

Back 14

range: 20 - 20,000 Hz

lowest threshold: 2,000 - 4,000 Hz

Front 15

What would happen to air conduction and bone conduction, respectively, in a person with a middle ear infection and what other problems cause these same symptoms?

Back 15

AC: threshold increases (more dB needed to perceive sound)

BC: no change; same holds true for excess wax or a ruptured tympanic membrane

Front 16

What is a decrease in both air and bone conduction a common sign of and what is the clinical term associated with it?

Back 16

aging

presbycusis (decrease in conduction especially evident with high frequencies)

Front 17

What can cause a notch in hearing loss located around a specific set of frequencies?

Back 17

tramua (i.e. shotgun blasts close to the ear)

Front 18

What frequencies are considered ultrasound and which frequencies are used in a clinical setting?

Back 18

ultrasound: > 20kHz

clinical setting: > 1 MHz

Front 19

Where is sound picked up when the oval window moves?

Back 19

in the vestibule in the inner ear

Front 20

What is the key distinguishing feature between perilymph and endolymph?

Back 20

perilymph: high Na+

endolymph: high K+

Front 21

At what point does the endolymph of the auditory and vestibular systems connect?

Back 21

ductus reuniens

Front 22

What structure connects the scala vestibuli and scala tympani and where does this communication occur?

Back 22

helicotrema - located at the apex of the cochlea

Front 23

How is the ionic concentration difference between the peri- and endolymph maintained and where is the K+ of the endolymph secreted?

Back 23

maintained through tight junctions all around the endolymph; K+ is secreted by the stria vascularis (through Na+/K+-ATPase)

Front 24

What are the receptor cells of the inner ear?

Back 24

hair cells

Front 25

What ligament attaches the basilar membrane to the bone?

Back 25

spiral ligament

Front 26

What is located in the spinal ganglion?

Back 26

cell bodies of the cochlear nerve (mainly innervate IHC)

Front 27

How many layers of outer hair cells are there and what are they attached to?

Back 27

3-5 layers

attached to a layer of supporting cells (Dieter's cells)

Front 28

What are the protrusions of the hair cells and what are they in contact with?

Back 28

sterocilia - in contact with the tectorial membrane

Front 29

How is the arrangement of stereocilia different when comparing IHC and OHC?

Back 29

IHC: linear

OHC: V or W shaped

Front 30

What are the connections between the stereocilia of hair cells called?

Back 30

tip links

Front 31

How does movement of the basilar membrane result in action potentials down the cochlear nerve (= sound transduction)?

Back 31

movement of the basilar membrane causes the Organ of Corti to move; deflection of sterocilia causes an influx of K+ into the IHC; depolarization than leads to an influx of Ca2+, this is turn caused by fusion of synaptic vesicles which can generate an action potential

Front 32

By what mechanisms is the balance of K+ and Ca++ restored after depolarization of the IHC?

Back 32

Ca2+ sensitive K+ channels; Ca2+ transporters; mitochondrial uptake of Ca2+; voltage-sensitive K+ channels

Front 33

After K+ is extruded from the IHC, how does it go from the perilymph back into the endolymph?

Back 33

it is taken up by supporting cells (Dieter cells) which then transport it to the stria vascularis

Front 34

What do 95% of the afferent nerve fibers of the auditory nerve innervate?

Back 34

IHC

Front 35

What does an overdose of kanamycin lead to?

Back 35

damage to hair cells (also damage to the kidney)

Front 36

What happens to the inner ear following noise exposure?

Back 36

folding over of sterocilia, fusion of sterocilia, breakage of tip links

Front 37

In what syndrome does the patient present with hypertelorism, patches of white pigmentation of the skin, and a forelock of white hair, and how is this associated with hearing?

Back 37

Waardenburg syndrome - also associated w/ severe hearing loss

Front 38

What causes the severe hearing loss in Waardenburg syndrome?

Back 38

faulty migration of melanocytes to the stria vascularis (melanocytes come from the neural crest cells)

Front 39

What is the most common syndromic cause of deafness and what other problems is it associated with?

Back 39

Pendred Syndrome

also associated w/ goiter (since the affected gene - pedrin gene - codes for iodide/chloride transporter)

Front 40

Which gene mutation is responsible for 30-50% of profound hearing impairment (non-syndromic)?

Back 40

Connexin 26 gene (gap jcns)

Front 41

What aspect of the hair cell is affected in Usher's syndrome and why does this syndrome also affect the eyes?

Back 41

tip links and other connections b/w sterocilia (due to a genetic defect), connections b/w sterocilia use similar components as those b/w photoreceptors and RPE cells (thus resulting in blindness and deafness)

Front 42

Through what structure is a cochlear implant inserted to get into the cochlea?

Back 42

through the round window into the scala tympani

Front 43

What happened in clinical trails after adenovirus-mediated transfection of transcription factor Atoh1?

Back 43

the sterocilia of the hair cells regenerated (after destruction by kanamycin exposure)

Front 44

When playing a high frequency sound, what parts of the cochlea become activated?

Back 44

only the most proximal portion (base) up to the frequency of sound (low frequencies are not recorded since they are picked up deeper in the cochlea)

Front 45

What is lost when the outer hair cells are destroyed?

Back 45

30 dB of noise sensitivity

Front 46

How do the OHC affect the IHC?

Back 46

when the sterocilia on the OHC move, a current is generated in the OHC; this current then creates a mechanical twitch (NOT through an actin-myosin) in the OHC which affects the IHC

Front 47

When a cell is transfected with the prestin gene, what results?

Back 47

the cell becomes motile (in response to sound)

Front 48

By what mechanism is aspirin hypothesized to affect hearing?

Back 48

by interfering with OHC motility

Front 49

How is OHC function tested?

Back 49

by measuring otoacoustic emissions (sound generated by OHC)

can be used to differentiate b/w OHC/IHC/ANF defects

Front 50

What is the electrical analog of the mechanical vibration of the OHC called and what is it used for?

Back 50

cochlear microphonic (CM): used to check OHC integrity

Front 51

Embryologically, what do the inner ear, middle ear, and outer ear form out of, respectively?

Back 51

inner: otic vesicle (ectodermal invagination)

middle: 1st pharyngeal pouch

outer: first pharyngeal cleft

Front 52

What is the purpose of the incus, malleus, and stapes?

Back 52

amplification of sound waves (transmitted from the tympanic membrane to the oval window)

Front 53

What is the inner ear completely surrounded by?

Back 53

petrous temporal bone

Front 54

What are the two muscles associated with the middle ear and what is their purpose?

Back 54

tensor tympani: tenses tympanic membrane

stapedius: suppresses excessive movement of stapes

Front 55

What causes tensor tympani and stapedius to contract, and which nerves are associated with each?

Back 55

reflexively activated by loud sound

Tensor Tympani: CN V

Stapedius: CN VII

Front 56

What is the major concern regarding persistent infection of the middle ear?

Back 56

scelorsis of the synovial joints b/w the ossicles

Front 57

What is the posterior extension of the middle ear?

Back 57

mastoid air cells

Front 58

What fluid is contained within the bony labyrinth and membranous labyrinth, respectively?

Back 58

bony labyrinth: perilymph (similar in composition to CSF)

membranous labyrinth: endolymph

Front 59

What do each of the semicircular ducts of the vestibular apparatus end in?

Back 59

an ampulla

Front 60

What are the utricle and saccule connected with, respectively?

Back 60

utricle: semicircular canals

saccule: cochlea

Front 61

What does the endolymphatic duct contact after ending in the endolymphatic sac?

Back 61

dura mater

Front 62

What are the three semicircular ducts?

Back 62

superior, posterior, lateral

Front 63

Where are cristae located and what do they respond to?

Back 63

inside of the ampullae of the semicircular ducts - respond to the movement of fluid from within the semicircular ducts

Front 64

What structures are found within the utricle and saccule?

Back 64

macule

Front 65

Which receptors respond to angular acceleration?

Back 65

the cristae in the semicircular ampullae

Front 66

What type of epithelium makes up the membranous labyrinth?

Back 66

squamous to cuboidal epithelium

Front 67

What happens to the epithelium of the membranous labyrinth as it approaches the maculae?

Back 67

becomes pseudostratified (and eventually columnar as it hits the macula)

Front 68

What are the stereocilia of the macula embedded in and what lies on top of that?

Back 68

a gelatinous material covered by otoliths (=otolithic membrane)

Front 69

What are the hair cells of the cristae embedded in?

Back 69

gelatinous cupula

Front 70

What is each of the turns of the cochlea surrounded by?

Back 70

bone

Front 71

What is the central core of bone in the cochlea called?

Back 71

modiolus

Front 72

What length determines the responsiveness to different movements of the perilymph generated by various sound frequencies?

Back 72

length of basilar membrane

Front 73

What happens to the length of the basilar membrane as you travel from the base of the cochlea to the apex?

Back 73

it becomes longer

Front 74

What is the bony extension called that arises from the modiolus and extends laterally to give attachment to the basilar membrane?

Back 74

osseous spiral lamina

Front 75

What structures define the tunnel of Corti?

Back 75

inner pillar cell, outer pillar cell

Front 76

Which cells are the transducers of vibration for the outer hair cells?

Back 76

supporting cells (aka phalangeal cells)

Front 77

Which cells insert their stereocilia into the tectorial membrane?

Back 77

OHC

Front 78

What does the tectorial membrane attach to and what is its embryologic origin?

Back 78

limbus laminae spiralis - ectodermal in origin

Front 79

What structures are the spikes (I-V) on an auditory brainstem response graph associated with, respectively?

Back 79

I: cochlear nerve
II: cochlear nucleus
III: superior olive
IV: lateral lemniscus
V: inferior colliculus

Front 80

Which peaks on the ABR graph are most reliable?

Back 80

I, III, V

Front 81

Which hair cells contain prestin?

Back 81

OHC

Front 82

What happens to the ABR threshold and the DPOAE threshold in prestin knockout mice?

Back 82

ABR: jumps up ~50 dB

DPOAE: jumps up ~60 dB or disappears completely; (also, CM is reduced)

Front 83

How does the brain distinguish between a 500 Hz sound at 20 dB vs. a 500 Hz sound at 50 dB?

Back 83

as the intensity increases, the rate of action potentials generated by the cochlear fiber associated with frequency will go up

Front 84

How is rate-place code conveyed to the brain?

Back 84

rate encodes intensity

place encodes frequency

Front 85

Besides increasing the firing rate of a specific fiber, what other effect will occur when the intensity of a sound is increased?

Back 85

the population of fibers sending action potentials will increase (= population code for intensity)

Front 86

How does phase-locking of auditory nerve fibers encode frequency?

Back 86

the brain counts the interval b/w action potentials (since they are only generated during the positive part of the wave) and takes the reciprocal (= interval codes)

Front 87

What happens to the range of frequencies that a single hair cell generates an action potential at as the intensity increases?

Back 87

it increases as well

Front 88

By what mechanisms is frequency of a stimulus determined by the auditory system?

Back 88

place code and interval code

Front 89

By what mechanisms is intensity of a stimulus determined by the auditory system?

Back 89

rate code and population code

Front 90

How does the auditory system localize sound in space (binaural cues)?

Back 90

by comparing the intensity and temporal difference b/w the two ears

Front 91

What is the temporal difference between a stimulus reaching both ears when the stimulus is placed at the side of the head?

Back 91

600 microseconds

Front 92

When moving a sound from in front of the head, what change in angle from the center can humans detect?

Back 92

3 degrees

= 30 microseconds of temporal difference

Front 93

Where in the CNS does integration of binaural cues mainly occur?

Back 93

medial superior olive (= dominent cell group)

Front 94

At which frequencies are timing cues useful?

Back 94

below 1500 Hz (above 1.5 kHz the system cant phase-lock)

Front 95

At what frequency does the human head begin to cast an acoustic shadow?

Back 95

above 1000 Hz (translates into a wavelength of about 1 foot)

Front 96

What aspects of sound are used to determine the direction of sound when comparing high and low frequency?

Back 96

high frequency: intensity

low frequency: time

Front 97

Where in the CNS are intensity cues analyzed?

Back 97

lateral superior olive (very small area)

Front 98

By what mechanism is noise filtered from signals generated by the hair cells?

Back 98

cells in the superior olive send out efferents that affect the auditory nerve fibers (either directly on OHC or axoaxonic IHC)

Front 99

How do efferent fibers interact with the outer hair cells and what is their function?

Back 99

synapse directly on the cell body - thought to have a protective fucntion against loud sounds (and used to filter out noise)

Front 100

What percent of information about the world is generated by the eye?

Back 100

70 - 80%

Front 101

What are the three major functions of the eyes?

Back 101

vision

control of light access/usage

special circulation (maintain intraocular pressure)

Front 102

Embryologically, what does the optic vesicle grow out of?

Back 102

diencephalon (forebrain)

Front 103

What is the critical period for eye development?

Back 103

3-10 weeks

Front 104

What does the primary optic vesicle grow out of?

Back 104

optic stalk

Front 105

What occurs when the growth of the primary optic vesicle comes close to the skin ectoderm?

Back 105

it induces formation of the lens vesicle from the skin ectoderm (= invagination)

Front 106

What is the end of the optic vesicle called when the lens vesicle begins the form?

Back 106

optic cup

Front 107

As the optic cups begins to assume its goblet shape, what happens to the lens vesicle?

Back 107

it pinches off to form the lens

Front 108

What characterizes the outer layer and inner layer, respectively, of the optic cup after invagination?

Back 108

outer layer: a single layer of cells

inner layer: differentitates substantially (forms the retinal cells)

Front 109

What does the optic stalk become as axons grow into it?

Back 109

optic nerve

Front 110

What is the vascular region surrounding the retina called?

Back 110

uvea

Front 111

What regions comprise the uvea?

Back 111

iris

ciliary body

choroid

Front 112

From what embryological layer are the uvea and corneosclera derived?

Back 112

mesoderm

Front 113

What is the rigid outer wall surrounding the eye made up of?

Back 113

sclera and cornea

Front 114

What types of connective tissue are the cornea and sclera composed of, respectively?

Back 114

cornea: dense, regular CT

sclera: dense, irregular CT

Front 115

When is the central artery of the retina a branch of?

Back 115

opthalmic artery

Front 116

What borders the posterior chamber of the eye?

Back 116

anterior: iris

Lateral: ciliary body

Posterior: vitreous body

Front 117

Which layer of the eye gives attachment to the various eye muscles?

Back 117

sclera

Front 118

What are the inner and outer epithelia of the cornea composed of, respectively?

Back 118

inner: squamous/low cuboidal

outer: stratified squamous (non-keritinized)

Front 119

How is the cornea innervated?

Back 119

by undifferentiated nerve endings from V1

Front 120

Are fibers running in from the eye to the brain myelinated or unmyelinated?

Back 120

both: from the retina they begin as unmyelinated and then become myelinated when they enter the optic nerve

Front 121

What does the dura mater attach to as it approaches the back of the eye?

Back 121

sclera

Front 122

How is increased intracranial pressure seen in the eyeball?

Back 122

increased pressure of the CSF in the subarachnoid space surrounding the optic nerve causes compression of the retinal vein which presents as papilledema

Front 123

What is the main cell type found in the iris?

Back 123

fibroblasts (iris also has a very rich vascular supply)

Front 124

What are the two main functional components of the iris?

Back 124

constriction and dilation of the pupil (via constrictor and dilator pupillae)

Front 125

What are the zonules?

Back 125

suspensory ligaments of the lens (connect lens to ciliary processes)

Front 126

What is the corneoscleral junction also known as?

Back 126

limbus

Front 127

What is the continuation of the corneal epithelium called as it covers the sclera?

Back 127

conjunctiva

Front 128

What does the aqueous humor consist of?

Back 128

plasma without protein

Front 129

What structure is found in the corneoiridial junction and what is its purpose?

Back 129

canal of schlemm = corneal drainage site

Front 130

Through what structures is aqueous humor drained?

Back 130

trabecular meshwork --> canal of schelmm --> scleral veins

Front 131

Where is aqueous humor produced?

Back 131

in the retina covering the ciliary processes (both the inner non-pigmented layer and outer pigmented layer)

Front 132

What is the attachment of the ciliary muscle called?

Back 132

scleral spur

Front 133

What is caused by excess production or decreased drainage of aqueous humor and what clinical sign is associated with this pathology?

Back 133

glaucoma - alteration in the anatomy of the optic nerve head (cup-to-disc ratio)

Front 134

What is the biggest problem caused by glaucoma?

Back 134

compression of nerve fibers leading to their destruction and subsequent blindness

Front 135

What cell layer developed from the outer rim of the optic cup?

Back 135

pigmented cell layer of the retina

Front 136

What layer is found just outside of the pigmented cell layer of the retina and what is its function?

Back 136

choriocapillaris: supplies nutrients to the pigmented cell layer and the outer segments of the rods and cones

Front 137

What is the site of highest visual acuity in the eye and what characterizes this site?

Back 137

fovea centralis: contains a large number of cones (and no rods)

Front 138

What part of the eye is the important element in the bending of light rays?

Back 138

the interface b/w air and cornea (lens is uded for fine tuning)

Front 139

What is the transition from ciliary body to neural retina called?

Back 139

ora serrata

Front 140

What is the approximate ratio of rods: cones in the retina?

Back 140

20:1

Front 141

What are the three cells found in the retina from outer to inner?

Back 141

photoreceptor cells

bipolar cells

ganglion cells

Front 142

What is found between the layer of rod/cone nuclei and the bipolar cell layer?

Back 142

outer plexiform layer

(vs. inner plexiform layer lying b/w bipolar cell layer and ganglion cell layer)

Front 143

Between which two layers does a retinal detachment normally occur?

Back 143

b/w the pigmented cell layer and the outer segment of rods and cones (the embryologic separation of inner and outer optic cup)

Front 144

In which layer of the retina are the amacrine cells and horizontal cells found?

Back 144

bipolar cell layer

Front 145

Between what two layers do the radial glia of the retina extend?

Back 145

inner portion of the nerve fiber layer and outer portion of the layer of rod/cone nuclei

Front 146

Where do the retinal arteries and veins run in the central portion of the eye?

Back 146

b/w the nerve fiber layer and vitreous body (so they dont obscure vision) - as they move more peripherally they start to run through the nerve fiber layer)

Front 147

As light enters the lens, what two factors determine the amount of bending the light will undergo?

Back 147

the strength of the lens and the difference b/w the refractive indices of air and the lens

Front 148

What happens to the lens strength as the radius of the lens decreases?

Back 148

increases (inverse relationship)

Front 149

What happens to the lens strength as the difference between refractive indices decreases?

Back 149

decreases (direct relationship)

Front 150

How much lens strength do the refractive surfaces of the eye yield?

Back 150

60 D

Front 151

Why does two thirds of the optic refraction occur in the cornea?

Back 151

the refractive indices of air (1.000) and cornea (1.376) are further apart than those of aqueous humorr (1.336) and the lens (1.413)

Front 152

When looking at the "reduced eye", what is the uniform index of refraction and what is the standard image distance?

Back 152

IR: 1.333

object distance = 15 mm

Front 153

How is the retinal image size calculated in the "reduced eye"?

Back 153

(object size * 15mm)/ (object distance)

Front 154

What percent of adults have emmetropia?

Back 154

30% (= perfect vision)

Front 155

What is the clinical name for short-sightedness and what can be the cause?

Back 155

myopia - caused by aberrant eyeball shape

Front 156

What is hyperopia and where does the image project in this case?

Back 156

far-sightedness - image projects behind the eye

Front 157

What is a lens called that has different refractivity (curvature) in different meridians?

Back 157

astigmatism

Front 158

How do corneal scarring and cataracts affect light?

Back 158

they scatter it (cataracts also reduce the total amount of light coming through)

Front 159

What can vitreous opacities create?

Back 159

shadows in the visual field

Front 160

At what object length does accommodation begin and what is the age-related pathology associated with accommodation?

Back 160

at about arm's length

age-related lack of accomodation is called presbyopia

Front 161

How many diopters of accommodation can a child add and how many can a person in their forties add?

Back 161

Child: 14D

forties: 2D - caused by a stiffening of the lens

Front 162

What are our photopic, scotopic, and mesopic light ranges and which retinal cell are used predominantly in each

Back 162

photopic: daylight (cone-dominant vision)

scotopic: darkness (rod-dominant vision)

mesopic: in b/w (mixed rod/cone vision)

Front 163

What is the rod photopigment and what part of this pigment become activated when a photon strikes it?

Back 163

Rhodopsin: 11-cis retinal at residue 296 undergoes a conformational change

Front 164

What does the chromophore (11-cis retinal) change into when light strikes it and at what wavelength is this conversion optimal?

Back 164

all-trans retinal - occurs optimally at 500 nm

Front 165

How many iodopsins function in the retina and what are their optimal wavelengths?

Back 165

three

S - cone (short/blue): 420 nm

M - cone (mediun/green): 534 nm

L - cone (long/red): 564 nm

Front 166

Why can we use cones to determine color, but not rods?

Back 166

since there is only one type of rod we have nothing to compare it to and it can only give us an idea of brightness; however, we have three types of cones, and by comparing the activation of each of them the brain interprets the differences as color

Front 167

What are the prefixes that describe the L, M, and S-cones and what suffix is used to describe a deficiency and an absence, respectively?

Back 167

L-cone: protan-

M-cone: deuteran

S-cone: tritan-

deficiency: -omaly

Absence: -opia

Front 168

What color can a deuteranope not see?

Back 168

green (only has L-cone and S-cone function)

Front 169

What does monochromacy refer to?

Back 169

a person who has only one functional type of cones (rare)

dichromacy refers to someone with two functional types of cones

Front 170

Why are males more susceptible to color vision deficits?

Back 170

the L-cone and M-cone genes are coded on the X chromosomes

(S-cone is on chromosome 7)

Front 171

What is the most common x-linked recessive vision deficit and what is the only type of vision deficit that has a dominant pattern of inheritance?

Back 171

X-linked: deuteranomaly (mild) - 5%

Autosomal dominant: trutanopia

Front 172

What are the times associated with the fast component and slow component of light adaptation?

Back 172

fast: seconds

slow: minutes

Front 173

How does the decrease in threshold differ between rods and cones when entering a dark room?

Back 173

cones: decrease 100 - 1,000 times within 5 minutes

rods: decreases 10,000 times within 35 minutes

Front 174

What structures in the eye cause scotomas and why do we normally not perceive them?

Back 174

optic nerve and blood vessels (obscure vision) - we dont perceive them because the visual cortex fills the gaps

Front 175

What is the yellow area around the fovea called?

Back 175

macula

Front 176

What is particular about the retinotopic organization of the eye?

Back 176

it is upside down and reversed

Front 177

Where on each eye does light from the right visual hemifield project?

Back 177

temporal hemiretina of left eye; nasal hemiretina of right eye

Front 178

Light from where travels in the right optic tract?

Back 178

left visual hemifield

Front 179

Where do the axons in the optic tract travel to?

Back 179

lateral geniculate body, superior colliculus, pretectal region, suprachiasmatic nucleus of hypothalamus

Front 180

Where in the CNS are conscious visual perception and control of eye movements located, respectively?

Back 180

conscious visual perception: lateral geniculate body

eye movements: superior colliculus

Front 181

What functions are performed in the pretectal area and the suprachiasmatic nucleus of hypothalamus, respectively?

Back 181

pretectal area: pupillary reflex

suprachiasmatic nucleus: circadian variation

Front 182

What is the normal visual pathway and how does it compare to the "blindsight" pathway?

Back 182

normal: retina --> LGB --> area 17 --> area 18 --> higher centers

blindsight (i.e. defectice area 17): retina --> superior colliculus --> pulvinar --> area 18 --> higher centers

Front 183

What are the two important retinal ganglion cell subtypes and where does each project to?

Back 183

Parasol (M-cells): to magnocellular layers of LGN

Midget (P-cells): to parvocellular layers of LGN

Front 184

Which layers of the LGN are called the parvocellular layers and which are the magnocellular layers?

Back 184

Parvocellular: III - VI

Magnocellular: I - II

Front 185

Which ganglion cell subtype prefers high-resolution, slow, color input?

Back 185

midget ganglion cells (P-cells)

vs. parasol ganglion cells (M-cells) preferring low-resolution, fast, motion, achromatic input

Front 186

Where in the LGN would a lesion result in the inability of a patient to detect motion?

Back 186

Layers I and II (M layers)

Front 187

What happens to retinotopic organization in the LGN?

Back 187

it is preserved

Front 188

Which layers of the LGN contain contralateral inputs?

Back 188

I, IV, VI - whereas ipsilateral input is contained in layers II, III, V

Front 189

In which part of the calcarine fissure is the contralateral lower visual quadrant located?

Back 189

upper bank

vs. lower bank containing contralateral upper visual quadrants (i.e. its flipped and contralateral)

Front 190

What would a lesion affecting Meyer's loop in the temporal lobe result in?

Back 190

loss of contrallateral upper visual quadrant (= contralateral superior quadrantanopia)

Front 191

What part of the visual cortex represents the fovea?

Back 191

the most posterior part (the more anterior in the cortex, the more peripheral the input from the retina)

Front 192

The loss of what structure signifies the boundary between area 17 and 18?

Back 192

stria of genarri

Front 193

Where in the visual cortex do the magnocellular and parvocellular layers of the LGN project to, respectively?

Back 193

magnocellular (I-II): project to IV-Calapha

Parvocellular (III-VI): project to IV-Cbeta

Front 194

What are ocular dominance columns?

Back 194

ipsilateral/ contralateral segregations in the visual cortex

Front 195

What processes are associated with the ventral (temporal) pathway of the visual cortex and the dorsal (parietal) pathway, respectively?

Back 195

ventral/temporal: object processing ("what")

dorsal/parietal: motion processing ("where"

Front 196

What extra-striate areas are the P cells (midget cells) associated with?

Back 196

ventral/temporal areas (=object processing)

Front 197

What test is used for manual visual field mapping?

Back 197

Goldmann perimetry testing

Front 198

What is the pathology called in which only the central portion of vision is affected (common problem)?

Back 198

age-related macular degeneration

Front 199

Which part of the visual field is affected in retinitis pigmentosa, diabetic retinopathy, and left field homonymous hemianiopia with macular sparing?

Back 199

retinitis: everything except the central portion

diabetic: streaks of vision loss all over visual field (scotomas)

hemianiopia: entire left with minus central portion

Front 200

What type of vision loss would accompany a pituitary tumor growing through the optic chiasm?

Back 200

bitemporal hemianopia

Front 201

What lesions are possible causes of contralateral homonymous hemianopia?

Back 201

optic tract; optic radiation; lower and upper banks of calcarine fissure

Front 202

How is the corticobulbar tract related to eye movement?

Back 202

indirectly - there is no direct relationship b/w the CBT and CN III, IV, VI nuclei

Front 203

Lesions to what brain structures can cause nystagmus?

Back 203

CN VIII, vestibular nuclei, MLF, brainstem, cerebellum

Front 204

What is fast movement of the eye called?

Back 204

saccade (400-800 degrees/second)

Front 205

What two types of movement are associated with nystagmus?

Back 205

slow pursuit movements and saccades

Front 206

What area of the cerebral cortex is responsible for driving the saccadic movements?

Back 206

frontal eye fields (located in the middle frontal gyrus, anterior to premotor cortex - incidental w/ area 8)

Front 207

What are the main direct inputs for the brain stem saccadic generator?

Back 207

frontal eye fields and intermediate superior colliculus

Front 208

What does the modulatory circuit of voluntary eye movement (saccades) consist of and what is its general effect?

Back 208

caudate and SNpr - has an inhibitory effect on eye movement

Front 209

What parts of the cerebral cortex are associated with slow pursuit movement and what is the speed of eye movement generated by this system?

Back 209

occipital-temporal-parietal cortex

50 degrees/second

Front 210

Where in the cortex does information about visual tracking go after leaving the striate cortex?

Back 210

prestriate motion areas: middle temporal and medial superior temporal association areas

Front 211

Which part of the brain serves as the major metric for measuring the velocities of smooth tracking movements?

Back 211

cerebellum

Front 212

What is the major integrating area that drives motor activity?

Back 212

PPRF (pontine gaze center)

Front 213

What are the movements called that change the focus between near and far vision and what is their associated speed?

Back 213

vergence movements - 20 degrees/second

Front 214

What kind of eye movement operates independent of the PPRF?

Back 214

vergence movements

Front 215

What type of eye movements are used to maintain focus on a particular object while smoothly rotating the head?

Back 215

compensatory eye movements

Front 216

Where is the primary input generated for compensatory eye movement?

Back 216

cristae ampularis of semicircular ducts (respond to angular rotation)

Front 217

What are the static vestibular structures and what is their main function?

Back 217

maculae in utricle and saccule - proprioceptice fcn (help maintain balance, equilibrium, and posture)

Front 218

When the head rotates horizontally what happens to the impulse frequency in the antagonistic horizontal semicircular ducts?

Back 218

one side will see inhibition of firing followed by a spike of action potentials; the other side will see a spike of action potentials followed by a drop and subsequent impulse inhibition

Front 219

Which vestibulospinal tract is responsible for coordinating head movements?

Back 219

medial vestibulospinal tract

(vs. lateral vestibulospinal tract coordinating posture)

Front 220

Where do the ascending pathways from the vestibular nuclei into the MLF travel?

Back 220

nucle of CN III, IV and VI

Front 221

Besides excessive input from the vestibular system, what else can cause vertigo and what is the mechanism associated with them?

Back 221

excessive intake of alcohol, infection, allergic reaction, Meniere's disease - effects due to local release of histamines causing buildup of excess fluid in the labyrinths

Front 222

What autonomic symptoms accompany excessive or abnormal vestibular output?

Back 222

pallor, cold sweating, naseua, vomiting

Front 223

Which stimuli can cause a leftward nystagmus?

Back 223

leftward head movements

cold water in opposite ear w/ warm water in same ear (COWS); bars moving to the right (optokinetic test)

Front 224

Where in the brainstem are the horizontal and vertical gaze centers located, respectively?

Back 224

horizontal: CN VI nucleus and IL PPRF (paramedian pontine reticular formation)

Vertical: midbrain reticular formation (not as well defined but includes the riMLF)

Front 225

Where in the cortex are horizontal eye movements initiated?

Back 225

frontal eye fields

(--> corticobulbar tract --> PPRF --> abducens nucleus)

Front 226

Besides inhibiting abduction of the IL eye, what other deficit will damage to the abducens nucleus produce?

Back 226

adduction of the CL eye (b/c of connections b/w CN VI nucleus and the CL CN III nucleus via the MLF)

Front 227

A lesion of what structure will produce similar effects as a lesion to the PPRF?

Back 227

IL abducens nucleus

Front 228

Through what structures does the pathway from the frontal eye fields to the oculomotor nuclei pass?

Back 228

corticobulbar tract and vertical gaze centers (midbrain reticular formation)

Front 229

What does stimulation of the frontal eye field lead to?

Back 229

CL conjugate deviation of the eye

Front 230

What distinguishes a right abducens nerve palsy from a right abducens nucleus palsy, clinically?

Back 230

in the right abducens nucleus palsy, adduction of the left eye will also be inhibited (besides abduction of the right eye)

Front 231

What is the most common site of damage in MS regarding the visual system and what clinical signs are associated with it?

Back 231

internuclear ophthalmoplegia: demyelination of MLF - causes problems w/ adduction of the IL eye and nystagmus of CL eye during abduction

Front 232

What structures are affected in the 1 and 1/2 syndrome?

Back 232

MLF and abducens nucleus on the same side

Front 233

A tumor of what structure can cause problems with vertical gaze?

Back 233

pineal tumor - affecting midbrain (esp. tectum)

Front 234

What is the general area associated with horizontal gaze problems?

Back 234

Pons (PPRF, CN VI)

Front 235

What is the most commonly damaged area associated with nystagmus?

Back 235

vestibular nuclei in the medulla (if there are no problems with vertical or horizontal gaze)

Front 236

When looking at the optic disc, which arteries can be seen?

Back 236

central retinal artery slitting up into retinal arteries

Front 237

What is the major blood supply to the outer segments of the rods and cones and where does this supply come from?

Back 237

choriocapillaris - derived from ciliary arteries via choroidal arteries

Front 238

What are examples of microscopic and macroscopic level electrical events in the eye?

Back 238

microscopic: photoreceptor membrane potentials

macroscopic:electroretinogram (ERG - from cornea) and visually evoked potentials (VEP - from scalp)

Front 239

How are the rod photoreceptor discs created and where do they end up?

Back 239

created by the folding and pinching off of plasma membrane

then they move up to the outer segment of the rod where they are released

after release they are degraded by the RPE cells

Front 240

How does the outer segment of the cone differ from that of the rod (besides their characteristic shape)?

Back 240

the discs of the cone are not free-floating as they are in the rods

Front 241

What is the resting potential of the "dark current" and how is this generated?

Back 241

- 40 mV

generated by a steady influx of Na+, efflux of K+, as well as active Na+/K+ transport

Front 242

What is the end-result of light hitting rhodopsin?

Back 242

hyperpolarization of the photoreceptor

Front 243

By what mechanisms does light hitting rhodopsin cause hyperpolarization of the photoreceptor?

Back 243

activated rhodopsin causes GTP to bind transducin --> transducin binds cGMP PDE which converts cGMP to 5' GMP; the subsequent lack of cGMP inhibits the cGMP-gated Na+ channels --> a decrease in Na+ influx leads to hyperpolarization of the photoreceptor

Front 244

What is the amplification associated with phototransduction?

Back 244

rhodopsin causes GTP to bind transducin 500x; the PDE-transducin-GTP complex converts1000 cGMP to 5'GMP per second; this leads to an overall depletion of cGMP of 500,000 molecules per second (Ramsden says 10^5/s)

Front 245

What does hyperpolarization of the photoreceptor cell lead to?

Back 245

a decrease in glutamate release

Front 246

What type of potential is associated with the photoreceptors and bipolar cells?

Back 246

graded potential

(vs. ganglion cell which uses action potentials)

Front 247

What concept explains why we don't have very good visual acuity at night?

Back 247

many rods converge on a single bipolar cell (i.e. the subsequently activated ganglion doesnt know which rod was activated)

Front 248

What does a foveal cone synapse on?

Back 248

one off-bipolar cell and one on-bipolar cell

Front 249

What type of polarization do the on-bipolar cells respond to?

Back 249

depolarization

(vs. off-bipolars responding to hyperpolarization)

Front 250

What is the purpose of having an off-bipolar and an on-bipolar cell and what does each synapse on?

Back 250

improving the signal-noise ration - they synapse on off- and on- midget ganglion cells

Front 251

What happens to the dendritic fields of both the parasol and midget cells when moving peripherally on the retina?

Back 251

they increase (thus decreasing visual acuity)

Front 252

How much vision loss would a person experience after losing all midget cells?

Back 252

from 20/20 to 20/100

Front 253

After synapsing on a bipolar cell where does the signal from a rod travel?

Back 253

rod --> rod bipolar --> amacrine --> cone bipolar --> ganglion --> optic nerve

Front 254

What is the main function of horizontal cell and how does it accomplish this function

Back 254

exert a lateral inhibitory effect ("center-surround" or "surround inhibition") - when activated,the horizontal cell releases GABA over a large area, thus inhibiting everything around the activated photoreceptor

Front 255

In an on-center ganglion cell, what happens to ganglionic action potentials in response to a peripheral light spot?

Back 255

they decrease since the periphery of an on-center ganglion cell has an inhibitory effect (think of the donut-like organization)

Front 256

What is the response seen when shining a large spot of light over the entire receptive field of an off-center ganglion cell?

Back 256

nothing (excitatory and inhibitory effects cancel each other out)

Front 257

How does the response of ganglion cells differ from that of "simple" cells in the primary visual cortex?

Back 257

ganglion cells: donut-shaped response area

simple cell: respond to particular orientation of stimulus (e.g. vertical bar vs. horizontal bar)

Front 258

How does the response of "simple" and "complex" cells differ regarding stimulation of their receptive fields?

Back 258

simple: oriented stimulus must be presented in an optimal location of their RF for maximal stimulation

complex: oriented stimulus can be presented anywhere in their RF for maximal stimulation (so long as the orientation is good)

Front 259

What do cells in V1 respond to preferentially in comparison to cells in the LGN/retina?

Back 259

larger RFs (such as lines and edges) - whereas cells in the LGN/retina prefer small spots of light and color differences

Front 260

What type of information is processed in areas V2/V4 and the inferior temporal cortex, respectively?

Back 260

V2/V4: combination of lines/edges, shape ocmponents, 3-D sensitivity

inferior temporal: faces, object components

Front 261

What happens to the receptive fields when moving further up the hierarchy of the visual system?

Back 261

they increase

Front 262

What is needed for distant electrical fields to be generated by the brain?

Back 262

summation of organized, coincident, and co-localized synaptic input

Front 263

When using electroretinography (ERG), what are the a-wave and b-wave associated with?

Back 263

a-wave: photoreceptor response

b-wave: other retinal cells

Front 264

In which disease is the scotopic response of ERG absent?

Back 264

retinitis pigmentosa (absence of scotopic response indicates a problem with the rods)

Front 265

In which disease is the photopic response of ERG absent?

Back 265

cone dystropy (absence of phototopic response indicates a problem with the cones)

Front 266

How is optic neuritis seen on a visually evoked potential (VEP)?

Back 266

a delayed response will be seen in the lead associated with information coming from the optic nerve

Front 267

What is the name of the earliest evolved part of the cerebral cortex and which functional areas are part of it?

Back 267

Palaeocortex = olfactory cortex in parahippocampal gyrus

Front 268

What are the two components of the allocortex?

Back 268

Palaeocortex and the archicortex (hippocampus)

Front 269

What volume of the brain is occupied by neocortex and percent of that volume consists of neuropil (i.e. dendrite and axons)?

Back 269

half of the brain volume is neocortex - 80% of that is neurophil

Front 270

What is traversed, respectively, when moving in a radial and tangential direction in the cortex?

Back 270

Radial: cortical layers

Tangenital: cortical areas

Front 271

What are the four named cortical layers and which numbered layers are contained within each?

Back 271

Molecular Layer (L1)
Supragranular layer (L2-3)
Granular Layer (L4)
Infragranular Layer (L5-6)

Front 272

What characterized the molecular layer?

Back 272

a cell-sparse layer in which all cells are inhibitory

Front 273

Which layers contain pyramidal cells and which layers are classified by the morphology of their pyramidal cells?

Back 273

All layers except L1

Specifically: L2-3: small-medium sized pyramidal cells and L5: large pyramidal cells

Front 274

What types of cells are located in layers 4 and 6 of the neocortex, respectively?

Back 274

L4: small stellate cells

L6: polymorphic cells

Front 275

What distinguishes agranular neocortex and which cortical areas are agranular?

Back 275

has no apparent Layer 4

examples are primary motor cortex (area 4) and premotor cortex (area 6)

Front 276

What do most granular areas of the neocortex have in common?

Back 276

they are primary sensory regions (also includes prefrontal cortex - areas 8, 9, 10)

Front 277

Which are the primary cortical areas and what characterizes them?

Back 277

S1: (3, 1, 2)
V1: (17)
A1: (41)
M1: (4)
they are all unimodal and organized topologically

Front 278

Which are the secondary cortical areas and what characterizes them?

Back 278

V2 (18)
A2 (42)
Premortor and SMA (6)
receove input from primary cortical areas, are still unimodal (complex), but topological order is distorted

Front 279

Which are the higher ("associational") cortical areas and what characterizes them?

Back 279

Superior Parital (5, 7)
Prefrontal (8, 9, 10)

receive input from primary and secondary cortical areas, are multimodal, and do not have topological order

Front 280

What characterizes the morphology of excitatory neurons in the cortex?

Back 280

Spiny Dendrites: Pyramidal shape (except for spiny stellate cells)

Front 281

What do all excitatory synapses on excitatory neurons impinge on?

Back 281

Dendritic Spines

vs. inhibitory synapses forming on dendritic spines, shafts, and somata

Front 282

What characterizes a neuron with smooth or sparsely-spiny dendrites?

Back 282

it is inhibitory

Front 283

Where do the spiny dendrites of the pyramidal cell come off?

Back 283

at the cell body: basal dendrites

From the apex: apical dendrite

along the apical dendrite: oblique dendrites

At the end of the apical dendrite: apical tuft

Front 284

How does the pyramidal cell make local connections?

Back 284

via axon collaterals

Front 285

With what pathways do supragranular pyramidals make connections?

Back 285

Associational and commissural pathways (i.e. only corticocortical connections)

Front 286

Where do most of the infragranular pyramidals project to and what are some examples?

Back 286

subcortical areas

Deep Layer V: corticotectal, corticostriatal, corticospinal

Layer VI: corticothalamic

Front 287

What are spiny stellate neurons derived from and where do they make their connections to?

Back 287

modified pyramidal cells (lost apical dendrite/shortened axon):
main input from sensory thalamocortical fibers
main output is local to upper cortical layers (i.e. layers closer to pia)

Front 288

What percent of cortical neurons are inhibitory, in what layers are they found, and where do they project to?

Back 288

25%
Found in all layers
Axons only travel locally (i.e. they fcn as local inhibitory interneurons)

Front 289

Where do the following inhibitory neurons synapse on: basket cells, Martinotti cells, and chandelier cells?

Back 289

Basket Cells: somata and proximal dendrites

Martinotti Cells: distal dendritic tufts

Chandelier Cells: intial segment of axon

Front 290

Where and from what are cortical neurons generated?

Back 290

in the ventricular wall, they are generated by asymmetric division of progenitor cells

Front 291

What are the cells called that form the "railway" for migrating neurons and span the zone between the ependymal layer and the pial surface?

Back 291

Radial Glial Cells

Front 292

What does the inside-out lamination of cortical neurons lead to?

Back 292

A layering scheme in which the oldest neurons are found in the deep layers of the cortex and the youngest in the superficial layers

Front 293

What gene mutation causes periventricular heterotopia (PH), in what sex is it found, and what are the clinical manifestations associated with this disease?

Back 293

Mutation in Filamen A gene (responsible for the initiation of neuronal migration)
X-linked so only heterzygous females will be viables
causes late onset seizures due to clumps of periventricular neurons which failed to migrate

Front 294

What are lissencephaly and pachygyria, respectively?

Back 294

Lissencephaly: "smooth brain" with no gyri or sulci

Pachygyri: Fewer than normal gyri

Front 295

A mutation of which protein causes migrating neurons to "fall off" the radial glia too early creating a band of gray matter underneath the cortical white matter (in heterozygous females)?

Back 295

Doublecortin (DCX): a microtubule-associated proteins

Affected gene is X-linked causing lissencephaly or pachgyria and mentral retardation in male carriers, causes double cortex (subcortical laminar band heterotopia) in female carries

Front 296

Besides causing facial and other abnormalities, what gene important for neuronal migration is affected by Miller-Dieker Syndrome and what are the associated deficits?

Back 296

LIS1 gene (chromosome 17): codes for a microfiliament-associated protein, mutations causes Type-1 Lissencephaly b/c protein is involved in maintaining the proper speed of migration

Front 297

Which protein is responsible for the termination of neuronal migration, which cells in which layer secrete it, and what results if the associated gene is mutated?

Back 297

Reelin: extracellular matrix proteins, secreted by Cajal-Retzius cells in layer 1

without Reelin, earlier-born neurons stay attached to the radial glial, blocking the migration of later-born neurons --> results in inverted cortical lamination and lissencephaly

Front 298

How is local intracortical information transfer oriented and what concept does this give rise to?

Back 298

Radial (vertical), giving rise to cortical columns; each vertical column is a sepatate inforamation processing unit responding only to a particular receptive field; each receptie field is thus processed in a parallel fashion by cortical columns making for extremely rapid processing

Front 299

In what functional area of the thalamus are the principal nuclei located?

Back 299

Isothalamus

(vs. allothalamus containing CM and other midline nuclei, also, a third functional area contains the reticular nuclei)

Front 300

Where do the intralaminar and midline nuclei of the thalamus receive input from, where do they project to, and what are their presumed functions?

Back 300

Input: basal ganglia, cortex, cerebellum, spinal cord

output: basal ganglia, cortex (diffuse-mostly L1)

thought to function in motor planning and the processing of painful sensations

Front 301

Where do the principal nuclei of the thalamus project to exclusively?

Back 301

Neocortex: layer 4 and layer 3 (of 4 is absent) - they project point-to-point and topological

Front 302

Which are the ventral tier nuclei of the thalamus, which are the dorsal tier nuclei, and what are their respective cortical connections?

Back 302

Ventral Tier: VA, VO, VL, VPL/VPM, MGN, LGN - connected with primary and unimodal areas

Dorsal Tier: anterior (and LD), MD, pulvinar (and LP) - connected with associated cortical areas

Front 303

Which thalamic nucleus receives input from the prefrontal cortex, amygdala, olfactory cortex, and basal ganglia, and projects back to the prefrontal cortex?

Back 303

Medial Dorsal nucleus (MD)

Front 304

Into what nucleus of the thalamus do the mamillothalamic tract and fornix travel and where does this nucleus project to?

Back 304

anterior nucleus - anterior nucleus and LD have reciprocal connections with the cingulate gyrus

Front 305

Where do the pulvinar and LP receive their main input from and where do they project to?

Back 305

Pulvinar and LP have reciprocal connections with the parieto-occipital cortex; there is also a small input from the superior colliculus into the pulvinar which is relayed to area 18

Front 306

What are the respective inputs and outputs of VA, VO, and VL?

Back 306

VA: SNpr --> prefrontal cortex (area 8, 9, 10)

VO: basal ganglia (GPm) --> premotor/SMA (area 6)

deep cerebellar nuclei --> M1 (area 4)

Front 307

How are thalamocortical neurons different from the pyramidal neurons of the cortex?

Back 307

they have ONLY long connections and NO local connections; (they are all glutaminergic multipolar neurons)

Front 308

When the cortical target of thalamocortical relay neurons is destroyed, what results?

Back 308

the thalamocortical relay neurons undergo retrograde degeneration

Front 309

Where do the reciprocal corticothalamic projections originate and what characterizes them?

Back 309

originate in L5-6, they are excitatory, projecto IL, and topological

Front 310

Which is the only thalamic nucleus that is purely GABAergic and where is it located?

Back 310

reticular thalamic nucleus - forms a thin shell surrounding the entire thalamus

Front 311

What are the inputs and outputs of the reticular thalamic nucleus (RTN)?

Back 311

inputs: from thalamocortical and corticothalamic tracts (both glutaminergic)

outputs: to thalamic nuclei (GABAergic)

Front 312

Information from which cortical areas is integrated in the superior colliculus?

Back 312

S1 (3, 1, 2)
A1 (41, 42)
V1 (17)

Front 313

What type of waves are seen on an EEG in an awake person with their eyes closed?

Back 313

Alpha waves (~ 10 Hz) - also seen in comatose patients

Front 314

What causes strong waves on an EEG?

Back 314

synchronous and spatially aligned thalamocortical synaptic currents in large populations of cortical pyramidal neurons

Front 315

In which two states of consciousness is the EEG "activated" (low-amplitude/high-frequency) and what differentiates those two states?

Back 315

Wakefulness and REM sleep

In wakefullness we have full muscle control whereas during REM sleep there is muscle atonia, saccades, and dream

Front 316

In which state of sleep is the EEG "deactivated" (high-amplitude/low-frequency) and what other signs are associated with this state?

Back 316

slow-wave sleep: also presence of muscle tone and intact reflexes

Front 317

What type of EEG activity is seen during an epileptic seizure?

Back 317

synchronized EEG (very high amplitude); also tonic-clonic bursts or spike-and-wave acitivty

Front 318

What types of waves are seen on EEG in every state of sleep, respectively?

Back 318

Awake: Beta
Relaxed: Alpha
Stage 1: Theta
Stage 2/3: Sleep spindle/ K complexes
Stage 4: Delta
REM: Beta

mnemonic: (at night) BATS Drink Blood --> BATSDB

Front 319

What are the frequencies associated with each of the wave types?

Back 319

Delta: < 4 Hz
Theta: 4-7 Hz
Alpha: 7-14 Hz
Beta/Gamma: > 14 Hz

Front 320

How do the actions of thalamus differ between the awake/attentive state and other states (e.g. drowsiness, sleep, some types of comas, petit-mal seizures)?

Back 320

Awake: high-fidelity relay (passes everyting on)

other: pacemaker (gates input)

Front 321

What happens to the overall potential of the thalamus during sleep and what is the result?

Back 321

it slowly hyperpolarizes (with each sleep stage it hyperpolarizes more)
This hyperpolarization increases the calcium conductance thus lowering AP threshold; when a stimulus now arrives at the thalamus it does not trigger a Na+ AP, but instead a Ca ++ AP

Front 322

How does the Ca++ AP differ from the Na+ AP?

Back 322

it is much slower

Front 323

What happens during sleep, when a Ca++ AP is triggered?

Back 323

as the cell depolarizes it initiates a synchronous burst of Na+ APs which shows up as a large amplitude wave on EEG

Front 324

What causes the oscillatory nature of the EEG spikes during sleep?

Back 324

When a burst of APs reach the cortex, descending corticothalamic tracts are activated; these tracts then activate RTN which causes inhibition of the thalamus, thus keeping the thalamus from causing another burst of APs in the cortex until the next cycle

Front 325

Why don't the EEG spikes reach out consciousness?

Back 325

there is a lack of informational content b/c of simulataneous and stereotypical firing of cortical neurons

Front 326

What effects do NE, 5-HT, and ACh have on the thalamus?

Back 326

excitatory (they depolarize it during the wakeful state keeping the memb potential at - 50 mV)

Front 327

What monoamine is produced in the tuberomamillary nucleus (TMH)?

Back 327

Histamine

Front 328

What neuropeptide hormone is produced in the lateral hypothalamus (LH)?

Back 328

Orexin (hypocretins)

Front 329

What amino acid neurotransmitter is produced in the VLPO (ventral lateral preoptic area)?

Back 329

GABA

Front 330

What structures are referred to as the "sleep center" and the “wake center", respectively?

Back 330

sleep center: VPLO

Wake center: LH and TMH

Front 331

Which structure is referred to as the "master sleep center" and what happens when it is activated?

Back 331

VLPO - sends inhibitory signals to the hypothalamic arousal centers ("wake centers"), slowly causing them to shut down

Front 332

Where do the hypothalamic arousal centers exert their effect and what is this effect?

Back 332

on the locus cerulus (NE), raphe nuclei (5-HT), and on the mesopontine REM centers (ACh) - the effects are all excitatory

Front 333

What happens to the mesopontine REM centers as sleep progresses?

Back 333

in early sleep stages, the bioaminergic nuclei (NE/5-HT) cause inhibition of the mesopontine REM centers

however, at some point the bioaminergic nuclei become completely inhibited and are thus unable to inhibit the mesopontine REM centers

this causes the mesopontine REM centers to become active leading to inhibition of motor nucleus (via reticulospinal neurons)

this is why muscles become atonic during REM sleep

Front 334

Input from what area causes the characteristic eye movements of REM sleep?

Back 334

Mesopontine REM centers (PPT/LDT) - also cause muscle atonia (via reticulospinal glycinergic neurons in the medulla) and activates dreaming

Front 335

What happens to the thalamus when we go from non-REM to REM sleep?

Back 335

ACh input depolarizes the thalamic neurons, generating forebrain arousal

Front 336

What does a mutation in the orexin gene or an autoimmunity to orexin producing neurons lead to?

Back 336

narcolepsy - loss of orexin causes uncontrolled entry from waking directly into REM sleep

Front 337

What are some symptoms often associated with narcolepsy?

Back 337

excessive daytime sleepiness (EDS)
cataplexy (sudden loss of muscle tone during awake state)
sleep paralysis (profound paralysis that persists for a few mintures after waking)

Front 338

What is seen in REM sleep behavior disorder and in what population does this occur most frequently?

Back 338

REM state muscle atonia is lacking causing ppl to act out their dreams - usually seen in older males

this is different from somnambulism ( = non-REM sleep walking and sleep terrors in children)

Front 339

What defines a seizure and what are the sites where seizures occur?

Back 339

a transient episode of synchronous and rhythmic firing in a large population of neurons - usually in the cerebral cortex (neocortex, paleocortex, hippocampus) and amygdala

Front 340

What defines epilepsy?

Back 340

a disorder of recurrent seizures

Front 341

What are the two main classifications of seizures and what are their subtypes?

Back 341

Partial seizures:
- Simple (no alteration of consciousness)
- Complex (with alteration of consciousness)

General Seizures:
- primarily generalized (originates bilaterally, no discernable focus)
- secondarily generalized (begins as a partial seizure, then generalizes)

Front 342

What is an example of a secondarily generalized seizure?

Back 342

"Jacksonian March" (seizure traveling up motor homunculus) leading to a tonic-clonic, "grand-mal" seizure

Front 343

What is the term used to describe continuous generalized seizures with no regaining of consciousness?

Back 343

status epilepticus (= life-threatening situation)

Front 344

How can an epileptic focus be identified on EEG and what are some causes of a focus?

Back 344

visible as interictal (= b/w seizures) spikes - an epileptic focus from traumatic injury, stroke, tumor, congenital defect, and acute inflammation

Front 345

How is an epileptic focus contained by normal physiological mechanisms and what happens for it to cause a full-blown seizure?

Back 345

an surround inhibition is generated around the epileptic focus through normal mechanisms; when this surround inhibition is breached, a seizure will be initiated

Front 346

Through what pathways do seizures spread from one cortical area to another?

Back 346

through the associational and commissural axons of pyramidal cells in the epileptic focus

Front 347

What differentiates the tonic and clonic phases of a "grand-mal" seizure?

Back 347

tonic: continous firing of cortical neurons (incl. motor cortex) causes muscles to contract non-stop leaving the person in a rigid state

clonic: some inhibition transforms the tonic output to the more rhythmic clonic firing in which the person has convulsions

Front 348

Which anti-epileptic drugs function by blocking Na+ channels during abnormally prolonged and high-frequency firing activity?

Back 348

Phenytoin (dilantin)

carbmazapine (Tegretold)

lamotrigine

Front 349

Which anti-epileptic drugs function by affecting GABA through either allosteric interactions, blocking the membrane GABA transporter, or inhibiting GABA break-down?

Back 349

Allosteric: barbiturates, benzodiazepines

transport: tiagabine (Gabitril)

break-down: vigabatrin

Front 350

What is the characteristic EEG finding with Absence (Spike-and-Wave) Epilepsy (SWE) and how does the treatment for this type of epilepsy differ?

Back 350

3 Hz oscillations in the thalamocortical circuit - b/x SWE is caused by excessive inhibition of the thalamocortical circuits by the RTN .GABAergic enhancers would only worsen the seizures; therefore, blockers of the low-threshold Ca currents (like ethosuximid) are prescribed instead

Front 351

Why are benzodiazepines effective in treating SWE?

Back 351

they enhance the mutual inhibition b/w the RTN neurons, thereby destroying their synchrony

Front 352

How do we determine to which hemisphere cerebral functions have lateralized?

Back 352

by using Wada test: intracarotid sodium amobarbital procedure - the procedure shits down one side of the brain; then lateralization is determined by loss of fcn

Front 353

In Broca's research, hemiparesis on which side of the body was found to correlate with language impairments?

Back 353

Right side (since Broca's area is most often lateralized to the left hemisphere)

Front 354

What results after cutting the corpus callosum?

Back 354

the hemispheres are unable to communicate with each other internally

Front 355

Which functions are normally found in the left hemisphere and which in the right?

Back 355

Left: speech, writing, lexical and syntactic language, sequential and analytical skills (arithmetic, muscical)

right: spatial abilities, control of attention, prosodic aspects of language (e.g. rhythm, stress, intonation), rudimentary speech, complex muscial ability

Front 356

Which cerebral functions are found in both hemispheres?

Back 356

stereognosis, analysis of visual fields

Front 357

What are the main functions of the parietal lobe?

Back 357

CL somatosensory, stereognosis; language (left hemisphere); spatial relations (right hemisphere); sensory integration for motor planning

Front 358

Where is the lesion commonly in spatial neglect syndrome?

Back 358

right parieto-occipital cortex

Front 359

What are the main functions associated with the temporal lobe?

Back 359

hearing; language (left hemisphere); olfaction (limbic cortex); object recognition (e.g. faces) ID and naming

Front 360

What do temporal lesions result in?

Back 360

agnosias (= difficulty in recognizing, identifying, and naming object)

Front 361

What is prosopagnosia and in what cortex is the associated lesion located?

Back 361

inability to recognize faces - lesion in inferior temporal cortex

Front 362

How do we determine to which hemisphere cerebral functions have lateralized?

Back 362

by using Wada test: intracarotid sodium amobarbital procedure - the procedure shits down one side of the brain; then lateralization is determined by loss of fcn

Front 363

In Broca's research, hemiparesis on which side of the body was found to correlate with language impairments?

Back 363

Right side (since Broca's area is most often lateralized to the left hemisphere)

Front 364

What results after cutting the corpus callosum?

Back 364

the hemispheres are unable to communicate with each other internally

Front 365

Which functions are normally found in the left hemisphere and which in the right?

Back 365

Left: speech, writing, lexical and syntactic language, sequential and analytical skills (arithmetic, muscical)

right: spatial abilities, control of attention, prosodic aspects of language (e.g. rhythm, stress, intonation), rudimentary speech, complex muscial ability

Front 366

Which cerebral functions are found in both hemispheres?

Back 366

stereognosis, analysis of visual fields

Front 367

What are the main functions of the parietal lobe?

Back 367

CL somatosensory, stereognosis; language (left hemisphere); spatial relations (right hemisphere); sensory integration for motor planning

Front 368

Where is the lesion commonly in spatial neglect syndrome?

Back 368

right parieto-occipital cortex

Front 369

What are the main functions associated with the temporal lobe?

Back 369

hearing; language (left hemisphere); olfaction (limbic cortex); object recognition (e.g. faces) ID and naming

Front 370

What do temporal lesions result in?

Back 370

agnosias (= difficulty in recognizing, identifying, and naming object)

Front 371

What is prosopagnosia and in what cortex is the associated lesion located?

Back 371

inability to recognize faces - lesion in inferior temporal cortex

Front 372

What are the main functions associated with the frontal lobe?

Back 372

personality, strategic planning, motor execution, working memory, rational decision making, processing of emotions, balancing of risk and reward

Front 373

What type of behavior can be seen in patients with frontal lobe lesions?

Back 373

sucking behavior afer stroking of cheek (i.e. infantile behavior)

Front 374

What did the Phineas Gage anecdote elicit?

Back 374

Frontal lobe lesions can cause dramatic personality changes

Front 375

What behavior does the Wisconsin Card Sorting test elicit?

Back 375

perservation (= lack of response initiation)

Front 376

What frontal lobe test is used to check working memory?

Back 376

delayed response test

Front 377

What defines arousal and awareness and how do they relate to sleep/coma/anesthesia, vegetative state, minimally conscious state, and locked-in syndrome, respectively?

Back 377

Arousal: state of being awake

Awareness: ability to interact meaningfully with one's environment

Sleep/coma/anesthesia: no arousal, no awareness

Vegitative state: high arousal/ no awareness

Minimally conscious state: high arousal/ low awareness

Locked-in state: high arousal/ high awareness

Front 378

In what type of coma is there not a problem with the brain, but the person nevertheless appears to be comatose?

Back 378

psychogenic coma - can be faked or due to psychiatric problems

Front 379

What is the oculocephalic reflex and is it present in a healthy person?

Back 379

reflex in which the eys move opposite the direction in which the head is turned, thus maintaining a fairly steady gaze

NOT seen in the healthy person (also called doll-head maneuver)

Front 380

What type of coma results from damage to the medial rostral brainstem and what abnormal findings are associated with it?

Back 380

structural (focal) coma
EEG: low frequency
PLR: compromised
OCR: non-conjugate
Caloric: asymmetric (also, person loses arousal AND awareness)

Front 381

What (ab)normal findings are associated with a metabolic/pharmacologic/multifocal coma and what distinguishes the light type from the deep type?

Back 381

light: depressed EEG, PLR present, conjugate OCR, conjugate tonic response to caloric test (also, no awareness)

Deep: flat or depressed EEG, PLR present, no OCR, conjugate tonic or no response to calcoric test (also, no awareness AND no arousal)

Front 382

How does the response in the comatose patient change to caloric testing and why?

Back 382

(COWS --> WOCS)
Since the patient will not show nystagmus, the slow phase will now determine which way the eyes travel; cold water will therefore draw the eyes to the IL ear in a slow movement (and warm water will draw it to the CL ear)

Front 383

Where is the damage located with a "locked-in" state and which function is retained?

Back 383

caudal brainstem (pons) - person is only able to move eyes vertically; all other muscles are compromised (however, arousal and awareness are retained)

Front 384

What percent of brain metabolism is maintained during coma (as compared to normal consciousness) and which comatose state is the exception?

Back 384

around 50% - except with locked-in state, in which about 90% of brain metabolism maintained

(lowest % is found in the persistant vegitative state)

Front 385

When does a vegetative state become persistent?

Back 385

after one month

Front 386

How long must there be a loss of awareness and arousal for a coma to be present and damage to what structures must be associated with it?

Back 386

> 1 hours; must be following either widespread cortical gray/white matter or focal, bilateral damage to medial rostral BS and/or diencephalon

Front 387

Lesions in which area of the brainstem are most often associated with coma?

Back 387

bilaterally in posterior rostral pontine tegmentum - medially part (includes: raphe nuclei, locus cereuleus, laterodorsal tegmental nucleus (ACh), pontis oralis (Glu) and parabrachial nucleus (Glu))

Front 388

In general, how do the outcomes compare for comatose patients, due to structural, metabolic, and pharmacologic causes, respectively?

Back 388

metabolic: worst

structural: better

Pharmocological: best

Front 389

What are examples of focal compressive structural brain damage and how does this cause coma?

Back 389

examples:
epidural/subdural hematoma, tumor
the increase in intracranial pressure can lead to herniation of the BS, in effect causing compression of BS structures and coma

Front 390

What is an example of diffuse compressive structural brain damage and by what mechanism will this cause coma?

Back 390

subarachnoid hemorrhage: leads to rapid increased intracranial pressure which constricts the vascular supply; this then causes massive ischemic cell death and coma

Front 391

What are examples of focal and diffuse destructive structural brain damage, respectively?

Back 391

focal destructive: brainstem infarct/hemorrhage

diffuse destructive: closed head trauma

Front 392

Which specific causes of coma have the worst prognosis?

Back 392

global anoxia: drowning, CO poisoning

global ischemia: cardiac arrest, massive stroke

Front 393

Lesions in which parts of the brain stem are NOT associated with coma?

Back 393

bilateral caudal pons, unilateral rostral pons, bilateral medulla

Front 394

What are uncal herniation and central herniation examples of?

Back 394

symmetric intracranial mass effects in compressive coma

Front 395

What findings are associated with the early and late stages of uncal herniation?

Back 395

early: IL dilated pupil, doll's head maneuver, conjugate tonic response to caloric test (OCR and caloric test can also be dysconjugate), motor response to noxious stimulus, babinski

Late: hyperventilation (or Cheyne-Stokes), fixed pupil size, impaired doll's head maneuver, impaired caloric testing, decerebrate rigidity

Front 396

What is the key difference between the uncal herniation and the central herniation?

Back 396

uncal herniation involves compression of CN III, thus leading to a unilateral pupillary dilation whereas with central herniation the pupils are bilaterally constricted (early phase)

Front 397

How does age and time spent in coma affect the outcome of coma from traumatic brain injury?

Back 397

age: older = worse

time: longer = worse

(child has 60% of regaining consciousness after traumatic injury)

Front 398

When is a persistent vegetative coma regarded as permanent?

Back 398

if the cause is metabolic, after 3 months

if the cause is traumatic, after 12 months

Front 399

What three requirements must be determined before declaring a person brain dead?

Back 399

careful determination that all brain functions ceased
determination of the cause ofthe cessation
determination that the cause renders the process irreversible

Front 400

Why is it essential to determine the cause of brain death?

Back 400

fully reversible "brain death" can be due to a massive sedative overdoes (i.e. pharmological coma)

Front 401

Cessation of which functions are necessary for declaring brain death and which are not?

Back 401

necessary: brain activity (no response to noxious stimuli), respiration (apnea), BS reflexes (pupils, ocular movement, facial sensation/motor responses)

NOT necessary: spinal reflexes, heartbeat

Front 402

What are the main inputs/outputs from the hypothalamus?

Back 402

inputs: limbic cortex, amgydala, brainstem

outputs: brainstem reticular formation

Front 403

What are the two main functions of the hypothalamus and what characterizes each?

Back 403

integration of visceral, endocrine, homeostatic, sensory and cognitive - affective information

coordination: uses internal signals to regulate the internal and external envirnoments

Front 404

Which tract sends information into the paraventricular nucleus of the hypothalamus?

Back 404

tracts of solitary nucleus (i.e. visceral info)

Front 405

From what areas does cognitive-affective information enter the hypothalamus?

Back 405

frontal, orbitofrontal, anterior cingualte cortices, and basal forebrain limbic structures

Front 406

Which hypothalamic cell bodies are visualized by Nissl stain?

Back 406

cell bodies of Meynert's nucleus

Front 407

Embryologically, what is the preoptic nucleus derived from?

Back 407

Telencephalon (NOT diencephalon) - however, since its fcn is intertwined with outher hypothalamic nuclei is has been grouped with them

Front 408

Which hypothalamic nucleus has the medial forebrain bundle (MFB) running through it?

Back 408

lateral hypothalamic nucleus (MFB runs from the forebrain through the hypothalamus to brainstem structures)

Front 409

Which hypothalamic nucleus controls reproductive and maternal behaviors?

Back 409

preoptic nucleus (its development is under the control of estrogen and testosterone during critical periods)

Front 410

Which hypothalamic nucleus is dimorphic with sexual orientation (in men) and which specific cell group is involved?

Back 410

interstitial nuclei of the anterior hypothalamus

- specifically, group 3 (more than twice as large in heterosexual men)

Front 411

How does the size of the bed nucleus of the stria terminalis differ in heterosexual males and females, and how does it differ between a homosexual male and a male-to-female transsexual?

Back 411

Heterosexual: larger in males

Homosexual/Transsexual: larger in homo

size does not dpend on sexual preference, but instead it depends on gender

Front 412

Where is the periventricular nucleus (PVN) located, what are its inputs/outputs and what is its function?

Back 412

bilaterally adjacent to the third ventricle

input: solitary tract

output: BS/SC, median eminence (CRF), posterior pituitary

Functions: production of oxytocin/ADH, osmosensitivity, lactation/milk production, stress response

Front 413

What does a lesion to the periventricular nucleus lead to, and what syndrome is a mirror-image to it?

Back 413

lesion: diabetes insipidus

mirror-image: SIADH (syndrome of inappropriate ADH)

Front 414

Which hypothalamic nucleus is located next to the optic chiasm (not above), what are its inputs/outputs, and what is its function?

Back 414

supraoptic nucleus (SON)

input: from BS

outputs: posterior pituitary

functions: release of oxytocin/ADH (lesions would causes similar symptoms as those found with a lesion of the PVN)

Front 415

Although the PVN and SON have similar functions, which specific function is more prominent in the SON?

Back 415

initiation of maternal behavior - also orgasm

Front 416

Which hypothalamic nucleus is located above the optic chiasm, what are its inputs/outputs, and what are its functions?

Back 416

Suprachiasmatic nucleus (SCN)

input: from retina

output: SCN --> pineal --> IML --> SCG --> pineal

functions: circadian rhythm, melatonin synthesis

Front 417

What will happen to the APs from the SCN after their connections with the retina are lesioned?

Back 417

their internal pacemaker activity will ensure that they continue to fire, regardless of input (when the lesion is to the SCN itself, circadian rhythms are lost)

Front 418

Which part of the hypothalamus is known as the "cooling system" and how does it achieve this function?

Back 418

anterior hypothalamic area - fcn through vasodilation and increased respiration

Front 419

Which substances are released from the arcuate nucleus?

Back 419

DA (= prolactin release inhibitory hormone)

LH-RH (= GnRH)

GH-RH

Front 420

Which hypothalamic nucleus is known as the center for feeding and aggression and what do lesions to this nucleus cause?

Back 420

Ventromedial nucleus

lesions cause overeating and rage

Front 421

What does a lesion of the lateral hypothalamic (LH) area lead to?

Back 421

undereating - LH also regulates sympathetic neurons in the spinal cord

Front 422

Which part of the thalamus is known as the "heating system"?

Back 422

Posterior Hypothalamus - fcns through vasoconstriction and shivering

Front 423

What are the mammillary bodies part of, what is their function, and what pathology is associated with them?

Back 423

part of the limbic system
functions in memory consolidation

damage leads to Korsakoff's psychosis (thiamine (B1) deficiency in alcoholics)

Front 424

What two groups of structures does the medial forebrain bundle connect?

Back 424

basal olfactory region, orbitofrontal cortex, entorhinal cotex, septal nuclei, BS nuclei, PAG, dorsal motor nucleus of X

Front 425

Which structure traverses the hypothalamus in the periventricular area and what are its origins/destinations?

Back 425

dorsal longitudinal fasciculus;

connects preoptic area, PVN, LH to the PAG, RF, Raphe, DMNX, nucleus ambiguus, IML

Front 426

What type of dysfunction will be seen when there is damage to the medial forebrain bundle or the dorsal longitudinal fasciculus?

Back 426

autonomic dysfunction

Front 427

In general, which areas of the hypothalamus are associated with the sympathetic and parasympathetic nervous system, respectively?

Back 427

sympathetic: lateral/posterior

parasympathetic: anterior/medial

Front 428

What are the key characteristics of Horner's syndrome and what can cause it?

Back 428

enopthalmos, vasodilation, anhydrosis, miosis, ptosis;

causes: injury to cervical sympathetic system, reticular formation, peripheral sympathetic pathways

Front 429

How do the Cannon-Bard theory and the James-Lang theory differ regarding early theories of emotion?

Back 429

Cannon-Bard: stimulus --> brain (fear) --> viscera (=emotional response)

James-Lang: stimulus --> viscera (= emotional reponse) --> brain (fear)

Front 430

What structures grossly encompass Papez circuit?

Back 430

hippocampus --> fornix --> mammillary body --> mammillothalamic tract --> anterior nucleus of thalamus --> cingulate cortex (diffuse) --> parahippocampal gyrus --> hippocampus

Front 431

Besides those found in Papez circuit, what other structures comprise the limbic system?

Back 431

septal area, orbitofrontal cortex, BS autonomic nuclei, prefrontal cortex, amygdala, nucleus accumbens, hypothalamus, dorsomedial thalamus, olfactory cortecx

Front 432

What structures are involved in executive oversight for when and where to release survival related behaviors?

Back 432

prefrontal, orbitofrontal, anterior cingulate cortices

Front 433

Neurons in which structures are directly in charge of survival related behavior (and emotions)?

Back 433

hypothalamus, septal nuclei, medial and basolateral amygdala

Front 434

Which structures are part of the relay for smell and which are involved in conscious perception of smell?

Back 434

relay: parahippocampal gyrus, uncus, amtgdala, entorhinal cortex

conscious: dorsomedial thalamus, orbitofrontal cortex

Front 435

Which structures are associated with associational learning and memory, respectively?

Back 435

associational learning: amgdala, mesiotemporal cortex, bed nucleus of stria terminalis

memory: hippicampus, mesiotemporal cortex

Front 436

At what age does the prefrontal cortex finish development?

Back 436

25

Front 437

What do lesions and stimulation of the orbitofrontal cortex lead to, respectively?

Back 437

lesions: reduce aggression, emotional responsiveness, and olfaction

stimulation: increase plasma cortisol and EEG arousal

Front 438

What functions are associated with the prefrontal cortex (think Phineas Gage)?

Back 438

executative control of emotional responses; weighs consequences of actionsl seat of personality and reflection; parenting

Front 439

What is capsulotomy and what does it lead to?

Back 439

cutting the connections b/w the dorsomedial nucleus of the thalamus and the orbitofrontal lobe

leads to docileness and flat affeect (also destroys relay for smell)

Front 440

What do Brodmann's areas 24, 25, 32, 33 comprise, where do its inputs arise from and where do its outputs go?

Back 440

anterior cingulate gyrus

inputs: parahippocampal gyrus, orbitofrontal gyrus, auditory cortex

outputs: amygdala, prefrontal cortex, medullary autonomic and visceral motor areas

Front 441

What does stimulation of the cingulate gyrus cause?

Back 441

"Arrest reaction" (inhibition of respiratory movements = vigilance), sexual behaviors, OCD (anxiety)

Front 442

What is the "pleasure center" of the brain?

Back 442

septal area

Front 443

What part of the septal apparatus is important in addiction?

Back 443

nucleus accumbens

Front 444

Which structure makes up the archicortex and what functions are associated with it?

Back 444

hippocampus - important for remembering where good and bad things happen; knowing the location of oneself and things in space

Front 445

What common problems are associated with the hippocampus?

Back 445

common site of epileptiform activity

lesions lead to deficits in short-term memory, anterograde amnesia, and deficits in memory consolidation

Front 446

What can cause a stress response and which structure mediates this response?

Back 446

any internal or external stimulus, which is perceived as threatening - mediated by the amygdala

Front 447

From what major areas does the amygdala receive its input?

Back 447

association cortex, thalamus, hypothalamus, BS reticular formation

Front 448

What are the direct and indirect outflow pathways of the amygdala and which structures do they include?

Back 448

Direct/Ventral amygdalafugal pathway: hypothalamus, dorsomedial thalamus, cingulate gyrus, BS autonomic centers; indirect/stria terminalis: bed nucleus of stria terminals, nucleus accumbens, hypothalamus

Front 449

What is the most common mental health problem in the US?

Back 449

anxiety disorders (person is most vulnerable to develop these due to pre- and postnatal stress)

Front 450

What are the three primary nuclei of the amygdala associated with the fear circuit?

Back 450

lateral (input), basolateral, central (output)

Front 451

What differentiates the high road and the low road by which sensory input reaches the amygdala, and which is mostly associated with anxiety disorders?

Back 451

high road: through sensory cortex (conscious)

low road: bypasses sensory cortex (unconscious) - chronic activity of the low road may underlie anxiety disorders

Front 452

Where do the outputs from the central nucleus of the amygdala go and what does each do?

Back 452

lateral hypothalamus: sympathetic effect

DMN of vagus: parasympathetic effects

central gray: freezing

nucleus reticularis pontis caudalis: startle reflex

periventricular nucleus: corticotropin releasing factor secretion

Front 453

What limbic structure is involved in face recognition?

Back 453

amygdala

Front 454

What is the pathophysiology of Urbach-Wiethe Syndrome and what does it result in?

Back 454

genetically based lipid storage disease that destroys the amygdala - leads to difficulty identifying fearful emotion from facial expression

Front 455

Which structure signals the amygdala that the dangerous situation is over ("extinction")?

Back 455

prefrontal cortex

Front 456

What is the most effective treatment for anxiety disorders?

Back 456

cognitive behavior therapy (activates prefrontal cortex) and medication (SSRI, diazapam, propranolol, cycloserine)

Front 457

What is psychic blindness and of which syndrome is this characteristic?

Back 457

a compulsion to examine every object tactilely and visually as well as a compulsive ingestion of non-food objects --> found in Kluver-Bucy syndrome (bilateral ablation of the amgydala); also presents with fearlessness, tameness, and hypersexuality

Front 458

Which hemisphere is more involved in facial emotion expression?

Back 458

Right Hemisphere - can be seen by looking at people's smiles (bigger on the left side)

Front 459

What happens to the observer when looking at a facial expression?

Back 459

the person has perceptual, somatovisceral, and motoric reexperiencing of the relevant emotion

Front 460

What is the relationship between basal motor activity and emotional judgments?

Back 460

adopting specific emotional postures will lead to experiencing the associated emotions

Front 461

What does damage to the orbitofrontal olfactory area lead to?

Back 461

a loss of conscious olfaction

Front 462

Where does the emotional response to odor occur and what about the memory of where the odor was encountered?

Back 462

emotional response: amygdala

memory: hippocampal formation

Front 463

Where do the projections from the primary olfactory cortex travel?

Back 463

dorsomedial thalamus, hypothalamus, amygdala, entorhinal cortex

Front 464

What is the clinical word describing the lack of a sense of smell?

Back 464

anosmia

Front 465

Seizures in which area of the cortex are often preceded by hallucinations of taste or smell?

Back 465

anterior temporal lobe

Front 466

Which important nucleus degenerates in Alzheimer's disease and what is its associated neurotransmitter?

Back 466

meynert's nucleus (aka substantia innominata) - ACh: has widespread cortical innervation

Front 467

What is the most common symptom reported by patients with cerebral cortex or subcortical dysfunction?

Back 467

memory problems

Front 468

In the simplest sense, what do encoding, consolidation, and retrieval refer to?

Back 468

encoding: getting info in

consolidation: putting info away

retrieval: getting information out

Front 469

What are the structures involved in encoding, consolidation, and retrieval, respectively?

Back 469

encoding: thalamus (MD and anterior nuclei), frontal lobe

Consolidation: mesial temporal lobes, hippocampus, fornix

Retrival: frontal lobes

Front 470

What are some key clinical syndromes which affect encoding?

Back 470

Wernicke's Korsakoff; Thalamic strokes;
End-stage Alzheimer's disease

Front 471

What are the characteristic signs associated with Wernicke's encephalopathy and what is the key sign of the subsequent Korsakoff's psychosis?

Back 471

Wernicke: acute confusion, eye movement problems

Korsakoff: dense amnesia

Front 472

What type of disease is associated with the loss of long-term memory and personal information?

Back 472

Psychiatric disease (whereas loss of short-term memory loss is often affected by neurological damage)

Front 473

464. What are possible causes of Wernicke's Korsakoff and what lesions are common with this disease?

Back 473

Alcoholism or bulimia leading to thiamine (Vit. B1) deficiency - lesions in MD of thalamus and mamillary bodies

Front 474

What do patients with Wernicke's Korsakoff of thalamic strokes do to compensate for their short-term memory loss?

Back 474

Confabulate bizarre stories

Front 475

What diseases affect consolidation?

Back 475

Alzheimer's disease, complex-parial seizures, anoxia, herpes encephalitis, paraneoplastic limbic encephalitis, closed head injury

Front 476

In what disease do antibodies from a neoplasm (usually in the lungs) travel to the limbic system causing acute inflammation?

Back 476

Paraneoplastic limbic encephalitis

Front 477

A lesion in which part of the limbic system causes the most severe amnesia?

Back 477

Hippocampus

Front 478

What is the treatment of herpes encephalitis and what results if the disease is found late?

Back 478

Acyclovir - herpes encephalitis progresses quickly causing destruction of the temporal lobes and limbic system; thus severe amnesia and death follow if treated too late

Front 479

What can a colloid cyst of the 3rd ventricle lead to?

Back 479

Hydrocephalus --> surgery to remove the cyst may lead to bilateral damage to the fornix --> significant short-term memory problems

Front 480

What can damage to the anterior portion of the corpus callosum lead to?

Back 480

"Alien-hand syndrome" - because of a disconnect between the frontal lobes, one of the patient's hands will appear to have a mind of its own

Front 481

Lesions in what part of the brain will affect retrieval and what are some examples of diseases causing such lesions?

Back 481

Frontal lobe lesions; Frontal disconnection (subcortical): Parkinson's, Huntington's, AIDS, Progressive Supranuclear Palsy, Chronic Ischemic disease, MS

Front 482

What triad of symptoms is associated with Parkinson's disease?

Back 482

Resting tremor, bradykinesia, rigidity

Front 483

What structure degenerates initially in Huntington's disease and what are the initial symptoms often seen?

Back 483

Caudate nucleus - initial symptoms: behavioral changes, anxiety, obsessive-compulsive behaviors

Front 484

With what disease are Dawson's Fingers present on an MRI?

Back 484

MS - looks like fingers reaching up to the corpus callosum

Front 485

How can closed head injury lead to retrieval problems?

Back 485

Either through direct damage to the frontal lobe or through shear injury causing separation of gray and white matter in the frontal lobe

Front 486

What is the pathology seen in CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)?

Back 486

Subcortical lacunar infarcts along with severe small vessel white matter changes (happens at a young age - 30s)

Front 487

A lesion in which part of the limbic system causes the most severe amnesia?

Back 487

Hippocampus

Front 488

What is the treatment of herpes encephalitis and what results if the disease is found late?

Back 488

Acyclovir - herpes encephalitis progresses quickly causing destruction of the temporal lobes and limbic system; thus severe amnesia and death follow if treated too late

Front 489

What can a colloid cyst of the 3rd ventricle lead to?

Back 489

Hydrocephalus --> surgery to remove the cyst may lead to bilateral damage to the fornix --> significant short-term memory problems

Front 490

What can damage to the anterior portion of the corpus callosum lead to?

Back 490

"Alien-hand syndrome" - because of a disconnect between the frontal lobes, one of the patient's hands will appear to have a mind of its own

Front 491

Lesions in what part of the brain will affect retrieval and what are some examples of diseases causing such lesions?

Back 491

Frontal lobe lesions; Frontal disconnection (subcortical): Parkinson's, Huntington's, AIDS, Progressive Supranuclear Palsy, Chronic Ischemic disease, MS

Front 492

What triad of symptoms is associated with Parkinson's disease?

Back 492

Resting tremor, bradykinesia, rigidity

Front 493

What structure degenerates initially in Huntington's disease and what are the initial symptoms often seen?

Back 493

Caudate nucleus - initial symptoms: behavioral changes, anxiety, obsessive-compulsive behaviors

Front 494

With what disease are Dawson's Fingers present on an MRI?

Back 494

MS - looks like fingers reaching up to the corpus callosum

Front 495

How can closed head injury lead to retrieval problems?

Back 495

Either through direct damage to the frontal lobe or through shear injury causing separation of gray and white matter in the frontal lobe

Front 496

What is the pathology seen in CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)?

Back 496

Subcortical lacunar infarcts along with severe small vessel white matter changes (happens at a young age - 30s)

Front 497

What defines aphasia?

Back 497

Loss of the ability to produces and/or comprehend language

Front 498

What are the five parts of the clinical assessment for aphasia and what is the main purpose of the assessment?

Back 498

spontaneous speech (fluent vs. non-fluent), comprehension, repetition, fluency (phonemes vs. semantics), naming - purpose is localizing the lesion

Front 499

What are paraphasias and what are the two main subtypes

Back 499

incorrect words or non-words

subtypes: semantic (word with similar meaning) and literal/phonemic (word with same sound) paraphasias

Front 500

\How is comprehension tested clinically?

Back 500

by giving a complex conditional command

e.g. "with your left hand touch your nose, after touching your right ear" or "if the lion ate the tiger, did the tiger die"

Front 501

How is fluency tested clinically?

Back 501

by asking the pt to name as many words as possible that start with a specif letter (phonemes) or as many words as possible within a certain category (semantics)

Front 502

What is the classification of aphasias based on?

Back 502

Stroke data (meaning that a tumor causing aphasia would not follow the same patterns)

Front 503

What happens in Broca's aphasia to each of the following functions: spontaneous speech, comprehension, repetition, naming, motor, and sensory?

Back 503

spontaneous speech: nonfluent
comprehension: intact repetition: impaired
naming: impaired
motor: hemiplegia
sensory: intact

Front 504

What happens in Wernicke's aphasia to each of the following functions: spontaneous speech, comprehension, repetition, naming, motor, and sensory?

Back 504

spontaneous speech: fluent, paraphasias, jargon
comprehension: impaired
repetition: impaired
naming: impaired
motor: intact
sensory: intact

Front 505

What is the key difference between Broca's and Wernicke's aphasia?

Back 505

Broca's: spontaneous speech is damaged (also, hemiplegia)

Wernicke's: speech comprehension is damaged

Front 506

What is the most striking defect in a conduction aphasia?

Back 506

repetition is notable imparied (due to a lesion of the arcuate fasciculus)

Front 507

How does a transcortical motor aphasia differ from Broca's aphasia?

Back 507

repetition is intact in an echolalic manner (o.e. the lesion is not in Broca's area)

Front 508

Where will a lesion have to be localized in order for repetition to be impaired?

Back 508

Sylvian fissure (lateral fissure)

Front 509

What differentiates a transcortical motor aphasia from a transcortical sensory aphasia?

Back 509

The motor aphasia will be due to a lesion located more anteriorly (disconnection of SMA, from motor speech) whereas the sensory aphasia lesion will be located more posteriorly (lesion of parietal/temporal jcn posterior to Wernicke) both are away from the lateral fissure

Front 510

Which function is most obviously impaired in subcortical aphasias (i.e. lesion in left thalamus/basal ganglia)?

Back 510

naming (if it's more posterior, comprehension will be impaired)

Front 511

What structure connects Broca's and Wernicke's area?

Back 511

arcuate fasciculus

Front 512

What is anomia and where will the lesion be located to produce this deficit?

Back 512

problem with naming, lesion can be anywhere in the left hemisphere (lateral temporal and anterior temporal cortices are most common site)

Front 513

What will a lesion of the occipital cortex cause if it clips the splenium of the corpus callosum?

Back 513

alexia without agraphia (pt can write a sentence, but not read what he/she just wrote) - although letter-by-letter reading is still intact

Front 514

A lesion in what area will cause agraphia?

Back 514

angular gyrus

Front 515

The image of the retina of an object in the visual field is

Back 515

left-right reversed
superior-inferior inverted

Front 516

About half of the visual cortex is devoted to input from the

Back 516

fovea

Front 517

The Parvocellular pathways (P-channels) conveys information about

Back 517

fine detail vision, color vision

Front 518

• The absence of both pupillary reflex responses from the right eye, but the presence of both responses in the left eye would indicate

Back 518

the afferent limb of the right eye is damaged, the efferent limb of the right eye and left eye is intact

Front 519

Saccadic eye movements

Back 519

conjugate
rapid jumps
visual acuity depressed
eyes provide main sensory input

Front 520

Smooth-pursuit eye movements

Back 520

conjugate
smooth and precise
visual acuity good
eyes provide main sensory input

Front 521

Eye movements to adjust from far to near vision:

Back 521

vergence
smooth and precise
visual acuity good
eyes provide main sensory input

Front 522

Eye movements to compensate for head movements

Back 522

conjugate,
smooth and precise
visual acuity good
semicircular canal provides main sensory input

Front 523

A lesion in the optic tract will cause a loss of vision in

Back 523

the left half of both eyes

Front 524

An increase in the firing frequency of the afferent neurons innervating the left hoizontal semicircular canals could be due to

Back 524

a left-ward rotation of the head
the cessation of a right ward head rotation
irrigating the left outer ear canal with warm water during a caloric test

Front 525

The illusion of spinning, known as vertigo can be caused by

Back 525

meniere's syndrome
middle ear infection
excessive intake of alcohol

Front 526

the eyeball develops embryologically from which tissues

Back 526

neural tube
head mesoderm
surface ectoderm of the head

Front 527

What part of the eye develops embryologically from the neural tube

Back 527

neural retina

Front 528

What part of the eye develops embryologically from the head mesoderm

Back 528

outer two layers

Front 529

What part of the eye develops embryologically from the surface ectoderm of the head

Back 529

lens

Front 530

What is production/circulation/drainage sequence of the aqueous humor

Back 530

ciliary processes --> posterior chamber --> pupil --> anterior chamber --> cama; pf Schlemm --> episcleral veins

Front 531

Collagen fibers run in precisely parallel layers, at 90 degrees to identical fibers in adjacent layers, in which part of the eye

Back 531

cornea

Front 532

In histological sections of the ear, one may encounter in the middle ear cavity what?

Back 532

facial nerve
stapedius muscle/tendon
stapes
geniculate ganglion

Front 533

Which two structures meet at te limbus of the eye

Back 533

pupillary constrictor and pupillary dilator

Front 534

where do the scala vestibuli and scala tympani communicate with each outher

Back 534

helicotrema

Front 535

What are in direct contact with the cupula of the cristae ampullares

Back 535

endolymph
stereocilia of hair cells

Front 536

labyrinthine channerls typically are interconnected, which spaces and caivities are in communication with each other

Back 536

utricle
cochlear duct
semicircular duct
endolymphatic duct

Front 537

what is the sequence for light that enters the eye and passes through the retina to reach the outer segments of rods and cones

Back 537

lens --> nerve fiber layer --> ganglion cell layer --> bipolar layer --> outer plexiform layer --> outer nuclear layer

Front 538

Consolidation occurs in the

Back 538

hippocampus

Front 539

the conscious sense of smell is encoded in the

Back 539

orbitofrontal cortex

Front 540

horner's syndrome is characterized by

Back 540

constricted pupil

PAM

Front 541

What deficit is common to all types of aphasia

Back 541

repetition

Front 542

repetition is predominantly impaired in which type of aphasia

Back 542

conduction

Front 543

the phototypical subcortical dementia with retrieval based memory problems is

Back 543

Parkinson's disease

Front 544

confabulation is commonly observed in

Back 544

Wernicke's Korsakoff

Front 545

a limitation of fMRI is

Back 545

motion artifact

Front 546

the typical area of activation in functional imaging studies of working memory is

Back 546

dorsolateral prefrontal cortex
anterior cingulate gyrus
posterior, inferior parietal

Front 547

a pt who scores above avg. on a test of immediate recall, below avg. on delayed recall, and perfect on recognition testing is demonstrating what type of memory problems

Back 547

retrieval

Front 548

consolidation based memory problems are commonly observed in

Back 548

Herpes encephalitis

Front 549

a pt with decreased encoding of visual material is likely to have

Back 549

right thalamic lesion

Front 550

repetition is notably preserved in which type of aphasia

Back 550

transcortical

Front 551

a pt with decreased encoding of visual material is likely to have

Back 551

right thalamic lesion

Front 552

repetition is notably preserved in which type of aphasia

Back 552

transcortical

Front 553

a pt with nonfluent speech, intact comprehension, impaired repetition, impaired naming and a left hemiplegia has which type of aphasia

Back 553

conduction

Front 554

the hemisphere encoding and retrieval asymmetry model (HERA) suggests that encoding is taken care of by the

Back 554

left frontal lobe

Front 555

dreaming is accompanied by activity in

Back 555

cholinergic bs nuclei

Front 556

cortical area 4 is

Back 556

agranular cortex

Front 557

reproductive behaviors

Back 557

preoptic area

Front 558

polyuria

Back 558

supraoptic nucleus

Front 559

heating area

Back 559

posterior hypothalamic nuclei

Front 560

humans are most sensitive to frequencies in the range of

Back 560

1-4 kHz

Front 561

which hair cells have contractile ability

Back 561

OHC

Front 562

which hair cells are innervated by auditory nerve fibers

Back 562

IHC

Front 563

which hair cells have stereocilia embedded in the tectorial memb

Back 563

OCH

Front 564

which hair cells are located over the osseous spiral lamina

Back 564

IHC

Front 565

which hair cells are located nearest the modiolus

Back 565

IHC

Front 566

which hair cells have sterocilia connected by tip links

Back 566

OHC and IHC

Front 567

which hair cells are though to generate otoacoustic emissions

Back 567

OHC

Front 568

which hair cells are easily damaged by aminoglycoside antibiotics

Back 568

OHC

Front 569

which hair cells dont regnerate following damage by loud sounds

Back 569

OHC and IHC

Front 570

which hair cells have supporting cells also called Dieter's cells

Back 570

OHC

Front 571

Wave IV of the brainstem auditory evoked response is associated with

Back 571

the inferior colliculus

Front 572

Which wave time interval in the brainstem auditory evoked response is a useful diagnostic tool

Back 572

b/w wave I and V

Front 573

what is the function of the pinna

Back 573

acts as an amplifier by funneling sound in the ear canal

Front 574

what is direction-dependent filtering of sound by the pinna useful for

Back 574

localizing sounds

Front 575

is the tympanic memb larger than the oval window

Back 575

yes

Front 576

how are tranductions channels in the ear opened

Back 576

by stretching the sterocilia memb

Front 577

what would you find in a pt whose MRI revealed a large acoustic neuroma on the left side

Back 577

otoacoustic emissions are normal in both ears

Front 578

cats mounting cats mounting cats mounting cats maby be seen in experimental animals with bilateral surgical removal of

Back 578

amygdala

Front 579

a pt whose diseased is charactreized by a series of episodic neurological deficits disseminated in time and space is likely to have

Back 579

MS

Front 580

among patient groups, seizure disorders occur relatively frequently in

Back 580

aging patients (> 60)

infants and young children

Front 581

a hypothetical young pt suffers from a severe motor disorder (dystonia) that appeared and was diagnosed shortly after birth; its a non-progressive, at least up to the present age of 11

Back 581

cerebral palsy

Front 582

what are brain mapping invasive techniques

Back 582

electrical stimulation
depth electrode recording
post mortem examination of tissue
WADA testing

Front 583

when testing for the babinski sign in a very spastic pt (e.g. severe cerebral palsy), the response often includes

Back 583

dorsiflexion of toes (upgoing toes)
fanning of toes
withdrawal of leg from stimulus

Front 584

relatively common cause of dizziness in pts include

Back 584

menieres
benign paroxysmal positional vertigo
acoustic neuroma

Front 585

the interstitial nucleus of cajal and the interstitial nucleus of the MLF, both found in the midbrain help regulate/control

Back 585

vertical eye movement

Front 586

cells near (or mixed with) cells of the abducens nucleus project to and supply CL MR motor neurons, thus a lesion in the facial colliculus actually causes

Back 586

IL facial paralysis
IL paralysis of abduction of eye
CL failure of adduction during conjugate eye movement of eyes

Front 587

complex partial seizures most often arise in the

Back 587

temporal lobe

Front 588

pts with MS often have extra problems with weakness and other symptoms during

Back 588

hot weather

Front 589

pts with memory deficits due to thalamic damage often have damage due to

Back 589

posterior cerebral artery and braches

Front 590

a pt was "soap opera" amnesia, who loses many facts about their personal life, is likely to suffer from

Back 590

psychosos

Front 591

when you swim underwater the refractive power of the eye is drastically reduced because

Back 591

the index of refraction of water is very close to that of the cornea

Front 592

the crystalline lens supplies only about 1/3 of the refractive power of the eye, its real importance lies in the fact that

Back 592

it can change its radius and curvature and thus vary its focal length

Front 593

as we grow older our ability to accommodate to near vision declines; this is due to

Back 593

a decrease in the elasticity of the crystalline lens and is called presbyopia

Front 594

the terminal endings of the retinal rods make synaptic connections with

Back 594

horizontal cells and bipolar cells in the outer plexiform layer of the retina

Front 595

the circular receptive field of the horizontal cell is due to

Back 595

the converging inputs of the receptor cells in that region of the retina

Front 596

complex cortical cells of areas 17 and 18 receive direct input from

Back 596

the simple cortical cells in area 17

Front 597

the "arrest" reaction occurs when animals are presented with

Back 597

novel environmental stimuli

Front 598

peduncularpontine nucleus neurotransmitter is

Back 598

ACh

Front 599

raphe nucleus neurotransmitter is

Back 599

serotonin

Front 600

reticular thalamic nucleus neurotransmitter is

Back 600

GABA

Front 601

tuberomammillary nucleus neurotransmitter is

Back 601

histamine

Front 602

corticospinal neurons are in which cortical layer

Back 602

L5

Front 603

spiny stellate neurons are in which cortical layer

Back 603

L4

Front 604

corticothalamic neurons are in which cortical layer

Back 604

L6

Front 605

alpha EEG rhythms have a clinical frequency of

Back 605

8 - 13 Hz

Front 606

beta EEG rhythms have a clinical frequency of

Back 606

13 - 30 Hz

Front 607

gamma EEG rhythms have a clinical frequency of

Back 607

4 - 8 Hz

Front 608

delta EEG rhythms have a clinical frequency of

Back 608

1 Hz

Front 609

theta EEG rhythms have a clinical frequency of

Back 609

9 Hz

Front 610

objects in the temporal crescent of the left visual hemifield project an image onto the

Back 610

nasal hemirentina of the left eye

Front 611

the physiological blind spot is

Back 611

where the axons of the retinal ganglion cells leave the eye
in the temporal hemiretina of each eye

Front 612

the magnocellular pathway conveys information about

Back 612

movement in the visual field

Front 613

a lesion in myer's loop on the left side will cause a loss of vision in which parts of the VF's

Back 613

upper right quadrant of both eyes

Front 614

what advantage is associated with PET rather than an fMRI study

Back 614

chemical specificity

Front 615

fMRI works by

Back 615

detecting an increase in flow of oxygen to an activated brain region
detecting regional transient differences in the brain's information processing

Front 616

fMRI results are determined by

Back 616

radiactive time constant

Front 617

if a pt with intractable epilepsy underwent section of the corpus callosum, what perceptual deficit might you expect to see

Back 617

difficulty naming an object presented in the left-sided peripheral vision

Front 618

temporal resolution of fMRI allows measurements of brain activity changes in the order of

Back 618

days
hours
minutes
seconds

Front 619

vestibular system signals indicating head position and movement arise from specialized "patches" or clusters of neuroepithelial (hair) cells in the membranous labyrinth, how many of these patches are present in a normal human head

Back 619

10

Front 620

the endolymphatic duct is a connected extension of the membranous labyrinth which ends close to the cranial cavity, to what end might one surgically open and thus connect this duct with the subarachnoid space

Back 620

to relieve pressure within the cochlear duct

Front 621

after destruction of the left superior cervical ganglion

Back 621

the left pupil is constricted

Front 622

the outer layer of the optic cup develops from

Back 622

pigment layer of the retina

Front 623

the majority of pts with unilateral hearing loss have problems localized to the

Back 623

middle or inner ear

Front 624

seizure activity

Back 624

is prone to originate in the temporal lobe
is often preceded by unpleasent olfactory hallucinations

Front 625

aqueous humor is secreted into the posterior chamber of the eye by secretory cells that cover the

Back 625

ciliary processes

Front 626

dementia can be

Back 626

static
reversible
progressive

Front 627

intact reptition is associated with which type of aphasia

Back 627

transcortical

Front 628

deficits encoding new info are most likely associated with a stroke in the

Back 628

thalamus

Front 629

broca's aphasia produces

Back 629

nonfluent speech
impaired repetition
impaired naming

Front 630

a cardiac arrest with a clinically significant period of anoxia will produce which type of memory problems

Back 630

consolidation

Front 631

in the anoxia of cardiac arrest lasts long enough to affect memory and produce hippocampal sclerosis, an additional possible outcome is

Back 631

temporal lobe seizures

Front 632

herpes encephalitis primarily affects the

Back 632

temporal lobes

Front 633

pick's disease begins with

Back 633

personality change

Front 634

drugs to treat alzheimer's disease work on which neurotransmitter system

Back 634

ACh

Front 635

damage to the midbrain (esp. tectum) is most likely to cause

Back 635

problems with vertical eye movements

Front 636

hair cells of the inner ear use similar (but not identical) structural mechanisms to alter membrane potential and thus, nt release, which receptor site's hair cells lack true cilia (kinocilia)

Back 636

organ of corti

Front 637

the spiral ganglion comprises bipolar neurons housed within the

Back 637

modiolus

Front 638

finds rewarding drugs

Back 638

nucleus accumbens

Front 639

knows where our car keys are

Back 639

hippocampus

Front 640

severance leasds to emotional "flatness", docility

Back 640

anterior limb of internal capsule

Front 641

needs thiamine to fcn properly

Back 641

amygdala

Front 642

scared of things

Back 642

amygdala

Front 643

relays "gut reactions" to hypothalamus

Back 643

nucleus tract solitarius

Front 644

dry, hot face

Back 644

superior cervical ganglion lesions

Front 645

sexual behaviors

Back 645

preoptic nucleus

Front 646

orgasm

Back 646

oxytocin

Front 647

regulation of the anterior pituitary gland

Back 647

arcuate nucleus

Front 648

regulation pineal cland

Back 648

retinal ganglion cells

Front 649

regulation of the posterior pituitary gland

Back 649

paraventricular nucleus

Front 650

the size of the retinal image of an object in the visual field is inversely related to the

Back 650

distance of the object

Front 651

what does the absolute threshold of vision approach

Back 651

the theoretical limit of one photon

Front 652

what is the only direct effect that light has on the visual pigments is

Back 652

to isomerize the chromophore, retinal, from its 11-cis forms to its all-trans form

Front 653

the receptive fields of bipolar cells are concentric circular areas of the retina where illumination of the central region produces either a hyperpolarization or a depolarization and illumination of the surrounding are is antagonistic to

Back 653

central stimulation

Front 654

a simple cortical cell in area 17 is sensitive to lines and edges with a specific orientation located in

Back 654

the center of its receptive field

Front 655

in general, the visual cortical cells are most sensitive to

Back 655

appropriately oriented lines and edges which are moving

Front 656

the main fcn of the tympanic memb and the ossicles of the inner ear is to

Back 656

increase the efficiency of transmission of sound from the air-filled outer ear to the fluid-filled cochlea

Front 657

high frequency sounds cause the basal end of the basilar memb to vibrate to a greater extent at which end

Back 657

apical end

Front 658

the intensity of a sound is coded by

Back 658

the number of afferent firing APs and by the rate at which each fiber is firing

Front 659

high frequency neurons in the superior olive excited by one ear and inhibited by the other are sensitive to

Back 659

interaural intensity differences

Front 660

the medial geniculate nucleus is reciprocally connects with cortical area

Back 660

41

Front 661

callosal projection neurons are likely to be younger than

Back 661

corticospinal neurons

Front 662

layer 5 is larger than layer

Back 662

4

Front 663

broadmann's cortical areas are defined based on

Back 663

cell size and density in different layers

Front 664

pre-ictal aura may preced

Back 664

simple partial seizures
complex partial seizures
secondary generalized seizures

Front 665

inhibitory neurons of the cerebral cortex

Back 665

layer 3 non-spiny basket cell
a axo-axonic chandelier cell

Front 666

reflex nystagmus can be induced by which procedures

Back 666

watching alternating black and white bars rotate in front of our eyes
sitting on a rotating chair with our eyes open
irrigating the outer ear canal with warm water during a caloric test

Front 667

vestibular neurons provide sensory info for postural control and balance with descending projections to the spinal cord via

Back 667

lateral vestibulospinal tract
medial longitudinal fasciculus

Front 668

an enlarging pineal tumor that compresses the tectum of the midbrain has neurological problems that are likely to include

Back 668

difficulty looking up
hydrocephalus

Front 669

ptosis of the eyelid could follow some form of damage to which structures

Back 669

ophthalmic a.
medullary reticular formation
cervical symp trunk
levator palpebrae superioris muscle

Front 670

degeneration of the nucleus basalis (of Meynert) has been implicated in the etiology of

Back 670

Alzheimer's disease

Front 671

in the absecence of natural photic stimuli humans have a diurnal cycle of about

Back 671

25 hours

Front 672

establishing conditioned fear using a tone-footshock depends on an intact

Back 672

amygdala
auditory pathways to the amygdala somatosensory system

Front 673

the area of the primary visual cortex devoted to the fovea is

Back 673

retinotopically organized
about 1/2 of the total area of the primary visual cortex
located at the posterior aspects of the primary visual cortex

Front 674

conjugate eye movements are essential for normal visual function. What are "control center" for generation of conjugate movement of the 2 eyes

Back 674

PPRF

Front 675

the horizontal cells respond with slow hyperpolarization when

Back 675

any region of its circular receptive field is illuminated with white light

Front 676

the amacrine cells and the retinal ganglion cells are the only cells in that retina that produce

Back 676

action potentials

Front 677

head and neck injuries are a serious complication of some types of

Back 677

generalized seizures

Front 678

stimulation of the cingulate gyrus influences

Back 678

respiration

Front 679

wakefullnes and REM sleep have which types of waves

Back 679

beta waves (14 - 80 Hz)

Front 680

main target of thalamocortical terminals

Back 680

cortical layer 4

Front 681

main source of corticospinal tract fibers

Back 681

cortical layers 5/6

Front 682

contralateral hemineglect is in which lobe

Back 682

parietal

Front 683

prosopagnoisa (deficit in face recognition) is in which lobe

Back 683

temporal

Front 684

innappropriate social behavior is lesion in which lobe

Back 684

frontal

Front 685

pt cant respond verbally to verbal instructions but can demonstrate comprehension of verbeal instructions

Back 685

Broca's aphasia

Front 686

Purkinje cells has what type of action on the CNS

Back 686

inhibitory

Front 687

non-spiny cortical neuron has what type of action on the CNS

Back 687

inhibitory

Front 688

GABA has what type of action on the CNS

Back 688

inhibitory

Front 689

a spiny stellate cell in layer 4 of the primary somatosensory cortex has what type of action on the CNS

Back 689

excitatory

Front 690

a thalamocortical relay neuron has what type of action on the CNS

Back 690

excitatory