Ifc Week 3

Front 1

har cell receptors are:

Back 1

extremely sensitive *mechanoreceptors*

Front 2

hair cells are found in the:

(3)

Back 2

1. ampulla of the semicircular canals

2. macula of the otolith organs

3. cochlear duct

Front 3

endolymph is high in:

Back 3

K+

Front 4

endolymph surrounds:

(2)

Back 4

the vestibular and cochlear apparatuses

Front 5

perilymph:

(2)

Back 5

1. CSF-like

2. high in Na+

Front 6

hair bundles:

(4)

Back 6

1. 20-200 stereocilia

2. + one kinocilium

3. are the *tops* of hair receptor cells

4. detect motion/sound by their movement

Front 7

stereocilia are actually:

Back 7

microvilli (actin-based)

Front 8

the kinocilium is made from:

Back 8

MT's

Front 9

(afferent =

Back 9

away from the receptor, toward CNS)

Front 10

tip links =

Back 10

tiny fibers that connect the top of one stereocilium to the *side* of another

Front 11

tip links run from:

Back 11

short to tall

Front 12

hair cells participate in:

Back 12

mechano-electric transduction

(movement => electrical signal)

Front 13

**when stereocilia are at rest, a small amount of:**

Back 13

NT is released

=> basal rate of firing of CN 8

Front 14

movement of the hair bundle toward the TALL end =>

Back 14

opening of ion channels => depol of hair cells => inc. in NT's released to CN 8 fibers => increased rate of firing of CN 8

Front 15

movement of hair bundles toward their SHORT end =>

Back 15

closing of ion channels => hyperpolarization of hair cells => LESS NT released => decreased activity of CN 8

Front 16

movement of hair cells toward the sides =>

Back 16

no response

Front 17

the channels found on stereocilia are:

Back 17

**stretch-activated** channels

Front 18

15% of a hair bundle's channels are open at:

Back 18

rest

Front 19

**with movement of hair bundle toward the tall end, tip links are pulled:**

Back 19

TAUT => more channels open => depol of hair cells

Front 20

**with movement of hair bundle toward the SHORT end, tip links are:**

Back 20

SLACK => decrease in channels open => hyperpolarization of hair cells

Front 21

hair cells are SUPER _____________ to _____________

Back 21

sensitive;

movement

Front 22

hair cell channels are located within the stereocilia, are large, and allow ANY cation to pass through; with that said, the reason hair cells depolarize is b/c these channels allow the passage of _______, specifically

Back 22

K+

Front 23

hair bundles ALWAYS project into:

Back 23

endolymph

Front 24

K+ flows into hair cells despite a difference in amount of K+ on either side because:

Back 24

of the massive *electrical* gradient:

+80 outside hair cell, -60 inside, 0 on the other side, near nerve

Front 25

what do the 3 semicircular ducts detect?

Back 25

**rotation/angular acceleration**

Front 26

in the semicircular canals, hair cells are found in each ampulla; they stick up from:

Back 26

the crista, into the cupulla

Front 27

cupulla =

Back 27

gelatinous mass

Front 28

rotation => displacement of cupula =>

Back 28

movement of hair bundles => depol of hair cells

Front 29

what runs from each crista?

Back 29

CN 8 fibers

Front 30

semicircular ducts work in:

Back 30

PAIRS

Front 31

rotation in one direction:

(2)

Back 31

depolarizes hair cells on one side while inhibiting hair cells on the other

Front 32

in general, the otolith organs detect:

Back 32

**linear** acceleration

Front 33

linear acceleration =

(2)

Back 33

1. tilting head back and forth

2. accelerating forward or backward in a straight line

Front 34

specifically, the saccule detects:

Back 34

**vertical** motion

Front 35

the utricle specifically detects:

Back 35

horizontal motion

Front 36

VOR makes eyes:

Back 36

*counter*the direction of head movement, in order to keep eyes on a fixed point

- uses CN 6/MLF pathway

Front 37

oscillopsia =

Back 37

absence of VOR

Front 38

result of oscillopsia:

Back 38

movement of head causes a continual shift in the center of gaze

Front 39

pathway for conscious perception of vestibular info: ducts/otolith organs =>

Back 39

vestibular ganglia => vestibular nuclei => thalamus => cortex

Front 40

what commonly causes vertigo and nystagmus?

Back 40

damage to vestibular pathway

( => different levels of activity between left and right side, resulting in vertigo and nystagmus )

Front 41

vertigo =

Back 41

sensation of spinning or whirling

Front 42

nystagmus =

Back 42

rhythmic oscillations of the eyeball

Front 43

Meneire's disease symptoms:

(4)

Back 43

1. "fullness" in the ear

2. tinnitus

3. acute attacks of vertigo/nystagmus

4. hearing loss

Front 44

causes of hair cell loss:

(5)

Back 44

1. genetics (many forms)

2. infections

3. acoustic trauma

4. presbyacusis

5. ototoxic drugs

Front 45

"ototoxic" = toxic to the organs of:

(3)

Back 45

1. hearing,

2. balance,

or

3. CN 8

Front 46

examples of ototoxic drugs:

Back 46

1. aspirin

2. quinone

3. cis-platinum

4. -mycin AB's

Front 47

temporary threshold shift =

Back 47

temporary decrease in hearing sensitivity, due to broken tip links

- which can recover in hours

Front 48

hair cells can be *killed* with:

Back 48

severe noise

- **once dead, gone forever**

Front 49

dB scale: every increase in 10 dB ~~

Back 49

10-fold increase in sound intensity

Front 50

prolonged exposure of sound over _____ dB damages hearing

Back 50

90 dB

Front 51

pure tone =

Back 51

single frequency

- low tone = low frequency

Front 52

frequency =

Back 52

waves per second

Hz = cycles per second

Front 53

human frequency range =

Back 53

20 - 20,000 Hz

Front 54

most sounds are NOT pure, but:

Back 54

complex

Front 55

***consonants are heard at _________ frequencies***

Back 55

HIGH

Front 56

presbyacusis =

Back 56

progressive loss of hearing due to old age

Front 57

what frequency are vowels heard at?

Back 57

LOW

Front 58

presbyacusis: hearing is first lost at:

Back 58

HIGH frequencies

=> hard to distinguish consonants

Front 59

external ear =

Back 59

funnel

Front 60

role of the pinna:

Back 60

localizes sound in the vertical axis

Front 61

middle ear transfers sound energy from:

Back 61

air to fluid

Front 62

the middle ear also protects against loud sounds, via:

(2)

Back 62

1. tensor tympani muscle

2. stapedius muscle

Front 63

how do the tensor tympani and stapedius protect the ear?

Back 63

at about 80 dB, they tense the malleous and the stapes, repectively

Front 64

loss of TT and stapedius =>

Back 64

hyperacusis

Front 65

hyperacusis =

Back 65

abnormal sensitivity to sound

Front 66

***conductive deafness ~~ damage to:***


(2)

Back 66

outer OR middle ear

Front 67

examples of conditions causing conductive deafness:

(4)

Back 67

1. wax

2. perforated ear drum

3. infections

4. cysts of the middle ear

Front 68

results of conductive deafness:

(2)

Back 68

1. hearing loss at ALL frequencies

2. but hearing by *bone conduction is preserved*

Front 69

***sensorineural deafness ~~ damage to***

(2)

Back 69

1. hair cells

or

2. associated neurons

Front 70

results of sensorineural deafness:

(2)

Back 70

1. loss of HIGH frequency hearing

2. bone conduction is NOT preserved

Front 71

scala medi =

Back 71

cochlear duct

Front 72

organ of Corti =

(3)

Back 72

inner and outer hair cells, the tectorial membrane into which they project, and the spiral ganglion fibers to which they communicate

Front 73

the organ of Corti rests on:

Back 73

the BM

Front 74

how many rows of IHC's and OHC's does the organ of Corti contain?

Back 74

ONE row of IHC's,

THREE rows of OHC's

Front 75

the BM ~~ *tonotopy*; a particular piece of the BM will:

Back 75

move in response to a particular frequency

Front 76

the BM is NARROW at:

Back 76

the base

Front 77

the BM is WIDE at:

Back 77

its apex

Front 78

***how many cochlear nerve afferents does EACH IHC contact?***

Back 78

10 cochlear afferents


meanwhile, **10 OHC's contact only ONE cochlear nerve afferent**

Front 79

IHC's take ____% of all cochlear nerve afferents

Back 79

90%

Front 80

apart from talking to afferents, ***OHC's also RECEIVE strong efferent innervation; they convert voltage changes into:***

Back 80

physical movement

- called reverse/electro-mechanical transduction

Front 81

electro-mechanical transduction of the OHC's =>

Back 81

otoacoustic emissions

Front 82

otoacoustic emissions =

Back 82

the production of sound BY the ear

Front 83

significance of otoacoustic emissions:

Back 83

since deafness ~ an inability to evoke otoacoustic emissions, testing for them = **quick screen for deafness in infants**

Front 84

***loss of OHC motility =>

(3)

Back 84

1. 30-40 dB decrease in hearing sensitivity

2. decreased **frequency discrimination**

3. loss of otoacoustic emissions

Front 85

another thing that otoacoustic emissions do:

Back 85

boost sensitivity

Front 86

otoacoustic emissions are NOT:

Back 86

tinnitus

Front 87

tinnitus can result from certain drugs =>

Back 87

switch drugs out immediately

Front 88

tinnitus sometimes presents in patients whose:

Back 88

cochlear nerves are severed

Front 89

***place coding:***

Back 89

each cochlear nerve fiber connects to a specific part of the BM

Front 90

***significance of place coding:***

Back 90

every cochlear afferent is sensitive to a particular frequency

- called the "best frequency"

Front 91

increase in sound ampitude recruits:

Back 91

more fibers

Front 92

**frequency coding:**

Back 92

a nerve receiving 100 Hz will FIRE at 100 Hz in response

Front 93

**frequency coding fails at:**

Back 93

HIGH frequencies

- too fast for the afferent to fire

Front 94

***ALL cochlear afferents participate in ____________________, while fibers responsible for LOW frequency (~20) also use _____________________***

Back 94

place coding;

frequency coding

Front 95

**in sensorineural deafness due to hair cell loss, neurons in the cochlear ganglion are spared; this allows for: ____________________**

Back 95

**cochlear implants**

Front 96

cochlear implants stimulate cochlear afferents __________, to make up for lack of hair cells

Back 96

DIRECTLY

Front 97

2 different mechanisms for localizing sound in the **horizontal plane**:

(2)

Back 97

1. loudness difference (~LSO)

2. time delay (~MSO)

Front 98

***UNILATERAL deafness implicates:***

(3)

Back 98

1. cochlea

2. 8th nerve

3. cochlear nuclei

- any higher up, and BOTH sides would be affected

Front 99

auditory pathway: sound from one ear =>

Back 99

cochlea => cochlear ganglion => SO's on BOTH sides => LL's on BOTH sides => inferior colliculi => MGN's => primary auditory cortex on both sides

Front 100

**the primary auditory cortex is organized tonotopically: specific parts of the cortex correspond to:**

Back 100

specific parts of the BM

Front 101

simple motor path: UMN =>

Back 101

LMN => skeletal muscle

Front 102

UMN's

(2)

Back 102

1. mediate *voluntary* control of movement

2. **located in cortex AND BS**

Front 103

LMN's

(3)

Back 103

1. directly innervate skeletal muscle

2. **located in the ventral horn and CN motor nuclei** in BS

3. mediate BOTH voluntary and involuntary movement

Front 104

"involuntary movement" =

Back 104

**reflexes**

Front 105

additionally, other regions like __________________________________ modulate movements

Back 105

the BG and the cerebellum

- both communicate with the cortex

Front 106

pyramidal system =

(2)

Back 106

1. UMN's in the motor and premotor cortex

2. + the axons that link them to the LMN's

Front 107

extrapyramidal system =

Back 107

the BG

Front 108

of the 5 major descending motor pathways, 3 arise from neurons in the cortex:

Back 108

1. LCST

2. VCST

3. cortibulbar tract

Front 109

"bulbar" ~~

Back 109

the medulla

Front 110

ALL 5 major motor pathways are composed of:

Back 110

only ONE neuron

Front 111

***motor pathways innervating LMN's that control DISTAL musculature will:***

Back 111

DECUSSATE before synapsing on the LMN's

Front 112

***motor pathways innervating LMN's that control AXIAL musculature are:***

Back 112

BILATERAL

Front 113

corona radiata =

Back 113

axons of cortical neurons, on their way to the internal capsule

Front 114

***LCST***

(4)

Back 114

1. responsible for MOTOR to CONTRALATERAL, DISTAL musculature

2. **decussates at the CAUDAL medulla**

3. travels in the DL funiculus of the SC

4. synapses in the ventral horn

Front 115

***VCST***

(4)

Back 115

1. motor to TRUNK, BILATERALLY

2. TWO axons go down, one decussates at the CAUDAL medulla

3. travel through the AM funiculus in the SC

4. synapse in the ventral horn

Front 116

where does the internal capsule become the cerebral peduncles?

Back 116

at the midbrain

- continue as the pyramids in the medulla

Front 117

***Corticobulbar tract***

(4)

Back 117

1. originates in facial region of each precentral gyrus

2. motor to CN motor nuclei controlling **all muscles in the face**

3. ***bilateral input*** to CN motor nuclei from each precentral cortex
(except for CN 7 and CN 12 - unilateral)

4. decussates THROUGHOUT BS

Front 118

**vestibulospinal tract:**

(4)

Back 118

1. ~~ balance

2. motor FROM vestibular nuclei straight down through BS

3. ipsilateral only - does NOT decussate

4. travels through anterior tract in front of VH

Front 119

vestibular nuclei are found:

Back 119

in lower pons/upper medulla

Front 120

**hypothalamospinal tract:**

(3)

Back 120

1. goes from hypothalamus straight down through BS/SC, via DL funiculus

2. synapses onto IML in thoracolumbar region

3. ipsilateral only - does NOT decussate

Front 121

while traveling in the BS, the hypothalamospinal tract travels with:

Back 121

the ALS tract

Front 122

while traveling in the SC, the hypothalamospinal tract travels with:

Back 122

the LCST

Front 123

Brown-Sequard Syndrome =

Back 123

severance of axons in one-half of SC

Front 124

Brown-Sequard Syndrome: signs =

(4)

Back 124

1. loss of FT/V/P ipsilaterally

2. loss of P/T contralaterally

3. loss of voluntary movement to distal musculature ipsilaterally

4. presence of Horner's syndrome ipsilaterally

Front 125

reflexes are generally fine in Brown-Sequard, b/c:

Back 125

the LMN's outside of that SC region aren't affected

Front 126

***UMN Syndrome =

Back 126

LCST damage anywhere between cortex and LMN***

Front 127

initial signs of UMNSyn =

Back 127

flaccid paralysis

Front 128

later signs of UMN Syndrome:

(4)

Back 128

1. Babinski's sign

2. spasticity

3. loss of voluntary fine movement

4. contralateral weakness

Front 129

Babinski's sign: toes:

Back 129

go up

Front 130

spasticity includes:

(3)

Back 130

1. increased tone

2. hyper-reflexia

3. clonus

Front 131

clonus =

Back 131

a series of involuntary, rhythmic, muscular contractions and relaxations

Front 132

2 kinds of LMN's:

Back 132

1. alpha MN's

2. gamma MN's

Front 133

alpha MN's:

(3)

Back 133

1. reside in the ventral horn

2. form the neuron part of motor units

3. get 3 major inputs

Front 134

3 major inputs to alpha MN's:

Back 134

1. interneurons

2. sensory afferents from muscle spindles

3. UMN's from brain

Front 135

why are alpha MN's called the final common pathway?

Back 135

you CANNOT MOVE without activating them

Front 136

muscle spindles are:

(2)

Back 136

1. intrasfusal (modified) muscle fibers in parallel with extrafusal (regular) fibers

2. with group 1a sensory afferents arranged around them

Front 137

**what do gamma MN's innervate?**

Back 137

the intrasfusal fibers of muscle spindles

Front 138

reflex arc: muscle stretch =>

Back 138

spindles move => 1a sensory afferents carry info to inhibitory interneuron and alpha MN => alpha MN fires to contract a muscle, interneuron fires to relax the antagonist muscle

Front 139

**one significant role of gamma MN's is to:

Back 139

give spindles gain

- i.e. make them taut so as to increase their sensitivity

Front 140

why is spindle gain so important?

Back 140

when a muscle is contracted, muscle spindles are SLACK

=> **won't fire** when muscles are contracted

gamma MN's give them tightness so that they continue to fire despite the length of the muscle

Front 141

reduced inhibition of gamma MN's partially explains:

Back 141

hyper-reflexia that results from UMN damage

Front 142

muscle spindles also participate in a negative feedback loop, e.g.

Back 142

beer glass

- deviations from the desired length are inhibited

Front 143

reflex: stepping on a nail causes:

(2)

Back 143

the stepping knee to flex

and the other knee to extend, preserving balance

**can be elicited in coma patients**

Front 144

each muscle fiber within a motor unit has the same:

(2)

Back 144

physiological and metabolic characteristics

Front 145

motor units come in a range of:

Back 145

sizes

Front 146

***fasciculation = ***

Back 146

contraction of an entire motor unit due to discharge of SICK LMN

- visible through the skin

Front 147

most human tissue contains a mixture of:

Back 147

the 3 muscle fiber types

Front 148

**degeneration of one nerve causes the nerve next to it to:**

Back 148

sprout

=> healthy nerve takes over the degenerated one's muscle fibers

=>=> ***those fibers change from one type to the other***

Front 149

significance of fiber-type grouping:

Back 149

***muscle fiber type is partially under MN control***

and is plastic

Front 150

LMN syndrome: 7 signs

Back 150

1. weakness *including speech and swallowing*

2. hypo-reflexia

3. fasciculations

4. fibrillations

5. muscle atrophy

6. fiber-type grouping

7. dec. muscle tone

Front 151

***fibrillation = ***

Back 151

*spontaneous* activity of a denervated muscle FIBER

Front 152

muscle atrophy occurs due to lack of:

Back 152

electrical activity

Front 153

***amyotrophic lateral sclerosis = ***

(2)

Back 153

slow degeneration of LMN's in SC and BS,

and degeneration of UMN's

Front 154

ALS =>

(3)

Back 154

1. muscle wasting

2. fasciculations

3. hyper-reflexia

Front 155

why does hyper-reflexia occur in ALS?

Back 155

b/c of loss of controlling UMN's

Front 156

ALS results in:

Back 156

pregressive degeneration/death in 3-5 years

Front 157

**hallmark of ALS** =

Back 157

tiny angular muscle fibers

(atrophic)

Front 158

10% of ALS patients have:

Back 158

a family history

Front 159

one cause of ALS: mutations in the RNA binding protein SOD1, which is:

Back 159

TOXIC to MN's

Front 160

spinal muscular atrophy =

Back 160

degeneration of LMN's in SC and BS BEFORE birth

Front 161

SMA is caused by:

Back 161

deletions or duplications in survival MN gene proteins (SMN's) that are *critical to MN survival*

Front 162

UMN's =

Back 162

cortex or BS neurons that initiate muscle contraction

Front 163

***BS UMN pathwyas terminate in:***

Back 163

MEDIAL regions of the IM zone/VH

Front 164

***BS UMN pathways are responsible for:***

Back 164

controlling LMN's related to POSTURE

Front 165

***cortex UMN pathways terminate in:***

Back 165

the LATERAL regions of the VH

Front 166

**cortex UMN pathways also synapse in:**

Back 166

the BS reticular formation

=> motor cortex mediates posture via reticulospinal tract

Front 167

***cortex UMN's are responsible for:***

(2)

Back 167

1. PRECISE movements

2. posture

Front 168

***many voluntary movements require:***

Back 168

associated **postural** contractions

- to keep you steady

Front 169

i.e. when arm muscles contract, leg muscles contract automatically;

Back 169

both direct AND indirect CST pathways are involved

Front 170

Betz cells:

(3)

Back 170

1. largest cells of cortex

2. pyramidal (projection) neurons

3. but only account for a minority of axons in the CST

Front 171

***most CST neurons correspond to a ____________ movement, represented ______________________***

Back 171

**specific**

topographically

Front 172

the lateral region of the premotor cortex responds to:

Back 172

external cues

Front 173

the medial region of the premotor cortex responds to:

Back 173

internal cues

Front 174

neurons fire in anticipation of:

Back 174

movement

Front 175

neurons also fire when:

Back 175

*watching* a movement

~~ learning by imitation

Front 176

**decorticate posture:**

(2)

Back 176

1. elbows flexed

2. knees extended

Front 177

**decorticate posture is the result of:**

Back 177

damage ABOVE the midbrain

Front 178

**decerebrate posture:**

(2)

Back 178

1. neck, elbows, knees extended

2. hands and feet pointing in

Front 179

***decerebrate posture is the result of damage to:***

Back 179

descending tracts in the BS

Front 180

hereditary spastic paraplegia is caused by:

Back 180

gene mutations

Front 181

UMN's control BOTH:

Back 181

skilled movements AND postural adjustments

Front 182

general role of the cerebellum:

Back 182

error detection and correction

- it *refines* movements

Front 183

***spinocerebellum*** is responsible for:

Back 183

motor execution

Front 184

***the vermis, within the spinocerebellum, is specifically responsible for:***

Back 184

**gait and posture**

Front 185

***the cerebrocerebellum is responsible for:***

Back 185

motor **planning**

Front 186

the vestibulocerebellum is made up of:

(2)

Back 186

the nodulus and flocullus

Front 187

***the vestibulocerebellum is responsible for:***

(2)

Back 187

eye movements and balance

Front 188

cerebellar peduncles ~~

(2)

Back 188

incoming AND outgoing

Front 189

which cerebellar peduncle is the largest?

Back 189

the middle one

Front 190

***deep cerebellar nuclei are ALL:***

Back 190

output

Front 191

***each cerebellar hemisphere regulates movements of which side?***

Back 191

the ipsilateral side

Front 192

4 inputs to the cerebellum:

Back 192

1. frontal and parietal cortex via thalamus

2. superior colliculi

3. sensory from SC and **vestibular nuclei**

4. inferior olives

Front 193

**cerebrocerebellum =>

Back 193

dentate nucleus => premotor cortex (motor planning)

Front 194

**spinocerebellum =>

Back 194

interposed AND fastigual nuclei => motor cortex and BS
(motor execution)

Front 195

the spinocerebellum adjusts:

Back 195

limb movements

Front 196

**vestibulocerebellum =>

Back 196

vestibular nuclei => LMN's of SC and BS

(balance)

Front 197

inferior cerebellar peduncles ~~ output to:

(3)

Back 197

1. superior colliculi

2. reticular formation (posture)

3. vestibular nuclei (balance)

Front 198

cerebellum projects to PPRF, sup. colliculi, and vestibular nuclei; disruption of these pathways =>

Back 198

nystagmus

Front 199

ataxia =

Back 199

lack of control of movements

Front 200

intention tremor =

Back 200

uncoordinated movements of the extremities

Front 201

intention tremor ~~ damage to:

Back 201

**cerebrocerebellum**

Front 202

gait ataxia is the result of damage to:

Back 202

the vermis

Front 203

dysarthria =

Back 203

impaired ability to articulate words

Front 204

Purkinje cells:

(2)

Back 204

1. output cells of the cerebellum

2. ***shape output of deep nuclei*** (via inhibition)

Front 205

mossy fibers come from:

Back 205

pontine nuclei

Front 206

climbing fibers come from:

Back 206

the inferior olives

Front 207

both mossy and climbing fibers:

(2)

Back 207

1. are excitatory

2. shape the output of the Purkinje cells

Front 208

patients with cerebellar degeneration CANNOT:

Back 208

learn to correct movement errors

Front 209

blood flow increases 2-4 seconds prior to a movement in:

(3)

Back 209

1. motor cortex

2. premotor cortex

3. cerebrocerebellum

Front 210

***spino-cerebellar ataxias are the result of:***

Back 210

degeneration of tracts

Front 211

most spino-cerebellar ataxias ~~ :

(2)

Back 211

1. AD

2. trinucleotide repeats

Front 212

trinucleotide repeats are either:

Back 212

untranslated (DNA/RNA problem)

or translated (protein problem)

Front 213

what kind of trinucleotide repeat problem are most spino-cerebellar ataxias?

Back 213

the **translated** kind

Front 214

2 examples of acquired cerebellar disease:

Back 214

1. MS

2. alcohol intake

Front 215

MS results in damage to cerebellar:

Back 215

inflow/outflow

=> intention tremor, gait ataxia, nystagmus

Front 216

acute alcohol consumption =>

Back 216

problems with cerebellar signals getting through

Front 217

chronic alcohol consumption =>

Back 217

marked atrophy of the cerebellum

Front 218

which CN's correspond to pharyngeal arches 1, 2, 3, and 4-6?

Back 218

arch 1 = CN 5

arch 2 = CN 7

arch 3 = CN 9

arch 4 = CN 10

Front 219

which of the CN's have motor innervation?

Back 219

every one of them except for:

CN 1, 2, and 8

Front 220

***CN UMN decussate at:***

Back 220

the level of the LMN

Front 221

CN *MOTOR* nuclei get _________________ cortical input

Back 221

***BILATERAL***

Front 222

which CN's have parasympathetic motor functions?

(4)

Back 222

CN 3, 7, 9, and 10

Front 223

parasympathetic motor CN targets:

(3)

Back 223

1. SM

2. cardiac muscle

3. glands

Front 224

basic CN parasympathetic motor circuit: CN nucleus in BS =>

Back 224

parasympathetic ganglion in wall of organ

Front 225

damage to spinal accessory nucleus => weakness in:

(2)

Back 225

1. ipsilateral shrugging

2. *contralateral* turning of head (b/c SCM is responsible for contralateral rotation)

Front 226

***special condition of facial expression innervation: the forehead gets:***

Back 226

BILATERAL innervation from UMN's,

but lower region gets ONLY CONTRALATERAL innervation

Front 227

which CN do you need to CLOSE your eye?

Back 227

CN 7

Front 228

which CN do you need to OPEN your eye?

Back 228

CN 3

Front 229

3 nuclei of the midbrain:

Back 229

occulomotor,

EW,

trochlear nucleus

Front 230

3 nuclei of the pons:

Back 230

motor nucleus of 5,

abducens,

facial nucleus

Front 231

3 nuclei of the medulla:

Back 231

nucleus ambiguous,

dorsal motor of 10,

hypoglossal

Front 232

**from the trochlear nucleus, CN 4:

(2)

Back 232

1. decussates

2. exits dorsally

Front 233

hypoglossal problem - tongue points:

Back 233

**to the side of the lesion**

Front 234

which CN motor nuclei is the PCA responsible for?

(3)

Back 234

occulomotor, EW, and trochlear

Front 235

which CN motor nucleus is the AICA responsible for?

Back 235

the facial nucleus

Front 236

which CN motor nucleus are the pontine vessels responsible for?

Back 236

the abducens nucleus

Front 237

which CN motor nuclei is PICA responsible for?

(2)

Back 237

dorsal motor of 10

and

nucleus ambiguous

Front 238

which CN nucleus is the anterior spinal artery responsible for?

Back 238

the hypoglossal nucleus

Front 239

memory is characterized in 2 ways:

Back 239

1. Declarative

2. Nondeclarative

Front 240

declarative memory ~~

(4)

Back 240

1. things you can recollect

2. daily episodes

3. words' meanings

4. history

Front 241

nondeclarative memory ~~

Back 241

motor skills, associations, e/t else

Front 242

what kind of memory is consolidated into long-term memory?

Back 242

working memory

Front 243

***anterograde amnesia = ***

Back 243

INABILITY to FORM new memories

Front 244

**retrograde amnesia** =

Back 244

difficulty RETRIEVING memories

Front 245

the hippocampus is ESSENTIAL to form:

Back 245

**declarative** memories

Front 246

if the hippocampus is removed, the result is:

Back 246

severe **anterograde** amnesia

- couldn't remember anything from 1953 on

Front 247

what's responsible for memory?

Back 247

synaptic connections

Front 248

short-term, declarative memory is found in:

Back 248

the hippocampus and related structures

Front 249

long-term, declarative memory is stored in:

Back 249

a variety of cortical areas

Front 250

long-term, nondeclarative memory is stored in:

(4)

Back 250

1. cerebellum

2. BG

3. premotor cortex

4. other motor areas

(short-term nondeclarative storage is hard to pinpoint)

Front 251

loss of memory is proportional to:

Back 251

the extent of damage to the cortex

Front 252

the brain is ALWAYS changing; changes in synaptic connections =>

Back 252

changes in memory

Front 253

short-term plasticity =

Back 253

a change in synaptic efficacy lasting **less than 1 hour**

Front 254

long-term plasticity is:

(4)

Back 254

1. activity -dependent

2. rapidly induced

3. input-specific

4. enduring

Front 255

with LTP, the EPSP is made:

Back 255

stronger

Front 256

how can we change a synapse, presynaptically?

(3)

Back 256

1. increase NT/vesicles

2. improve vesicle fusion

3. dec. reuptake

Front 257

how can we change a synapse, post-synaptically?

(3)

Back 257

1. inc. postsynaptic receptors

2. improve receptor properties

3. improve membrane properties

Front 258

in general, we can also:

Back 258

create more synapses to increase memory

Front 259

in order for NMDA receptors to open:

(2)

Back 259

1. glutamate must bind

2. depolarization must be great enough to displace Mg2+

Front 260

NMDA R's allow passage of:

(3)

Back 260

Na+, K+, and ***Ca2+***

Front 261

LTP induction: NMDAR activation =>

Back 261

Ca2+ influx => activation of protein kinases => increase in number/function of AMPA receptors => LTP

Front 262

***LTD induction is exactly the same as LTP induction, except that:

Back 262

the number/function of AMPAR's is DECREASED

Front 263

***whether LTP or LTD occur depends on:***

Back 263

**how much Ca2+ enters**

Front 264

*large* influx of Ca2+ =>

Back 264

LTP

- small amount of Ca2+ => LTD

Front 265

Ca2+ is very tightly:

Back 265

regulated

Front 266

the brain atrophies with age -

Back 266

in general, no specific area

Front 267

brain diminishment with age is NOT:

Back 267

neuronal death, but atrophy

=> changes in strength and number of connections

Front 268

brain atrophy begins at:

Back 268

10 y.o

Front 269

Alzheimer's affects:

Back 269

ALL areas of the brain. but especially the hippocampus

Front 270

what's the ONLY kind of memory that actually increases with age (after 20 y.o.)?

Back 270

vocabulary memory

Front 271

limbic system circuit: hippocampus =>

Back 271

fornix => hypothalamus => mammillothalamic tract => anterior thalamic nuclei => cingulate gyrus => parahippocampal gyrus/entorhinal cortex => hippocampus

Front 272

hippocampus/parahippocampus ~~

Back 272

the antero-medial Temporal lobe

Front 273

loss of hippocampus/parahippocampus =>

Back 273

mostly anterograde amnesia,

sometimes retrograde

Front 274

amygdala ~~

(3)

Back 274

1. fear

2. aggression

3. emotions

Front 275

3 areas that correspond to mood states, mood disorders, and addiction:

Back 275

1. ventral tegmental area

2. mesocorticolimbic pathway

3. nucleus accumbens/ventral striatum

Front 276

mood states, mood disorders, and addictions often depend on:

(2)

Back 276

1. DOPA

2. SER

Front 277

SER comes from:

Back 277

raphe nuclei of BS

Front 278

NOREPI comes from:

Back 278

locus coeruleus of pons

Front 279

ACH comes from:

Back 279

the PAG

Front 280

Karsokoff's syndrome =

Back 280

loss of mammilary bodies due to alcoholism

=> loss of memory

Front 281

BG =

Back 281

feedback loop that activates planned movements and suppresses unwanted movements

Front 282

**the cortex will NOT generate a movement without:**

Back 282

input from the VA/VL thalamus

Front 283

striatum =

Back 283

caudate + putamen = input region of BG

Front 284

what's the output region of the BG?

Back 284

GPi

Front 285

2 inputs to BG:

Back 285

1. cortical to striatum via glutamate

2. SNpc to striatum via DOPA

Front 286

***GPi's relationship to the Va/VL thalamus:***

Back 286

GPi tonically inhibits it

Front 287

the caudate ~~

Back 287

eye movements

Front 288

the putamen ~~

Back 288

limb movements

Front 289

the direct pathway of the BG allows:

Back 289

movements

- uses D1 receptors

Front 290

the indirect pathway inhibits:

Back 290

movement

Front 291

****DOPA is ALWAYS:****

Back 291

**pro-movement**

- D1 receptors encourage the direct pathway,

- D2 receptors silences the indirect pathway

Front 292

the BG selects intended movement via:

Back 292

the direct pathway, and suppresses unwanted movement via the indirect

Front 293

the BG has projections to many different parts of the CNS; for example, one loop ~~

Back 293

planning and attn.

another regulates transition from one mood to another

Front 294

medium spiny neurons of the striatum:

(4)

Back 294

1. >75% of all striatum cells

2. GABAnergic

3. cortical neurons form excitatory synapses onto them

4. dopaminergic afferents modulate the excitatory cortical input

Front 295

decrease in DOPA =>

Back 295

less direct, more indirect pathway

Front 296

chorea =

Back 296

rapid, unwanted torsion movements

Front 297

Huntington's chorea:

(4)

Back 297

1. degeneration of the ***medium spiny nerves of the striatum***

2. trinucleotide repeat disease

3. AD

4. onset in 30's

Front 298

hemiballismus =

Back 298

**ipsilateral** flailing of the extremities

Front 299

hemiballisumus is due to:

Back 299

lesion of subthalamic nucleus

=> removes cortical inhibition of VA/VL

Front 300

Parkinson's:

(3)

Back 300

1. bradykinesia

2. mutations, MPTP toxins are associated

3. L-dopa is the treatment

Front 301

Parkinson's is due to:

Back 301

progressive loss of **dopaminergic** neurons in the substantia nigra

Front 302

another treatment for Parkinson's = DBS; electrodes are placed in:

Back 302

ironically, the GPi or subthalamic nucleus

Front 303

essential/familial tremor:

(2)

Back 303

1. AD

2. worse when limbs are held

Front 304

tardive dyskinesia =

Back 304

oral-lingual chorea

(delayed onset)

Front 305

tardive dyskinesia is a side-effect of:

Back 305

anti-psychotic medications

Front 306

tourettes (tics) ~~

Back 306

excessive activity of BG loops

Front 307

dystonia =

Back 307

unwanted contraction of muscles