Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuro > Unit III week 1 > Flashcards

Unit III week 1 Flashcards

1
Q

Brainstem Function (3)

A

1) Conduit functions
2) Integrative functions
3) Cranial nerve functions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Conduit function of brainstem

A

transit and processing stations for ascending and descending pathways between cerebrum, cerebellum, and spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Integrative Functions of brainstem

A

“Keeps you alive” - integrative functions, consciousness, sleep-wake cycle, muscle tone, posture, respiratory and cardiovascular control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Cranial Nerve Functions of brainstem

A

home of cranial nerves 3-12 and their nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Local signs

A

clues to where lesion in brainstem is based on the levels CNs exit brainstem

Long tracts = meridians of longitude, CNs are parallels of latitude

Can figure out lesion based on long tract deficits + CN deficit

CN SIGN appears IPSILATERAL to lesion, LONG TRACT signs are CONTRALATERAL

Lesions in medial part of brainstem result in completely different deficits than a lateral lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Inferior cerebellar peduncle

A

conveys spinal cord information to cerebellum and interconnects cerebellum with vestibular nucleus and inferior olive

Carries contralateral inferior olive, ipsilateral spinocerebellar, and ipsilateral vestibular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Middle cerebellar peduncle

A

route by which information from cerebral cortex gets to cerebellum via pontine nuclei

carries info from contralateral pontine nuclei to dentate nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Superior cerebellar peduncle

A

route by which the cerrebellum gets information back to the cerebral cortex via the thalamus

Carries info from dentate nuclei to contralateral thalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cerebral peduncle

A

structures at the front of the midbrain which arise from the front of the pons and contain the large ascending (sensory) and descending (motor) nerve tracts that run to and from the cerebrum from the pons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Medial and lateral division of the spinal cord:

Alar vs. Basal plate
Visceral vs. non-visceral portion

A

Alar plate → sensory, more lateral basal plate → motor, more medial

Visceral portion: closest to sulcus limitans
Visceral motor → lateral to somatic motor, medial to somatic sensory

Non-visceral portion: lateral to visceral portion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Corticospinal tract review

A

Internal capsule → corticospinal tract in cerebral peduncles → split up in pons, separated by pontine nuclei, and then come together again to reform corticospinal tract → Medulla, corticospinal tract in pyramid → decussation at spinomedullary junction → ventral horn of spinal cord to a-motor neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Dorsal Column-Medial Lemniscus review

A

Sensory info comes in → Fasciculus gracilis (legs), Cuneatus (arms) → first synapses in medulla at nucleus gracilis/cuneatus → cross → pons, ML slips and forms a mustache (upper arms more medial), just below mustache is trapezoid body (crossing fibers of auditory pathway) → VPL of thalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Anterolateral (spinothalamic) review

A

Synapse in spinal cord dorsal horn, cross in spinal cord, and then doesn’t stop until it reaches the top → pain is more lateral than other tracts in medulla → spinothalamic tract is lateral to medial lemniscus thalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Sound

A

series of pressure waves of alternating compression (increased density) and rarefaction (decreased density) of air molecules

Tells us WHAT and WHERE (direction and distance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Intensity

A

increase of intensity in a sound is when the air is compressed more forcefully during peak compression each cycle → increased density of air

“Loudness” = pressure at peak of compression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

dB SPL = decibels of sound pressure level

equation

A

dB SPL = 20 x Log (P1/P2)

P2 = standardized reference pressure, 20x10^-6 (micro Pascals)

P1 = pressure of the tested sound

Sound above 120 dB → permanent hearing loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Frequency

A

number of times per second that a sound wave reaches peak of rarefaction (or compression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Quantification of hearing loss

A

determining for each ear, and at different frequencies, the smallest dB SPL a subject can just detect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

External ear

A

pinna, external auditory meatus, bounded by tympanic membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Function of external ear

A

Pinna collects sound, funnels it toward auditory meatus, provides acoustical cues to spatial location of sound source

Pressure waves then move tympanic membrane

Rarefaction → TM bulges out
Compression → TM presses in

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Middle ear

A

ossicular chain (malleus, incus, stapes)

Moved by movement of tympanic membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Inner ear includes the _______ and _________

A

cochlea and semicircular canal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Acoustic impedance mismatch

A

Air-fluid boundary causes most acoustic energy to be reflected away, water → high impedance, air → low impedance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What allows us to overcome the acoustic impedance mismatch

A

Middle ear allows us to overcome impedance mismatch

1) P=F/A → Area of tympanic membrane 20x that of stapes → low amplitude vibrations falling onto large tympanic area concentrated into large amplitude motions of much smaller stapes footplate

2) Orientation of middle ear bones confer levering action resulting in larger force
→ almost completely overcomes air-fluid impedance mismatch problem

Impedance mismatch is a problem if fluid fills middle ear → otitis media

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Sensorineural hearing loss

A

damage to or loss of hair cells and/or nerve fibers

involves cochlea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Common causes of sensorineural hearing loss (4)

A

1) Excessively loud sounds
2) Exposure to ototoxic drugs (diuretics, aminoglycoside antibiotics, ASA, cancer therapy drugs)
3) Age (presbycusis) - lose high frequency hearing, as we age
4) Genetic causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Conductive hearing loss

A

degraded mechanical transmission of sound energy through middle ear.

Areas involved: external ear, tympanic membrane, middle ear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Common causes of conductive hearing loss (7)

A

1) Filling of middle ear with fluid during otitis media
2) Otosclerosis - arthritic bone growth impedes ossicle movement
3) Malformation of ear canal (swimmer’s ear, cauliflower ear)
4) Perforation/rupture of tympanic membrane
5) Interruptions of ossicular chain
6) Static pressure in middle
7) cholesteatoma (skin cyst that acts in tumor-like way)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How can you differentiate conductive vs. sensorineural hearing loss?

A

Can overcome conductive hearing loss by placing tuning fork against bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Tonotopic map

A

frequency-wise arrangement of tones or frequencies along length of BM (and is preserved through the auditory pathway into the primary auditory cortex)

Key for determining IHC sensitivity at different spots along BM → each IHC will respond best to a certain frequency determined by mechanical properties of BM at that particular location

Sound FREQUENCY = primary stimulus attribute mapped along cochlea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

BM at apex vs. base

A

BM more flexible, wider, and thicker at APEX
→ LOW FREQUENCY VIBRATION

BM thinner narrower, and more rigid near oval and round window at BASE of cochlea
→ HIGH FREQUENCY VIBRATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

3 compartments of the cochlea

A

scala vestibuli, scala media, scala tympani

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Basilar membrane (BM)

A

separates scala media and scala tympani

Mechanical properties of BM key for discrimination of sound frequency

IHCs attached to BM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Organ of corti

A

sits on top of BM and in scala media

Contains inner hair cells (IHC) attached to BM that transduce sound into electrical signals

Each cross section = 1 IHC and 3 outer hair cells (OHC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Helicotrema

A

hole in BM at apex of cochlea, connects scala tympani to scala vestibuli, relieves pressure → both have perilymph

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How sound elicits movement of BM

A

1) Stapes hits OVAL WINDOW (during peak of compression) → oval window bulges into SCALA VESTIBULI = “traveling wave”
2) → downward movement of BM to relieve compression
3) → compress fluid in SCALA TYMPANI → ROUND WINDOW bulges out towards middle ear (pressure relief)

Opposite happens with rarefaction - round bulges in, oval bulges out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the “traveling wave”

A

generated by stapes hitting oval window - reaches max amplitude at certain location along length of BM

Particles itself are NOT traveling with wave, just going up and down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Hair cell:

A

sensory receptor responsible for detecting sound pressure and converting mechanical vibration into a membrane potential change (transduction)

16,000 hair cells per cochlea

Arranged in 4 rows - row of 3,500 IHCs, 3 outer rows with 12,55 OHCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Stereocilia

A

located on apical surface of IHC

Change membrane potential of hair cell

Bending of stereocilia → altered gating of transduction channels near tips of individual hairs

Connected by tip links

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Resting potential of IHC, driving potential of IHC and mechanism of depolarization vs. hyperpolarization

A

Resting potential of IHC = -50mV, never “at rest”

Push stereocilia bundle in direction TOWARD longest stereocilia, pull trap door open with tip links → DEPOLARIZATION

Push stereocilia bundle in direction AWAY from longest stereocilia, slams trap door shut with tip links → HYPERPOLARIZATION

Driving potential of 130 mv (-50 → +80 mV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Endolymph

A

K+ rich fluid filling scala media, bathes stereocilia on apical end of hair cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Stria vascularis

A

epithelium on side of scala media, actively pumps K+ into endolymph to maintain high [K+] → ENDOCOCHLEAR POTENTIAL

(+80mV positive potential in scala media, endolymph positive with respect to perilymph)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

MUTATION in gap junction subunit, connexin 32 causes what?

A

collapse of endocochlear potential, congenital deafness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Perilymph

A

ionic composition similar to blood (high Na, low K+), fills scala vestibuli and scala tympani

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Tip-Links

A

connect apex of stereocilia to shank of next (taller one) - key role in opening and closing of mechanically gated channels at tips of stereocilia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Tectorial membrane

A

Generates shearing force (between basilar and tectorial membrane) that results in bending of hair cells

Directly attached to outer hair cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Auditory nerve fibers

A

afferent fibers located at basal end of hair cells

Cell bodies in SPIRAL GANGLION

Project to cochlear nucleus of brainstem

Hair cell depolarizes → open Ca2+ basolateral channels → synaptic vesicles release glutamate → excitation of afferent axon → AP sent to second order neurons in brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Cochlear amplifier

A

Efferent innervation from central auditory system act upon OHCs to amplify movements of BM

OHCs respond to changes in voltage with a change in length = “Electromotile”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

mechanism of cochlear amplifier

A

OHCs respond to changes in voltage with a change in length = “Electromotile”

Voltage sensitive PRESTIN protein → change length of OHC

→ OHC pulls BM toward or away from tectorial membrane → changes mechanical frequency selectivity of BM

→ Contributes 50 dB of cochlea’s sensitivity to sound
OHC enhances movement of BM in a frequency dependent manner

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Medial olivocochlear neurons (MOC)

A

efferent neurons, innervate OHCs

Sense context of sound environment

Act as feedback control to change cochlear sensitivity via OHCs

*Use ACh

Adjust sensitivity of cochlea by changing properties of OHCs so you can function with correct auditory sensitivity in loud vs. quiet environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Clinical importance of OHCs

A

Sensorineural deafness due to damage of OHCs
OHCs more sensitive to damage from abx and loud sound

Streptomycin, gentamycin → block transduction channel of OHCs and can kill OHCs, resulting in deafness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Spiral Ganglion Cells

A

aka auditory nerve (8th CN), innervates hair cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Type I ANFs

A

innervate IHC, myelinated
Make up 95% of ANFs
10-30 ANFs innervate a single IHC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Type II ANFs

A

innervate OHC, not myelinated

1 ANFs innervate 10 OHCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Frequency tuning curve

A

sound response of a single ANF where the number of APs fired per sec plotted vs. sound frequency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Characteristic frequency

A

sound to which fiber is maximally sensitive, dictated by place on BM

Fibers have specific frequency selectivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Four properties of ANFs

A

1) frequency of sound encoded by place along cochlear BM where afferent fiber innervates an IHC (ANFs have topographic map of sound frequency)
2) Rate code
3) Phase lock
4) Temporal pattern of APs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Rate code property of ANFs

A

sound intensity encoded via increases in NT release and increases in rate neuron fires APs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Phase lock property of ANFs

A

neurons tend to fire APs only at particular phases of ongoing sound waveform, only LOW frequency sounds (below 1.5kHz)

Important for pitch perception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What two properties of ANFs are crucial for pitch perception?

A

pitch perceived by place of stimulation along basilar membrane and by phase locking (timing of APs with waves)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Auditory neuropathy

A

patients have normal hearing, but can’t hear with ambient noise

Normal OHC function, but absent/abnormal auditory brainstem response

Problem with neural transmission from IHC to ANFs or in ANF function

ANFs have lost ability to phase lock → deficit in discriminating/understanding speech

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Temporal pattern property of ANFs

A

Temporal pattern of AP in ANFs determine pitch of sounds with frequencies below 1 kHz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

otoacoustic emissions

A

outer hair cells also produce sounds that can be detected in the external auditory meatus with sensitive microphones

used to screen newborns for hearing loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

General pathway of the auditory system

Information proceeds from the _________ to __________ cells and the VIIIth nerve afferents in the ear

→ _________ nuclei

→ many cross in the ___________ to the ________ in brain stem

→ Then all ascending fibers stop in the _____________ in the midbrain and the _____________ in the thalamus

→ cortex in the ____________ gyrus.

*All auditory afferents synapse in cochlear nuclei and thalamus.

A

Information proceeds from the ORGAN OF CORTI to SPIRAL GANGLION cells and the VIIIth nerve afferents in the ear

→ COCHLEAR nuclei
→ many cross in the TRAPEZOID BODY to SUPERIOR OLIVE in the brain stem

→ Then all ascending fibers stop in the INFERIOR COLLICULUS in the midbrain and the MEDIAL GENICULATE BODY in the thalamus

→ cortex in the SUPERIOR TEMPORAL gyrus.

*All auditory afferents synapse in cochlear nuclei and thalamus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Cochlear nuclei (2)

located where in brainstem?

position in pathway of auditory information

A

spiral ganglion cells bifurcate upon entering brainstem to innervate nuclei on dorsal and lateral aspects of INFERIOR CEREBELLAR PEDUNCLE of ROSTRAL MEDULLA

1) Branch innervates VENTRAL COCHLEAR NUCLEUS (VCN)
- -> Some then cross midline to trapezoid body

2) Branch innervates DORSAL COCHLEAR NUCLEUS (DCN)
- -> Some then cross midline to dorsal acoustic stria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

After synapsing in the cochlear nuclei, the auditory tracts regroup as ________ and ascend to ________________

A

Tracts regroup as lateral lemniscus → ascend to inferior colliculus of midbrain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Inferior colliculus

A

receives direct projections from cochlear nuclei and multisynaptic input from pontine nuclei (superior olivary complex) = obligatory relay center of ascending auditory info

Right IC represents sound on LEFT side of body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Along the way up to midbrain, many axons terminate in various nuclear complexes in pons

These pontine regions are known as what?

A

Superior Olivary Complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

After synapsing in the inferior colliculus, auditory nerve fibers do what?

A

Inferior colliculus → ipsilateral medial geniculate in thalamus and contralateral inferior colliculus and medial geniculate

Medial geniculate → primary auditory cortex (A1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Primary auditory cortex (A1)

A
  • Part of superior temporal gyrus
  • Cochleo-topic (tonotopic) map found on cortical surface

-gets input from the MGN of thalamus

Brodmann’s area 41

Tonotopic map

  • Neurons responding to lower frequencies located anteriorly
  • Neurons responding to higher frequencies located posteriorly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Unilateral lesions ROSTRAL to cochlear nuclei cause what?

Lesions CAUDAL to cochlear nucleus and those including the CN produce what?

A

Unilateral lesions ROSTRAL to cochlear nuclei do NOT produce unilateral deafness

CAUDAL lesions and those including the CN produce unilateral deafness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Sound localization

A

computed centrally in auditory system based on neural representations of spectral and temporal characteristics of acoustic stimuli arriving at the two ears

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Three main acoustical cues for sound source localization

A

1) Interaural time differences (ITD)
2) Interaural level differences (ILD)
3) Spectral cues (monoaural spectral shape)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Interaural time differences (ITD)

A

physical separation in space of ears → different times of arrival of sound at two ears

Cue to horizontal location of sound

encoded in Medial Superior Olive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Interaural level differences (ILD)

A

ears separated by an obstacle (the head) → acoustic shadow for high frequencies

encoded in Lateral Superior Olive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Duplex theory of sound localization:

A

Low frequencies → ITDs

High frequencies → ILDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Spectral cues - Monaural spectral shape

A

arise from direction and frequency dependent reflection and diffraction of pressure waveforms of sounds by pinna that result in broadband spectral patterns, or shapes, that change with location

Primarily for high frequency sounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Medial superior olive (MSO)

A

ITDs encoded in Medial superior olive (MSO) - nucleus of superior olivary complex

MSO contains input from CONTRALATERAL ear (already crossed in trapezoid body), so projects IPSILATERALLY up to auditory midbrain

MSO receives excitatory input from both ears via cells of anteroventral cochlear nucleus (AVCN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

anteroventral cochlear nucleus (AVCN)

A

AVCN receive excitatory inputs from ANFs

AVCN organized tonotopically

sends output to MSO and LSO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

3 properties of input to MSO neurons

A

1) Phase-locked neural responses of ANF/AVCN neurons carry timing info to MSO
2) MSO neurons = coincidence detectors
3) Axons of AVCN cells input to MSO form delay lines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

MSO neurons as coincidence detectors

A

maximal response when AP from AVCN cells from L ear coincides with R ear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

MSO and delay lines

A

Axons of AVCN cells input to MSO form delay lines due to differences in neural path length from AVCN to MSO → differences in neural conduction times to MSO

Projection to contralateral MSO = longer path length than ipsilateral MSO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

These 3 properties of input to MSO allows for what?

A

All 3 → *Allows for a place code for the horizontal location of sounds in terms of timing between the two ears

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Lateral superior olive (LSO)

ipsilateral vs. contralateral LSO inpus

A

ILDs encoded by Lateral superior olive (LSO) - nuclei of superior olivary complex

Ipsilateral ear input to LSO conveyed via ANF synapses with AVCN cells → ipsilateral LSO

Contralateral ear input to LSO conveyed from AVCN → across midline to neurons of medial nucleus of trapezoid body (MNTB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

calyx of Held

A

AVCN synapse onto MNTB = calyx of Held = LARGEST synapse in entire CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

medial nucleus of trapezoid body (MNTB) neurons

A

Contralateral ear input to LSO conveyed from AVCN → across midline to neurons of medial nucleus of trapezoid body (MNTB)

AVCN synapse onto MNTB = calyx of Held = LARGEST synapse in entire CNS

MNTB neurons = glycinergic → inhibitory effect on LSO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Net result of LSO inputs…

A

ipsilateral excitation and contralateral inhibition of LSO neurons allowing computation of difference between intensity of sounds present at the two ears

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Dorsal Cochlear Nucleus

what happens if you lesion this?

A

Spectral cues encoded in Dorsal Cochlear Nucleus → across midline to excitatory synapse on inferior colliculus

Lesion → can’t tell if sound is above or below you, but can still localize in horizontal plane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Inferior colliculus represents sound where?

A

IC represents sound in contralateral hemisphere, and MSO, LSO and DCN reconverge at contralateral IC

Unilateral lesions in IC or above → deficits in sound source localization for sources contralateral to lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Secondary auditory cortex A2

A

Brodmann’s area 42

Surrounds A1

Does not have tonotopic organization

Includes Wernicke’s Area → understanding and processing spoken language

→ Wernicke’s Aphasia = general impairment in language comprehension but not language production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Mental status exam includes:

A

1) Arousal and attention - level of consciousness, digit span, serial events
2) Memory - orientation, three words at 5 minutes, remote events
3) Language - fluency, comprehension, repetition, naming, reading, writing
4) Visuospatial function - clock drawing tests for hemineglect
5) Mood and affect - inquiries about feelings, observations of affect
6) Complex cognition - executive function, similarities, proverbs, judgement, insight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Aphasia

A

acquired disorder of language resulting from damage to brain areas subserving linguistic capacity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Dysarthria

A

disorder of speech due to motor system involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Dysphonia

A

disorder of voice related to laryngeal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Amnesia

A

impaired recent memory, with deficit new learning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Handedness and cerebral language dominance

A

Language is lateralized usually to LEFT hemisphere - 99% of right handers and 67% of left handers are left dominant → great majority of people are left dominant for language

Ambidextrous people may have mixed language dominance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Right hemisphere contributions to language

A

Automatic speech - expletives, angry outbursts

Prosody - inflection of speech with emotion

Music - subserved by right hemisphere > left

Humor, Metaphor

Recovery - mediated in part by right hemisphere - can rewire itself to become linguistically competent again

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Assessment of aphasia includes assessment of… (5)

A

Spontaneous speech - nonfluency is characterized by labored, effortful speech and less than 6-word phrases

Auditory comprehension - poor comprehension is defined by performing less than 4 step verbal commands

Repetition - “No ifs, ands, or buts”

Naming - Common (e.g. pen) and less common (e.g. crystal of a watch) objects

Reading/writing - a short passage or sentence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

All patients with aphasia have what kind of impairment?

A

All patients with aphasia have NAMING impairment - inability to name common items = most sensitive indicator of language impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Broca’s aphasia

repetition, naming, comprehension, and fluency

A

“non-fluent” aphasia

aphasia with nonfluent speech and good comprehension

Poor repetition and naming

Left hemisphere - Broca’s area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Wernicke’s aphasia

repetition, naming, comprehension, and fluency

A

fluent aphasia

fluent speech and poor comprehension

Poor repetition and naming

Left hemisphere - Wernicke’s area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Conduction aphasia

repetition, naming, comprehension, and fluency

where is the lesion?

A

loss of repetition and naming in presence of preserved fluency and comprehension

Left hemisphere - Arcuate fasciculus - white matter tract connecting Wernick’es and Broca’s areas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Global aphasia

repetition, naming, comprehension, and fluency

where is the lesion?

A

disabling disruption of all aspects of language

Left hemisphere - Perisylvian region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Panic Disorder

A

sudden overwhelming episodes of anxiety that include both somatic and psychic elements, along with worry about either the implication of the attack or about having future attacks

Can occur with or without agoraphobia (fear to leave the house)

Onset typically early adulthood, 2x more in females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Symptoms of panic disorder

A

palpitations, pounding heart, tachycardia, SOB, sensation of smothering, sweating, trembling/shaking, feeling of choking, chest pain/discomfort, nausea, dizziness, feeling faint, paresthesias, chills/hot flashes, derealization/depersonalization, fear of losing control or going crazy, fear of dying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Differential diagnosis - what else could be causing panic disorder?

A 
Hyper/hypothyroidism
Hyperparathyroidism
Mitral valve prolapse, cardiac arrhythmias, coronary insufficiency
Pheochromocytoma
Hypoglycemia
True vertigo
Drug/alcohol withdrawal
Cannabis intoxication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Treatments of panic disorder

A 
Benzodiazepines
Tricyclic antidepressants
Monoamine oxidase inhibitors
SSRIs, SNRIs
Cognitive behavioral therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Generalized Anxiety Disorder

A

excessive worry and more generalized somatic symptoms of anxiety (worry, anxiety, tension)

75-90% comorbid with other psych disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Treatments of GAD

A

Benzos, Buspirone, TCAs, MAOIs, SNRIs, SSRIs, CBT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Social Phobia

A

overwhelming anxiety in situations where one would have to interact with others, be center of attention, or perform in front of others - NOT “shyness”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Treatment of social phobia

A

benzos, B-blockers, MAOIs, SSRIs, CBT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Obsessive-Compulsive Disorder

A

Obsessions: recurrent, persistent thoughts, images, or impulses that are intrusive and cause anxiety

Compulsions: repetitive behaviors or mental acts that are performed in order to reduce anxiety

High comorbidity with Tourette’s Disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Pathophysiology of OCD

A

relative imbalance between direct and indirect basal ganglia pathways, with tendency toward greater direct basal ganglia tone

→ thalamic disinhibition → further activation of orbitofrontal cortex → push even more toward direct pathway tone

→ driven circuit which leads to “capture” of cognitions and behaviors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Treatment of OCD

A

Clomipramine, SSRIs, atypical antipsychotics, CBT, neurosurgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Biological theories of anxiety (2)

A

Dysregulated sympathetic system - locus coeruleus, dysregulated noradrenergic function

GABA-benzodiazepine system - Decreased BZD receptor binding in hippocampus and prefrontal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Neurocircuitry of fear in anxiety

A

1) Fear generation → amygdalo cortical interactions

Anxiety = fear generation is trigger happy

2) Fear extinction → orbitofrontal cortex and prefrontal cortex

Anxiety = fears never extinguished

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Characteristic audiogram in conductive hearing loss

A

shows DIFFERENCE between air conduction line and bone conduction line** → how we distinguish a conductive hearing loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Neural hearing loss

causes and areas involved

A

Causes:

1) 8th nerve tumors - vestibular schwannoma (acoustic tumor)
- 6% of all intracranial tumors

2) Auditory neuropathy
3) Multiple sclerosis

Areas involved: 8th cranial nerve, central pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Neural hearing loss

signs/audiogram

A

Asymmetry of hearing between two ears, and reduced speech perception scores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Audiogram - what to look for, what is normal

A

0 = normal hearing threshold of a young adult

1) Should have normal bone conduction and air conduction
2) Should have good clarity at decibel level adequate for patient → if not, then probably something neural wrong (schwannoma, etc.)
3) Should have symmetry between ears

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Presbycusis

A

gradual, progressive, bilateral hearing loss caused by degenerative physiologic changes associated with aging

Decreased hearing threshold sensitivity

Decreased ability to understand suprathreshold speech

Central auditory process impairment

**most significant drop off is at high frequencies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Noise exposure causes what pattern on audiogram

A

baseline, then a drop, and then return to baseline at high frequency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

are syndromic or non-syndromic mutations more common in congenital hearing loss?

A

non-syndromic (Connexin26/GJB2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Endolymphatic hydrops

A

Pathologic condition, idiopathic

Expansion/distension of endolymphatic compartment of inner ear

Recurrent episodes of vertigo, sensorineural hearing loss, tinnitus, and aural fullness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Disordered inner ear fluid homeostasis

some causes

A

causes dysfunction of stria vascularis and loss of endocochlear potential

1) Vascular dysfunction and/or vasculitis
2) Systemic metabolic disorders: DM, hyperthyroidism, renal failure, arteriosclerosis
3) Immune system disorders: lupus, Cogan’s syndrome, sarcoidosis, Wegener’s granulomatosis, autoimmune inner ear disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What are the two otolith organs?

A
  1. Utricle

2. Saccule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What are the sensory epithelia of the otolith organs?

A

Maculae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Utricle location

A

Floor of vestibule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Saccule location

A

hangs vertically on lateral wall of vestibule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

The utricle senses what?

A

portion of the head with respect to gravity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

The saccule senses what?

A

linear acceleration in vertical direction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Maculae contain ___ cells and ____ overlaid with ___

A

contain hair cells and supporting cells, with apical surface overlaid with gelatinous mass (otolithic membrane)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Name of crystals that overlie hair cells in maculae and what are they composed of?

A

Otoconia

Composed of calcium carbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Maculae assist with ___ detection and ____ changes= “___” receptors

A

gravity
postural
“static” receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Epithelia of utricle and saccule are oriented at ___ angles of one another

A

right angles

Therefore, they are activated buy different signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Hair cell axes of polarity in utricle and saccule

A

Hair cell axes of polarity are opposite in utricle and saccule

→ maximum excitation (depolarized) of one group of hair cells, while opposing hair bundle orientations maximally inhibited (hyperpolarized)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Saccule hair bundles oriented facing ____ from _____ (central region of epithelium) while utricle hair bundles face ____

A

AWAY

Striola

TOWARDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Function of Maculae

A

Detect linear acceleration (change in velocity) of head and position with respect to gravity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Semicircular canal organs

A

3 - horizontal, anterior, and posterior canals

organized in orthogonal planes to each other and allow detection of movements in yaw, pitch, and roll axes (angular acceleration)

140
Q

How do semicircular canals on one side work with those on the contralateral side? (2)

A
  1. Horizontal canals on L and R work together - while one is maximally stimulated the other is maximally inhibited
  2. Posterior canal on one side works with anterior canal from other side
141
Q

Ampulla

A

welling at one end of each canal with specialized patch of epithelium, “crista” → contain sensory hair cells

142
Q

Hair bundles of the ampulla project into ___ (gel like substance)

A

cupula

143
Q

____ moves cupula and stimulates hair cells in the __________→

i.Firing rate will increase, and then adapt (due to _________)

A

Endolymph
crista ampullaris
endolymph inertia

144
Q

Function of semicircular canals

A

Detect angular accelerations and decelerations

Does NOT sense continued motion (adaptation)
- Because cupula has returned to its normal position

145
Q

Membranous labyrinth

A

connective tissue surrounds sensory organs, which in turn is encased by the bony labyrinth within petrous portion of temporal bone

146
Q

Each hair cell has bundle of ___ filled ____ projecting from apical surface in staircase like pattern

A

actin filled stereocilia

147
Q

Kinocilium

A

Tallest cilium within on one side of hair bundle

a.Give the hair cell directional polarity - towards kinocilium is depolarization, away is hyperpolarization

148
Q

Tip Links

A

connect adjacent cilia, and their lower end to an ion channel

149
Q

Hair bundle bathed in ____ (___ K+, ___ Na and Ca2+), but base of hair cell bathed in _____ (____ K+, ____ Na and Ca2+)

A

endolymph
High, Low

Perilymph
Low, High

150
Q

Hair cells are found where?

A

Ampulla of semicircular canals, saccule, and utricle

151
Q

Types of hair cells in vestibular system

A

Type I hair cells: have an afferent nerve terminal encasing most of the basolateral surface of the cell

Type II hair cells: bouton type synapses and efferent innervation that innervates hair cells

152
Q

Vestibular pathway

A

movement accessory structure (cupula in semicircular canal, otoliths in saccule/utricle) pushes on hair bundle → depolarize → modulate release of NT from hair cell → act on afferent vestibular nerves, cause APs to fire at higher frequency in nerve fiber

Vestibular nerve –> flocculonodular lobe and vestibular nuclei

153
Q

Vestibular afferent nerves at rest

A

fire APs even at rest

154
Q

Cell bodies of vestibular afferent nerves located in ______ ganglion → project to ______

A

Scarpa’s

ipsilateral vestibular nucleus

155
Q

Location of vestibular nuclei

A

located at border of caudal pons and rostral medulla

156
Q

Four vestibular nuclei

A
  1. Superior
  2. Inferior
  3. Medial
  4. Lateral
157
Q

Superior and medial vestibular nuclei receive fibers from

A

Semicircular canals

158
Q

Superior and medial vestibular nuclei project to what?

What is the function of these neurons?

A

ascending information via medial longitudinal fasciculus (MLF) →

1) oculomotor nuclei
2) trochlear nucleus
3) abducens nucleus
4) cervical motor neurons of neck musculature

Coordinates eye and head movements

-Gaze control

159
Q

Descending/inferior vestibular nuclei receive inputs from (5)

A

saccule, utricle, and semicircular canals, spine, and cerebellum

160
Q

Descending/inferior vestibular nuclei project to

A

vermal cerebellum, reticular formation, and other brainstem centers

161
Q

Utricles project to (3)

A

lateral, medial, inferior vestibular nucleus

162
Q

Spine and cerebellum project to which vestibular nucleus?

A

lateral

163
Q

Semicircular canals project to which vestibular nuclei?

A

medial and superior

164
Q

Second order cells in vestibular nuclei project to what three main places

A

1) flocculo-nodular lobe of cerebellum
2) Ascend via MLF (to occulomotor, abducens, and trochlear nuclei)
3) Descend via MLF and LATERAL VESTIBULOSPINAL TRACT –> ventral horn of spinal cord (postural reflexes)

165
Q

Vestibular Occular Reflex (VOR)

A

during head rotation, vestibular system signals how fast head is moving and oculomotor system responds to keep visual field stable

166
Q

VOR:

Move head left → endolymph ____-> hair cells excited on ____, inhibited on ____

A

endolymph moves in opposite direction to rotation → hair cells excited on LEFT, inhibited on RIGHT

167
Q

VOR: (moving head to LEFT)

Vestibular afferent fibers synapse in _____ nucleus

______ nerve innervates medial rectus on _____ side (excite, contract)

At same time, get excitatory signal from ____ horizontal canal via ____ nerve to excite lateral rectus muscle on ____ eye

A

Vestibular

Occulomotor
LEFT

LEFT
6th (Abducens)
Right

168
Q

Nystagmus

A

involuntary eye movements that occur during the VOR

169
Q

Neurochemistry of Parkinson’s Disease

A

Loss of substantia nigra dopaminergic cells → reduce dopamine input to striatum
-dopamine = excitatory to striatal neurons → reduce inhibitory input to globus pallidus and thus lose “disinhibition” thalamus

Loss of dopamine synthesis

Loss of regulated release

“Lewy Bodies” with a-synuclein protein precipitate

170
Q

L-Dopa

A

Provides useful clinical benefit for 5-20 years after diagnosis

–> Early smooth motor control produced by L-Dopa is replaced by fluctuations in clinical state, ranging from freezing spells, to wild dyskinetic movement

When quality of L-Dopa response fails, other drugs provide only partial improvement

Oral absorption, crosses BBB

Converted to dopamine in brain, but much of L-Dopa systemically is decarboxylated in intestine, liver, and peripheral organs

**→ take L-Dopa with carbidopa

171
Q

Carbidopa

A

peripheral decarboxylase inhibitor

blocks decarboxylase in intestine and peripheral organs, but does NOT cross BBB
→ Reduces L-dopa requirements by 90%

172
Q

Dopamine Receptor Agonists

A

directly stimulate dopamine receptors in caudate/putamen - most are D2 agonists

173
Q

Dopamine Receptor Agonists drug names (2)

A

Pramipexole (Mirapex) - D2 + D3 agonist

Ropinirole (Requip) - D2 agonist

174
Q

Drugs that facilitate release of endogenous dopamine:

A

Amantadine

175
Q

Anticholinergic drugs for Parkinson’s

A

Less effective than L-Dopa
Used for initial therapy of tremor

Balance the overactivity of inhibitory cholinergic interneurons in striatum caused by lack of dopamine

176
Q

Drug names of Anticholinergic drugs for Parkinson’s (3)

A

Benztropine
Diphenhydramine (Benadryl)
Trihexyphenidyl

*can make you constipated and cause difficulty to empty your bladder

177
Q

Monoamine oxidase inhibitors for Parkinson’s

2 drug names also

A

prevent breakdown of dopamine → prolong D action

Selegiline
Rasagiline

178
Q

Catechol-o-methyltransferase inhibitors for Parkinson’s

2 drug names also

A

Prevent breakdown of L-dopa and dopamine by COMT

Drug Name:
Tolcapone
Entacapone

179
Q

Surgical treatment for Parkinson’s (2)

A

1) Fetal dopamine cell transplants to treat Parkinson’s
2) Placing pacemaker stimulating electrodes in certain basal ganglia nuclei, including globus pallidus, subthalamic nucleus, and thalamus

180
Q

Ways to treat Parkinson’s

A

1) L-DOPA + Carbidopa **most important
2) Dopamine receptor agonists
3) Facilitate endogenous release of dopamine
4) Anticholinergic drugs
5) Monoamine oxidase inhibitors
6) Catechol-o-methyltransferase (COMT) inhibitors
7) Surgical treatment

181
Q

How does dopamine deficiency block movement?

No dopamine for D1 Receptors?

No dopamine for D2 Receptors?

A

No dopamine for D1 Receptors → reduces GABA in striatum → more GABA in GP interna → thalamus inhibited → movement blocked in cortex

No dopamine for D2 receptors → striatum releases more GABA → reduces GABA in GP externa → increases GABA release in GP interna → thalamus inhibited → movement blocked

182
Q

Dopamine normally does what in regards to movement

A

Normally dopamine turns up direct pathway and turns down indirect pathway

→ Dopamine facilitates movement

183
Q

Hyperkinesis

A

moving too much
Chorea, tics, dystonia, restless legs, myoclonus
Tremor

184
Q

Tremor

A

rhythmic oscillatory movement produced by alternating or synchronous contraction of antagonist muscles

Positional: resting, action (intentional), postural (with sustained posture)

Frequency: fast or slow
Regular or jerky

185
Q

Hypokinesia

A

not moving enough

Parkinsonism

186
Q

Most common movement disorders in adults and in kids

A

Adults: Restless leg syndrome, essential tremor, parkinson disease

Children: Tics

187
Q

Dystonias

A

[esp. Wilson’s disease]

Pathophysiology:
-Co-contraction of muscle agonists and antagonists → sustained muscle contractions causing twisting, abnormal postures

Can be associated with tremor

Mobile, static, task specific, exercise induced, diurnal

Can be task specific: e.g. writers cramp

188
Q

Treatment of dystonias (5)

A 
Anticholinergic
Muscle relaxants
Benzos
Botulinum toxin injections
Deep brain stimulation
189
Q

Tics

A

brief intermittent movements or sounds

Sudden, abrupt, transient

Repetitive and coordinated

Vary in intensity, repeated at irregular intervals

May resemble gestures, normal behavior

Most common in children

190
Q

Essential tremor

A

Postural and kinetic tremor (NOT at rest)

Affects hands, arms, head, voice

191
Q

Treatment of essential tremor (6)

A

B-blockers, primidone, topiramate, gabapentin, clonazepam, deep brain stimulation

192
Q

Tourette’s syndrome

Diagnostic criteria (3)

A

1) Age of onset less than 16 years
2) Motor and vocal tics

Motor = grimacing, blinking, nose twitching, hopping, clapping, throwing, head banging

Vocal = grunts, throat clearing, barks, sniffing, shouting

3) Lasts > 1 year

193
Q

Treatment of Tourette’s Syndrome

A

Educate family, patient, school
Support groups
Treat OCD, ADHD, tics (only if interfering with life)
CBT

194
Q

Motor symptoms of Parkinson’s

A 
Resting tremor (may not have tremor!)
Bradykinesia/akinesia
Rigidity
Postural instability
Hypophonia, dysphagia
DOES NOT involve muscle weakness!
195
Q

Some nonmotor symptoms of Parkinson’s

A

Depression, anxiety, cognitive impairment

Autonomic instability (orthostatic hypotension, bladder dysfunction, constipation, erectile dysfunction)

Sleep disturbances

Sensory changes (muscle cramps, pain, paresthesias)

196
Q

Atypical parkinsonian disorders include…

A

1) Lewy Body Dementia
2) Progressive supranuclear palsy
3) Multiple systems atrophy
4) Drug-induced parkinsonism
5) Vascular parkinsonism
6) Posttraumatic parkinsonism
7) Postinfectious parkinsonism

197
Q

Chorea

A

irregular, brief, dancing-like, jerky

198
Q

Huntington’s disease key findings

A

Chorea-athetosis, dementia and psychiatric illness

199
Q

Progressive supranuclear palsy

A

Progressive, onset >50 years
Impaired eye movements = CANNOT DOWNGAZE
Early onset of postural instability

200
Q

Psychogenic movement disorders are characterized by what? (9)

A

1) SUDDEN ONSET
2) waxing and waning
3) Do not respond to meds, but DO respond to placebo/psychotherapy

4) Selective disability
Inconsistent - changing movement amplitude, frequency, and direction

5) Combination of movement disorders
6) Movement increases with attention and decreases with distractibility
7) Evidence of depression or somatization
8) History of similar disorder in family
9) Medical professional

201
Q

Motor unit

A

a-motor neuron and the muscle fibers it innervates
Each muscle fiber only innervated by one motor neuron
Muscle fibers in a motor unit are the same type

202
Q

Small motor unit

A

Small a-motor neuron → innervate small number of muscle fibers → small force

Preferentially innervate slow twitch muscle fibers

Requires less input to cause a depolarization and AP

Important for sustained activities (maintaining posture)

Degenerate in ALS

203
Q

Large motor unit

A

a-motor neuron → innervate many muscle fibers → large force

Preferentially innervate fast twitch glycolytic muscle fibers, quick to fatigue (running, jumping)

Require more input to drive them - recruited later with larger currents

204
Q

Motor neuron pool

A

population of a-motor neurons that innervate the muscle fibers within a single muscle

205
Q

Size principle for recruitment of muscles

A

Systemic recruitment of smaller to larger motor units - generates graded forces

Orderly recruitment of increasingly forceful motor units because small neurons have HIGH input resistances

→ given synaptic current induces larger voltage change in a small motor neuron compared to a large motor neuron

206
Q

Types of muscle cells (4)

A

1) Tonic
2) Slow twitch
3) Fast twitch oxidative
4) Fast twitch glycolytic

207
Q

Tonic muscle fibers

A

non-spiking muscle fibers, shorten extremely slowly, efficiently generate isometric tension with low fatigability

208
Q

Slow twitch muscle fibers

A

generate APs to twitch, fatigue very slowly, high concentration of myoglobin and many mitochondria

209
Q

Fast twitch oxidative muscle fibers

A

activate quickly, many mitochondria so fatigue moderately slowly

Make up the “Fast Fatigue-Resistant” Motor units

210
Q

Fast twitch glycolytic muscle fibers

A

activate quickly, fatigue rapidly, few mitochondria - depend on anaerobic glycolysis ATP generation

Make up the “Fast Fatigable” Motor units

211
Q

Exercise/Chronic stimulation can effect muscle fibers how?

A

can shift motor unit phenotype from fast to slow → slows fatigability, increases endurance capacity

212
Q

A-motor neurons

A

output of local circuits that control muscle = final common pathway

Innervate striated muscle

Cell bodies in ventral horn of spinal cord and brainstem cranial motor nuclei

Have somatotopic organization

213
Q

Somatotopy of a-motor neurons

A

Medial-Lateral somatotopy:

  • Lateral musculature innervated by laterally situated motor neurons
  • medial musculature innervated by medially situated motor neurons

Rostrocaudal somatotopy: Cervical and lumbar enlargements due to more muscles innervated at those levels

214
Q

Muscle tone

stretch reflex influence on tone?

Y-motor neuron activation influence on tone?

A

defined as resistance to muscle stretch - important for walking, standing, running, etc.

Stretch reflex provides resistance to stretch → enhances tone

Y-motor neuron activation → top-down regulation of muscle tone

215
Q

Hypotonia

A

condition of decreased muscle tone due to damage to Ia sensory afferents innervating spindles or a-motor neurons innervating muscle

216
Q

Hypertonia

A

due to damage to descending motor pathways that influence spinal cord premotor circuits

217
Q

Muscles Spindles

A

proprioceptor embedded within a muscle, composed of muscle fibers

Aka intrafusal muscle fiber - runs PARALLEL with force-generating extrafusal muscle fibers

Preferentially signals muscle stretch

Important for maintaining muscle tone - Feedback system for maintaining muscle strength

Use group Ia and group II fibers (large, fast)

Innervated by y-motor neurons

218
Q

Group Ia fibers synapse on ___________ in the spinal cord and cause ______________ in response to stretch

A

Ia → synapse on a-motor neurons in spinal cord → trigger muscle contraction of homonymous muscle fiber in response to stretch

219
Q

Group Ia fibers

A

large and fast
used by muscle spindles

Have a non-zero firing rate under baseline conditions → maintenance of muscle tone

Can signal passive stretch by increasing firing rate and passive shortening by decreasing firing rate

220
Q

Y-motor neurons

A

special motor neurons that innervate intrafusal muscle fibers

During voluntary contraction, a and y motor neurons fire together → shorten extrafusal AND intrafusal muscle fibers together → maintains spindle sensitivity to stretch

Do not directly interact with Ia fibers→ not engaged during reflexive contractions

221
Q

Golgi tendon organs

A

collagen structures at junction of muscle and tendon

-made up of capsule and collagen fibrils

Innervated by Ib fibers

In SERIES with muscle and tendon

Important for stabilizing contractions

Not contractile, not innervated (by y-motor neurons)

Feedback system for maintaining muscle force

Preferentially sensitive to muscle TENSION rather than passive stretch

222
Q

How are golgi tendons activated?

A

Preferentially sensitive to muscle tension rather than passive stretch:

Passive stretch lengthens muscle before straining the tendon

During muscle contraction, force increases tension on collagen strands → causes them to fire AP

Participate in negative feedback regulation of muscle tension

223
Q

Stretch Reflex Circuit

A

“knee-jerk” reflex
Monosynaptic

Hammer tap → stretch muscle spindle→ stimulate Ia sensory axons → activate a-motor neuron in spinal cord → contract stretched muscle

224
Q

Reciprocal innervation of Ia fibers

A

Ia fibers also innervate other inhibitory interneurons → inhibit other motor neurons → inhibit opposing antagonist muscle

–> activate contraction in one muscle, and relaxation in opposing muscle

225
Q

Rapid error correction in movements

A

mismatch between expected and actual muscle stretch detected rapidly and used to correct errors in motor output

226
Q

what would happen if you picked up a big box, labeled “Books” that you expected to be be heavy but was actually really light?

A

→ exert lots of force, highly active firing of a/y motor neurons and shortening of muscle and spindle

BUT if box is actually empty, muscles would shorten too quickly relative to spindle (spindle is floppy) and mismatch will cause Ia spindle afferent to drop firing rate

→ rapid reduction in a-motor neuron drive → reduce muscle contraction

227
Q

What happens if the box is heavier than we expect?

A

Heavier than we expect → muscle spindle stretches more than muscle fibers → increase Ia spindle firing → increase contraction of muscle fibers via a-motor neurons

228
Q

Extensor-flexor coupling circuits

A

Ib afferents innervate GTOs → GTOs directly innervate inhibitory and excitatory interneurons in spinal cord

Protects musculature from over exertion by relaxing the synergist (homonymous) muscle and contracting the antagonist

229
Q

Crossed-extensor reflex

-what happens when you step on a tack?

A

Cutaneous sensory receptors (nociceptors in case of stepping on a tack) innervate spinal interneuron motor networks

→ coordinate extensor relaxation and flexor contraction on same side as stimulus and converse extensor contraction and flexor relaxation on contralateral side

230
Q

Central Pattern Generator

what do you not need for central pattern generation?

Where is the “control center”

A

neural networks that can produce patterned, rhythmic outputs in absence of sensory or central input - coordinate complex movements

Used in locomotor patterning

Sensory and descending input from upstream motor centers can modify CPG output, BUT SENSORY is NOT NECESSARY for CPGs to generate organized rhythmic motor output

Resides in mesencephalic locomotor center

231
Q

Reticular formation

where does the reticulospinal tract project?

A

collection of loosely connected areas in midbrain tegmentum (ventral midbrain)

Reticulospinal tract: send axons ipsilaterally and innervate medial part of ventral horn

232
Q

Modulatory functions of reticular formation

A

Modulatory functions: cardiovascular, respiratory control, and sensorimotor reflexes, eye movement, sleep-wake regulation, and coordination of limb/trunk movement

233
Q

Premotor functions of reticular formation (3)

A

1) Regulate locomotor speed via Input from mesencephalic locomotor region - initiator of CPG activity
2) Anticipatory responses to voluntary movement (e.g. flex legs before lifting weight, anticipating change in center of balance)
3) Important for posture, balance and anticipatory movements

234
Q

Vestibulospinal tract/Vestibular nuclei

informs brain of what? (4)

Sensory info detected by ___________ and sent via _____________ to ________________

A

informs brain of head position, orientation, and motion - important for protective responses to falls

Sensory info detected by semicircular canals and sent via 8th cranial nerve to vestibular nuclei

235
Q

Vestibular nuclei sends info via what 3 pathways?

Each pathway is responsible for what?

A

1) Medial vestibulospinal tract to medial spinal cord
→ regulate head orientation and neck muscle activation

2) Lateral vestibulospinal tract to lateral motor pools
→ control proximal limb musculature

3) descending projections to cranial nuclei III (oculomotor), IV (trochlear, and VI (abducens)
→ regulate eye movement

236
Q

Vestibulo-Occular-Reflex

A

produces eye movements that counter head movements to keep gaze fixed

Absent VOR indicates brainstem damage

237
Q

VOR pathway:

Vestibular nuclei –> projects __________ to ___________

Abducens nuclei ________

On side contralateral to activated vestibular neuron/ nucleus what happens?

On side ipsilateral to activated vestibular neuron/ nucleus what happens?

A

Vestibular nuclei → project BILATERALLY to ABDUCENS NUCLEI

Abducens nuclei CROSS again:

On side contralateral to activated vestibular neuron/ nucleus…
-axons excite motor neurons that contract lateral rectus of contralateral eye and medial rectus of ipsilateral eye

On side ipsilateral to activated vestibular neuron/ nucleus
-axons inhibit motor neurons that control medial rectus muscle of contralateral eye and lateral rectus of ipsilateral eye

238
Q

Superior colliculus/Tectospinal tract

aka colliculospinal tract

A

midbrain structure responsible for orienting gaze and body position

Computes a map merging auditory and visual space onto body coordinates

Descending projections of colliculospinal tract target motor neurons that control axial musculature of neck (e.g. turn head/upper torso towards siren going off)

239
Q

Descending pathways for control of finger movement

Descending pathways for control of axial musculature

A

Lateral corticospinal tract

Ventral corticospinal tract

240
Q

Primary Motor Cortex (M1)

A

Brodmann’s Area 4 in precentral gyrus of cerebral cortex

Pyramidal neurons of layer five → spinal cord via corticospinal tract

Critical for voluntary action

241
Q

Corticospinal tract pathway

A

Internal capsule → cerebral peduncle (ventral midbrain)

→ collateralize (branch while continuing their course) in pons

→ pyramids (caudal medulla), where most axons cross

→ lateral corticospinal tract or ventral corticospinal tract:

242
Q

lateral corticospinal tract

A

→ direct synapse on a-motor neurons for hand and finger movement

→ spinal cord local circuit interneurons to innervate motor neurons in ventral horn

243
Q

ventral corticospinal tract

A

axons remain ipsilateral, innervate ipsilateral axial and proximal limb muscles

244
Q

Premotor Cortex

A

just anterior to primary motor cortex

Fewer descending projections, but still make up 25% of corticospinal tract

Involved when movement is initiated by an external cue

245
Q

Supplementary motor cortex

A

involved in self-cued movements

Highly active during mental rehearsal of movement

246
Q

“Mirror neuron” activity

A

selective neural responses in response to subject watching an action with an intended consequence

Role in empathy and learning

247
Q

Organizational principle of motor cortex

A

“Motor Maps”

1) Disproportionate M1 Surface area devoted to controlling musculature used in fine motor tasks
2) Movements, not muscles are mapped

248
Q

Motor cortical plasticity is used in stroke recovery how?

A

Stroke → damage motor cortex → acute impairments in ability to control affected area

Over time, areas adjacent to damaged cortical region can sprout new connections and subserve motor control of affected body part → functional recovery

249
Q

Practice and motor cortical plasticity

A

repeated performance of a given action leads to expansion of that region of cortex

250
Q

Three functional divisions of the cerebellum

A

1) Cerebrocerebellum = lateral hemispheres
2) Spinocerebellum = vermal and paravermal regions
3) Vestibulocerebellum = flocculo-nodular lobe

251
Q

Three main fiber bundles of cerebellum

A

Inferior Cerebellar Peduncle: major input
Middle Cerebellar Peduncle: major input
Superior Cerebellar Peduncle: major output

252
Q

Three cortical layers of cerebellum

A

molecular
purkinje
granule

253
Q

Paired central nuclei of deep cerebellum (4)

A

1-3) Interposed nucleus - dentate, globose, emboliform

4) Fastigial nucleus

254
Q

Three main deficits with cerebellar lesion

A

synergy, equilibrium, tone

NO loss of muscle strength or sensation

255
Q

Flocculo-Nodular Lobe: aka vestibulocerebellum

receives input from __________ and outputs to _____________

Important for what main functions (2)

A

vestibular nuclei and 8th cranial nerve directly (NO connection to deep cerebellar nuclei)

vestibular nuclei of brainstem

Important for axial control, vestibular control (balance, eye movements, VOR, VCR, VSR)

256
Q

Vermis projects to _________ nucleus → ________ and ___________

Information then descends via the ____________

A

Fastigial nucleus (DCN)

Vestibular nucleus and pontine reticular formation (bilaterally)

medial descending system

257
Q

Medial descending system is made up of the ______________ and ___________.

It carries information form the _______ to control what?

A

lateral vestibulospinal tract and pontine reticulospinal tract

carries information from the vermis

→ control of axial musculature, posture, and balance, and integration of head and eye movements
(Axial (trunk) musculature represented along vermis)

258
Q

Paravermis projects to the ____________ nuclei and then travels via the ______________ to the ___________ and _________

A

interpositus nuclei →

via Superior Cerebellar Peduncle

contralateral red nucleus and Va/Vl Thalamus

259
Q

The paravermis sends descending motor output via what?

Paravermis receives input from where?

A

LATERAL descending system - rubrospinal tract

Input from spinal cord

260
Q

Function of paravermis

A

→ Fine tune movement of limbs

Distal limbs represented stretching out into paravermal regions

**right cerebellum controls right hand

261
Q

Flocculonodular lobe

functional region?
Principal input?
Deep nucleus?
Principal destination?
function?
A

functional region - vestibulocerebellum

Principal input - vestibular sensory cells

Deep nucleus - vestibular

Principal destination - axial motoneurons

function - axial control, vestibular reflex (balance, eye movement)

262
Q

Vermis

functional region?
Principal input?
Deep nucleus?
Principal destination?
function?
A

functional region - spinocerebellum

Principal input - Visual, auditory, vestibular, somatosensory

Deep nucleus - Fastigial

Principal destination - medial systems

function - axial motor control (posture, locomotion, gaze)

263
Q

Paravermis

functional region?
Principal input?
Deep nucleus?
Principal destination?
function?
A

functional region - spinocerebellum

Principal input - spinal afferents

Deep nucleus - interposed

Principal destination - lateral system, red nucleus

function - distal motor control

264
Q

Lateral hemisphere

functional region?
Principal input?
Deep nucleus?
Principal destination?
function?
A

functional region - cerebrocerrebellum

Principal input - cortical afferents

Deep nucleus - dentate

Principal destination - integration areas

function - initiation, planning timing

265
Q

The cerebellar deep nuclei carry what information

A

Provide major output pathway of cerebellum

Cerebellar outputs from deep nuclei of medial regions (vermis, vestibulocerebellum) → modulate medial descending pathways (vestibulospinal tracts, reticulospinal tracts, tectospinal tracts)

Cerebellar outputs from deep nuclei of lateral regions (paravermis and vestibulocerebellum) → modulate rubrospinal and corticospinal outputs

266
Q

Neocerebellum (aka cerebrocerebellum) projects to the ___________ nucleus and then to _____________ to influence what cortical regions?

A

Projects to dentate nucleus → contralateral ventrolateral thalamus → influence cortex regions (primary motor and premotor cortex)

→ higher level coordination of movements (planning, initiation of movement)

267
Q

The cerebrocerebellum receives input form where?

A

pontine gray matter:

Axons from cortex synapse on ipsilateral neurons in basal pons → pontine neurons send axons contralaterally to cerebellar hemispheres

268
Q

Sensory input into cerebellum and descending cerebellar output are __________, while tracts between cerebellum and cortex __________

Thus, the right cerebellum deals with what side of the body and what side of the motor cortex?

A

uncrossed

decussate

→ Right cerebellum deals with right (ipsilateral) body, and must communicate with left (contralateral) motor cortex

269
Q

Cerebellar lesions result in loss of __________ but NOT _______ or __________

A

Cerebellar lesions result in loss of coordination but NOT sensation or strength

270
Q

Modest lesion to cerebellar cortex vs. lesion of large region of cortex or deep nuclei

A

Modest lesions to cerebellar cortex have little obvious motor effect and to do so, must involve large regions of cortex or lesion underlying deep nuclei

271
Q

Deficits that arise from cerebellar damage (6)

A

HANDS Tremor

Hypotonia: anterior lobe injury

Ataxia: loss of coordination or timing of muscles

Nystagmus - Extraocular muscle deficit → nystagmus

Dysarthria - Slurred speech

Stance and gait problems

Tremor

272
Q

Ataxia

A

Loss of coordination or timing of muscles

Dysmetria: inability to bring limb to required/desired point in space
Dysdiadochokinesia: impaired rapid alternating movements
Decomposition of movements

273
Q

Tremor associated with cerebellar damage

A

Intention tremors perpendicular to direction of limb motion, increasing oscillations as limb approaches target

274
Q

Cellular constituents of cerebellar cortex (5)

A

Stellate cells, Basket cells, Purkinje cells, Granule cells, and Golgi cells - divided into three layers

275
Q

Cerebellar cortex:

Molecular layer

A

uppermost layer

contains large numbers of:

1) parallel fibers
2) dendrites of Purkinje cells
3) scattered inhibitory neurons (Stellate cells and basket cells)

Parallel fibers interact with dendrites of multiple Purkinje cells

Each purkinje cell is in contact with many parallel fibers

276
Q

Cerebellar cortex:

Purkinje Cell Layer

A

contains cell bodies of Purkinje cells
ONLY output from cerebellar cortex is via Purkinje cells

Purkinje cell output inhibits cells of deep nuclei

277
Q

Cerebellar cortex:

Granular Layer

A

many small granule cells whose processes extend superficially to become parallel fibers in molecular layer

278
Q

Stellate Cells and Basket Cells

A

excitation of basket and stellate cells by parallel fibers results in inhibition of neighboring Purkinje cell = Lateral Inhibition

Inhibition of Purkinje cell → disinhibition of deep cerebellar neurons

279
Q

Purkinje cells are inhibitory or excitatory?

A

Purkinje cell output inhibits cells of deep nuclei

280
Q

Input to the cerebellar cortex comes from ____________ and ___________

A

mossy fibers and climbing fibers

281
Q

Mossy fibers come from where?

A

arise from several different sources (depends on functional zone they innervate)

1) Clarke’s column (nucleus gracilis) in spinal cord - relay proptioceptive information from lower extremities
2) Lateral cuneate nucleus in caudal medulla (relaying proprioceptive information from upper extremities
3) Vestibular nuclei
4) Pontine nuclei (pontine nuclei send axons to contralateral middle cerebral peduncle –> cerebral cortex)

282
Q

Mossy fibers

A

Come from three functional regions to innervate cerebellar cortex

Diverge extensively, excite large number of granule cells that then excite Purkinje cells, Stellate cells, and Basket cells via parallel fibers

Many parallel fibers must sum to generate a single AP in a Purkinje cell = Simple Spike

283
Q

Simple spike

A

Many parallel fibers must sum to generate a single AP in a Purkinje cel

Generated by mossy fiber input

284
Q

Climbing fibers originate in __________ and travel via _________ cerebellar penduncle to make direct contact with _________

A

CONTRALATERAL inferior olivary nucleus

CONTRALATERAL inferior

Purkinje cells

285
Q

Climbing fiber and Purkinje cell interaction

A

Each climbing fiber contacts one Purkinje cell - very powerful synaptic contact

Single AP in climbing fiber → burst of spikes in Purkinje cell = Complex Spike

286
Q

Complex Spike

A

Single AP in climbing fiber → burst of spikes in Purkinje cell

287
Q

Cerebellar cortex has cells that receive two distinct inputs

A

1) One is modality-specific input (i.e. balance, limb position, eye-hand coordinates) that represent a copy of the reflex input
→ MOSSY FIBERS

2) Another input from the inferior olivary nucleus, signals errors and unexpected responses in reflex activity
→ CLIMBING FIBERS

288
Q

Together, the input from the mossy fibers (modality specific) and climbing fibers (unexpected responses) generate what?

A

→ together generate an output that modifies the gain of the reflex in question

289
Q

what happens when a purkinje cell is simultaneously depolarized by a mossy fiber and a climbing fiber?

A

Plasticity:

If there is simultaneous depolarization of Purkinje cell between mossy fiber (copy of sensory signal) and climbing fiber (inferior olivary nucleus) there is a WEAKENING of a signal (LTD) and modulation of cerebellar output

290
Q

When ________ detects a discrepancy between planned and actual motor performance, it generates what?

A

INFERIOR OLIVE

generates climbing fiber activity (error signal) that modulates cerebellar function

→ Long-term depression of sensitivity to mossy fiber input (reduced simple spike frequency)

291
Q

Putamen

A

Sensorimotor cortex projects to putamen

Projects to its own subsection of GP → VA thalamus → motor cortex, especially supplementary motor area (SMA)

292
Q

Caudate

A

Input widely from frontal association cortex (frontal lobes)

Sends info to its own region of GP → dorso-medial thalamus → association cortex

293
Q

Nucleus Accumbens

A

caudal juncture between caudate and putamen

Processes info from paleo-cortex

Part of limbic system - emotional and drive-related behavior

294
Q

What happens when Dopamine stimulates D1 receptors?

A

Dopamine stimulates D1 receptors in striatum → releases GABA in striatum → reduces GABA in GP interna → disinhibit thalamus → movement allowed in cortex

= direct pathway

295
Q

What happens when dopamine stimulates D2 receptors?

A

D2 dopamine receptors project to GP externa (inhibits)→ stops inhibiting STN → STN excited → activates GPi → inhibits thalamus → turns of thalamo-cortical activity (decreases movement)

= Indirect Pathway

296
Q

Substantia nigra

A

dopamine rich

Receives projections from striatum (C and P)
-Striatum releases GABA and inhibits substantia nigra

Projects back to caudate and putamen via PARS COMPACTA neurons that contain and release dopamine

Projects to thalamus via PARS RETICULA

297
Q

Substantia nigra and parkinson’s

A

Dopamine in striatum is EXCITATORY

Parkinson’s = degeneration of substantia nigra, loss of dopamine input = paucity of movement

298
Q

Subthalamic nucleus

A

Input from external segment of GP → release GABA, inhibit subthalamic nucleus

Projects to external and internal segment of GP → excitation of internal segment of GP

299
Q

Major source of input to basal ganglia?

A

Cerebral cortex

300
Q

Parkinson’s vs. Huntington’s

direct vs. indirect pathway activity

A

Direct pathway facilitates movement, indirect pathway inhibits movement

Parkinson’s = activity in direct pathway reduced relative to indirect pathway → paucity of movement

Huntington’s = activity in indirect pathway reduced → hyperkinetic disorder

301
Q

Out put of basal ganglia

A

Basal ganglia output via thalamus which inhibits motor cortex function, until thalamus is “disinhibited” by GP

302
Q

Huntington’s disease symptoms

A

Chorea: continuous rapid movements of face, tongue, or limbs

Athetosis: slow, writhing, ceaseless movements of hand, lips, tongue, neck, and foot

303
Q

Huntington’s disease pathophysiology

A

AD mutation on 4th chromosome, CAG triplet repeat 17 to 34 times

Possible due to too much dopamine or glutamate excitotoxicity

304
Q

Direct path from cortex to basal ganglia

A

Cortex → input nuclei (Caudate and Putamen) → output nucleus (Globus Pallidus interna) → Thalamus (VA/VL for motor portion, DM for cognitive/associational)

305
Q

Cellular actions in basal ganglia

A

activation of motor control signal is achieved by release from inhibition (disinhibition), NOT by direct excitation

306
Q

Cells in layer ________ of cerebral cortex send axons to synapse in _______________ where they release ___________

A

Cells in layer 5 of cerebral cortex (output cells) send axons to synapse in basal ganglia → release GLUTAMATE to excite cells in Caudate or Putamen

307
Q

(direct pathway)

Cells in caudate or putamen send axons to __________ where they release _______ and cause what?

GP cells → send axons to ________ → release _________ –> _________ thalamus → thalamus _______ firing and ________ cortical neurons

A

Cells in C or P send axons to globus pallidus → release GABA, inhibit GP cells

GP cells → send axons to thalamus → release LESS GABA, disinhibit thalamus → thalamus increases firing and excites cortical neurons

308
Q

GP cells are continuously acting on the thalamus how?

A

GP cells continuously inhibit thalamus in absence of cortical input = emergency brake on your car - must release break and “disinhibit” car when you want to go

“Disinhibit” ONLY those specific corticospinal commands appropriate to behavioral task

309
Q

Stroke in subthalamic nucleus → ?

A

hemiballismus

310
Q

hemiballismus

A

Lose excitation to inhibitory neurons of globus pallidus → thalamus disinhibited → motor programs inappropriately initiated

Symptoms: flailing movements of arm and leg on one side

311
Q

Deep stimulation treatment of Parkinson patients

A

Implantation of electrodes into subthalamic nucleus or into internal segment of globus pallidus to stimulate the neurons in these parts of the basal ganglia

Used to treat patients who still receive benefit from meds, but are disabled by fluctuations between their on and off medication states

312
Q

Feedback controller

A

e.g. thermostat with heater and cooler turned on when temp crosses a certain threshold

Slow, tends to overshoot the mark in both directions

313
Q

Feedforward controller

A

system that predicts change in room temperature → activate heater preemptively, counteracting coming temperature drop

Involves using sensory data to calculate a state coming at some future time

314
Q

Adaptive feedforward control

A

feedforward system with error signal information

Error signal:

EX) window is opened→ predicts temp drop, heats house. Then measure temperature, and if it is off from desired → ERROR SIGNAL

Instructs system to perform more or less heating for the same inputs the next time around

Calibration process continues in case the system changes

315
Q

Parietal Association Cortex

A

Visual “Where” pathway (from dorsal stream from occipital visual cortex) provides visual info about target/limb position and joint position sense information from somatosensory cortex combine → integrated by parietal cortex

  • This integrated information is fed to premotor cortices (frontal lobe) → calculate difference between current and desired location → issue command for desired changes in joint angles to primary motor cortex
  • Contains an internal model that specifies certain PREDICTIONS
316
Q

Prism Adaptation

A

effect of prisms on a reaching movement

Changes system such that predictions of the system are no longer valid → system must be RECALIBRATED

CNS able to adapt to this change

Adaptation takes only a few trials when prisms are applied for a short time, but correcting post adaptation after effect can take much longer if prisms are worn for weeks or months

317
Q

Prism adaptation in patients with cerebellar damage

A

fail to show this adaptation

When prisms on → consistently point beyond target

When taken off → no post-adaptation after effect, right back on target

318
Q

Corticopontine fibers descend via _____________ → pontine grey →________ fibers that travel via _________ cerebellar peduncle and innervate _________________

A

(LEFT) internal capsule

mossy

middle

contralateral (RIGHT) cerebrocerebellum

319
Q

Parietal cortex role in mossy fiber input to cerebral cortex

A

Parietal cortex contributes a large amount to these corticopontine fibers
→ mossy fiber input is a reflection of current state of parietal cortical mapping between visual and proprioceptive signals

320
Q

Mossy fibers in right cerebrocerebellum synapse with ________ cells –> __________ that synapse with array of _______ cells

–> output to __________ via ________ cerebellar peduncle

–> ____________ and then __________

A

Mossy fibers synapse with granule cells → parallel fibers that synapse with array of Purkinje Cells

→ output to (RIGHT) dentate nucleus via superior cerebellar peduncle

→ across decussation to (LEFT) VA/VL thalamus

–> (LEFT) motor and premotor cortices

321
Q

Inferior olivary nucleus sends ________ fibers to _______ cells via the ________ cerebellar peduncle

A

climbing

Purkinje cells

Inferior

322
Q

Climbing fibers from ION generate burst of complex spikes in response to __________

A

unexpected change - spike activity returns to normal once you adapt

323
Q

Simultaneous discharge of olivary climbing fibers and parallel fibers leads to…

A

changes in synaptic strengths (Long Term Depression) of parallel-Purkinje synapses

324
Q

Inferior olivary nucleus as a comparator

A

Compares expected state (conveyed by deep cerebellar nuclei as a reflection of parietal network) with the observed state (conveyed by visual/proprioceptive feedback)

325
Q

NO CHANGE in ION activity would result if…

A

Proprioceptive and visual feedback are exactly what current parietal network predicts → reflection of parietal network conveyed to ION would cancel out proprioceptive and visual feedback

326
Q

Error signal from ION would result if…

A

Feedback was different from expected state

Error signal proportional to magnitude of difference between observed and expected states

Conveyed via climbing fibers to cerebellar cortex → complex spikes in Purkinje cells

Parallel fiber synapses that are active simultaneously with climbing fiber-induced complex spike undergo Long Term Depression

→ the ensemble that was active in erroneous movement has been deactivated and new ensemble conveys revised reflection of parietal cortex’s mapping of visual/proprioceptive coordinates to motor cortices

→ Predictions about which limb position will achieve which visual coordinate has been updated and motor system has adapted to new conditions

327
Q

Reflex error correction - picking up something heavier than expected

A

Muscle will be stretched and muscle spindle will discharge in proportion to magnitude of error

→ discharge signal conveyed to inferior olivary nucleus and transmitted to cerebellum as error signal that reconfigures the network that uses perceptions of object to generate predictions about motor commands required to lift it

328
Q

Reward activates _______ cells in ___________ and __________

A

dopaminergic cells

substantia nigra and VTA

329
Q

Dopamine in the substantia nigra and VTA does what?

A

→ dopamine facilitates and strengthens activity in specific circuit between cortex, striatum, GP, thalamus, and cortex

Symbol that anticipates reward can come to drive dopamine release

Prediction area about reward in substantia nigra is used to modify connectivity of cortico-striatal circuits - reinforce certain networks to exclusion of others

330
Q

How does SN and VTA know about what to expect in reward?

A

Splotches in striatum correspond to striosomes with separate projections from direct/indirect pathway that project to dopaminergic cells in SN

-these are GABAergic cells, so striosome inhibits dopaminergic cells in SN = Efference Copy

SN is mirror of striatal activity

Compares current vs. expected conditions

331
Q

Comparator in basal ganglia vs. cerbellum

A

Basal ganglia:
comparator = Substantia Nigra and VTA

Cerebellum:
comparator = Inferior olivary nucleus

Comparator generate a signal (Error signal) if observed outcome differs from predicted → uses signal to instruct and change circuit

332
Q

Mismatch between expected and observed rewards causes what?

A

Unpredicted reward STRONGLY activates medium spiny neurons

→ increase dopamine release into striatum → alter plasticity of cortico-striatal networks so networks that correctly predicted the error will be reinforced and those that do not correctly predict error will be diminished

→ recalibration of direct and indirect pathways so that revised network conveyed to VTA/SNc will now predict the reward and VTA/SNc will no longer discharge in response to discrepancy until next unexpected reward occurs

333
Q

Cerebellum and basal ganglia both have _________ projection neurons that act as pattern recognizers

Cerebellum = ?

Basal ganglia = ?

A

GABAergic

Cerebellum → Purkinje cells of cerebellar cortex

Basal ganglia → medium spiny cells of striatum

334
Q

Medium spiny cells of striatum

A

Medium spiny cells project directly to SNc/VTA (ventral tegmental area) dopaminergic neurons and convey a reflection of the current state of the corticostriatal network to the SNc/VTA dopaminergic neurons

Convey network’s current predictions about reward

Similar to GABAergic cells from deep cerebellar nuclei in cerebellar pathway

335
Q

Extrapyramidal signs

A

abnormal movement, posture, or muscular tone, NOT paresis or sensory loss

336
Q

Basal ganglia disorders result in what deficits? (3)

A

1) Tremor (resting)

2) Hypokinetic - rigidity, bradykinesia
Rigidity → lead pipe or cogwheel feeling

3) Hyperkinetic - chorea, athetosis, akathisia
- Spasticity → “clasp-knife”, velocity dependent increase in tension

337
Q

What happens with a lesion of midline cerebellum?

A

Lesions of midline (vermis) → impair coordination of stance and gait, axial truncal posture, and equilibrium

338
Q

What happens with cerebeller lesion of paravermis?

A

Lateral lesions impair the ipsilateral limb

339
Q

Stroke in paramedian branches of anterior spinal artery or vertebral artery causes what symptoms?

A

MEDIAL deficits

1) Motor (contralateral hemiparesis)
2) Medial lemniscus (contralateral deficit in vibration and touch)
3) Hypoglossal ipsilateral tongue deviation

340
Q

PICA stroke causes what symptoms (4)

A

LATERAL deficits

1) Spinocerebellar –> ataxia, dysmetria
2) Sympathetic dysfunction –> Horner syndrome (ipsilateral)
3) Dysphagia/Hoarsness (Nucleus Ambiguus, Vagal nerve problem)
4) Spinothalamic –> contralateral body, ipsilateral face pain and temperature deficit

341
Q

AICA stroke causes what symptoms (5)

A

LATERAL deficits

1) Facial nucleus –> ipsilateral facial paralysis
2) Cochlear nucleus –> ipsilateral hearing loss
3) Spinothalamic –> contralateral body, ipsilateral face pain and temperature deficit
4) Vestibular nucleus –> ipsilateral vestibular problems
5) Ataxia (spinocerebellum)

342
Q

Basilar artery stroke causes what symptoms?

A

Causes locked in syndrome

Complete paralysis except vertical eye movements

343
Q

Interposed nucleus of cerebellum –> ___________ –> _________ and ________

A

CONTRALATERAL red nucleus

inferior olive and rubrospinal tract

344
Q

Fastigial nucleus of cerebellum –> _________ and _________ and gets input from _________

A

BILATERAL vestibular nuclei and reticular formation

input from vestibular afferents

345
Q

Dentate nucleus of cerebellum –> _________

Input to dentate nucleus from ______

A

CONTRALATERAL VA/VL thalamus

input form pontine nuclei

Neuro (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions