Neuroanatomy Test 3

Front 1

LGN Cortical Target & Brodmann number

Back 1

Primary Visual Cortex (17)

Front 2

MGN Cortical Target & Brodmann number

Back 2

Primary Auditory Cortex (41, 42)

Front 3

VPL Cortical Target & Brodmann number

Back 3

Primary Somatosensory Cortex (3,1,2), D, M

Front 4

VPM Cortical Target & Brodmann number

Back 4

Primary Somatosensory Cortex (3,1,2) V, L

Front 5

VL Cortical Target & Brodmann number

Back 5

Primary Motor Cortex (4)

Front 6

VA Cortical Target & Brodmann number

Back 6

Premotor Cortex (6)

Front 7

Intralaminar Nuclei Cortical Target & Brodmann number

Back 7

Diffusely to cortex, heavily to striatum

Front 8

Pulvinar and LP Cortical Target & Brodmann number

Back 8

association cortices of parietal, temporal, and occipital lobes

Front 9

Medial Dorsal Nucleus Cortical Target & Brodmann number

Back 9

Association cortices of frontal lobe (prefrontal cortex)

Front 10

LD/A Cortical Target & Brodmann number

Back 10

Cingulate Cortex

Front 11

VPI (Ventral Posterior Inferior nucleus) Cortical Target & Brodmann number

Back 11

primary vestibular cortex (2)

Front 12

VPM^m Cortical Target & Brodmann number

Back 12

Primary gustatory cortex (43)

Front 13

cortical target of the one that has no input from thalamus

Back 13

primary olfactory cortex, not in neocortex

Front 14

Source and Afferent tract to LGN

Back 14

Retina ganglia-> optic tract/optic chiasm

Front 15

Source and Afferent tract to MGN

Back 15

inferior colliculus->brachium of inferior colliculus

Front 16

Source and Afferent tract to VPL

Back 16

1)Dorsal horn->STT->VPL

2) Dorsal column->medial lemniscal->VPL

Front 17

Source and Afferent tract to VPM

Back 17

Descending nucleus of V, Main sensory nucleus of V->trigeminothalamic nucleus->VPM

Front 18

Source and Afferent tract to VL

Back 18

Deep cerebellar nuclei->brachium conjunctiva->VL

Front 19

Source and Afferent tract to VA

Back 19

globus pallidus, substantia nigra pars reticulata->thalamic fasciculus->VA

Front 20

Source and Afferent tract to intralaminar nuclei

Back 20

1)dorsal horn->STT->

2) globus pallidus/SNc reticulata->thalamic fasciculus->

Front 21

Source and Afferent tract to Pulvinar and LP

Back 21

1)Retina ganglia->optic tract->

2) Superior colliculus->tecto-thalamic tract->

Front 22

Source and Afferent tract to medial dorsal nucleus

Back 22

amygdaka, hypothalamus, other thalamic nuclei->medial dorsal nucleus

Front 23

Source and Afferent tract to LD/A

Back 23

mammillary nucleus of hypothalamus->mammillothalamic tract->LD/A

Front 24

Source and Afferent tract to VPI

Back 24

vestibular nuclei->VPI

Front 25

Source and Afferent tract to VPM^m

Back 25

pontine taste area->VPM^m

Front 26

Source and Afferent tract to primary olfactory cortex

Back 26

olfactory nerve (receptor cells in nose)->olfactory bulb->olfactory tract->primary olfactory cortex

Front 27

Association area pathway

Back 27

Primary sensory area->unimodal association area->multimodal association area

Front 28

What is CM?

Back 28

inside an internal medullary lamina, called an intralaminar nuclei; CM largest of these nuclei

Front 29

what are the internal medullary lamina?

Back 29

bundles of fibers running between thalamic nuclei

Front 30

Neuron innervation and muscle control?

Back 30

any muscle with fine control has more neurons innervating it at motor neuron level; to have voluntary control, need more descending pathways to it

Front 31

What is the ventral stream? And dorsal stream?

Back 31

Ventral- "what"
Dorsal- "where" and "how"

Front 32

Visual association pathway

Back 32

Brodmann area 21 (unimodal)->inferior parietal lobule (multimodal)

Front 33

auditory association pathway

Back 33

Brodmann area 22 (unimodal)->prefrontal cortex(multimodal)

Front 34

special sensory association pathway

Back 34

Brodmann area 7 (unimodal)->paralimbic system (multimodal)

Front 35

Function of infweioe parietal lobule

Back 35

cognitive functions
can have dysfunction of any higher functions with lesions here

Front 36

Function of prefrontal cortex

Back 36

personality (example of dyfunction: Phineas Gage)

Front 37

Function of paralimbic system

Back 37

emotional, motivational, memory

Front 38

What is a motor unit?

Back 38

one motor neuron (motoneuron) + all muscle fibers innervated by that motoneuron

Front 39

Ratio of motoneurons: muscle fibers of most muscles

Back 39

1 motoneuron: 150 muscle fibers

Front 40

Ratio of motoneurons: muscle fibers for large muscles

Back 40

1:1000 (like leg)

Front 41

Ratio of motoneurons: muscle fibers in small precise muscles

Back 41

1:2-3 (like larynx)

Front 42

Ratio of motoneurons: muscle fibers for very fine muscles

Back 42

1:3-6 (like eye muscles)

Front 43

How can we increase force of contraction of muscles?

Back 43

increase number of motor units active or increase frequency of activation of motor units

Front 44

control of motor elements in periphery which we need fine control over_?

Back 44

requires more of NS devoted to it

Front 45

Who came up with the idea of the "final common path" and what is it?

Back 45

Sherrington
final common path= all inputs funneled to a motor output (motoneurons of ventral horn of spinal cord and motoneurons of somatic motor cranial nerve nuclei)

Front 46

4 symptoms of an LMN lesion?

Back 46

1) areflexia
2) flaccid paralysis (no muscle tone)
3) atrophy
4) fibrillations (muscle fibers twitching spontaneously, seen on EMG, membrane extra-sensitive to AcH)

Front 47

most ventral medial motor neurons function?

Back 47

axial muscles (trunk)

Front 48

most lateral motor neuron function?

Back 48

limb muscles (only in enlargement areas- C5-T1, L4-S2)

Front 49

more lateral than axial muscle motor neurons?

Back 49

C5-C6 diaphragm muscles (phrenic nerve)and the S1-S2 pudendal nucleus (urinary and rectal sphincter)

Front 50

more medial than limb muscles?

Back 50

pelvic girdle muscles

Front 51

which is more dorsal- extensor or flexor muscles?

Back 51

flexor

Front 52

connection percentages?

Back 52

90% premotor interneurons
5% corticospinal tract
5% dorsal root ganglion cell axons for monosynaptic reflexes

Front 53

premotor interneurons on axial muscle motor neurons?

Back 53

may have collaterals to motor neurons on toher side so we can activate or inhibit muscles on both side of trunk
some can simultaneously be activating medial motor neurons above and below that segment so we can move trunk forward and backward

Front 54

where else can we have premotor interneurons?

Back 54

synapsing on most lateral ventral motor neurons (for limbs)

Front 55

what's the general rule about where pathways end either medially or laterally?

Back 55

medially-located interneurons often end controlaterally, while lateral pathways often end bilaterally (ipsilateral)

Front 56

What are the medial descending pathways?

Back 56

1) superior colliculus->tectospinal tract
2) vestibular nuclei->vestibulospingal tracts
3) pontine tegmentum->pontine-reticulospinal pathways
4) meduall->meduallary-reticulospinal pathway
5) corticospinal tract

Front 57

What are the laterally descending pathways?

Back 57

1) red nucleus->rubrospinal tract
2) primary motor cortex->corticospinal tract (90% laterally descending)

Front 58

What is the function of the tectospinal tract?

Back 58

visual reflexes of neck

Front 59

What is the function of the vestibulospinal tract?

Back 59

respond to movement and equilibrium when we move our head

Front 60

Where does the corticobulbar tract peel off to innervate other areas (like CN III)?

Back 60

at level of basis pedunculi

Front 61

What other pathways does the internal capsule consist of?

Back 61

corticobulbar and corticospinal tracts come through it

Front 62

cranial nerves and nuclei that corticobulbar tract innervate

Back 62

all contralateral unless indicated otherwise
III, IV, V (can be bilateral), VI, VII (upper face, bilateral), VII (lower face, contralateral), Ambiguus (IX, X; some bilateral), XI (contralateral in area that innervates trapezoid), XII

Front 63

What is usual the primary loss in stroke patients?

Back 63

at medulla level, combination of motor and sensory losses (usually corticospinal fibers, medial lemniscus, and maybe STT)

Front 64

What happened when monkey corticospinal tracts were transected bilaterally at the level of the pyramids?

Back 64

all movements normal except use of individual fingers; could no longer do pegboard trick

Front 65

What happened when only the medially descending pathways were transected bilaterally?

Back 65

postural changes of trunk and limbs, prolonged inability to right themselves, severe deficits in steering of axial and proximal limb musculature; could pick up something with whole hand

Front 66

What happened when only the laterally descending pathways were unilaterally transected?

Back 66

could right themselves, no postural changes, but had to move whole body to move arm

Front 67

What kind of damage usually results in UMN symptoms?

Back 67

stroke in internal capsule

Front 68

What are the immediate, but transient symptoms of UMN damage?

Back 68

1) flaccid paralysis on contralateral side
2) areflexia

Front 69

What are the longterm symptoms of UMN damage?

Back 69

1) hyperreflexia on contralateral side
2) spasticity (increased resistance to passive movement, effects flexor muscles in upper body and extensor muscles in lower body); results in clasp knife
3) Babinski sign (dorsal splaying of toes, seen in infants because not yet myelinated)
4)diminshed abdominal reflex
5) diminished Cremasteric reflex in males (retraction of testicles)

Front 70

Why are UMN damage symptoms more more dramatic than the results of the monkey experiments?

Back 70

1) more pathways in internal capsule (like corticotectal fibers, corticoreticular fibers, corticospinal and corticobulbar, corticorubral fibers
2) might have interrupted ascending pathways too

Front 71

What is damage in LMN symptoms?

Back 71

somatic motoneurons (the final common pathways)

Front 72

What structures are active when you do a movement as opposed to movements involving advanced thoughts?

Back 72

When you do a movement, motor cortex active.
When you have to plan for a movement, the basal ganglia and premotor cortex active.

Front 73

How does information flow to initiate a movement?

Back 73

cortex layers->basal ganglia->thalamus->premotor cortex

Front 74

What are the 3 loops within the basal ganglia?

Back 74

1) SNc pars compacta->striatum
2) external pallidum->subthalamic nucleus->internal pallidum
3) internal pallidum->intralaminar nuclei->striatum->cortex

Front 75

What is the direct pathway from the striatum to GPi/SNr and what cotransmitter is involved?

Back 75

The direct pathway involves D1 dopamine receptors from the SNc, the cotransmitter is substance P, goes directly with no intermediary

Front 76

What is the indirect pathway from the striatum to GPi/SNc and what is the cotransmitter involved?

Back 76

Striatum->GPE (inhibitory)->STN (inhibitory->GPi/SNr (excitatory)
- cotransmitter is enkephalins
- involves D2 dopamine receptors from the SNc

Front 77

What cells are involved in Parkinson's Disease?

Back 77

degeneration of dopamine cells in substantia nigra pars compacta

Front 78

symptoms of Parkinson's Disease?

Back 78

1) tremor at rest but not during movement
2) rigidity of muscles (Cogwheel- only give way partially to pressure)
3) akinesia- relative inability to move, problems with initiating movement, masked facial expressions (mimicked by decreasing substantia nigra dopamine cells)

Front 79

What kind of drugs are used to treat Parkinsons?

Back 79

- L-DOPA (crosses BBB, as opposed to dopamine, turns into dopamine in the brain) with carbidopa (inhibits uptake of L-DOPA in periphery)
- MAOI (inhibits MAO from making dopamine inactive) with L-DOPA, ex: Deprenyl

Front 80

What is the problem with drugs given to treat Parkinsons?

Back 80

over time you lose more cells and need more drugs to be effective, which causes more side effects

Front 81

What treatments besides drugs are there to treat Parkinsons?

Back 81

- surgery making lesion in one of these pathways
- deep stimulation by electrically stimulating and changing pattern of activity in nuclei
- transplanting piece of adrenal gland into brain, not clear it has longterm benefits
- transplant piece of SNc pars compacta into brai near striatum from aborted fetuses
- stem cell research making cells into dopamine

Front 82

What is the effect of losing connections with the SNc on the pathway involved in Parkinsons disease?

Back 82

decreases inhibition in direct pathway on the SNr/GPi and increases excitation in indirect pathway on SNr/GPi which results in increased inhibition on the thalamus and decreased excitation of the cortex which results in decreased excitation of the brain stem and spinal cord
i.e. volume control decrease

Front 83

What is the effect of losing D2 receptors in the striatum on the pathway involved in Huntington's disease?

Back 83

a decreasing effect of the indirect pathway resulting in decreased excitation of the GPi/SNR causing decreased inhibition of the thalamus and thus increase excitation of the cortex and increased excitation of the brain stem and spinal cord
i.e. volume control increase

Front 84

What are the symptoms of Huntington's disease?

Back 84

1) Choreaform movement- unwanted movement, abnormal, jerky
2) later dementia and personality changes (most commit suicide or die of this)

Front 85

How is Huntington's Disease transmitted?

Back 85

- genetic
- autosomal dominant gene (50/50 kids will get)

Front 86

What does the gene involved in Huntington's disease produce and what is the damage done to cause this?

Back 86

- gene produces Huntingtin
- triplets CAG gene repeats 34 times or more and codes for glutamine; more repeats you have earlier and more rapidly disease will progress
- may be transcription for neurotrophic factors and have loss of neurons for those that need these factors

Front 87

What cells are lost in Huntington's Disease?

Back 87

- neurons of striatum, especially those of the D2 receptors
- causes larger lateral ventricles because smaller caudate nucleus

Front 88

What is unusual about the amount of cells in the cerebellum?

Back 88

it makes up 10% of the volume of the brain, but 50% of the cells in the brain reside here

Front 89

How many lobules does the cerebellum have and how are they divided?

Back 89

- 10 lobules
- divided into anterior, posterior, and flocculonodular lobes

Front 90

What is the midline area of the cerebellum called?

Back 90

vermis (meaning "worm")

Front 91

What is the area surrounding the vermis of the cerebellum called?

Back 91

cerebellar hemispheres with intermediate and lateral zones

Front 92

What is the center of the flocculus called?

Back 92

nodulus

Front 93

What are other names for the 3 lobes of the cerebellum?

Back 93

1) anterior= spinocerebellar lobe
2) posterior= ponto-cerebellar lobe (from pontine cells)
3) flocculonodular lobe= vestibular lobe (from vestibular ganglion and nuclei)

Front 94

What does the cerebellum arise from?

Back 94

alar plate

Front 95

Where does the inferior olivary nucleus and pontine nucleus arise from?

Back 95

alar plate

Front 96

What are the 3 layers of the cerebellar cortex?

Back 96

1) Molecular layer
2) Purkinje cell layer
3) granular cell layer

Front 97

What kind of cells are in the molecular layer of the cerebellar cortex, are they inhibitory or excitatory, and where is the layer located?

Back 97

- most surface layer of cerebellum
- consists of stellate cells and basket cells, which both inhibit Purkinje cells

Front 98

What kind of cells are in the Purkinje cell layer of the cerebellar cortex, are they inhibitory or excitatory, and where is the layer located?

Back 98

- this layer is one cell thick, deep to the molecular layer
- consists of Purkinje cells
- their axons go down to synapse on deep white matter, inhibitory

Front 99

What kind of cells are in the granular layer of the cerebellar cortex, are they inhibitory or excitatory, and where is the layer located?

Back 99

- deepest layer
- large density of granule cells;they have parallel fibers which are excitatory when they sum on Purkinje cells
- Golgi cells here too, inhibit granule cells

Front 100

What are the mossy fibers and where do they go?

Back 100

-spinal, trigemino, pontine, and vestibular cells give rise to this afferent pathway into cerebellum
- collateral on deep white matter (excitatory) and synapse on granule cells (excitatory)

Front 101

What are the climbing fibers and where do they go?

Back 101

-spinal cord, cerebral cortex, vestibular nuclei->inferior olivary nucleus
- collateral on deep white matter cells (excitatory) and synapse/branch on Purkinje cells (excitatory)

Front 102

What is corollary discharge?

Back 102

of descending pathways, causes change in information in muscle spindle and input back is different, relayed through VL nucleus

Front 103

What kind of problems does one have with damage to the cerebellum?

Back 103

- coordination, balance, and equilibrium problems
- if damage to flocullonodular lobe or parts of vermis, have problems with unsteadiness and balance (ataxia of ait) and tend to fall towards side of lesion
- if have damage to cerebellar hemispheres, have problems with limb musculature (intention tremor- jerking to speed up/slow down; decomposition of movement, dysmetria- failing to meet target); problems with using flexor and extensor at same time, slurred speech, dysarthria (inability to articulate speech)