Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

103 Cards in this Set

  • Front
  • Back
LGN Cortical Target & Brodmann number
Primary Visual Cortex (17)
MGN Cortical Target & Brodmann number
Primary Auditory Cortex (41, 42)
VPL Cortical Target & Brodmann number
Primary Somatosensory Cortex (3,1,2), D, M
VPM Cortical Target & Brodmann number
Primary Somatosensory Cortex (3,1,2) V, L
VL Cortical Target & Brodmann number
Primary Motor Cortex (4)
VA Cortical Target & Brodmann number
Premotor Cortex (6)
Intralaminar Nuclei Cortical Target & Brodmann number
Diffusely to cortex, heavily to striatum
Pulvinar and LP Cortical Target & Brodmann number
association cortices of parietal, temporal, and occipital lobes
Medial Dorsal Nucleus Cortical Target & Brodmann number
Association cortices of frontal lobe (prefrontal cortex)
LD/A Cortical Target & Brodmann number
Cingulate Cortex
VPI (Ventral Posterior Inferior nucleus) Cortical Target & Brodmann number
primary vestibular cortex (2)
VPM^m Cortical Target & Brodmann number
Primary gustatory cortex (43)
cortical target of the one that has no input from thalamus
primary olfactory cortex, not in neocortex
Source and Afferent tract to LGN
Retina ganglia-> optic tract/optic chiasm
Source and Afferent tract to MGN
inferior colliculus->brachium of inferior colliculus
Source and Afferent tract to VPL
1)Dorsal horn->STT->VPL

2) Dorsal column->medial lemniscal->VPL
Source and Afferent tract to VPM
Descending nucleus of V, Main sensory nucleus of V->trigeminothalamic nucleus->VPM
Source and Afferent tract to VL
Deep cerebellar nuclei->brachium conjunctiva->VL
Source and Afferent tract to VA
globus pallidus, substantia nigra pars reticulata->thalamic fasciculus->VA
Source and Afferent tract to intralaminar nuclei
1)dorsal horn->STT->

2) globus pallidus/SNc reticulata->thalamic fasciculus->
Source and Afferent tract to Pulvinar and LP
1)Retina ganglia->optic tract->

2) Superior colliculus->tecto-thalamic tract->
Source and Afferent tract to medial dorsal nucleus
amygdaka, hypothalamus, other thalamic nuclei->medial dorsal nucleus
Source and Afferent tract to LD/A
mammillary nucleus of hypothalamus->mammillothalamic tract->LD/A
Source and Afferent tract to VPI
vestibular nuclei->VPI
Source and Afferent tract to VPM^m
pontine taste area->VPM^m
Source and Afferent tract to primary olfactory cortex
olfactory nerve (receptor cells in nose)->olfactory bulb->olfactory tract->primary olfactory cortex
Association area pathway
Primary sensory area->unimodal association area->multimodal association area
What is CM?
inside an internal medullary lamina, called an intralaminar nuclei; CM largest of these nuclei
what are the internal medullary lamina?
bundles of fibers running between thalamic nuclei
Neuron innervation and muscle control?
any muscle with fine control has more neurons innervating it at motor neuron level; to have voluntary control, need more descending pathways to it
What is the ventral stream? And dorsal stream?
Ventral- "what"
Dorsal- "where" and "how"
Visual association pathway
Brodmann area 21 (unimodal)->inferior parietal lobule (multimodal)
auditory association pathway
Brodmann area 22 (unimodal)->prefrontal cortex(multimodal)
special sensory association pathway
Brodmann area 7 (unimodal)->paralimbic system (multimodal)
Function of infweioe parietal lobule
cognitive functions
can have dysfunction of any higher functions with lesions here
Function of prefrontal cortex
personality (example of dyfunction: Phineas Gage)
Function of paralimbic system
emotional, motivational, memory
What is a motor unit?
one motor neuron (motoneuron) + all muscle fibers innervated by that motoneuron
Ratio of motoneurons: muscle fibers of most muscles
1 motoneuron: 150 muscle fibers
Ratio of motoneurons: muscle fibers for large muscles
1:1000 (like leg)
Ratio of motoneurons: muscle fibers in small precise muscles
1:2-3 (like larynx)
Ratio of motoneurons: muscle fibers for very fine muscles
1:3-6 (like eye muscles)
How can we increase force of contraction of muscles?
increase number of motor units active or increase frequency of activation of motor units
control of motor elements in periphery which we need fine control over_?
requires more of NS devoted to it
Who came up with the idea of the "final common path" and what is it?
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)
4 symptoms of an LMN lesion?
1) areflexia
2) flaccid paralysis (no muscle tone)
3) atrophy
4) fibrillations (muscle fibers twitching spontaneously, seen on EMG, membrane extra-sensitive to AcH)
most ventral medial motor neurons function?
axial muscles (trunk)
most lateral motor neuron function?
limb muscles (only in enlargement areas- C5-T1, L4-S2)
more lateral than axial muscle motor neurons?
C5-C6 diaphragm muscles (phrenic nerve)and the S1-S2 pudendal nucleus (urinary and rectal sphincter)
more medial than limb muscles?
pelvic girdle muscles
which is more dorsal- extensor or flexor muscles?
connection percentages?
90% premotor interneurons
5% corticospinal tract
5% dorsal root ganglion cell axons for monosynaptic reflexes
premotor interneurons on axial muscle motor neurons?
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
where else can we have premotor interneurons?
synapsing on most lateral ventral motor neurons (for limbs)
what's the general rule about where pathways end either medially or laterally?
medially-located interneurons often end controlaterally, while lateral pathways often end bilaterally (ipsilateral)
What are the medial descending pathways?
1) superior colliculus->tectospinal tract
2) vestibular nuclei->vestibulospingal tracts
3) pontine tegmentum->pontine-reticulospinal pathways
4) meduall->meduallary-reticulospinal pathway
5) corticospinal tract
What are the laterally descending pathways?
1) red nucleus->rubrospinal tract
2) primary motor cortex->corticospinal tract (90% laterally descending)
What is the function of the tectospinal tract?
visual reflexes of neck
What is the function of the vestibulospinal tract?
respond to movement and equilibrium when we move our head
Where does the corticobulbar tract peel off to innervate other areas (like CN III)?
at level of basis pedunculi
What other pathways does the internal capsule consist of?
corticobulbar and corticospinal tracts come through it
cranial nerves and nuclei that corticobulbar tract innervate
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
What is usual the primary loss in stroke patients?
at medulla level, combination of motor and sensory losses (usually corticospinal fibers, medial lemniscus, and maybe STT)
What happened when monkey corticospinal tracts were transected bilaterally at the level of the pyramids?
all movements normal except use of individual fingers; could no longer do pegboard trick
What happened when only the medially descending pathways were transected bilaterally?
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
What happened when only the laterally descending pathways were unilaterally transected?
could right themselves, no postural changes, but had to move whole body to move arm
What kind of damage usually results in UMN symptoms?
stroke in internal capsule
What are the immediate, but transient symptoms of UMN damage?
1) flaccid paralysis on contralateral side
2) areflexia
What are the longterm symptoms of UMN damage?
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)
Why are UMN damage symptoms more more dramatic than the results of the monkey experiments?
1) more pathways in internal capsule (like corticotectal fibers, corticoreticular fibers, corticospinal and corticobulbar, corticorubral fibers
2) might have interrupted ascending pathways too
What is damage in LMN symptoms?
somatic motoneurons (the final common pathways)
What structures are active when you do a movement as opposed to movements involving advanced thoughts?
When you do a movement, motor cortex active.
When you have to plan for a movement, the basal ganglia and premotor cortex active.
How does information flow to initiate a movement?
cortex layers->basal ganglia->thalamus->premotor cortex
What are the 3 loops within the basal ganglia?
1) SNc pars compacta->striatum
2) external pallidum->subthalamic nucleus->internal pallidum
3) internal pallidum->intralaminar nuclei->striatum->cortex
What is the direct pathway from the striatum to GPi/SNr and what cotransmitter is involved?
The direct pathway involves D1 dopamine receptors from the SNc, the cotransmitter is substance P, goes directly with no intermediary
What is the indirect pathway from the striatum to GPi/SNc and what is the cotransmitter involved?
Striatum->GPE (inhibitory)->STN (inhibitory->GPi/SNr (excitatory)
- cotransmitter is enkephalins
- involves D2 dopamine receptors from the SNc
What cells are involved in Parkinson's Disease?
degeneration of dopamine cells in substantia nigra pars compacta
symptoms of Parkinson's Disease?
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)
What kind of drugs are used to treat Parkinsons?
- 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
What is the problem with drugs given to treat Parkinsons?
over time you lose more cells and need more drugs to be effective, which causes more side effects
What treatments besides drugs are there to treat Parkinsons?
- 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
What is the effect of losing connections with the SNc on the pathway involved in Parkinsons disease?
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
What is the effect of losing D2 receptors in the striatum on the pathway involved in Huntington's disease?
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
What are the symptoms of Huntington's disease?
1) Choreaform movement- unwanted movement, abnormal, jerky
2) later dementia and personality changes (most commit suicide or die of this)
How is Huntington's Disease transmitted?
- genetic
- autosomal dominant gene (50/50 kids will get)
What does the gene involved in Huntington's disease produce and what is the damage done to cause this?
- 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
What cells are lost in Huntington's Disease?
- neurons of striatum, especially those of the D2 receptors
- causes larger lateral ventricles because smaller caudate nucleus
What is unusual about the amount of cells in the cerebellum?
it makes up 10% of the volume of the brain, but 50% of the cells in the brain reside here
How many lobules does the cerebellum have and how are they divided?
- 10 lobules
- divided into anterior, posterior, and flocculonodular lobes
What is the midline area of the cerebellum called?
vermis (meaning "worm")
What is the area surrounding the vermis of the cerebellum called?
cerebellar hemispheres with intermediate and lateral zones
What is the center of the flocculus called?
What are other names for the 3 lobes of the cerebellum?
1) anterior= spinocerebellar lobe
2) posterior= ponto-cerebellar lobe (from pontine cells)
3) flocculonodular lobe= vestibular lobe (from vestibular ganglion and nuclei)
What does the cerebellum arise from?
alar plate
Where does the inferior olivary nucleus and pontine nucleus arise from?
alar plate
What are the 3 layers of the cerebellar cortex?
1) Molecular layer
2) Purkinje cell layer
3) granular cell layer
What kind of cells are in the molecular layer of the cerebellar cortex, are they inhibitory or excitatory, and where is the layer located?
- most surface layer of cerebellum
- consists of stellate cells and basket cells, which both inhibit Purkinje cells
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?
- 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
What kind of cells are in the granular layer of the cerebellar cortex, are they inhibitory or excitatory, and where is the layer located?
- 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
What are the mossy fibers and where do they go?
-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)
What are the climbing fibers and where do they go?
-spinal cord, cerebral cortex, vestibular nuclei->inferior olivary nucleus
- collateral on deep white matter cells (excitatory) and synapse/branch on Purkinje cells (excitatory)
What is corollary discharge?
of descending pathways, causes change in information in muscle spindle and input back is different, relayed through VL nucleus
What kind of problems does one have with damage to the cerebellum?
- 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)