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74 Cards in this Set

  • Front
  • Back
Motor Cortex location in frontal lobe
back end of frontal lobe
Precentral Gyrus

Premotor Cortex

Supplemental Motor Area
motor strip, primary motor cortex
PreMC-in front of precent. refines motor mvmt
SMA-top, medially- refines motor mvt
Raw Motor output

Precentral Gyrus (motor cortex)

Basal Ganglia and Cerebellum
what type of neruons are in the CST and motor cortex areas?
Upper Motor Neurons
where is the CST at the decussation of the pyramids?
CST winds up in the dorsal part of lat funiculus

goal=talk to alpha motor neuron
mouth- lateral
feet/legs- medial

Big Lips/Face/Hands-a lot dedicated to these parts
3 Homunculi
1. precentral gyrus
2. postcentral gyrus
3. Premotor Cortex
Brodman's Areas
dfft parts of cortex w/ dfft histological differences

3layered piece
cortex is primarily 6 layers

Hippocampus, more ancient
Layer 5
most important
contains Betz cells
main pyramidal cells, give rise to CST
Brodman Area 4
precentral gyrus (primary motor cortex-PMC). main motor output.

control individual mvmt of muscles
Force of Contraction and Timing of Contraction are dependent on?
relative to what is happening in the cortex

freq of firing of individual Betz Cells

M1 UMN from precent gyrus. neuron to muscle contraction has lag (ms)
Brodman Area 6
Pre Motor Cortex (PreMC)
refines motor mvmt, controls complex mvmt
Timing: PreMotor Neruon fires when?
before the M1 (main motor neuron)
Main outputs of PreMC (area 6)

what inputs INTO PreMC
1. Main=Area 4
2. some directly to ventral horn
3. some to reticulspinal path
-axial and prox musc

*Posterior Parietal Cortex
Fxn of Post Parietal Cortex
1. input into PreMC
2. fxn in Tone (Gamma MN)
3. goes to reticulospinal neurons
Supplemental Motor Area(SMA)
-location, brodman area
medial aspect of hemisphere
still brodman area 6
-just like PreMC
function of SMA (MII) neurons

anomaly of SMA
motor planning
precedes firing of PreMC
just thinking of moving will fire MII
what is the SMA in close prox to
the limbic lobe
Flow of Timing of motor firing
1. SMA (MII)
2. PreMN
3. MI
4. Contraction
Primary Motor Cortex neurons (PMC) receive input from

1. SMA (MII)
2. PreMC
3. Primary Sensory Areas
4. Post Parietal
5. Thalmus VA/VL
-also receives
6. Cerebellum
7. Basal Ganglia
in cortex
in ventral horn
LMN+all the muscle cells it innervates
EMG can detect

at rest
max act
diseases of LMN and UMN
recording needle in muscle itself


neve damaged or alpha motor neuron is dead

can have damage to both LMN/UMN
what happens when a muscle cell is denervated?
secrete substances that attract nearby intact nerve endings
other nerves can reconnect that muscle cell
if renervation doesnt happen, 2 things are possible....
1. fibrillations
2. fasiculations
muscle atrophy/shrinkage occurs
use EMG
NOT visible to naked eye
Partially denervated muscle
at rest, get fibrillations (positive sharp waves)
tic intermittent at rest
NOT visible
need EMG
sick/dieing motor neuron that is STILL connected to muscle...
muscle will be irritated-fires on its own

visible to naked eye
represent irritated/sick motor unit
do NOT need emg
seen in ALS or Polio before you see atrophy
when do i need an EMG?

when do i not need an EMG
to see fibrillations

to see fasiculations
Fasiculations of the Tongue
seen in ALS
skeletal hands
very weak
will become a serpintine tongue after wasting
no phys contact
rel Ach
what does the muscle tissue do to accomodate the NMJ?
microscopic indendations to inc surface area of receptors
what happens to jxnl folds in M.G.?
they flatten out
amt of Ach rec is decreased

autoimmune disease to Ach rec
Botulinum Toxin

large portion
small portion
clostridium botulinum

fools the buton into taking it in
protease that eats a docking protein
botulinum toxin

Type A
Type B
all small portions are protenacous

cut synaptobrevin(VAMP)
cut SNAP25
effects of botulinum toxin..
neuron cant rel Ach anymore
terminal does not fxn
grows rootlets to reattach
symptoms of LCST lesion
contralateral body weakness
lose fine motor control
lose contralateral lower face
lose contralateral tongue (CBT)

spare axial muscles(VCST)
Lesion to PreMC
slow jerky movements
difficult in visually guided tasks

*very rare*
what usually accompanies a preMC lesion?
a concurrent lesion to PMC
Lesion to SMA results in
losing your motor memory
What is perseverative behavior and what is it associated with?
repeating motor tasks over and over

assoc w/ lesions to SMA
Normal Pressure Hydrocephalus
pressure is abnormal during sleep
pressure bangs up against ventricles and hits lets/bladder
3 Ws of NPH
1. wacky- forgetful, not psychotic
2. wet- loss of bladder fxn
3. wobbly- more of an apraxic gate, espec when starting to walk
what do NPH patients appear to be like? exception....

whats another name for apraxic gate?
Parkinson's Patients

magnetic gate
treatment for NPH
put a shunt in to relieve night-time CSF pressure spikes

small window of opportunity
Lesion to Post Parietal Cortex(PPC)
rare to have motor complaints if just PPC. but usually with PMC
Hemi-neglect arm/leg
ususally nondominant hemi, so left hand neglected
Parietal Lobe controls what
3-Dimensional Space map
Premotor for eyes is called what?
Frontal Eye Fields (FEF)
infront of homunc for eyes
what does the FEF talk to?
to PPRF on opp side
PPRF talks to ipsiVI + contraIII
allows eyes to work laterally
what gets from PPRF to opposite CNIII?
MLF-medial long fasiculus
lesion in lft MLF->problems w/ left CNIII
look laterally, problem with medial rectus in lft eye, converge and everything is ok. what is this called?
Intranuclear opthlmolegia(IOP)
usual areas affected in MCA stroke
1. FEF
2. precentral gyrus
3. postcentral gyrus
is person is looking AWAY from paralyzed side, what does that mean?
they are looking toward damaged cortex
if damage is in pons w/ pyramidal fassicles affected, person is looking toward damaged side, why??
if lesion in Lft Pons, hitting Lft CST. rt side paralyzed

look to right b/c lft PPRF is damaged- lft lat rectus gone
and lft MLF is damaged- rt med rectus is gone--->therefore eyes look right
associated with damage right after pathways have left the cortex
Herniation-pushing brain down
decerebrate or decorticate
happens first. closer to cortex
motor lesion of IC or cortex
spastic hemiplegia
'looks like an O'
lesions b/w red nuc and vestib nuc
gamma rigidity
hyperpronation and extension
is the CST all motor?
40% Betz cells from Area 4
20% from Area 6
40% from PPC
*some sensory is in CST
CST path
post limb of IC
ducussates at pyramidal dec
80-90% crosses to lateral funiculus
10-20%stays Ipsi in ventral funiculus
down to ventral horn of SC
Corticobulbar Tract (CBT)
Area 4 and Area 6
pass thru Genu of IC
goes to all motor nuclei in brain stem
gets most bilaterally
lesion of CBT
lower face paralysis
sometimes contralat tongue
Corticorubral Tract

what is the main output of CRT?
Areas 4+6
UMN for Red Nuclei
-part of Mollaret's Triangle
Rubrospinal Tract
Rubrospinal Tract
crosses and goes to
1. torso
2. head
3. upper arm
facilitates upper limb flexor MN
where does the RubroST synapse
on interneurons in Rexed Laminae 5, 6, and 7
primarily of cervical cord

its a little VENTRAL to LCST in lateral funiculus
what pathway is cervical dystonia associated with?
person's head is twisted
Rubrospinal Tract
Corticoreticular pathway
Area 4+6
post limb of IC
synapse on pontine and medullary reticular fomrations Bilat
Reticulspinal Tract synapses where
Rexed Laminae 7, 8, 9

goes to torso, head, and forearm alphaMN
Primary involvement of Reticulospinal tract
gama tone and reflexes
preganglionic sympathetic neurons in CV regulation
-via talking to IMLCC
what is near the Reticulospinal tract in the SC
overlaps with Spinothalamic Tract
pain illicits racing heart rate and inc BP
which pathways have direct control over movement?
Corticospinal (CST)
Corticobulbar (CBT)
which paths modulate motor performance via neural loops involv cerebellum and BG

relay paths