01 JULY 2019 Flashcards
end of chapter 13 all of ch. 14
function of nonspecified motor tracts:
low degree of voluntary control:
job: to lower threshold for UMN so can more quickly established an AP
primary motor cortex comes from
precentral gyrus in….. frontal lobe
corticobrainstem tract:
controls CNs and face throat neck
**high degree of voluntary control since from cortex
the primary motor cortex has a
motor homonulus : which is like a sensory homonulus
what are 3 broad conditions of UMN
- UMN completely cut off from LMN
- UMN intact but tonically overactive
- cortical damaged but brainstem UMN ok
when the UMN is cut off from the LMN it is a
complete spinal cord injury
when UMN is intact but tonically overactive it is an example of
Parkinson’s
when the cortical is damaged but the brainstem is ok that is an example of
stroke:
paralysis in the MT (UMN) is different because:
everything below it is “cut off” you can not get any sensory or motor sensation to contract M
paresis in the MT (UMN) is different because:
the brain stem is still functioning but the cortex is not so you can still “think to move”
neural degeneration could mean
Parkinson’s dx
glial degeneration could mean
multiple sclerosis
the premotor area is where you
plan anticipatory postural control movements
supplementary motor area is where you
- plan bi manual movements
2. plan / execute activities w/ sequence
an example of a fx task from supplementary motor area is
playing a sequence on the piano
example of fx task from the premotor area
why you don’t fall over when you walk and trip
name the two cortical motor areas:
- premotor area
2. supplementary motor area
decerebrate is
tonic extensors of arms and legs:
decorticate is
tonically overactive flexors in arms and legs
which is worse? decerebrate or decorticate
decerebrate
muscle overactivity three things:
- reduction of cortical control
- activity dependent which means Mm is overused
- may contribute to abnormal syngeries
activity dependent means:
occurs depending on activity
may be spastic when walking but not when sitting
overall muscle overactivity / overuse leads to
reduction of cortical control
when there is a reduction of cortical control
there is reduced fine motor movements only gross
because brainstem is making money moves
decerebrate cuts off the
head
decorticate cuts off the
cortex
which is more common? decerebrate or decorticate
decorticate
rigidity comes from
UMN overactivity
temporary hyptonia is
spinal shock
nerves get scared and go to sleep = no longer function
when motor neurons go into shock there is no
NO movement or reflex loop
when there is hyptonia there is
abnormal activity but UMN is still present
rigidity is when
your muscles have too much tone
hypertonia is
the muscle stretch is hyperreflexic / velocity dependent
= spasticity
= TOO MUCH CONTRACTION
spasticity refers to
the muscle stretch is hyper reflexic
difference in cerebral shock from spinal shock
spinal shock happens in spinal cord: neurons go to sleep
cerebral shock happen in the cerebrum much more severe ie from a stroke
hemiplegia
paraplegia
tetra plegia
hemi = half of body left/ right para = upper and lower tetra = all four
loss of “fractionated movement means that
you do not have full voluntary control of moving no more fractionated
abnormal cutaneous reflexes include
- babinski reflex
2. limb withdrawal
abnormal cutaneous reflexes means that
when UMN is cut at the spinal level the below part gets stronger
a UMN tells the LMN to relax when no UMN there is NO CHILL so contract a shit ton
babinski reflex means that
the UMN is cut off which makes LMN threshold lower = touch receptors can signal pain much easier so you don’t need a painful stimulus
muscle stretch hyperrelfexic
exaggerated reflex response to stretch when descending connection is missing or much reduced
clonus is
velocity dependent hypotonia that is repeated in response to a quick stretch
what are two types of clonus
- unsustained
2. sustained
unstained clonus means that
it repeats for a little bit then dies out
sustained clonus means that
the repetition keeps repeating
clasp-knife syndrome is when
initially strong resistance to stretch fades with a sustained stretch : like a pocket knife blade sliding back in
myoplasticity occurs because
there are plastic changes to a muscle because is is not moving
myoplasticity means there are
adaptive changes within a muscle itself
myoplasticity is an example of what type of atrophy:
disuse because loss of neuromusclar excitation not that they aren’t there
if you have a motor tract injury its atrophy of
disuse
if you have a motor neuron injury its atrophy of
denervation
increased stiffness in myoplasticity is due to
weak actin and myosin not “sticking” due to lack of movement when you don’t slide normally
therapeutic response is to “break up” = passive movement
what is the therapeutic response to increased stiffness in myoplasticity
passive movement = need to “break up” “sticky” actin and myosin heads over connecting
a contracture in myoplasticity is due to
loss of sarcomeres due to prolonged positioning
muscle won’t go because not able to bind
what is the therapeutic response to contracture in myoplasticity
move through passive ROM
