exam 1: UMN and LMN issue Flashcards
MD characterized by too little movement
paralysis
hypertonia
bradykinesia
what us paralysis
weakness
what are the two types of paralysis
UMN para
LMN para
both present very differently
what is UMN lesion characterized by - anatomy wise
lesion found in the descending motor tracts
cerebral cortex
BS
internal capsule
SC
but do not forget that the indirect pathways
UMN lesions that lead to paralysis
stroke
ALS
MS
traumatic brain injury
CP
SCI
UMN issues is characterized by
hypertonia - spasticity
hyper-reflexia
UMN muscle weakness
decrease in motor coordination
selective distribution of muscle weakness is often seen with what kind of issue
UMN lesion
UE selective distribution
abductor, external rotators and extensor are primarily effected
LE selective distribution
flexors (knee), internal rotators and DF
how soon do we see the effects of UMN issue
days to weeks
syneries
the CNS organizes movement patterns of functionally linked muscles to produce an intended action
Abnormal movement control is often observed as what
lack of isolated voluntary movement - moves with poor motor control
abnormal synergy movement patterns
The inability to isolate movement of a joint
How do we examine if someone has an abnormal movement synergy?
We ask them to voluntarily perform a movement or skill and analysis the movement that we observed. – this is movement analysis.
how do you treat abnormal synergy
Repetitive task practice, also if there is secondary soft tissue complications I address those impairments also.
do we see atrophy when we have spasticity
little to no
what is a positive babinki
toes flare up
LMN paralysis - is casued by
lesion of the nerve fibers travels fron the ventral horn of the SC
or
the cranial nerve motor nuclei to the relevant muscle
what is the main characteristic that we use to ID LMN issue
flaccid paralysis
signs of LMN issue
para is limited to segmental or focal pattern (root innervated pattern)
decrease muscle tone
hypo-reflexia
the present of fasculation or fibrillation
what is the muscle atrophy seen with LMN issue due to
loss of trophic influences of the cell body (AHC) on the muscle
fasciulation present as
muscle twitches
small groups of muscle fibers
does not denote patho
fibrillations present as
involuntary, unsynchronized patho contraction of muscle fibers
seen with EMG
example of patho the result from LMN lesion
ALS
guille barre syndrome
poliomyelitis
cauda equina syndrome
what is ALS
degeneration and scarring of motor neurons in the lateral aspect of the SCC, BS, and CC
neurodegenerative disease the combines LMN and UMN issues
what does ALS present with
peri nerve changes that leads to muscle atrophy or amytrophy
progressive motor dysfunction without sensory issues
cognitive impairments and ALS
frontotemporal lobar degeneration
what does hypertonia mean
to much tone
two types of hypertonia
spasticity
rigidity
spasticity is resistance to what kind of movements
passive
velo dependent
spasticity is secondary to what
UMN issue
patho of spasticity
increase afferent input to AMN - increasing stretch excitation
what causes the stretch reflex to fire
with any quick movement of the limb
how do you treat spasticity
cutting the peri nerve
inject the nerve with phenol
pharma interventions - baclofen, Bo-tox
stretching
positioning and splitting
motor re-education with task specific stregthing
what is rigidity due to
excess supraspinal drive acting on the AMN
characteristic of rigidity
spinal relfexes are typically normal
not velo dependent
involves agonist and ant
lead pipe rig
constant hypertonia felt throughout the ROM with passive movement
cog wheel rig
jerk responses of the muscle when force is applied to bend the limb
PD is due to what
death of cells in the midbrain (substantia nigra)- these convert AA to dope - which is the release to the striatum of the extrapyramidal motor system
treatment of rig
add component that involve twisting and reaching
act that require large rhythmic movement to go through ROM
what is bradykinesia
move slow
bradykinesia is due to a issue where
extrapyramidal region
brady is associated with what patho
parkinsons
what are example of too much movement
tremor
fasciulation
fibrillations
chorea
hemiballisum
tremor
type of shaking movement
what is a resting tremor
present when the muscle is resting
may go away when the muscle is activated
a tremor is a key sign of what disease
PD
intentional (action) tremor
oscillation that are exaggerated at the end of voluntary movements
the tremor will often go away with rest of effected muscles
what is action tremors seen with
cere issues
physiological tremor
normal - reflects the error of the system
fascuialtion are caused by what
anterior horn cell and motor unit firing without a command
chorea
movements and rapid and involuntary
non-sterotypical
semi/non purposeful
dance like
more distally involved
hemiballisum is a result of what
stroke of the subthalamic nucleus
how does hemi present like
rapid involuntary movements
non-purposeful
violet fling movement
more proximal involvement
ataxia
uncoordinated movement
hard time regulating forces, range and direction, and timing of movement
motor axtia
intergration of motor commands there is a dysfunction
sensory ataxia
sensory pathway are disrupted therefore there is not proprioceptive awareness
The role of the primary motor cortex
is to initiate and execute voluntary muscle movement
location of the primary motor cortex
precentral gyrus
where is the prefrontal cortex located
anterior frontal lobe
what is the prefrontal cortex involved in
memory, behavior, executive functions
subthalmic nucleus is part of what
the BG circuit
what is the role of the subthalamic nucleus
suppression of unwanted movement
