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abnormalities of muscle tone
flaccidity
none - low tone
common in stroke and SCI
no movment from MM
MMT grade of 0
tone
muscle resistance to passive stretch
current level of contractio
hypertonia
decrease tone
little resistance
need to be increase muscle
“beef them up”
addition of electrical stimulus
increased contrition to stabilize atrophy
normal
large range of “normal”
spasticity
rigidity
spasticity
abnormal increase in muscle tone or stiffness
interferes with movment and speech
cause discomfort or pain
caused by damage to nerve pathways in brain or SC that control muscle movment
broad definition that it is part of NS
imbalance of signals between CNS and muscles
presenting as intermittent or sustained involuntary activation of muscles
velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks
how it is measured
pathophysiology of spasticity
many theories and dicussion
supra spinal pathways
release of brain stem reflexes from cortical inhibition
overactivity of non-adrenergic pathways from locus coerulueus
overactivity of serotoninergic pathways from raphe nucleus
spinal cord
loss of recurrent inhibition, mediated my motor axon collaterals and Renshaw cells
loss of reciprocal inhibition, mediated by antagonistic muscle spindle afferents
inhibition of antagonist to remove tension
reduced inverse stretch reflex, mediated by GTO
reduced presynaptic inhibition of muscle spindle afferents
spinal motor neurone
denervation supersensitivty
collateral sprouting
muscles nad joints
shortening of sarcomeres
loss of elastic tissue
fibro-fatty deposits in muscles and tendons
byproduct of continual contraction of muscle
global withdrawal of inhibition of motor cortex
downstream effects
spasticity in Stroke
damage from M1 to corticospinal tract
activation of contralateral recticulospinal tract
over activation of motor neurons limiting control
mechanisms of increased muscle tone
enhanced sensisitiy of muscle spindles through activation of gamma efferent system
too much intrtafusal activation
causing increased chance of contraction
turn off allowing systems to come back allow for homeostasis
modulation of transmitter release at the synapse of the afferents with motoneuron through presynaptic inhibition
NT depletion at synapse of group 1a afferents with motoneuron
homosynaptic depression or post activation depression
assessment of spasticity
velocity dependent increase in tonic stretch reflexes with exaggerated tendon jerks, presenting as intermittent or sustained involuntary activation of muscles
MAS or Tardieu scale
MAS commonly used by doctors
does not involve quick movment when testing for spasticity
rehab preference ot use Tardieu scale
Modified Ashworth Scale (MAS)
performed by extending patients limb from max flexion to max extension
modified Ashworth scale is assessed while moving from extension to flexion
no increase in tone
slight increase in tone giving at “catch” when limb moved in flexion or extension
+ slight increase in muscle tone indicated by a catch followed by final resistance throughout range of motion
more marked icnrease in tone through most the ROM but limb is easily flexed
considerable icnrease in tone passivber movmement difficult
limb rigid flexion or extension
Tardieu scale
quality of muscle reaction
no resistance thought passive movment
slight resistance thoruoguht with no clear catch at precise angel
clear catch at precise angle followed by release
fatiguable clone (<10s) occurring at a precise angle
shakes and then moves onward
unfatiguable clonus (>10s) occurring at precise angel
joint immobile - cannot be moved
spasticity angle
angle of catch seems at velocity V2 or V3
full range off option achieved when muscle is at rest and tested at V1 velocity
velocity to stretch
as slow as possible
speed of the limb segment falling
with gravity
at fast rate
clasp-knife phenomenon
velocity-dependent build-up of reflex resistance
UMN lesion and GTO
Clonus
sustained reflex response triggered by tendon percussion
Spindle feedback
Exaggerated tendon jerk
asymmetric reflex response caused by abrupt mechanical disturbance
GTO
clinical signs of exaggerated cutaneous reflexes
flexor withdrawal reflex and extensor/flexor spasms
manifestations of severely damaged SC
nociceptor stimulus occurring within cutaneous spindle
Babinski response
toe extension elicited by stimulus on plantar surface of foot
indicating an UMN lesion
cutaneous reflex and UMN lesion
lead-pipe rigidity
sustained resistance to passive movement throughout the entire range of motion w/o fluctuations
caused by deficiency of signalling via D2 dopamine receptors in the brian
affects both agonist nad antagonist muscles resulting in increased muscle tone nad stiffness
cogwheel rigidity
jerky reisitnace ot passive moment resembling the movment of gears in a cogwheel
caused by low levels of dopamine acitvity in the brain
primarily affects the limbs, leading ot muscle stiffness
neurophysiology of rigidity
involves abnormalities in supra spinal drive nad interplay between UMN nad AMNs
excessive supra spinal drive from brain acts on AMNS resulting in increase muscle tone nad resistance ot movements
dopamine is crucial in modulating motor function and regulating muscle tone
reduction in dopamine disrupts the balance between inhibitor and excitatory pathways
leading to increased excitatory output form UMNs to AMNs and subsequent rigidity
abnormal porcessing of proprioceptive feedback and rigidity
proprioceptive feed ack from muscle spindles, GTO and joint receptors provides info about muscle neath, tension nada point position
rigidity involves distortion of proprioceptive signals
altered sensory processing leads to inappropriate and sustained muscle contractions
contributes to the resistance observed during passive movment
hypotonia
decrease muscle tone
characterized by reduced muscle tension and a “floppy” or “limp” feeling
different from muscle weakness
can result from damage to the brain, SC, nerves, or muscles
associated with various conditions
increased spasticity in incomplete SCI
compared to complete SCI
hippo therapy
horsetherapy
rhythmic movment of horse affects decreased spacticity
some lasting effect
hyporeflexia
decrease reflex response or diminished deep tendon reflexes
caused by damage to sensory, central or motor components of the reflex arc
commonly associated with lower motor neuron lesions
presents with flaccid paralysis, muscle paresis or paralysis, fibrillations, fasciculations, hypotonia nad hyporeflexia
contrasts with UMN lesions
spastic paralysis and hyperreflexia
areflexia
absence of neurologic reflexes
synonymous with hyporeflexia
indicates a lack of normal reflex repossess
associated with neurological disorders
eg. Guillain-Barré syndrome
immune triggered autoimmune disease
hemodialysis helps ot increase function