Abnormal Tone

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21 Terms

1
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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 

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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 

3
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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

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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

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spasticity in Stroke

  • damage from M1 to corticospinal tract

    • activation of contralateral recticulospinal tract

  • over activation of motor neurons limiting control

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mechanisms of increased muscle tone

  1. 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

  2. modulation of transmitter release at the synapse of the afferents with motoneuron through presynaptic inhibition

  3. NT depletion at synapse of group 1a afferents with motoneuron

    • homosynaptic depression or post activation depression

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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

8
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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

  1. no increase in tone

  2. slight increase in tone giving at “catch” when limb moved in flexion or extension

    1. + slight increase in muscle tone indicated by a catch followed by final resistance throughout range of motion

  3. more marked icnrease in tone through most the ROM but limb is easily flexed

  4. considerable icnrease in tone passivber movmement difficult

  5. limb rigid flexion or extension

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Tardieu scale

quality of muscle reaction

  1. no resistance thought passive movment

  2. slight resistance thoruoguht with no clear catch at precise angel

  3. clear catch at precise angle followed by release

  4. fatiguable clone (<10s) occurring at a precise angle

    • shakes and then moves onward

  5. unfatiguable clonus (>10s) occurring at precise angel

  6. joint immobile - cannot be moved

spasticity angle

  1. angle of catch seems at velocity V2 or V3

  2. full range off option achieved when muscle is at rest and tested at V1 velocity

velocity to stretch

  1. as slow as possible

  2. speed of the limb segment falling

    • with gravity 

  3. at fast rate 

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clasp-knife phenomenon

  • velocity-dependent build-up of reflex resistance 

    • UMN lesion and GTO

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Clonus

  • sustained reflex response triggered by tendon percussion 

    • Spindle feedback

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Exaggerated tendon jerk

  • asymmetric reflex response caused by abrupt mechanical disturbance 

    • GTO

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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

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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 

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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

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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 

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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

18
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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

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hippo therapy

  • horsetherapy

  • rhythmic movment of horse affects decreased spacticity 

    • some lasting effect 

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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

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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