Exam 1 Lecture 2 Pathophysiology of Tone part 2: Tone to end Flashcards

1
Q

What is tone?

A

•Muscle tone is the resting level of tension in a muscle in response to passive stretch

  • –Allows a muscle to make an optimal response to voluntary/reflexive commands
  • –Reflects balance of excitatory and inhibitory influences
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2
Q

How does damage to the CNS effect tone?

A

•Damage to central nervous system often results in an alteration in regulation of muscle tone

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3
Q

Hypotonia

What is it

Infants

Other symptoms

PT managment

A

–Decrease in resistance to passive limb manipulation

–Flaccid

  • •Infants have a floppy quality or “rag doll” appearance
    • –Arms and legs hang by sides
    • –Little or no head control
  • •Other symptoms include
    • –Difficulty with mobility, posture, breathing and speech, lethargy, ligament and joint laxity, and poor reflexes
  • •PT Management
    • –Developmental positions, strengthening, sensory stimulation, positioning and bracing, weight bearing
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4
Q

Hypotonia vs muscle weakness

A

Hypotonia is Not the same as muscle weakness

  • –True muscle tone is the ability of a muscle to respond to a stretch
    • •Low tone results in a slow ability to initiate a muscle contraction and an inability to maintain the contraction
  • –True muscle weakness is characterized by the force exerted by a muscle is less than expected
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5
Q

Hypotonia: causs

A

•Many causes though the underlying cause is often difficult to determine

  • –Trauma, environmental factors, or by genetic, muscle, or central nervous system disorders
    • •Down syndrome, muscular dystrophy, cerebral palsy etc
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6
Q

Hypotonia: development as an adult

A

Development as an adult may be associated with

  • –Cerebellar degeneration (such as multiple sclerosis, Friedreich’s ataxia, or multiple system atrophy)
    • •Neurons that control muscle coordination and balance, deteriorate and die
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7
Q

Is hypotonia or hypertonia more common?

A

Hypertonia is more common

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8
Q

Hypertonia

A

More common than hypotonia
–Increase in resistance to passive limb manipulation
–Damage to UMN and or descending pathways making afferent pathways more responsive
–Can be spastic (spacticity) or rigid (rigidity)

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9
Q

Pathological spread of reflexes

A
  • Sign of hyperactivity
  • Contraction of muscles that have different actions while eliciting a reflex
  • Contraction of thigh adductors while testing patellar reflex
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10
Q

What is spacticity?

A

Velocity dependent increase in resistance to a passive stretch

  • –Classified as a symptom of UMN syndromes
  • Can include
    • –Spastic paresis—spasticity combined with muscle weakness, often in someone with an incomplete SCI
    • –Spastic paralysis—absence of voluntary muscle control in someone with spasticity
  • Can result in secondary impairments in muscles and other tissues
    • Stiffness, contracture of muscle, tendon, joint
      • Spastic muscles seem to undergo intrinsic structural changes which explains why more tension is usually developed with spasticity over time when stretched relative to non spastic muscles
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11
Q

What is spastic paresis?

A

Spastic paresis—spasticity combined with muscle weakness, often in someone with an incomplete SCI

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12
Q

What is spastic paralysis?

A

Spastic paralysis—absence of voluntary muscle control in someone with spasticity

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13
Q

What are two things that clinicians recognize the same spasticity in?

A

–Clinicians also recognize that the same spasticity is triggered by the light touch or hair tug or a hitting a bump in a wheelchair

(I’m not sure what “also” is referring to here)

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14
Q

Clonus

A

hyperactive stretch reflex

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15
Q

Characteristics of spasticity following cerebral lesions

A

–Damage to corticobulbar fibers
–Decrease excitation of descending inhibitory pathways
–Extensors of LE & flexors of UE
–Easier to pharmacologically control

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16
Q

Characteristics of spasticity following spinal cord lesions

A

–Damage to all descending activity
–Flexor & extensor involvement
–More resistant to pharmacologic control

Must use different techniques than what we would use if it was a brain injury (for example, to break clonus)

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17
Q

Synergy Patterns of Extremities: Flexion

A

–Upper extremity

  • •Scapular retraction/elevation or hyperextension, shoulder abduction, external rotation, elbow flexion, forearm supination, wrist and finger flexion
  • Looks like primitive reflex

–Lower extremity

  • •Hip flexion, abduction, and external rotation, knee flexion, ankle dorsiflexion, inversion, and toe dorsiflexion
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18
Q

Synergy Patterns of Extremities: Extension

A

–Upper extremity

  • •Scapular protraction, shoulder adduction, internal rotation, elbow extension, forearm pronation, wrist and finger flexion

–Lower extremity

  • •Hip extension, adduction, and internal rotation, knee extension, ankle plantarflexion, inversion, and toe plantarflexion
19
Q

what are Synergy Patterns of Extremities?

A

A consistant pattern of spacticity that can be documented in one term (usually indicate UE, LE, or both)

Sometimes good

Sometimes bad

20
Q

Negative outcomes of Spacticity: (7)

A
  1. –Interference with mobility, transfers, ROM, and ADLs
  2. –May lead to heterotopic ossification- bone forms where should have a muscle
  3. –May cause pain and discomfort, possibly to the point of sleep disturbance
  4. –May lead to contractures or dislocations
  5. –Increase risk of skin breakdown
  6. –Bowel and bladder dysfunction
  7. –Decreased pulmonary function
21
Q

Positive outcomes of Spacticity: (6)

A
  1. –Maintain muscle tone
  2. –Help support circulatory functions
  3. –Assist with mobility, transfers and ADLs
  4. –Reduced osteopenia
  5. –Prevent formation/decrease risk of DVT
  6. –Sudden increase in spasticity can alert patient to other medical problems such as bladder infections, skin breakdown, or fever
22
Q

Things about Ashworth and Modified Ashworth Tests (11)

A
  1. –Clinical gold standard tests for spasticity
  2. –Evaluate muscle tone and stretch reflexes elicited by movement
  3. –Assess all joints in available ROM in same position for all joints
  4. –Perform movement opposite to muscle being tested
  5. –Compare both sides
  6. –Spasticity should be assessed during one quick movement and should not be repeated as this may loosen the muscle
  7. –Always use the highest measure
  8. –Do not perform long passive stretch or perform movement gently
  9. –Measure passive ROM as part of assessment
  10. –Additional grade was added (1+) for the Modified Ashworth to enhance sensitivity and accommodate hemiplegic patients who typically graded at the lower end of the scale
  11. –Does not address frequency or severity of spasms or influence on daily activities
23
Q

Contensts of the Ashworth Scale

A

Ashworth Scale

  • 0 -No increase in muscle tone
  • 1 -Slight increase in muscle tone, with the limb “catching” when it is flexed or extended
  • 2 –More marked increase in tone, but limb easily flexed
  • 3 –Considerable increase in tone; passive movement difficult
  • 4 –Limb rigid in flexion and extension
24
Q

Contents of Modified Ashworth Scale

A

Modified Ashworth Scale

  • 0 -No increase in muscle tone
  • 1 -Slight increase in muscle tone, manifested by a catch and release or by minimal resistance at the end of the range of motion when the affected limb) is moved in flexion or extension
  • 1+ -Slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remainder (less than half) of the ROM
  • 2 -More marked increase in muscle tone through most of the ROM, but affected limb) easily moved
  • 3 -Considerable increase in muscle tone, passive movement difficult
  • 4 -Affected limb) rigid in flexion or extension
25
Q

•Wartenberg Pendulum Test

A

For Spacticity: Can use test to help determine if interventions ore working well or not.

–Assesses responsiveness of knee extensor muscles to rapid, gravity assisted stretch

  • •Person is supine on table with knee and lower leg hanging over the edge
  • •Examiner grasps the heel of one foot, extends the knee, releases the heel and allows the lower leg to swing
  • •Joint angle during first swing of highest degree of knee flexion is measured
26
Q

Modified Terdieu Scale

A
  • •Tests for spasticity; commonly used in pediatrics
  • •R1 is first catch
    • –Resistance to maximal velocity stretch
  • •R2 is end of PROM
    • –Amount of muscle contracture/available length
  • •What is ideal? The closer together they are the less spasticity there is - closer to end range
  • •What is functional? The R1

Different than ashworth because it is for pediactrics

We want resistance to be as close to end range as possible (because we can just teach them to use the range before it catches)

Things before R1 is the functional range.

27
Q

Spinal Cord Assessment Tool for Spastic Reflexes (SCATS)

A

Spinal Cord Assessment Tool for Spastic Reflexes (SCATS)

  • Tests ankle clonus and flexor/extensor spasms in the lower extremities
  • Ankle Clonus—rapid, passive dorsiflexion
    • •0—no reaction;
    • •1—mild, <3sec;
    • •2—moderate 3-10 sec;
    • •3—severe >10 sec
  • Flexor Spasm—pinprick of 1 sec to medial arch of foot
    • •0—no reaction;
    • •1—mild, <10 deg gr toe ext OR <10 deg hip/knee flexion;
    • •2—moderate 10-30 deg hip/knee flexion;
    • •3—severe, >30 deg knee/hip flexion
  • Extensor Spasm—passive extension of knee and hip simultaneously
    • •0—no reaction;
    • •1—mild, <3sec;
    • •2—moderate 3-10 sec;
    • •3—severe >10 sec
  • All tested supine
28
Q

Spacticity: Medications for treatment

A

•Baclofen

  • –GABA agonist (gamma-Aminobutyric acid receptor)
  • –Oral, Intrathecal Pumps

•Benzodiazepines

  • –increase in GABA receptor affinity
  • –Limited use because of sedation
    • •Xanax, Paxal, Temazepam (Restoril)

•Dantrolene sodium (Dantrium®)

  • –Acts at muscle relaxant
  • –Generalized weakness

•Gabapentin (Neurontin®)

  • –Use limited by sedation•

Botulinum toxin type A

  • –One of the most effective in spasticity of cerebral or spinal origin
29
Q

Intrathecal Baclofen pump

A

Can insert pump directly into the spinal cord.

Can create a direct entry for bacteria into the spinal cord.

Want the tube running in to intrathecal? Area

Important to know where the pump is if the patient has it so we don’t disrupt it

30
Q

Spacticity: PT Managment

A

–Education regarding noxious stimuli, positioning, skin etc
–Positioning
–ROM and stretching and exercise program- maintain muscle length
–Motor control, weightbearing
–Standing frame- can get prolonged stretches
–Splinting/serial casting depending on joint and severity

Also:
–Muscle lengthening - agonist
–Muscle strengthening – antagonist
•Loss of strength for weeks to months
–Positioning
–Gait training
–Motor learning - constraint induced forced use

31
Q

Spacticity: Surgical Techniques

A

–Dorsal rhizotomy
–Tendon release

32
Q

•Dorsal Rhizotomy

A

A surgical technique for spacticity

–Some of dorsal roots are cut (to stop reflex arc)
–Nerve roots are stimulated via EMG to determine the nerve roots causing the spasticity
–Also can relieve assoc pain (may be done just for pain or skin irritation - like if clonus is causing rubbing)
–Paralysis of legs, bladder, and skin possible
–Strict eligibility requirements
–Most common in children with CP

33
Q

What is Rigidity?

A
  • Rigidity—an increase in muscle tone that causes resistance to passive movement throughout the whole range of motion, independent of velocity
  • Types of Rigidity
  • –Lead-pipe
  • –Cogwheel
  • –Claspknife
34
Q

What disease is rigidity associated with?

A

Parkinson’s Disease

35
Q

3 Types of Rigidity

A

•Types of Rigidity

  1. –Lead-pipe
  2. –Cogwheel
  3. –Claspknife
36
Q

Lead Pip Rigidity

A
  • –Seen especially in Parkinson’s disease
  • –Constant resistance to movement throughout the range of motion of a joint
  • –It is indicative of increased tone in all the sets of muscles around a joint
  • –Lead-pipe rigidity, as with other forms of Parkinsonian rigidity, may be more pronounced on one side
37
Q

Cogwheel Rigidity

A
  • –Alternative episodes of resistance and relaxation or ‘catches’ in ROM
  • –Teeth of the cog are analogous to the tensed parts of the tremor
  • –May be unilateral initially
  • –Antipsychotics medications can cause cogwheel rigidity
38
Q

Clasp Knife Rigidity

A

Clasp Knife

  • Describes the phenomenon in a rigid limb after an initial resistance to passive movement of a joint
  • There is a sudden reduction in tone and the limb moves quite freely through the rest of the range of the particular movement
39
Q

Comparison between Lead-pipe and Clasp-knife rigidty

A

•Comparison

  • –Lead-pipe rigidity persists throughout the range of movement of a particular joint, as distinct from clasp knife or cogwheel rigidity which varies through the range
40
Q

Decerebate Rigidity (general)

A

–Sectioning of the neural axis between the midbrain & brainstem in experimental animals or substantial brain damage above the brainstem in humans

–Caused by substantial brain damage in the midbrain
–Produces a profound extensor rigidity in both UE & LE
–Rigid extension of limbs and trunk, internal rotation of upper limbs and plantar flexion, head is extended

From Notes:

You see it in football games when something takes a fall. Brainstem injury.

Maybe look at a picture of it.

Usually means swelling, doesn’t usually lead to paralysis.

Usually a bad sign when pt is in respirator.

Will be on the test: differentiating between Decerebrate and Decorticate rigidity

41
Q

Describe Decerebrate Rigidity

A

–Caused by substantial brain damage in the midbrain
–Produces a profound extensor rigidity in both UE & LE
–Rigid extension of limbs and trunk, internal rotation of upper limbs and plantar flexion, head is extended

42
Q

Decortate Rigidity (general)

A

•Decorticate Rigidity

  • –Modeled in animals by sectioning the neuroaxis just rostral to the superior colliculi
  • –Higher lesion

–Damage to the brain, superior to the midbrain
–increase UE flexor tone & increase LE extensor tone
–Flexed limbs, extended neck and lower limbs and plantar flexion

43
Q

Describe Decortate Rigidity

A

–Damage to the brain, superior to the midbrain
– increased UE flexor tone & increased LE extensor tone
–Flexed limbs, extended neck and lower limbs and plantar flexion