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neuro > tone > Flashcards

tone Flashcards

1
Q

2

normal muscle tone

A
  • sufficient tension to allow movement but maintian stability
  • varies with posture and …?
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2
Q

2

what provides normal muscle tension?

A
  • neural - firing of nerves active muscle contraction and background activity even when the muscle is relaxed
  • non-neural- non-elastic structures within the muscle tendons; elastic properties and connective tissues
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3
Q

between 3 things

what interaction maintains tension?

A

extrafusal muscle fibres, spindles and golgi tendon organs

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4
Q

extrafusal muscle fibres

A

comprise the main bulk of muscle and form the major force-generating structure

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5
Q

3 where, contain?

intrafusal muscle fibers

A
  • buried in the muscle
  • contain the muscle spindles (afferent receptors for stretch)
  • contain contractile elements
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6
Q

2

reciprocal inhibition basic principle

A
  1. when a muscle spindle is stretched and the stretch reflex is activated
  2. the opposing muscle group must be inhibited to prevent it from working against the resulting contraction of the homonymous muscle
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7
Q

how is inhibition acomplished?

A

by an inhibitory interneuron in the spinal cord

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8
Q

reciprocal inhibition

what divides in the spinal cord

A
  1. The 1a afferent of the muscle spindle
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9
Q

where do the branches go and wha do they do

A
  • One branch innervates the alpha motor neuron that causes the homonymous muscle to contract, producing the reflex.
  • The other branch innervates the 1a inhibitory interneuron, which in turn innervates the alpha motor neuron that synapses onto the opposing muscle.
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10
Q

what does the interneurone prevent and why

A
  • it prevents the opposing alpha motor neuron from firing, thereby reducing the contraction of the opposing muscle.
  • Because the interneuron is inhibitory
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11
Q

5, 6 med

extrinsic factors affecting tone

A
  1. posture (BoS, CoG)
  2. temperature
  3. visual or auditory stimuli- affect alert state
  4. emotional states e.g anxiety
  5. medical factors
    * UTI’s
    * bowel impactation
    * skin irritation/ ulceration
    * ingrown toenail
    * increased sensory stimuli (clothes or orthoses)
    * pain
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12
Q

3

model of abnormal motor output

A
  1. under-active agonist
  2. over active antagonist
  3. shortened antagonist
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13
Q

model of abnormal motor output 2

A

over active antagonist
- increased tone/ spasticity
- may still be weak due to lack of voluntary drive

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14
Q

model of abnormal motor output 3

A

shortened antagonist
- stiffness and contracture

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15
Q

secondary adaptive changes UMN lesion

A
  • mechanical muscle stiffness
  • contractures (decreased range of movement)
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16
Q

Clinical presentation of UMN syndrome

weakness (underactive)

A

low tone

17
Q

Clinical presentation of UMN syndrome

spasticity (overactive)

A

High tone
neural

18
Q

Clinical presentation of UMN syndrome

2nd adaptive muscle and soft tissue

A

high tone
**non- neural **

19
Q

Nerve impulse

A
  • a small electrical potential generating a current that travels rapidly along the nerve fibre (See health sciences module for nerve conduction, velocities, nodes of ranvier, saltatory conduction etc.)
20
Q

voluntary movement

A
  • initiated by nerve impulses arising in the pre-motor and motor cortex.
  • complex interconnecting pathways connect the brain with the muscles to generate movement.
  • Feedback to the brain and spinal cord from many and varied types of sensory receptors enables movement to be controlled.
21
Q

Voluntary movement by definition

A

involves the conscious brain, but the basic building block of movement is the spinal reflex, onto which higher centres exert control. More about reflexes later.

22
Q

why can brain lesions cause symtoms on the opposide side of the body

A

some nerve impulses travel directly from the motor cortex to the spinal cord – pyramidal tracts (corticospinal tract) - majority cross over in the brain so that the right side of the brain controls the left side of the body and vice-versa – example stroke. Impulses arising in other parts of the brain, e.g. reticular formation, cerebellum, do not.

23
Q

spasticity definitions

A
  • velocity depended increase in tonic stretch reflexexs as one component of the upper motor neuron sydrome
  • disordered sensory-motor control, resulting from upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles
24
Q

what is spasticity

A
  • innapropriate muscle activity- often presents itself as an axaggerated stretch reflex or co-activation of opposing muscel groups
25
Q

stretch reflex

A
  • When muscle is stretched
  • firing of the 1a afferents
  • The 1a afferents have their cell bodies in the dorsal root ganglia of the spinal cord
  • send projections into the spinal cord, and make synapses directly on alpha motor neurons
  • that innervate the same (homonymous) muscle.
    .
    Thus, activation of the 1a afferent causes a monosynaptic activation of the alpha motor neuron that causes the muscle to contract.

stretch reflex is activated, it not only causes contraction of the synergistic muscles, but also caused relaxation i.e. has an inhibitory effect on the antagonist muscles.

26
Q

under-active agonist

A
  • derease neural drive to spinal neurons
  • muscle weakness/low tone
27
Q

over-active antagonist

A
  • increased tone/ spasticity
  • may still be weak due to voluntary drive
28
Q

shortened antagonist

A

stiffness and contracture

29
Q

assessment

handling

A
  • Avoid over handling reflex stimulating surfaces e.g. ball of foot and palm of hand
  • Use lumbrical grasp with firm contact throughout your whole hand i.e. avoid gripping with finger tips, so that its supportive but not painful (which would stimulate reflex response)
  • Make sure hands are warm as temperature really affects neuro patients
30
Q

assessment

Passive range of motion

A
  • Consider starting position, ideally well supported in supine to ensure accuracy and patient able to relax with minimal associated reactions or compensatory movement
  • Slowly move the joint through range, apply small traction force
  • Watch patient’s face
  • Make sure you know your anatomy and biomechanics – how far should this joint move? What is the normal range? Are there any muscles limiting ability to assess joint range specifically?
  • Take care with low tone joints – e.g. risk of damage / pain GH joint post-stroke
  • Take care if poor sensation – e.g. risk of joint damage if reduced proprioception
  • What is the ‘feel’ during movement? How much resistance? Does this change through range? Is there a catch?
  • What is the ‘feel’ at end of range?
31
Q

Assessment of hypertonia (spasticity):

A
  • Hypertonicity (spasticity) is present if resistance through range increases as speed increases or if a “catch” occurs as the velocity becomes fast enough
  • Sometimes there is also a “clasp-knife” response, this is where following the initial catch, there is a sudden reduction in resistance and movement returns through the rest of the available range
  • Rapid passive movements may also elicit spasm or clonus of muscle being stretched
  • Patients starting posture will affect result i.e. muscles partially stretched are more likely to elicit reflex e.g. hamstrings demonstrate greater reflex activity if start in hip flexion rather than hip extension
  • Recording the influence of starting posture on reflex response is important (it will also influence the starting postures used in treatments)
  • Consider other relevant factors i.e. tight clothing, medication, noxious stimuli (i.e. UTI)
32
Q

upper limb tone hypertonia test

A
  • Elbow flexors
  • Wrist flexors
33
Q

lower limb hypertonia test

A
  • Ankle plantar flexors (knee extension and knee flexion)
  • Knee extensors
34
Q

assess clonus in lower limb

A
  • Ask patient to relax
  • Support the knee in a partly flexed position
  • Quickly dorsiflex the foot and observe for rhythmic clonic movements
  • More than three rhythmic contractions of the plantar flexors is a positive response and indicates an UMN lesion
35
Q

initial assessment

A

in supine as it lowers tone and is a good position for patient and therapist
Assess again in sitting and in walking

36
Q
A

neuro (20 decks)

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