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Postural Control > UMNS > Flashcards

UMNS Flashcards

1
Q

What are the positive features of UMNS ?

A
  • Spasticity
  • Dystonia
  • Clonus
  • Spasm
  • Co-contraction
  • Associated reaction
  • Tendon reflex
  • Babinski sign
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2
Q

What are the negative features of UMNS ?

A
  • Weakness
  • Loss of dexterity and coordination
  • Fatigue
  • Sensory deficit
  • Postural control deficit
  • fasciculations
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3
Q

What are the bio mechanical features of UMNS

A
  • Contractures
  • muscle stiffness
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4
Q

What are the neural changes caused by UMNS ?

A

Positive and negative features.

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5
Q

What are the non neural changes caused by UMNS ?

A

Bio mechanical features (contractures and muscle stiffness)

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6
Q

How to assess muscular tone ?

A

Passive mobilization. But in doing so we evaluate both contractile and non contractile structures.

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7
Q

What is the viscoelastic tone ?

A

Résistance in the connective tissue. This tissue is not contractile so we cannot evaluate it.

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8
Q

How does the stretch reflex work ?

A

When the muscle is stretched (eg: hammer strikes tendon) they send an impulse via the sensory neurons to the relevant spinal cord segment. The nerve synapses with a second nerve within the spinal cord, with the alpha motor neuron to contract. This impulse does not need to travel to the brain. When stretch reflex is activated it causes contraction of synergistic muscles but also relaxation of the antagonist muscles (inhibitory effect from alpha motor neuron).

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9
Q

What are the dynamic components of positive features of UMNS ?

A

-Co-contractions
-Clonus
-Babinski sign
- associate reaction
- flexor shortness

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10
Q

What are the static components of the positive features of UMNS ?

A
  • spasticity
  • spastic distonia
  • spasm
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11
Q

Define spasticity

A

It is a sensorimotor disorder (not only motor) following an UMNS showing a sustained and involuntary muscle activity. We find abnormal muscle contraction at rest and in dynamic. It includes, hyper stretch reflex, spasm, clonus, muscular response at the stretch reflex velocity and position dependent, abnormal patterns and co-contraction.

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12
Q

What is spastic distonia ?

A

It the involuntary, sustained muscle activation at rest, in absence of phasic stretch or voluntary effort. Found in patient with damage to the basal ganglia or striatum. Spastic distonia fixes the limb in one position and it is not possible to change it during an activity. It needs to be treated with sensory informations.

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13
Q

What is spastic co-contraction ?

A

Involuntary muscular activity in the antagonist muscle during voluntary effort of the agonist, aggravated by antagonist stretch. The timing of contraction needs to be treated.

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14
Q

What are in broad terms the networks affected in spasticity ?

A
  • Corticospinal networks
  • Spinal networks
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15
Q

Describe the Patophysiology of spasticity

A

Spasticity is an adaptation to the primary lesion.

1) Lack of descending motor command accessing the motor neurons leads to motor behavioral hypo activity, which corresponds to a state of sensorimotor restriction.

2) Alteration of the balance of inhibition system in the reticular system.

3) Adaptives changes in the spinal neural network leading to an alteration of the sensory integration and non neural changes.

4) Muscle structural alterations (volume of fibers, type of fibers distribution, amount of intramuscular fat, function modification, sarcomeres modifications, connective tissue proliferation, pennation angle modification).

5) tendon atrophy

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16
Q

Which CNS lesions can cause spasticity ?

A
  • S1
  • M1
  • PMC
  • SMA
  • corona radiata
  • internal capsule
  • thalamus
  • midbrain
    In fact until the pyramidal decussation
17
Q

Describe the adaptations taking place in the spinal cord during UMNS

A

1) Changes occur at the presynaptic level, in the descending systems
2) Reduced info about muscle spindle contraction so muscle spindle recieve less sensory info because there is less possibility to contract the muscle.
3) Less inhibition since patient cannot feel sensory input from the muscle spindles.
4) As patient cannot record the change in tension there is an over reactivity coming from excessive output.

18
Q

What is clonus ?

A

Rhythmical contraction after an effort or during a change in muscle length.

19
Q

What are the two types of clonus ?

A

1) positive clonus: Comes after the cession when muscles have worked. We activated a new circuitry in the spinal cord by changing the corticospinal drive. We have to reinforce it to make plasticity happen.

2) negative clonus: is seen during the performance of an exercise and is caused by fatigue. Need to stop the cession.

So timing of clonus is essential.

20
Q

What is an associate reaction ?

A

Any atypical movement pattern (ex: flex the elbow to move the body) due to a lack of activation of axial muscle causing a lack of postural control.

21
Q

What is the cause of flexor shortness ?

A

Lack of anti gravity muscle activation.

22
Q

What are the muscle structural alteration in UMNS ?

A

Similar to aging. They are due to abnormal central neural innervation and disuse.

  • reduction of the volume of muscle fibers
  • change in the fiber type distribution (between fast contractile and slow contractile fibers)
  • increased amount of intramuscular fat
  • fonction modification
  • sarcomere modification
  • connective tissue proliferation
  • pennation angle modification
23
Q

What is the pennation angle, and why is it important for therapy ?

A

It is the alignment of muscle fibers relative to line of contraction. If the alignement of the muscle is not good so is the alignement of the body. This is why realignement of soft tissue is part of the therapy.

24
Q

Which non neural changes can cause muscle stiffness ?

A
  • intrinsic changes in muscular tissues
  • intramuscular connective tissue
  • alterations in the connection between epimysium and extra muscular tissues.
25
Q

How do non neural changes affect tendons ?

A
  • increased tendon length
  • lower tendon stiffness
  • higher mechanical hysteresis
  • reduction of cross-sectional area

So stretching will cause more tendon extension ! Don’t stretch.

26
Q

Describe the pathophysiology of tendon atrophy in UMNS

A

1) Spasticity
2) muscle atrophy
3) less movement of the tissues
4) muscular weakness
5) less tendon stiffness
6) less force transmission
7) less collagen in tendon
8) tendon atrophy

27
Q

Which is the most appropriate scale to assess spasticity

A

Modified Tardieu scale

28
Q

Which is the most appropriate scale to assess spasticity

A

Modified Tardieu scale

29
Q

What is diaschisis ?

A

Following acute, localized lesions of the CNS, arising from any cause, there are immediate depressions of neural synaptic functions in other areas of the CNS remote from the lesion. Diaschisis most commonly manifests itself by such neurological signs as impaired consciousness or cognitive impairment including dementia, dyspraxia, lack of coordination and sensory neglect. It is due to widespread depressions of local cerebral blood flow and metabolism extending far beyond the anatomical lesion. Most common form is cerebellar diaschisis.

30
Q

How to adapt treatment to diaschisis ?

A
  • Involve patient in the cognitive process: trigger attention, perception, memory and the ability to solve problems through the body (ex: tactile recognition or body positioning exercises).
  • Avoid excessive immediate physical stimulation: offer increasing complexity, starting with simple stimulations both in motor terms and cognitive terms.
31
Q

How to adapt treatment to diaschisis ?

A
  • Involve patient in the cognitive process: trigger attention, perception, memory and the ability to solve problems through the body (ex: tactile recognition or body positioning exercises).
  • Avoid excessive immediate physical stimulation: offer increasing complexity, starting with simple stimulations both in motor terms and cognitive terms.
32
Q

What causes spastic movement disorder ?

A

-Altered mechanical properties (= contractures)
-Paresis, muscle atrophy and weakness
-Impaired coordination of muscle activity
-Compensatory muscle contractions to maintain posture and stability
-Sustained involuntary muscle activation (=spastic distonia)

33
Q

What are the 12 recommandations for neurorehabilitation ?

A

1) Active patient participation is necessary
2) Physical aids should only be given when really necessary
3) Provide challenges that can support learning
4) Training should be of the responsibility of the patient
5) Train everyday for as long as possible
6) Ensure motivation and reward
7) Structure practice to optimize acquisition and retention
8) Improved function requires optimal consolidation
9) Less emphasis on spasticity and more on paresis
10) neurorehabilitation has effects late in life and long after primary injury
11) Consider other factors that influence learning and memory (ex: enough glucose intake during cession)
12) Individualization

34
Q

What are the 3 «ingredients» of learning process ?

A
  • Cerebellum is learning from error
  • Cortex is learning from repetition
  • Basal ganglia is stimulated by reward

Postural Control (4 decks)

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