UMN Syndromes and Muscle Tone Flashcards

(62 cards)

1
Q

Muscle performance includes these 3 components:

Disordered muscle performance is related to:

A

Strength, power, endurance ; inability of diseased/atrophied muscle to generate forces, and LMN disorders.

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2
Q

Aspects of motor control include:

A

dexterity, coordination, agility, & fractionated movement

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3
Q

What is always applicable to UMN disorders?

A

Motor control

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4
Q

Aspects of Impaired ______ can affect _______, and vice versa.

A

muscle performance; motor control

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5
Q

UMN Syndrome causes loss/impairment of _____ control of ______ .

A

UMN control of LMN

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6
Q

How does UMN Syndrome change motor control?

A

Paresis, Loss of fractionated movement, Abn reflexes, Changed tone (usually increase), Co-contraction & movement synergies.

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7
Q

Possible causes of UMN Syndrome

A

CVA, SCI, CP, trauma, tumor, etc. Anything disrupting descending motor tracts.

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8
Q

Define Paresis

A

Inadequate recruitment of LMN’s by UMN’s. Decreased agonist activation. EMG can show denervation.

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9
Q

Do muscles atrophy in UMN lesion?

A

Some do, but not as bad as in LMN lesion

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10
Q

2º Changes from Paresis

A

Muscle contractures with disuse (loss of sarcomeres). Disuse –> reorganizes sensory-motor cortex (maladaptive plasticity, learned non-use)

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11
Q

Loss of ability to activate individual muscles independently is …

A

Loss of fractionated movement

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12
Q

What segment has most impaired fractionated movement with UMN lesion?

A

The hand! Especially with loss of contralateral lateral C-S Tract

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13
Q

Why is ipsilateral innervation spared in stroke?

A

Because Brainstem-Spinal Cord tracts operate without contralateral cortical control.

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14
Q

What do Brainstem-Spinal Cord tracts primarily control?

A

Trunk and girdle muscle cross movements.

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15
Q

Why is it hard for stroke pt’s to isolate joint movements?

A

Because their limbs tend to move in flexion/extension synergies

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16
Q

What is an example of a post-stroke movement synergy?

A

Plantarflexion with knee flexion

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17
Q

True/false: downward response is normal in Babinski

A

TRUE

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18
Q

Light touch with UMN disorder can elicit …

A

muscle spasms, especially in spinal cord injury

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19
Q

Why is there an increase in DTRs with UMN disorders?

A
  1. upregulation of receptors associated with Ia afferents; 2. loss of UMN control of inhibitory local circuits
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20
Q

Hyperreflexia

A

Increased deep tendon reflexes (DTRs)

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21
Q

How many with UMN lesion will develop hyperreflexia?

A

Most, but not all.

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22
Q

What competes with recovering UMN to influence over LMN?

A

Ia afferents

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23
Q

Post-SCI: Relationship of DTR magnitude to recovery of muscle strength

A

Inverse relationship

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24
Q

Define clonus

A

Involuntary, rhythmic, repeating muscle contractions. Lost UMN input lets circuits in spinal cord run free.

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25
What induces clonus?
Muscle stretch - noxious/cutaneous stimuli - voluntary movement
26
How often is sustained clonus pathological?
Always!
27
When will Type II muscle spindle input elicit muscle contraction?
Post-UMN lesion, because descending IPSPs are not present. Allows for Tonic Stretch Reflex.
28
Clasp Knife Reflex
When a hyperreflexive muscle is slowly stretched, and reached a point when muscle relaxes. Caused by Type II MS, joint capsule fibers, and touch receptors.
29
Resistance to passive stretch is …
Muscle tone. Defined as change in force per change in length
30
Active factors of muscle tone
UMN firing and reflexes cause ACH-induced muscle contraction and cross-bridging
31
Intrinsic factors of muscle tone
weak actin-myosin bonds in muscle at rest
32
Passive factors of muscle tone
Titin (elastic structural protein which holds sarcomere together)
33
Why is resistance to slow stretch normally minimal?
No activation of quick-stretch Ia fiber. - Slow stretch reflex normally inhibited. - So no normal neural response to slow stretch. - Actin-myosin will let go with minimal resistance. - Passive elements (titin) give most resistance.
34
What is normal response to quick stretch?
DTR in 2+ range from Ia activation, - actin-myosin bonds don't have a chance to let go
35
How are contractures formed?
With immobilization, sarcomeres are lost at end of muscle. - Less titin overall, so muscle becomes stiffer. - also more actin-myosin bonds 2º inactivity
36
What is the purpose of a contracture?
Adaptive change, to generate optimal force at shortened length.
37
Hypertonia
Excess resistance to muscle stretch, caused by overactive neural input: - Hyperreflexia - Incr UMN activity
38
Myoplasticity
Change in muscle (stiffness) in response to changed activity level, prolonged positioning. Can be independent of hyperreflexia. Includes: - Contracture - Actin-myosin bonds - Atrophy of fast-twitch
39
Hypotonia
Decr resistance to passive movement. Movements generally impaired.
40
Causes of Hypotonia
Partial peripheral nerve damage. - Certain CNS lesions (Cb, CP of basal ganglia)
41
What is the most extreme form of Hypotonicity?
Flaccidity. - Complete loss of muscle tone, floppy limbs. - Happens with complete LMN lesions, or some acute CNS lesions
42
Research definition of Spasticity
Incr muscle tone, notable for velocity-dependent incr in phasic stretch reflex.
43
How is Hyperreflexia measured?
Clinically: DTRs (phasic stretch reflex). - Lab: H Reflex
44
Modified Ashworth Scale
Scale to measure spasticity, but really measures muscle stiffness. 0-5
45
Baclofen pump
Manages excessive tone via intrathecal release of Baclofen. Spreads locally.
46
Botulinin Toxin
Blocks release of ACH at motor endplate OR proximal nerve
47
Phenol
Blocks conduction of action potential at motor endplate OR proximal nerve
48
Oral spasticity reducing drugs
Baclofen, Benzodiazepines. - effects last several hours. - not specific to one muscle group. - general CNS depressants-GABA agonists
49
Examples of Benzodiazepines
Valium - Atavan - Zanax - Dantrium
50
Surgical treatments for excessive tone
Dorsal rhizotomy or phenol block of dorsal root. - muscle/tendon lengthening suergeries
51
What are 2 Basal Ganglia-related disorders of muscle tone?
Dystonia & Rigidity
52
Dystonia
Involuntary muscle contractions causing ABN twisting and postures. Sx vary w/ activity, posture, task, stress, fatigue. - Cause poorly understood.
53
Describe location & quality of Dystonic contractions
Affects any part of body. - Sustained, Tremulous, Intermittent, Rhythmic (STIR)
54
Rigidity
Dystonia with uniform resistance around a joint. - Non-velocity dependent incr to passive stretch, tonic
55
What is lacking in Rigidity?
Clasp-knife and hyperreflexia
56
Lead pipe rigidity
Resistance uniform throughout range
57
Cog wheel rigidity
Resistance interrupted by series of jerks. Seen in Parkinson's
58
Define tremor
rhythmic, involuntary oscillatory movement of a body part
59
Physiologic tremor
normally not visible
60
Resting
commonly seen in Parkinson's disease
61
Action tremor aka …
essential tremor. Basal ganglia reliated
62
Intention tremor
target related seen with Cerebellar disorders