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Neuroscience III > UMN Syndromes and Muscle Tone > Flashcards

UMN Syndromes and Muscle Tone Flashcards

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
Q

What induces clonus?

A

Muscle stretch - noxious/cutaneous stimuli - voluntary movement

26
Q

How often is sustained clonus pathological?

A

Always!

27
Q

When will Type II muscle spindle input elicit muscle contraction?

A

Post-UMN lesion, because descending IPSPs are not present. Allows for Tonic Stretch Reflex.

28
Q

Clasp Knife Reflex

A

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
Q

Resistance to passive stretch is …

A

Muscle tone. Defined as change in force per change in length

30
Q

Active factors of muscle tone

A

UMN firing and reflexes cause ACH-induced muscle contraction and cross-bridging

31
Q

Intrinsic factors of muscle tone

A

weak actin-myosin bonds in muscle at rest

32
Q

Passive factors of muscle tone

A

Titin (elastic structural protein which holds sarcomere together)

33
Q

Why is resistance to slow stretch normally minimal?

A

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
Q

What is normal response to quick stretch?

A

DTR in 2+ range from Ia activation, - actin-myosin bonds don’t have a chance to let go

35
Q

How are contractures formed?

A

With immobilization, sarcomeres are lost at end of muscle. - Less titin overall, so muscle becomes stiffer. - also more actin-myosin bonds 2º inactivity

36
Q

What is the purpose of a contracture?

A

Adaptive change, to generate optimal force at shortened length.

37
Q

Hypertonia

A

Excess resistance to muscle stretch, caused by overactive neural input: - Hyperreflexia - Incr UMN activity

38
Q

Myoplasticity

A

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
Q

Hypotonia

A

Decr resistance to passive movement. Movements generally impaired.

40
Q

Causes of Hypotonia

A

Partial peripheral nerve damage. - Certain CNS lesions (Cb, CP of basal ganglia)

41
Q

What is the most extreme form of Hypotonicity?

A

Flaccidity. - Complete loss of muscle tone, floppy limbs. - Happens with complete LMN lesions, or some acute CNS lesions

42
Q

Research definition of Spasticity

A

Incr muscle tone, notable for velocity-dependent incr in phasic stretch reflex.

43
Q

How is Hyperreflexia measured?

A

Clinically: DTRs (phasic stretch reflex). - Lab: H Reflex

44
Q

Modified Ashworth Scale

A

Scale to measure spasticity, but really measures muscle stiffness. 0-5

45
Q

Baclofen pump

A

Manages excessive tone via intrathecal release of Baclofen. Spreads locally.

46
Q

Botulinin Toxin

A

Blocks release of ACH at motor endplate OR proximal nerve

47
Q

Phenol

A

Blocks conduction of action potential at motor endplate OR proximal nerve

48
Q

Oral spasticity reducing drugs

A

Baclofen, Benzodiazepines. - effects last several hours. - not specific to one muscle group. - general CNS depressants-GABA agonists

49
Q

Examples of Benzodiazepines

A

Valium - Atavan - Zanax - Dantrium

50
Q

Surgical treatments for excessive tone

A

Dorsal rhizotomy or phenol block of dorsal root. - muscle/tendon lengthening suergeries

51
Q

What are 2 Basal Ganglia-related disorders of muscle tone?

A

Dystonia & Rigidity

52
Q

Dystonia

A

Involuntary muscle contractions causing ABN twisting and postures. Sx vary w/ activity, posture, task, stress, fatigue. - Cause poorly understood.

53
Q

Describe location & quality of Dystonic contractions

A

Affects any part of body. - Sustained, Tremulous, Intermittent, Rhythmic (STIR)

54
Q

Rigidity

A

Dystonia with uniform resistance around a joint. - Non-velocity dependent incr to passive stretch, tonic

55
Q

What is lacking in Rigidity?

A

Clasp-knife and hyperreflexia

56
Q

Lead pipe rigidity

A

Resistance uniform throughout range

57
Q

Cog wheel rigidity

A

Resistance interrupted by series of jerks. Seen in Parkinson’s

58
Q

Define tremor

A

rhythmic, involuntary oscillatory movement of a body part

59
Q

Physiologic tremor

A

normally not visible

60
Q

Resting

A

commonly seen in Parkinson’s disease

61
Q

Action tremor aka …

A

essential tremor. Basal ganglia reliated

62
Q

Intention tremor

A

target related seen with Cerebellar disorders

Neuroscience III (7 decks)

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