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Neuroscience > Clinical Aspects of Motor Systems > Flashcards

Clinical Aspects of Motor Systems Flashcards

1
Q

inability to produce a muscle contraction

A

Paralysis

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2
Q

ability to produce a muscle contraction but is much weaker than what we need

A

Paresis

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3
Q

What is atrophy due to unused muscles? what is atrophy due to a muscle losing its nerve innervation?

A

disuse atrophy; neurogenic atrophy

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4
Q

Occurs when LMN is more excitable than usual; produces an action potential which causes all m fibers in the motor unit to contract; visible m contraction but don’t produce a joint muscle

A

Fasciculations

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5
Q

LMN loss to m fiber; m fiber becomes more sensitive, spontaneously depolarize, and contract randomly; no visible twitch, but can be picked up on EMG

A

Fibrillations

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6
Q

What are involuntary movements (m contractions) that ALWAYS indicate a pathological condition?

A
  1. Fibrillations

2. Abnormal movements caused by dysfunction in basal ganglia

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7
Q

What can cause hypotonia?

A
  1. Damage of LMN - Transection of: Ventral root, Peripheral nerve, or
  2. Cutting sensory coming into Dorsal root ( DR Rhizotomy)
    - Injury to cerebellum will decrease tone but usually resolves
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8
Q

What are the two main types of hypertonia?

A
  1. velocity-dependent hypertonia (spasticity)

2. velicity-independent hypertonia (rigidity)

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9
Q

Tone that occurs in chronic injury to UMN or some basal ganglia disorders

A

hypertonia

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10
Q

Stretching a body part with hypertonia that is hard up until a point where it “gives”

A

Clasp knife phenomenon

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11
Q

What usually accompanies hypertonia?

A

hyperreflexia DTR

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12
Q

indicates damage to lateral corticospinal tract; quick DF in foot results in a reaction of alternating PF/ DF beats

A

Clonus

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13
Q

What type of rigidity shows high tone throughout entire muscle lengthening? what type of rigidity shows?

A

Lead-pipe rigidity (seen in parkinson’s);

Cog-wheel rigidity

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14
Q

rigidity due to severe brain lesion where entire brainstem is in tact and the lesion is superior to midbrain; results in UE flex, LE ext

A

Decorticate

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15
Q

Rigidity due to severe brain lesion at midbrain level; results in ext, UE, IR, PF

A

Decerebrate rigidity

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16
Q

Descending motor commands interrupted by injury to upper motor neurons; Lower motor neurons become temporarily inactivated; Hypotonia, Hyporeflexia; Resolves with time

A

Spinal or cerebral shock

  • spinal or cerebral depends on location of injury
  • appears as LMN injury; damaging UMN systems but see decreases in LMN fxning
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17
Q

What are some causes of disorders of LMNs?

A
  1. Trauma
  2. Infectious diseases (poliomyelitis)
  3. Degenerative diseases (ALS)
  4. Vascular diseases (diabetic polyneuropathy)
  5. Tumors
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18
Q

Where does the LMN injury occur in the nervous system?

A
  1. Ventral horn of the spinal cord
  2. Ventral root of the spinal cord
  3. Spinal/ Peripheral nerves
  4. Brain stem (nuclei to motor cranial nerves)
  5. Cranial nerves (peripheral nerve)
19
Q

What are the signs of LMN injury?

A
  1. Loss of reflexes to muscle
  2. Atrophy (rapid and severe)
  3. Flaccid paralysis (Hypotonicity)
  4. Fibrillations
20
Q

Virus damages LMN; As LMN are lost, m fibers has lost innervation; sprouting takes place to reinnervate m’s that have lost innervation; After time, a lot of stress happens to the remaining LMNs, so they begin to prune back innervations; Symptoms include weakness, fibrillations, sometimes pain

A

Post-polio syndrome

21
Q

Where does UMN injury occur in the nervous system?

A
  1. Cerebral Cortex
  2. Brainstem (Medulla, pons)
  3. Midbrain
  4. Diencephalon
  5. Lateral columns in spinal cord (some anterior too)
22
Q

What are the signs and symptoms of UMN injury?

A
  1. Abnormal cutaneous reflexes (babinski’s)
  2. Abnormal timing of muscle activation
  3. Paresis
  4. Muscle hyper stiffness (myoplastic stiffness)
  5. Clasp-knife response and clonus
  6. Fasciculations
23
Q

What are abnormal cutaneous reflexes that occur in UMN injury?

A
  1. Babiniski’s sign (normal until 6 m, also occurs after injury to corticospinal tract)
  2. Muscle spasms in response to normally innocuous stimuli
24
Q

What can contribute to the abnormal timing of muscle activation, contributing to movement problems?

A
  1. Delayed initiation of movement
  2. Rate of force development is delayed
  3. Muscle contraction time is prolonged (results in loss of power)
  4. Relationship of timing of activation of agonists and antagonists is altered (biceps may recover to full strength, but triceps activate at the same time, reducing overall force)
25
Q

Weakness; Inability to activate LMN; Loss of ability to fractionate movements (damage to lateral corticospinal tracts; also fine movements of hands)

A

Paresis

26
Q

Result due to changes in muscles ( from Loss of sarcomeres, increased weak binding of actin and myosin, and atrophy of muscle fibers)

A

Myoplastic hyper stiffness post stroke

27
Q

What are the changes in m fibers due to stroke (causing hyper stiffness)?

A

Muscle fiber diameter decreased

Selective atrophy of Type II fibers (fast twitch) - Slow twitch muscle more resistant to stretch

28
Q

What muscle fiber type do you lose after a stroke? after a spinal cord injury?

A

Type IIB; Type I

29
Q

During a complete SCI, all descending motor control lost below the level of the lesion. Spinal shock occurs at and below level of lesion. What symptoms are present below the level of injury after spinal shock resolves?

A
  1. Tone - increase
  2. Monosynaptic Reflexes - increase
  3. Polysynaptic Reflexes - decrease
  4. Voluntary muscle control – still lost
    - clonus and clasp-knife response also present
30
Q

Do you see hyperreflexia immediately after strokes or after time has passed?

A

after time has passed
- Hyperreflexia seen only in people with hemiplegia and severe contractors; Evidence suggests that hyperreflexia may result from contractures, not the other way around; Shortened muscles have an amplified stretch of muscle spindles during a stretch, producing a greater stretch reflex

31
Q

What S and S do you see in a complete SCI

A
  1. Tone - increase
  2. Monosynaptic Reflexes - increase
  3. Polysynaptic Reflexes - decrease
  4. Voluntary muscle control – still lost
    (when spinal shock resolves)
32
Q

Occlusion or hemorrhage of a blood vessel in the CNS; Most common site is the middle cerebral artery (supplies lateral sides of cerebral hemispheres)

A

Stroke

33
Q

Disrupts connections between the [lateral] cerebral cortex and the brainstem, spinal cord, and cerebellum; Damages adult upper motor neurons (corticospinal tracts): Paresis, Loss of fractionation of movement; Sensory and communication systems may also be damaged

A

MCA stroke

34
Q

What pathways are damaged in MCA strokes? what is its effect on motor systems?

A
  1. corticospinal
  2. lat reticulospinal (suppressed, not damaged, bc UMN unable to receive important info)
  3. med reticulospinal (activated)
  4. vestibulospinal
    - abnormal muscle inactivation
35
Q

What standing posture do you see with MCA strokes?

A
  1. Hemiparetic upper extremity (contralateral to injury)
    - Contracture
    - Weak actin-myosin bonds
    - Atrophy of type II muscle fibers
  2. Lower extremity:
    - Excessive extension in standing and walking
    - Changes in activation of different pathways
    - Paresis
    - Myoplastic hyperstiffness in specific muscles
36
Q

Gandevia studied MCA stroke pts with muscle weakness in one group of muscles on paretic side associated with weakness in antagonist muscle group. what did he find?

A
  • Distal muscles weaker than proximal muscles on both limbs

- In general, muscles on the non-paretic side were weaker than muscles in matched healthy subjects

37
Q

Congenital disorder of UMN that results in:

  • Abnormal tonic stretch reflexes at rest and while moving
  • Reflex irradiation - test reflex at one muscle and response spreads past that joint
  • Abnormal co-contraction of antagonist muscles
  • Lack of postural preparation prior to movement
A

Spastic CP

38
Q

Intervention that corrects learned non-use: Non-use leads to secondary consequences (Atrophy, Contractors); Used pts at least 1 year post-stroke; Constrain non-paretic limb; Specific exercises for paretic limb

A

Constraint-induced movement

  • basically, you make the person use the involved body part for 1-2 days of intense therapy
  • improved UE fxn in most pts with moderate impairments
  • cannot be done immediately after stroke bc it may increase lesion due to neuronal excitotoxicity; start with gentle then move to this after a while
39
Q

Other than constraint induced movement, what are some other techniques PTs may use for those with strokes?

A
  1. Movement against resistance
  2. Bicycling with high workloads
  3. Walking with partial weight supported (More symmetrical gait, More normal muscle activation patterns)
40
Q

Used to decrease muscle stiffness in Stroke and Spastic cerebral palsy; Also inhibits active muscle contraction; Injected into muscle and blocks release of Ach from presynaptic nerve terminal

A

Botulinum toxin

41
Q

Medicinal treatment for hyperreflexia post SCI that stimulates presynaptic release of GABA which activates GABA-B receptors; Inhibits stretch reflex pathways (Decreases calcium intake into presynaptic terminal of primary sensory afferent fibers, Stabilizes postsynaptic membrane)

A

Baclofen

- does NOT alter myoplastic stiffness (decreases reflex, not the action of contracting m)

42
Q

What are the positive effects of baclofen? negative effects?

A
  • Positive effects:
    1. Decreases spasms, pain and sleep disturbances
    2. Improves bladder function
    3. Increased mobility
  • Negative effects:
    1. Can reduce function if reflexive muscle contraction is used functionally (Stability, Mobility)
43
Q

What systems are damaged in ALS?

A
  1. Lateral activating systems
  2. Anterior horn neurons
    - damage to both UMN and LMNs
    - sensory and autonomic are usually normal

Neuroscience (19 decks)

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