Clinical Aspects of Motor Systems

Question 1

inability to produce a muscle contraction

Answer 1

Paralysis

Question 2

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

Answer 2

Paresis

Question 3

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

Answer 3

disuse atrophy; neurogenic atrophy

Question 4

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

Answer 4

Fasciculations

Question 5

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

Answer 5

Fibrillations

Question 6

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

Answer 6

1. Fibrillations

2. Abnormal movements caused by dysfunction in basal ganglia

Question 7

What can cause hypotonia?

Answer 7

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

Question 8

What are the two main types of hypertonia?

Answer 8

1. velocity-dependent hypertonia (spasticity)

2. velicity-independent hypertonia (rigidity)

Question 9

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

Answer 9

hypertonia

Question 10

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

Answer 10

Clasp knife phenomenon

Question 11

What usually accompanies hypertonia?

Answer 11

hyperreflexia DTR

Question 12

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

Answer 12

Clonus

Question 13

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

Answer 13

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

Cog-wheel rigidity

Question 14

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

Answer 14

Decorticate

Question 15

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

Answer 15

Decerebrate rigidity

Question 16

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

Answer 16

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

Question 17

What are some causes of disorders of LMNs?

Answer 17

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

Question 18

Where does the LMN injury occur in the nervous system?

Answer 18

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)

Question 19

What are the signs of LMN injury?

Answer 19

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

Question 20

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

Answer 20

Post-polio syndrome

Question 21

Where does UMN injury occur in the nervous system?

Answer 21

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

Question 22

What are the signs and symptoms of UMN injury?

Answer 22

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

Question 23

What are abnormal cutaneous reflexes that occur in UMN injury?

Answer 23

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

Question 24

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

Answer 24

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)

Question 25

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

Answer 25

Paresis

Question 26

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

Answer 26

Myoplastic hyper stiffness post stroke

Question 27

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

Answer 27

Muscle fiber diameter decreased | Selective atrophy of Type II fibers (fast twitch) - Slow twitch muscle more resistant to stretch

Question 28

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

Answer 28

Type IIB; Type I

Question 29

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?

Answer 29

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

Question 30

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

Answer 30

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

Question 31

What S and S do you see in a complete SCI

Answer 31

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

Question 32

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

Answer 32

Stroke

Question 33

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

Answer 33

MCA stroke

Question 34

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

Answer 34

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

Question 35

What standing posture do you see with MCA strokes?

Answer 35

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

Question 36

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?

Answer 36

- 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

Question 37

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

Answer 37

Spastic CP

Question 38

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

Answer 38

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

Question 39

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

Answer 39

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

Question 40

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

Answer 40

Botulinum toxin

Question 41

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)

Answer 41

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

Question 42

What are the positive effects of baclofen? negative effects?

Answer 42

- 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)

Question 43

What systems are damaged in ALS?

Answer 43

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