Neurophysiology Of Spacticity - 18 & 19

Question 0

Baclofen

Answer 0

Presynaptic mediated inhibition. Inhibits calcium influx and therefore suppresses release of excitatory neurotransmitter’s binds to GABA-B receptors.

Question 1

Define spasticity

Answer 1

Overactivity of neuromuscular systems interfering with voluntary motions secondary to upper motor neuron lesion. It is velocity dependent resistance to passive range of motion in one direction, generally antigravity mms

Question 2

Benzodiazepine or diazepam

Answer 2

GABA agonist increases inhibition in the brain stem and spinal cord. Binds GABA-A receptors to increase infinity for GABA in brain and spinal cord

Question 3

Tizanidine

Answer 3

Inhibits excitatory neurons throughout central nervous system by increasing inhibitory neurotransmitters and decreasing excitatory neurotransmitters

Question 4

Dantrolene

Answer 4

Directly inhibits skeletal muscle contraction by blocking calcium release from sarcoplasmic reticulum

Question 5

How is a temporary nerve block done?

Answer 5

Changing membrane permeability to sodium to stop nerve conduction using local anesthetics effects start quickly and last several hours

Question 6

How does neurolysis work?

Answer 6

Chemically destroy nerve tissues with alcohol or phenol, creates a lesion then degeneration occurs but the axon can regrow in 2 to 12 months

Question 7

How does chemodenervation work?

Answer 7

Botulinum toxin is injected directly into the muscle to block muscle contraction. Effects last for 3 to 6 months. Basically like Botox for wrinkles.

Question 8

Name the two mechanisms that produce neuromuscular overactivity

Answer 8

Absence of corticospinal inhibition onto lower motor neurons. Primarily Alpha and gamma motor neurons or interneurons that control motor neuron pools.

Brainstem upper motor neuron over activity

Question 9

Name the conditions that generally have spasticity

Answer 9

Cerebral palsy, spinal cord injury, brain injury, stroke, multiple sclerosis

Question 10

Describe what causes cerebral palsy

Answer 10

Damage to the corticospinal tract in development. Causes excess synapses to not be terminated in adolescence, leading to improper cocontractions of agonist, antagonist and synergistic muscles at the same time. Also causes loss of corticospinal tract inhibition of lower motor neurons and disinhibition of reticulospinal tract producing abnormal synergies

Question 11

What is the usual outcome after a stroke, what is damaged?

Answer 11

Unilateral corticospinal tract and medullary reticulospinal tract. This leads to reticulospinal tract over activity which leads to decreased cortical inhibition which then increases reticulospinal tract signals causing excessive muscle contraction synergies

Question 12

What happens after spinal cord injury?

Answer 12

Disinhibition of lower motor neurons below the lesion. Hyperreflexia, enhanced lower motor neuron excitability, therefore interneurons and lower motor neuron’s overreact to somatosensory input and increase sensitivity of muscle spindles

Question 13

Where does voluntary movement originate?

Answer 13

Motor cortex, basal ganglia, cerebellum, thalamus, brainstem, spinal motor neurons

Question 14

What is muscle tone?

Answer 14

Muscles are tonically active and have a general resting tension when not actively being used. Also refers to general muscle resting strength

Question 15

What does the amount of muscle tone depend on?

Answer 15

Discharge of alpha motor neurons, 1a spindle afferents. Discharge of gamma motor neurons, intrafusal tension. Reticular formation. Actin and myosin overlap.

Question 16

What is the clinically relevant spasticity definition by the SPASM?

Answer 16

Assuming that all involuntary activity involves reflexes, specificity is an intermittent or sustained involuntary hyperactivity of a skeletal muscle associated with an upper motor neuron lesion

Question 17

What are the two supra segmental contributions to the neurophysiology of spasticity? What do they do?

Answer 17

Pyramidal tract the precentral cortices control voluntary movement. Primary motor cortex is 40% and premotor cortex is 20%. Postcentral cortices is the somatosensory pathways which are proprioception, cutaneous, and nociceptive. Loss here causse hyperactive reflexes.

The extrapyramidal brainstem areas. Inhibitory is the medullary reticulospinal tract, and excitatory is the pontine reticulospinal tract and the vestibulospinal tract

Question 18

Lesions to which areas pertaining to the cortex will cause spasticity?

Answer 18

Large cortical areas that have to include the premotor cortex with the primary motor cortex, Corona radiate, and the internal capsule

Question 19

What symptoms will be seen from a lesion isolated in the motor cortex?

Answer 19

Flaccid paralysis and hyporeflexia

Question 20

What is FRA?

Answer 20

Flexor reflex afferent

Question 21

What fibers pass through the anterior limb of the internal capsule? What symptoms occur with a lesion here?

Answer 21

Fibers from the supplemental motor area therefore spasticity would result

Question 22

Explain the extrapyramidal inhibitory system.

Answer 22

It is the dorsal or medullary reticulospinal tract. It comes from the medullary reticular formation and it is inhibitory. It is closely controlled by the premotor cortex. It inhibits spinal stretch reflex FRA

Question 23

Explain the extrapyramidal excitatory system

Answer 23

It is the pontine reticulospinal tract and vestibulospinal tract from the large midbrain – pons – medullary reticular formation that is excitatory. It facilitates spinal stretch reflex and extensor tone, inhibits FRA under less cortical control

Question 24

Give a short summary of the suprasegmental contribution to spasticity

Answer 24

Less inhibition equals overall increase in motor neuron excitability

Question 25

Give a brief description of the Ashworth scale and the Tardieu scale

Answer 25

Ashworth is measured in a relaxed position and it is simple passive range of motion testing.

Tardieu measures the upper extremity in sitting and the lower extremity in supine. Different velocities are used and noted as V1, V2, or V3. The muscles are graded and given a score of X and the angle at which it is performed is given Y. Scores are written as V 1, 2, or 3 then X/Y