Neurophysiology Of Spacticity - 18 & 19 Flashcards

0
Q

Baclofen

A

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

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1
Q

Define spasticity

A

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

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2
Q

Benzodiazepine or diazepam

A

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

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3
Q

Tizanidine

A

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

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4
Q

Dantrolene

A

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

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5
Q

How is a temporary nerve block done?

A

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

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6
Q

How does neurolysis work?

A

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

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7
Q

How does chemodenervation work?

A

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

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8
Q

Name the two mechanisms that produce neuromuscular overactivity

A

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

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9
Q

Name the conditions that generally have spasticity

A

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

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10
Q

Describe what causes cerebral palsy

A

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

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11
Q

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

A

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

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12
Q

What happens after spinal cord injury?

A

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

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13
Q

Where does voluntary movement originate?

A

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

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14
Q

What is muscle tone?

A

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

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15
Q

What does the amount of muscle tone depend on?

A

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

16
Q

What is the clinically relevant spasticity definition by the SPASM?

A

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

17
Q

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

A

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

18
Q

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

A

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

19
Q

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

A

Flaccid paralysis and hyporeflexia

20
Q

What is FRA?

A

Flexor reflex afferent

21
Q

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

A

Fibers from the supplemental motor area therefore spasticity would result

22
Q

Explain the extrapyramidal inhibitory system.

A

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

23
Q

Explain the extrapyramidal excitatory system

A

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

24
Q

Give a short summary of the suprasegmental contribution to spasticity

A

Less inhibition equals overall increase in motor neuron excitability

25
Q

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

A

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