Spasticity Pathophysiology
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Transcript of Spasticity Pathophysiology
![Page 1: Spasticity Pathophysiology](https://reader033.fdocuments.net/reader033/viewer/2022061401/553608234a79593c148b487a/html5/thumbnails/1.jpg)
The Pathophysiology of The Pathophysiology of SpasticitySpasticity
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Upper Motor Neuron
• Negative Features– Weakness– Loss of dexterity
• Positive Features– Muscle “overactivity”
• Spasticity• Hyperactive tendon reflexes• Clonus• Flexor spasms
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Pyramidal…
• Pure pyramidal lesions: clumsiness, minimal weakness, mild decrease in DTRs followed by hyperreflexa, upgoing toes
• Spasticity and muscle overactivity do not occur
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vs. Parapyramidal…
• UMN syndrome mostly due to loss of inhibition of parapyramidal tracts: dorsal reticulospinal tract
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Excitatory vs Inhbitory
• Excitatory pathways also arise in brainstem: bulbopontine tegmentum, & fibres descend via medial reticulospinal tract
• & vestibulospinal fibres also have excitatory effect upon spinal reflexes, but not as important for spasticity
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Pathophysiology
1. Dorsal reticulospinal pathways (originating from VMRF) under cortical control– motor cortex facilitat this area -> increasing inhibitory
drive
2. Corticobulbar fibres lesion (either in cortex or internal capsule) -> withdraws cortical facilitation– -> mild decrease inhibitory drive and net increased
spinal cord activity
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…Pathophysiology
3. Partial spinal cord lesion: totally destroyed inhibitory pathways with preserved excitatory fibres -> leave spinal activity uninhibited– marked spasticity, hyperreflexia, flexor &
extensor spasms
• Complete SC lesion: inhib/excitatory– Spinal reflexes lose all supraspinal control
and eventually become hyperactive
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Classification of muscle overactivity in UMN syndrome
1. Spinal Reflexes
2. Efferent Drive
3. Disordered control of mvt
•Stretch•Nocicepive•Cutaneous
•Spastic dystonia?•Associated reactions?
•Co-contraction
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1. Spinal Reflexes
• A. Disinhibition of existing normal reflexes– Stretch: hyperreflexia– Nocicepive: flexor response
• B. Release of Primitive Reflexes– Cutaneous & Positive support reaction
• C. New reflex
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Spasticity
• Healthy tone at rest: muscle contraction contributes nothing to resistance– There is no tonic reflex at rest with no
pathology
Vs.
• Spasticity: increased muscle activity with stretch (tonic stretch reflex), velocity dependent
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Spasticity is…
• Sustained Stretch reflex
• Mediated by Ia afferents (predominantly in the muscle spindle)
• Velocity dependent
• Dynamic & Static component
• Length dependent
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Flexor Spasms
• Due to disinhibited normal flexor withdrawal reflexes
• Mechanism:– Flexor reflex afferents mediate polysynaptic
flexor reflexes
• Total cord transection: all suprapinal inhibitory influences lost, resulting in intense flexor spasms
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Clasp Knife Phenomenon
• Clasp Knife: tonic stretch reflex modified by flexor reflex afferents – Velocity dependent– Length dependent
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Efferent Drive
• Continuous muscle contractions in absence of 1) sensory feedback & 2) voluntary contraction– Spastic dystonia: ?Tonic supraspinal drive to
the alpha motor neurons
• Cat picture
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Associated Reactions
• Associated reactions: due to tonic efferent drive to the alpha motor neurones of the elbow flexors (form of spastic dystonia)– Related to effort– Synkinesis
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3. Disordered Control
• Disordered control of voluntary mvt, especially co-contraction– Normal vs pathological– Controlling reciprocal inhibition
• Reduced reciprocal inhibition– 1. Reduced inhibition -> pathological co-
contraction– 2. Excessive inhibition -> appearance of
weakness
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