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The Pathophysiology of Spasticity

Upper Motor Neuron


Negative Features
Weakness Loss of dexterity

Positive Features
Muscle overactivity
Spasticity Hyperactive tendon reflexes Clonus Flexor spasms

Pyramidal
Pure pyramidal lesions: clumsiness, minimal weakness, mild decrease in DTRs followed by hyperreflexa, upgoing toes Spasticity and muscle overactivity do not occur

vs. Parapyramidal
UMN syndrome mostly due to loss of inhibition of parapyramidal tracts: dorsal reticulospinal tract

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

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

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

Classification of muscle overactivity in UMN syndrome


1. Spinal Reflexes Stretch Nocicepive Cutaneous 2. Efferent Drive Spastic dystonia? Associated reactions? 3. Disordered control of mvt Co-contraction

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

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

Spasticity is
Sustained Stretch reflex Mediated by Ia afferents (predominantly in the muscle spindle) Velocity dependent Dynamic & Static component Length dependent

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

Clasp Knife Phenomenon


Clasp Knife: tonic stretch reflex modified by flexor reflex afferents
Velocity dependent Length dependent

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

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

3. Disordered Control
Disordered control of voluntary mvt, especially co-contraction
Normal vs pathological Controlling reciprocal inhibition

Reduced reciprocal inhibition


1. Reduced inhibition -> pathological cocontraction 2. Excessive inhibition -> appearance of weakness