The Pathophysiology of The Pathophysiology of SpasticitySpasticity

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

2. Efferent Drive

3. Disordered control of mvt

•Stretch•Nocicepive•Cutaneous

•Spastic dystonia?•Associated reactions?

•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 co-

contraction– 2. Excessive inhibition -> appearance of

weakness