Spasticity

Question 1

What is the definition of spasticity?

Answer 1

“Motor disorder characterised by a velocity dependent increase in stretch reflexes with exaggerated tendon jerks, resulting from hyperexitability of the stretch reflex”

Question 2

What are the clinical symptoms of spasticity?

Answer 2

• Increased muscle tone, clonus, spasms and hyperreflexia

- Exaggerated contraction which can be painful

Question 3

How does spasticity arise?

Answer 3

• Lesions in descending inputs from higher centres to the spinal cord
• Maladaptive changes in the spinal cord with the net effect of greater excitation or excitability of motor neurons
• Changes in MN properties or sensory inputs

Question 4

How can spasticity arise from altered sensory inputs?

Answer 4

Facilitation from 1a fibres in the monosynaptic reflex pathway

Question 5

What are treatments aimed to target changes in sensory inputs?

Answer 5

Pre-post synaptic inhibition through GABAB receptor include Baclofen which is a GABAb agonist leading to decreased Ca2+ influx and reducting neurotransmitter release and benzodiasepines that bind to post-synaptic GABAA receptors and depress moto neuron activity

Question 6

How can spasticity arise from changes to MN properties?

Answer 6

• Persistent inward currents which lead to plateau potentials can result in self sustained firing and the amplification of synaptic inputs
• These bouts of self-sustained firing can only be terminated though the application of a hyperpolarising stimulus

Question 7

How does the potassium chloride co-transporter KCC2 play a role in mainiting the inhibitory actions of glycine and GABA?

Answer 7

• These inhibitors act on glycine and GABA(A) receptors which open Cl- channels, which relies on neurons having a low intracellular Cl- concentration
• The co-transporter KCC2 maintains this low concentration