On the third day of WCNR 2018, an interesting spasticity symposium (co-organised by the Spasticity SIG) was conducted.
As per Dr Gerard Francisco, Professor and chair of PM&R, UTHEALTH Neuro recovery Research Center, TIRR Memorial Hermann:
Why did treatment outcomes vary?
- Similarities
- Assessment
- Clinical criteria for decision making
- Toxin
- Injection technique
- Therapy Program
Differences:
- Age
- Sex
- Chronicity of Stroke
- Location of stroke
- (No stroke volumetric information)
- Genetic make-up?
“Injuries to the insula, the thalamus, the basal ganglia, and white matter tracts ( internal capsule, corona radiata, external capsule, and superior longitudinal fasciculus) were significantly associated with severe upper limb post-stroke spasticity, said Dr Gerard Francisco.
Types of spasticity:
Intrinsic tonic
Exaggerated tonic stretch reflex
Neuronal changes
Changes in muscle properties
Intrinsic Phasic
- Reduced pre- synaptic la inhibition – hyperreflexia
- Recurrent activation of stretch reflex
Extrinsic
- Lack of inhibition of afferent peripheral input ( “flexor reflex afferents”) that mediate polysynaptic reflexes
Spasticity treatment options:
- Botulinum toxins
- Physical modalities and therapies
- Oral drugs
- Surgery
- Intrathecal therapies
- Phenol and alcohol injections
- Others
According to Dr Gerard Francisco, “No two spastic presentations and conditions are alike, so perhaps the underlying pathology may vary.”
On the question, why do outcomes of post-stroke spasticity management vary? He said, “Different underlying pathologies and mechanisms should inform treatment decisions.”