Upper motor neuron evaluation in multiple sclerosis patients treated with Sativex®

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Spasticity is one of the most common disabling symptoms in multiple sclerosis (MS), occurring in 40%–70% of patients with MS and showing increased severity as disease progresses.1 Spasticity is a motor disorder, characterized by a velocity‐dependent increase in muscle tone resulting from hyperexcitability of the stretch reflexes.2 The key to the increased excitability is the abnormal activity of muscle spindles, which show an intricate relation with the innervation of the extrafusal muscle fibers at spinal level, under the influence of the supraspinal inhibitory and facilitatory pathways.3 Although the pathophysiology of spasticity has been addressed in a number of studies during the past decades,4 the role of the pyramidal pathway in its determination is still unclear and, to date, the treatment of spasticity rests almost solely on empirical basis.
Recent studies have confirmed the clinical efficacy of Δ‐9‐tetrahydrocannabinol (THC) and cannabidiol (CBD) (Sativex®) for the treatment of MS‐related spasticity.5 The antispastic effect of cannabinoids is primarily mediated by CB1 receptors.10 Activation of CB receptors might also exert a neuroprotective effect through a CB1 receptor‐mediated inhibition of excitotoxicity and through a CB2 receptor‐mediated inhibition of neuroinflammation.11
In this study, we (i) assessed the functional and structural integrity of the upper motor neuron (UMN) in MS patients with and without spasticity and (ii) explored the evolution of UMN impairment longitudinally in patients under treatment with Sativex® to clarify the structural and electrophysiological correlates of Sativex® clinical effect.

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