Sativex Did Not Improve Spasticity Measures or Endocannabinoid Levels in MS Patients | Research

The takeaway

In 20 multiple sclerosis patients, the THC/CBD spray Sativex failed to improve spasticity on clinical or neurophysiological measures and did not alter endocannabinoid system markers.

Read this if you have MS and are considering cannabis-based treatments for spasticity.

Zero significant changes across all measured outcomes in 20 MS patients

What the researchers found

Twenty MS patients used Sativex (a THC/CBD oromucosal spray) and were assessed for changes in spasticity and endocannabinoid system markers.

Sativex failed to improve clinically measured spasticity. It also did not change stretch reflex excitability, a neurophysiological marker of spasticity.

On the biochemical level, Sativex did not affect the synthesis or degradation of the endocannabinoid anandamide. It also did not change the expression of CB1 or CB2 cannabinoid receptors on various types of peripheral lymphocytes.

Why it matters

While Sativex has been approved for MS-related pain in some countries, this study found no objective improvement in spasticity, suggesting the drug may not address all MS symptoms equally.

The numbers in context

20 MS patients were studied. Sativex contains both THC and CBD. No significant changes were found in any measured outcome.

How the study worked

This was an observational study of 20 MS patients receiving Sativex. Researchers measured clinical spasticity, stretch reflex excitability (neurophysiological), anandamide metabolism, and cannabinoid receptor expression on peripheral lymphocytes.

What this study cannot tell us

Small sample of only 20 patients. The study did not include a placebo control group. Peripheral lymphocyte markers may not reflect what is happening in the central nervous system.

How to read the evidence

Small uncontrolled observational study (n=20) without placebo comparison.

When this study was published

Published in 2009. Subsequent larger trials have provided more nuanced data on Sativex and MS spasticity, with some finding benefits on subjective but not always objective measures.

The bigger picture

This study highlights the gap between subjective symptom relief (reported in other studies) and objective clinical measurements. A drug can make patients feel better without producing measurable changes on clinical scales, raising questions about which outcomes matter most.

Questions still open

Why does Sativex appear to help some MS symptoms (pain) but not others (spasticity) on objective measures? Could longer treatment duration produce different results? Are peripheral endocannabinoid markers relevant to central nervous system effects?

Common questions

Does this mean cannabis does not help MS spasticity?

Not necessarily. Other studies have found subjective improvement in spasticity symptoms. This study focused on objective measures, and the disconnect between subjective and objective findings is itself an important research question.

Why were lymphocytes measured in a spasticity study?

Cannabinoid receptors are expressed on immune cells, and researchers wanted to see if Sativex altered the endocannabinoid system in measurable ways. The lack of change in peripheral markers does not rule out central nervous system effects.

Read the original research

Lack of effect of cannabis-based treatment on clinical and laboratory measures in multiple sclerosis.

Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 30(6), 531-4

View on PubMed ↗Publisher’s paper ↗

Citation

Centonze, Diego; Mori, Francesco; Koch, Giacomo; Buttari, Fabio; Codecà, Claudia; Rossi, Silvia; Cencioni, Maria Teresa; Bari, Monica; Fiore, Stefania; Bernardi, Giorgio; Battistini, Luca; Maccarrone, Mauro. (2009). Lack of effect of cannabis-based treatment on clinical and laboratory measures in multiple sclerosis.. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 30(6), 531-4. https://doi.org/10.1007/s10072-009-0136-5