DAVID BAKER, GARETH PRYCE, J. LUDOVIC CROXFORD, PETER BROWN,
ROGER G. PERTWEE, JOHN W. HUFFMAN & LORNA LAYWARD

Chronic relapsing experimental allergic encephalomyelitis (CREAE) is an
autoimmune model of multiple sclerosis. Although both these diseases are typified
by relapsing-remitting paralytic episodes, after CREAE induction by sensitization to
myelin antigens Biozzi ABH mice also develop spasticity and tremor. These
symptoms also occur during multiple sclerosis and are difficult to control. This has
prompted some patients to find alternative medicines, and to perceive benefit from
cannabis use. Although this benefit has been backed up by small clinical studies,
mainly with non-quantifiable outcomes, the value of cannabis use in multiple
sclerosis remains anecdotal. Here we show that cannabinoid (CB) receptor agonism
using R(+)-WIN 55,212,  9-tetrahydrocannabinol, methanandamide and JWH-133
(ref. 8) quantitatively ameliorated both tremor and spasticity in diseased mice. The
exacerbation of these signs after antagonism of the CB1 and CB2 receptors, notably
the CB1 receptor, using SR141716A and SR144528 (ref. 8) indicate that the
endogenous cannabinoid system may be tonically active in the control of tremor and
spasticity. This provides a rationale for patients' indications of the therapeutic
potential of cannabis in the control of the symptoms of multiple sclerosis, and
provides a means of evaluating more selective cannabinoids in the future.
 

Cannabinoids control spasticity and tremor in a multiple sclerosis model 

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