Cannabinoids

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related to muscle spasticity. Analgesic effects of both active drugs were similar
and both superior to placebo. It was noted that THC also significantly improved
the spasticity. No adverse effects were reported. Holdcroft et al. (1997) compared
oral THC (50 mg daily in divided doses) with placebo in a 6-week, double-blind,
crossover trial in a patient who required daily morphine to control chronic pain
associated with familial Mediterranean fever. The patient was allowed to take
morphine tablets as required, and although VAS pain scores remained similar in
the THC and placebo conditions, the morphine consumption was significantly
reduced (p<0.001) in the THC period.
This limited body of work was subjected to meta-analysis (Campbell et al. 2001),
and the authors reached the following conclusion:


Cannabinoids are no more effective than codeine in controlling pain and
have depressant effects on the central nervous system that limit their use.
Their widespread introduction into clinical practice for pain management
is therefore undesirable. In acute postoperative pain they should not be
used. Before cannabinoids can be considered for treating spasticity and
neuropathic pain, further valid randomised controlled studies are needed.

The validity of this conclusion was challenged by several correspondents to the
editor of the journal. For example, Iversen (2001), noting that “a wealth of animal
data support a role for cannabinoids in pain modulation” in contrast to the paucity
of controlled human studies available for review, criticised the authors for “coming
to a series of emphatic but ill-founded conclusions”.
A further study of oral THC in postoperative pain has also given negative
results (Buggy et al. 2003). THC 5 mg was compared with placebo in a randomised,
double-blind, single-dose study in 40 women who had undergone abdominal
hysterectomy. Measurement of summed pain-intensity difference at6hpostdose
revealed no difference between THC and placebo. However, there was also no
difference between the groups in the incidence of adverse events, so the negative
findings may be the result of a sub-therapeutic dose of THC.
Emerging evidence from basic science (e.g. Bridges et al. 2001; Fox et al. 2001;
and Walker and Hohmann, this volume) implies that cannabis may benefit neuro-
pathic pain. The 1997 National Institute of Health workshop on medical cannabis
concluded: “Neuropathic pain represents a treatment problem for which currently


available analgesics are, at best, marginally effective. Since∆^9 -THC is not acting by


the same mechanism as either opioids or NSAIDs [nonsteroidal anti-inflammatory
drugs], it may be useful in this inadequately treated type of pain.” The UK House
of Lords Science and Technology Committee (1998) came to a similar conclusion:
“... pain which originates from damaged nerves might respond to cannabinoids....
An example of such pain is phantom limb pain following amputation.... [There is]
anecdotal evidence that cannabis can relieve this pain [and] ... trials of cannabis
should be undertaken in such patients.”
Notcutt and colleagues (1997) reported their qualitative experience of the use of
nabilone (synthetic THC analogue) in the treatment of 43 patients with severe pain
resulting from MS, SCI and other sources of peripheral or central nerve damage,

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