Meinck, H M, et al, "Effect of Cannabinoids on Spasticity and Ataxia in Multiple Sclerosis." Journal of Neurology. 1989; 236: pp. 120-122.
The chronic motor handicaps of a 30-year-old multiple sclerosis
patient acutely improved while he smoked a marihuana cigarette. This
effect was quantitatively assessed by means of clinical rating,
electromyographic investigation of the leg flexor reflexes and
electromagnetic recording of the hand action tremor. It is concluded
that cannabinoids may have powerful beneficial effects on both
spasticity and ataxia that warrant further evaluation.
This study was prompted by a young man with multiple sclerosis (MS)
who used marihuana as a remedy for his various motor, micturition and
sexual handicaps. After smoking a marihuana cigarette on the ward, he
clinically. improved. He agreed to the beneficial effects of marihuana
being investigated by means of quantitative clinical and
This male patient, born in 1955, had had MS since 1983. At the time
of our experiments he was bound to a wheelchair because of severe limb
and gait ataxia and spastic tetraparesis. After micturition, his
residual urine volume was 100-150ml. He complained of impotence, with
erections lasting less than 5 min and lacking ejaculation. He tried a
marihuana cigarette in about 1984 and noted an instantaneous
improvement of his motor and sexual functions lasting for several days.
Since then, he regularly took some marihuana biscuits each week, which
enabled him to climb stairs, to walk on even ground, and to have
erections for more than 30min, allowing him a quite satisfactory sexual
From 12 October 1985 the patient abstained from all drugs, including
marihuana. He was hospitalized between 17 October and 25 October. On 22
October, one "experimental" marihuana cigarette was allowed, and
various electrophysiological experiments were performed as described
Clinical rating was performed daily by the same neurologist
and on 22 October before and after the "experimental" cigarette. Rating
comprised motor functions relevant to the electrophysiological tests
described below (see Fig. 1).
The flexor reflex was elicited by a painful electrical shock
to the foot sole and recorded from the quadriceps (Q), posterior biceps
(PB), gastroenemius (G) and tibialis anterior (TA) muscles. The EMG was
full-wave rectified, and eight consecutive reflexes were summated. Five
control series of eight consecutive reflexes each were run at intervals
of about 5 min. The patient was then asked to take one whiff of his
"experimental" cigarette, and further series of reflexes were run in
the manner described above (for details see ).
Finger movements were recorded in a standardized pointing task
performed before and after both the "experimental" cigarette and the
flexor reflex experiment. Basically, the recording device consisted of
a three-coil-transmitter system generating non-homogeneous magnetic
fields, and a miniaturized receiver coil attached to the finger tip.
When the finger moved through the magnetic fields a signal was induced
in the receiver coil, allowing the computation of the two- dimensional
movement trajectory (for details see ). Ten trials were performed
before and after marihuana smoking, each consisting of a pointing
movement of the right index finger over a 10-cm distance. The forearm
rested on a stable support, but the finger and hand could not reach the
Clinical rating showed a moderate deterioration of motor
functions between 17 October and 22 October (Fig. 1). On 22 October,
before the "experimental" cigarette, he was incapable of walking a few
steps even with support; his muscle force in the legs did not exceed
MRC grade 3. Muscle tone ranged between slightly and moderated
increased, and the leg deep tendon reflexes were exaggerated or clonic
with sustained ankle and knee clonus. The receptive field of the
Babinski sign covered the whole foot and the shin. Ataxia in the arms
was severe and could not be tested in the legs because of distinct hip
About 45 min after the marihuana cigarette, muscle force was
somewhat increased in the knee extensors and ankle flexors (but not in
the hip flexors), and muscle tone was reduced. The leg deep tendon
reflexes showed normalization, too, corresponding to a clear shortening
of the periods of clonus. The receptive field of the Babinski sign was
confined to the lateral foot sole margin. Ataxia in finger-nose testing
was moderate. After the flexor reflex experiment, the patient was able
to walk a few metres between the couch and his wheelchair with support.
Some of these improvements lasted beyond 23 October and even 24 October
The flexor reflex showed the desynchronized and prolonged
reflex pattern typical of spastic paresis (Fig. 2a; cf ). As soon
as 2 min after the whiff of the marihuana cigarette, a clear
attenuation of the reflex activity was noted. Attenuation was about
equal in all four muscles (20%-30% of the last three control
recordings) and progressed until 17 min after the whiff. A second whiff
(18 min after the first one) did not induce further reflex attenuation.
Single sweep recordings showed that the reflex attenuation after
marihuana was not due to enhanced habituation: after marihuana even the
first of the eight consecutive reflex responses was attenuated.
Electromagnetic recording of action tremor revealed a coarse 3
Hz hand and finger tremor with an amplitude between 1 and 3cm,
persisting throughout nearly the whole movement. Hours after the
"experimental" cigarette, action tremor was almost completely
abolished, although the movements were made at about the same speed
Our findings clearly show that there are indeed motor actions of
marihuana which were (a) reproducible in a laboratory situation most
exhaustive to the patient, (b) quantitatively assessable by means of
electrophysiological testing, and (c) in line with the results of
clinical rating. Our findings further correspond with earlier anecdotal
clinical reports [4, 6, 11, 14].
Little is known about the neurophysiological background of the
antispastic and antiataxic actions of marihuana seen in our patient.
However, some findings in experimental animals seem relevant to our
observations. Cannabinoids in higher dosages attenuate the monosynaptic
reflex [1, 2, 17, 18] principally corresponding to the attenuation of
both deep tendon reflexes and clonus in our patient (Fig. 1).
Polysynaptic reflexes were also attenuated after tetrahydrocannabinol
derivatives in experimental animals [1, 7, 20], fitting in well with
the narrowing of the receptive field of the Babinski sign (Fig. 1) and
with the results of our flexor reflex experiment. As cannabinoids have
analgesic properties [16, 20], attenuation of the pathological flexor
reflex in the present case could represent analgesic rather than
antispastic effects of the drug. However, analgesic effects are also
attributed to several antispastic drugs [10, 21] and, on the other
hand, classical analgesics such as opioids may improve spastic symptoms
. One might, therefore, indeed wonder whether both the antispastic
and analgesic actions of such drugs are in fact at least to a
substantial degree based on common neuronal mechanisms such as an
increase of presynaptic inhibition or a decrease of postsynaptic
excitation of multireceptive interneurones at various levels of the
neuraxis. Whatever the mechanism, the antispastic actions of marihuana
in both clinical rating and electrophysiological testing are similar to
those seen in spastic patients after either 0.3 mg tizanidine , 150
mg clonidine, or 10 mg diazepam (unpublished observations). The
important difference is that marihuana apparently also has antiataxic
actions (Fig. 2b; see also ) not ascribed to any antispastic drug.
The biochemical basis of the motor effects of marihuana is obscure.
Available data, although somewhat controversial, suggest that
cannabinoids release brain serotonin from its storage sites and block
its re-uptake , inhibit the synthesis of prostaglandins within the
CNS  and - in large doses - elevate brain acetylcholine and reduce
its utilization . The relationship of these neurotransmitters to
spasticity and ataxia is unknown: none of the well-established
antispastic drugs is thought to interfere with them; they are onlv
scarcely, if at all, found within the cerebellum .
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