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Narcissus and Daffodil

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342 D. Brown<br />

cortex <strong>and</strong> hippocampus, results in reduced levels of acetylcholine which are<br />

thought to be associated with loss of memory <strong>and</strong> disrupted cognition. Drugs that<br />

preserve acetylcholine by inhibiting its destruction by cholinesterase, such as<br />

neostigmine, rivastigmine, tacrine, metrifonate <strong>and</strong> galanthamine, can reduce<br />

AD symptoms <strong>and</strong> delay, but not halt, disease progression (Mucke, 1997). Several<br />

small trials <strong>and</strong> what amount to anecdotal reports provide an impression that<br />

galanthamine is useful in this respect <strong>and</strong>, because of this early promise, several<br />

larger <strong>and</strong> more carefully controlled trials are underway. This work is reviewed in<br />

the next chapter of this volume. Specific, non-AD applications are described<br />

below.<br />

Neurological injury<br />

Paskov (1986) reviews the use of galanthamine to treat a wide range of neurological<br />

disorders. Most of the evidence is anecdotal <strong>and</strong> unclear, but it is logical to<br />

expect that if the neurological injury involves a cholinergic pathway resulting in a<br />

reversible deficit or imbalance of acetylcholine, then galanthamine may be of use.<br />

Reversal of pathological paralysis<br />

In the 1960s, galanthamine was used, again in eastern European countries, to<br />

assist recovery from paralysis associated with poliomyelitis, neuromuscular disorders<br />

or neuromuscular diseases. Trigeminal neuralgia was managed with oral <strong>and</strong><br />

intramuscular administration <strong>and</strong> occasionally by infiltration. Doses of 15–25 mg/<br />

day were typically used (Kilimov, 1961a). Galanthamine was reported to produce<br />

motor function improvement in 15 of 25 children with muscular dystrophy (Pernov<br />

et al., 1961) <strong>and</strong> in patients with myasthenia <strong>and</strong> neuromuscular dystrophy (Pestel,<br />

1961). Sixteen of 20 patients with brain injuries (not specified) showed improvement<br />

on galanthamine (Kilimov, 1961b). Revelli <strong>and</strong> Grasso (1962) noted varying<br />

degrees of benefit in 49 of 52 patients suffering from post-febrile polio during a<br />

3-month trial of the drug at doses of 2.5–10 mg/day. Gopel <strong>and</strong> Bertram (1971)<br />

reported the use of galanthamine in an heterogeneous group of patients studied<br />

over a 30-month period, using subcutaneous doses of galanthamine in the range<br />

1.25–25 mg daily. Beneficial effects were seen in the following disorders, some of<br />

which were resistant to conventional therapy: facial paralysis (22 of 22); peripheral<br />

neuropathy (38 of 46); paralysis of central origin (11 of 12); progressive myodystrophy<br />

(1 of 2); poly/dermatomyositis (3 of 3) <strong>and</strong> multiple sclerosis (4 of 4). The<br />

authors stated that the drug was well tolerated.<br />

Gujral (1965) studied 100 patients with post-polio spinal paralysis, seven with<br />

muscular dystrophy <strong>and</strong> two with facial paralysis due to lower motor neurones.<br />

Galanthamine was administered as a series of courses of 40 subcutaneous injections,<br />

repeated after a 6- to 8-week interval, up to a maximum of three courses per<br />

patient. Total daily doses were related to age. Drug treatment was combined with<br />

physiotherapy; this may have confounded the results, as physiotherapy was<br />

already proven to be effective <strong>and</strong> was not administered uniformly. In any event,<br />

the results were far from conclusive. Only modest number of patients showed<br />

improvement with galanthamine. The author concluded that the drug was most<br />

likely to have a beneficial effect in early cases of post-polio paralysis (improvement

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