In Reply:—

We appreciate Dr. Gourlay's interest in our work. 1Of course, we are aware that clonidine, while diminishing sympathetic neural outflow both in volunteers 2and in opioid addicts, 3,4acts as an agonist on central α-receptors. We apologize for the typographical error that appears on page 571 of the original article.

We agree that antagonist supported detoxification from opioids during general anesthesia can restore opioid sensitivity. Accordingly, opioid receptor blockade, e.g. , by oral naltrexone, should be maintained in formerly addicted patients as long as possible to prevent both relapses as well as potentially fatal effects of further opioid intake. However, our patient experienced chronic pain with tolerance to the analgetic effects of administered opioids. Thus, antagonist supported detoxification was intended to restore opioid sensitivity, allowing continuation of analgesic therapy by administration of much lower opioid dosages while again achieving sufficient analgesia.

With respect to cost–benefit ratios, we expect by this procedure high rates of successful detoxification with markedly shortened hospitalization. 5,6Accordingly, this procedure seems to be economically attractive. However, a decrease in the number of relapses may not be expected, although little data are currently available.

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