One of the few truly long-term follow-up studies I have found regarding botulinum toxin type A (in this case Botox®) was out of Jordan, Turkey and the University of Cincinnati. In this study, chart reviews were performed on 32 patients who were being treated for hemi-facial spasm and blepharospasm and had had at least one Botox injection annually for at least 10 years (some patients had been treated for 20 years). The findings demonstrated a need for a slightly higher dose of Botox to be effective over time and a decrease in the number of adverse effects (i.e. complications) over time. No life-threatening or systemic complications were reported, only localized ones likely relating to the function of the drug at the site of injection. Several other studies with follow-up between 6-15 years have found similar results. The latter finding is likely a function of greater experience treating patients after many years and improved injection techniques. The former finding can be related to a number of potential causes.
Prolonged treatment with botulinum toxin type A has been shown to result in the development of neutralizing antibodies which are thought to decrease the efficacy of the toxin. Risk factors for the development of such antibodies are the formulation of the toxin, the frequency and dosage of the injections and the conditions for which the injections are being used. Decreased efficacy (and hence the need for higher doses) may also be a reflection of the progressive nature of the disease being treated. In other words, if the nerves are progressively injured by the disease process, they may require higher doses of Botox for clinical effectiveness. The take home message would be that Botox appears to be relatively safe and effective in long-term use although very few studies have been done to test this concept formally and none with occipital neuralgia. Therefore, in my hands botulinum toxin type A remains a diagnostic test which, if effective, means that no more botulinum toxin type A needs to be injected - the patient is a candidate for decompression. After all, in ON we are talking about a mechanical compression of the nerve(s) by a physical structure (muscle, fascia, blood vessels) and no amount of medicine will make that go away.