action of the injected solution (Combes and Clark, 1960; Sunderland, 1968), or neuritis may develop from progressive inflammatory and fibrotic changes (Tarlov et al, 1951). If the injury results from progressive inflammatory and fibrotic changes, there is usually a latent period before the onset of paralysis. The severity of neural damage is determined by the internal structure of the nerve at the site of injury and the amount of toxicity of the injected material (Sunderland, 1968). Most therapeutic agents in use could cause paralysis if injected into the wrong site (Ling and Loong, 1976). The committee did not consider such injuries to be adverse events associated with the toxoid.
The pathogenesis of brachial neuritis is not well understood. It has been suggested that this form of neuropathy may be a manifestation of a systemic or localized infectious disorder, possibly vital, or the result of an allergic or hypersensitivity reaction, such as that which may occur after vaccination, but this is far from conclusive (Tsairis et al., 1972). Although the pathogenesis of brachial neuritis is unclear, it is a well-defined clinical syndrome, and its occurrence following administration of tetanus toxoid has been described in the literature numerous times (Baust et al., 1979; Bensasson et al, 1977; Dittmann, 1981c; Getsbach and Waridel, 1976; Kiwit, 1984; Tsairis et al., 1972).
Two case reports in the literature link administration of tetanus toxoid to a peripheral mononeuropathy. Ling and Loong (1976) described a 47-year-old male who developed a left radial nerve palsy 2 weeks following a painful injection of tetanus toxoid into his left arm. This case was felt to be caused by direct injection of tetanus toxoid directly into the radial nerve. Blumstein and Kreithen (1966) described a 23-year-old who developed a complete radial nerve paralysis 7 hours following injection of tetanus toxoid into the right deltoid muscle. Cranial mononeuropathies have been described in three separate case reports. Eicher and Neundorfer (1969) reported a reversible paralysis of the left recurrent laryngeal nerve 8 days after receipt of a booster injection of tetanus toxoid. von Wirth (1965) described a patient who developed reversible deafness resulting from cochlear neuritis 5 days following receipt of a booster of tetanus toxoid. Hatter et al. (1971) described a 21-year-old man who developed deglutition paralysis and accommodation paresis 10 days following receipt of a tetanus toxoid booster. All of these cases, except those in which tetanus toxoid was injected directly into the nerve, were considered to have an allergic basis.
A number of case reports in the literature associate the development of brachial neuritis with administration of tetanus toxoid. Dittmann (1981c) provides an uncritical review of 12 cases of ''neuritis'' following receipt of