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Controlled trials are particularly important in evaluating treatment in a condition such as Guillain-Barre syndrome (GBS), which has a high incidence of spontaneous recovery. Nevertheless analysis of 904 cases published in the last 15 years indicates the need for improved treatment since only two-thirds of patients had recovered by the end of a year, while 7% had died [15].

Erythrocyte and plasma glutathione peroxidase levels were measured in 12 patients with multiple sclerosis, in 11 age- and sex-matched normal subjects, and in 12 similarly matched patients with other neurological diseases. No difference was found in the enzyme levels in the three groups, indicating that glutathione peroxidase deficiency is not a contributing factor in the aetiology of multiple sclerosis.

EXPERIMENTAL ALLERGIC NEURITIS (EAN) is a model of human acute inflammatory polyneuropathy, Guillain–Barre syndrome. It can be produced in several species of laboratory animal by immunisation with homologous or heterologous peripheral nerve emulsified in Freund's complete adjuvant1,2. After about two weeks the animals may develop signs varying from ataxia to paralysis and death. EAN has been produced using crude acid extracts of peripheral nerve3,4, but investigations into the neuritogenic properties of the component proteins of peripheral nerve myelin have yielded inconclusive results5–10. In experimental allergic encephalomyelitis (EAE), the central nervous system (CNS) counterpart of EAN, the encephalitogenic antigen has been shown to be a CNS myelin basic protein of molecular weight 18,000 (ref. 11). The three major proteins of peripheral nerve myelin, which together account for about 75% of the myelin protein, are usually referred to as P0, P1 and P2 (ref. 12). P0 is a glycoprotein of molecular weight 30,000 and P1 and P2 are both basic proteins with molecular weights of 18,000 and 12,000–14,000, respectively12–13. We describe here a reliable method for producing severe EAN in inbred Lewis rats with bovine intradural root material, and show that intact P2, the major basic protein of peripheral nerve myelin, is the responsible neuritogen.

Preliminary observations suggested that arterial and arteriolar necrosis in vasculitis of the peripheral nerve leads to local haemorrhage and subsequent deposition of haemosiderin. This pigment is more readily recognized in the nerve by the sensitive Perls' test for iron than by relying on recognizing its yellow colour. To support the use of iron staining as an index of vasculitis, in addition to necrosis and fibrin deposition, we obtained the following results from nerve biopsy and autopsy nerve specimens: vasculitis confined to PNS = 5/6 iron positive; polyarteritis nodosa and Wegener's granulomatosis = 4/5 iron positive; systemic lupus erythematosus 2/3 iron positive; rheumatoid disease 1/1 iron positive; acute Guillain–Barre syndrome and subacute or chronic demyelinating polyradiculoneuropathy = 12/12 iron negative; and other perivascular inflammation in the PNS (without evidence of vasculitis) = 2/2 iron negative. One case of Churg–Strauss syndrome showed no changes on nerve biopsy. Iron staining was also demonstrated in the kidneys of five or six patients with polyarteritis nodosa.