Experimental allergic neuritis was produced in 77 out
of 93 guinea-pigs injected intradermally with antigenic
emulsion containing human sciatic nerve and modified
Neurological features of the disease began approximately
17 days following the injection and these were characterised
by instability of posture following displacement, symmetrical
ataxia of gait and some weakness, especially of the hind
limbs. Weight loss usually accompanied the onset of
the clinical features in severe cases and only in these
animals was any constitutional upset evident. Animals
were graded according to their most severe clinical disability.
Specimens of sciatic nerve, spinal roots and ganglia as
well as parts of the spinal cord were examined histologically.
The most striking abnormalities in specimens from diseased
animals were found in the sciatic nerve trunk. These
consisted of focal areas of demyelination of varying severity
with relative sparing of axons. Cellular infiltration with
large and small mononuclear cells accompanied the
demyelination but this was not an invariable feature.
Spinal roots sometimes showed lesions, while lesions
in the root ganglia were rare. Sections of spinal cord
and other parts of the central nervous system were
The possible immunological mechanism in the pathogenesis
of the disease is discussed.
Electrophysiological observations were made in vitro on whole
sciatic nerves and in vivo on spinal roots supplying the medial
gastrocnemius muscle. In addition, single afferent fibres from t
his muscle were isolated by systematic dissection of dorsal root
filaments, identified as coming from muscle stretch receptors and
differentiated into muscle spindle and Golgi tendon organ afferents
by physiological methods. In all cases, observations were made on
normal control animals and the results compared with similar observations
on demyelinated nerves from animals with clinical features of
experimental allergic neuritis. In the demyelinated nerves,
experiments showed that conduction in some fibres was blocked,
others continued to conduct, but at reduced velocity and
finally some fibres appeared to conduct normally. The possible
reasons for these changes in conduction are considered in
relation to the normal mechanism of nerve impulse transmission.
A comparison is made between the clinical features, conduction
velocities and histological changes in guinea-pigs with
experimental allergic neuritis and it is concluded that, in
general, correlation is best in severely affected animals.
In the absence of pathological changes in the central nervous
system, neurological features of diseased animals have been
explained, on the basis of the defective conduction in the
Evidence is presented that some animals which made a complete
clinical recovery from the disease still had demonstrable
lesions in the peripheral nerves associated with defective
conduction. An analogy is made between this finding and
those found in apparently recovered cases of polyneuritis in
Maximum conduction velocity of the nerve to the medial
head of gastrocnemius is related to the size of the largest
fibres in the same nerve, measured from histological sections.
The result is contrasted with results from similar studies by
other authors and it is suggested that the myelinated nerves
of the cat conduct at a faster velocity per I
μ. diameter than those of either the rabbit, the guinea-pig or the rat.