. POLYNEURITIS Polyneuritis or multiple neuritis is seen in children after acute infectious diseases and poisoning, or as an idiopathic disease. From the cases reported it appears that diphtheria, scarlet fever (Seifert, Baselli, Itemak), mumps (Joffroy), whooping-cough alobius), influ enza, pneumonia and typhoid fever predispose to multiple neuritis. The most important poisons are alcohol, lead and arsenic. As an independent disease multiple neuritis has been observed not only sporadically but also in epidemic form as well as in association with poliomyelitis and poliencephalitis.
11-e will first consider the symptoms. of multiple neuritis such as they appear especially in the idiopathic form, after which the somewhat aberrant course observed in postcliphtheritic, alcoholic, saturnine and arsenical neuritis will be discussed.
Multiple neuritis (except after diphtheria, see below) is a very rare disease in childhood, particularly in comparison with acute inflammation of the brain and spinal cord, which are EO frequent at that period of life. The disease usually begins with weakness and pain in the extremities; the legs are generally attacked first. The child is easily fatigued, there is motor weakness, emaciation, especially in the muscles of the leg, and the deep reflexes are abolished. As the peroneal muscles are chiefly attacked by the disease in children, the gait, aside from the general weakness of the legs, becomes characteristic ancl is known as stepping gait. Electric irritability in the diseased muscles is usually dimin ished; sometimes the reactions of degeneration are present. Pain may either occur spontaneously in the legs, or may be elicited by pressure on the nerve trunks and muscles; widespread or localized hypermsthesia, more rarely anmsthesia, is frequently present. The skin reflexes are also, as a rule, diminished. In most cases the arms are attacked at a later period, when the paralysis of the legs is already quite marked. Again, the forearm and the hand are the parts chiefly involved; the muscles supplied by the radial nerve being frequently involved more than any others (individual muscles in the distribution of the diseased nerve may remain intact). Atrophy, electric irritability, the state of the reflexes, and the sensory disturbances are exactly the same in the arms as in the legs; but the motor and s.ensory paralysis in the arms is often much less
marked than in the lower extremities. The paralysis of the arms is sometimes accompanied by tremor. The palsy is always bilateral and usually uniform in intensity. Extension of the motor weakness to the muscles of the trunk is rare, weakness of the sphincters still more rare; sluggishness of the bowels is somewhat more frequent. The cranial nerves (ocular muscles), the pneumogastric and the phrenic are attacked only in exceptional cases in children. Trophic changes such as abnormal sweat secretion, cederna and changes in the skin sometimes occur. The occurrence of a polyneuritic psychosis (Korsakow) has, so far as I know, never been observed in children.
Multiple neuritis does not always exhibit the distribution described above; it rnay be limited to smaller territories (legs). Thus I have seen a bilateral paresis of the peroneal muscles develop spontaneously with pain, which could be interpreted only as a neuritis.
Multiple neuritis may come on suddenly' like a febrile disease and run an acute febrile course. Insidious onset, however, is more frequent; the disease reaching its acnie in from two to four weeks, and persisting at that point for several months. In favorable cases multiple neuritis in children lasts from several weeks to six months. Localized muscular atrophy and paralysis may persist after the disease has run its course, Death is very exceptional, although the primary disease to which the polyneuritis is clue may terminate fatally.
The pathology of multiple neuritis, in so far as the findings in adults can be applied to children, shows inflammatory degenerative disease of the peripheral nerves. It is not always easy even in the histologic pic ture to distinguish polyneuritis from nerve degeneration. Spinal changes in the form of poliomyelitic foci and degeneration of ganglion cells and fibres, which may also be present, must be ascribed to some toxic affec tion of the spinal cord. The changes in the spinal cord must be regarded as coordinate with the peripheral changes and not as the primary condition.