previous to this date, were both abundant and accurate, but the attention of the profession was not properly directed to it until its pathology and etiology were fully set forth by the labors of Joffroy, Leyden and Grainger Stewart, between the years 1879 and 1882. It is greatly to the credit of American medicine that, in the early days of our republic, we find the first concise and accurate account of the affection now called multiple neuritis. This account was furnished by Dr. James Jackson, of Boston, in the year 1822. His cases, many of which were women, were typical of alcoholic multiple neuritis, which for want of a better name, he called "arthrodynia a potu," thus recognizing one of the chief exciting causes. He distinctly states that the paralysis was in the muscles and not in the nerves, possibly meaning thereby that it was peripheral and not central. Some years later, Graves, of Dublin, and Chomel investigated together many cases and concluded the whole affection was peripheral and not due to central lesion. Again, from 1852 to 1855, Duchenne and other neurologists, not only recognized the alcholic form of neuritis, but proved that there were no lesions in the brain or cord to account for the paralysis. Neverthless, the motor and sensory disturbances were generally referred to the cord. As late as 1864, Dumesnil published contributions on the subject, in which a well-observed case was recorded, and upon which an autopsy was held. Microscopic examination discovered that the nerve trunks and their ramifications had undergone degeneration, and further examination showed no alteration in the spinal marrow. Even these well-established conclusions failed to receive much consideration. Earlier special treatises on neurology, such as Dr. W. A. Hammond's first edition of 1870, and others of that date, have no chapter on the subject. Since 1882, however, great attention has been bestowed on its study, and its bibliography has grown to large proportions.

This is not only an interesting and important affection, but a very grave and serious one, and by no means uncommon. Its characteristic features are the involvment of many or all the nerves in the body, the production of complete palsy of all the limbs, often a long and tedious illness before recovery, and sometimes a fatal termination; and also that a large number of exciting causes are responsible for its production.

Dr. Ross has given us a detailed classification of multiple neuritis, based partly on its course and progress in some forms, and partly on the varied etiological factors.

1.

2.

The idiopathic form, as in Landry's paralysis.

The toxic, which is subdivided into:

(a) Those cases due to diffusible stimulants, as alcohol, etc. (b) Those cases due to animal poisons, as diphtheria, typhoid, septicemia, syphilis, tubercle, beri-beri and leprosy. (c) Metallic poisons, lead, arsenic, etc.

(d) The endogenous, as gout, diabetes, etc.

3. The dyscrasic form, from cancer and other cachexia and vascular degenerations.

4. Sensory, vaso-motor and trophic, as found in ataxia and Raynaud's disease.

5. The irritative form, etc.

Our limits will only allow us to briefly discuss some of the toxic group, chiefly the alcoholic. Cases of multiple neuritis vary greatly in extent and intensity and in the final results. If the toxic cause has been operating for a long while, the case will be proportionately severe. If the respiratory nerves be involved, a fatal termination may rapidly ensue. If the system is broken down and visceral complications exist, the condition will be a very grave one. On the other hand, if the distribution is limited to a few groups and the exciting cause can be removed and the general health is fair, an easy course and short duration can be predicted.

The morbid anatomy in multiple neuritis is essentially the same as in isolated neuritis. The inflammation, which may be acute or chronic, sometimes attacks the axis cylinder, the myelin and the sheath of Schwann, constituting parenchymatous neuritis. Or the connective tissue may become primarily involved; interstitial neuritis. The important results in both instances being the impairment or abolition of the conducting power in the nerve, and finally the breaking up of the myelin and the complete degeneration of the axis cylinder.

It is well to remember the distinction between a nerve whose conductivity is lost by reason of a spinal lesion and one in which neuritis has occurred. In both cases the function may be equally lost.

Where it is due to disease of the grey matter of the ante

rior horns, the nerves proceeding from that center, degenerate downwards to the periphery; but in neuritis the inflammatory action begins in the nerve endings and extends upwards, the de— generation proceeding pari passu with the inflammation. As the nerve ceases to functionate, the muscular fibres supplied by it become flaccid and flabby, lose tone and very soon show atrophyThe normal faradic response is lost, and reaction of degeneration supervenes if recovery is long delayed. The remarkable feature in these apparently radical changes in nerve elements is the capacity of restoration through the process of regeneration, so that although the function has for months been destroyed, under favorable conditions a return to the normal often takes place.

The nature of the toxin influences somewhat the morbid change. Lead acting specially on the myelin. Leprosy producing the interstitial type, while alcohol and diphtheria most generally excite a parenchymatous type.

The causation in the various forms of polyneuritis is an attractive part of the subject; investigations of recent years discovering a wide range of etiology. Long before our knowledge was systematized the abuse of alcohol was admitted to be an active cause, and now we know that it is the most common of all. It is not the man who indulges in periodic sprees, drinking heavily for a few days; but the steady drinker, provided he drinks daily to excess, that becomes the victim of neuritis. Thus we find that women are more frequently the subjects than men, probably because when they acquire the habit it is a constant indulgence, but as Gowers suggests, it may also be because of some peculiarty in that part of their nervous structure. Those who in addition to hard drinking, are poorly fed, hard worked and exposed to the inclemency of the weather, become more often affectedAlcoholic neuritis is often accompanied by meningitis, and hepatic and renal disease from the same poison.

The next largest group of cases are those poisoned by absorption of lead in one way or another. The commoner forms of lead poisoning, as colic, constipation and wristdrop, are by no means all the bad effects of this absorption of the metal. The brain, the spinal cord and the peripheral nerves are often extensively implited. Those whose occupations bring them in close contact with the metal are liable, such as miners, smelters, the employees in

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paint factories, painters, plumbers and those who drink water impregnated with some of the salts of lead, are all more or less liable to some form of peripheral paralysis.

In many instances the infectious diseases, through the toxin generated in the system, produce these results. Diphtheritic toxins are the best recognized of these, and although this has been known for many years, only of recent years has its full importance been admitted. Tyyhoid fever, measles, smallpox, syphilis, septicemia and leprosy are now admitted to be responsible for a great many cases. It is doubted by some neurologists whether there is any purely rheumatic polyneuritis; and it is further a question whether cold and chilling can produce it. Most neurologists incline to the opinion that this chilling only presents a favorable condition for the development of some preexisting toxin.

Symptomatology.-As in all nervous diseases, we can best arrange the symptoms that belong to multiple neuritis in the spheres of motor, sensory, reflex-visceral and psychic activities.

Paralysis, slight or complete, is the common and conspicuous sign of multiple neuritis. This loss of power in the muscle supplied by the nerve undergoing inflammatory degeneration is of the flabby, flaccid type, and along with this loss of tone comes loss of reflexes, together with that impairment of nutrition ending in atrophy and final and complete destruction of the muscle fibre and the nerve endings.

These correlated phenomena are easily understood when we remember their physiologic relations, which are precisely the same, whether the destruction takes place at the polar end of the neuron, as in poliomyelitis, or in the peripheral end, as in multiple neuritis. The five changes in the muscular tissue, namely, paralysis, flaccidity, atrophy, loss of tendon reflex and changed electrical reaction, although not equally prominent in every case, are cardinal symptoms, which, if rightly observed, will usually establish the nature of the case. In addition, these symptoms will be usually bilateral and symmetrical, because the toxins circulating in the blood reach both sides alike.

Where the patient is still able to walk, a striking peculiarity in his gait will be observable, due to loss of power to raise the toes; and in order to clear obstacles in the way, the knee and hip

must be more flexed and the foot raised higher, quite different from the swinging motion of the hemiplegic. In some cases incoordination of the limbs occurs, while cramps and tremor are not exceedingly rare. Slow chronic contractions come on late in the case, especially in the hamstring muscles, giving the patient pain and distress.

The application of the Faradic and Galvanic currents are to be used in order to test changed reactions in the nerve and muscle.

Alterations in sensation are hardly ever absent in peripheral neuritis, although varying much in kind, in extent and intensity. Pain is an early symptom, but is much aggravated later, especially when the affection is due to alcohol. At times very sharp and quick, at other times burning and dull. It is located in the small nerve twigs, muscles and overlying skin. Along with pain, extreme tenderness is common-pressure over the course of the nerve, or squeezing the muscles, producing intense suffering. Paresthesia, in the way of tinglings and formications, is quite common, and you seldom meet a case where some variety of anesthesia is not present to some extent. The reflexes suffer in all cases of polyneuritis, the knee jerk being lost early.

Another and important symptom is the implication of some of the visceral nerves, chiefly the pneumogastric, giving rise to a weak and quickened action of the heart.

Multiple neuritis has two modes of access, in the one class of cases, the onset is abrupt and rapid; in the other class, insidious, slow and chronic. In the acute cases, a slight chill and febrile reaction may occur, and the disease may be fully established in a few days. In the alcoholic cases, the acute form is usually attended with great pain, followed very quickly by paralysis. In those cases of gradual onset, the patients keep up for some time, the paresis passing into complete palsy very slowly, or only continuing as paresis for a few months and then recovery occurs.

I think I can better exemplify the varieties, the progress and termination of multiple neuritis by citing four cases from my note book:

Some fifteen years ago I was called to see a man in his thirtyseventh year. I was informed that he had drank freely and constantly for the previous ten years, and that twice before had