spinal meningitis. The paralysis, contractures, and other late results of the myelitis are to be managed in accordance with the rules of practice in that disease.

Chronic Spinal Leptomeningitis.-The chronic form of inflammation of the soft spinal membranes is usually the sequential stage of an acute attack, but may follow alcoholism, syphilis, or tuberculosis. Its existence as a primary affection is open to some doubt, but a very slowly developed leptomeningitis may follow concussion, though it is impossible in such a case to exclude immediate slight histological injuries of which the later inflammation is a natural development. The formerly much used term "chronic meningitis," which was applied to every group of obscure subjective symptoms, however remotely referable to the spine, needs no mention.

The symptoms are practically those of the acute form much reduced in intensity, and are dependent upon similar causes. Pain in the back predominates, and spasm is insignificant or absent. The radiating neuralgic pains are especially pronounced, and paresthesia are prominent. Their distribution depends upon the nerve-roots involved and the location of the inflammation, which is much more circumscribed than in the acute form. The late manifestations are those due to neuritis originating in the roots, and myelitic symptoms are comparatively infrequent.

The anatomy of the disease is very little known, as opportunity for post-mortem examination rarely occurs, but more or less extensive fibrous thickening, or adhesions between the pia and dura which constrict the nerve-roots, may be found, and may girdle the cord. Degeneration of the spinal nerves traversing the lesion is not rare, and this accounts for the herpetic and other cutaneous symptoms which are occasionally noted. The prognosis will be guided mainly by the effect of treatment, but a complete recovery is very rare. Each case must be carefully estimated by itself.

The treatment in syphilitic cases consists in the heroic management of that disease, and iodids and mercury in small doses are also the most efficient drugs in non-luetic cases. General measures are of service, and persistent counterirritation over the spine, preferably by Paquelin's cautery, is the most valuable local measure. Sometimes rest in bed and the ice-bag to the spine are of distinct value. Sedatives and analgesics are often required.

Spinal Meningeal Hemorrhage.-Spinal meningeal hemorrhage is either extradural, in the vertebral canal, or subdural, within the dural sheath. It is frequently associated with intracranial hemorrhage and with hemorrhage into the substance of the cord, but also occurs independently.

Etiology.-Meningeal hemorrhage occurs frequently at birth in protracted and difficult labors, and is then almost invariably a part of a more extensive hemorrhage within the skull. It has been considered under the cerebral palsies of childhood. Spontaneous hemorrhage is very rare, but occurs in adult life at all ages. Disease of the meningeal vessels is sometimes the immediate cause, but in the great majority of cases it is induced by traumatism. It may be caused by direct blows

or falls upon the back, shock communicated through the lower limbs, vertebral fractures and dislocations, penetrating wounds and even by severe muscular spasm, as in tetanus, convulsions, and violent chorea. No doubt syphilis, arteriosclerosis, purpura, scurvy, and other hemorrhagic states favor it. The blood sometimes comes from a thoracic aneurysm which has eroded the vertebræ and ruptured into the spinal canal or dura, or from one situated on the vertebral or basilar arteries. Intracranial hemorrhage into the cerebral meninges may find its way below the foramen magnum, and in the same way a spinal hemorrhage may invade the cranium.

Morbid Anatomy.-In extradural cases the clot usually originates from the rich plexuses of veins that line the vertebral canal. It may be of considerable size and extend through the intervertebral foramina. The most common location is in the cervical region. The dura is stained and infiltrated, and the cord may exceptionally be compressed. Effusions of blood within the dura vary much in size. The blood usually comes from the pial vessels, and consequently, as a rule, involves the cord. Complete flooding of the dural sheath is almost always due to intracranial hemorrhage or rupture of an aneurysm. A small hemorrhage tends to remain localized and to surround the cord at the original point. It discolors and compresses the cord and after a few days produces inflammatory changes in the meninges. In the same way an annular myelitis may be induced.

Symptoms. The symptoms are practically the same in both extraand subdural hemorrhage. The onset is ordinarily abrupt and the early symptoms depend upon irritation of the meninges and nerve-roots. There is great pain in the back, which often radiates along the implicated nerves, girdling the body or running down the extremities. Tingling and formication are complained of, and paralytic symptoms below the level of the lesion, loss of power, and diminished sensation. Bladder and bowel symptoms shortly appear. There is ordinarily some spinal rigidity, which may develop into opisthotonos, and convulsions are not infrequent. Symptoms are gradually developed unless the hemorrhage is due to severe traumatism or to flooding of the vertebral canal by rupture of an aneurysm. In crushing injuries, spinal fractures, and dislocations the cord is almost invariably injured, and hemorrhage, if present, scarcely adds anything to the symptoms. From the onset to the full development of the paralytic features from one or two to forty-eight hours, or even more, may be required. The symptoms, therefore, greatly resemble those of spinal meningitis, which usually is added after a few days, and its invasion is often marked by a distinct aggravation of all the symptoms.

Cerebral symptoms are only present when the cranial contents are simultaneously affected. Death is likely to occur early when the symptoms have reached their height, or during the secondary meningitis.

Diagnosis. In cases of insidious onset without definite symptoms, the diagnosis at best can be but conjectural. When hemorrhage follows a traumatism, the distinguishing trait is a gradual development of the symptoms within a few hours. Injuries that affect the cord-substance

produce instantaneous loss of function, but a meningeal hemorrhage may be, and often is, associated with hemorrhage into the cord. From meningitis the chief distinction is the much more rapid development and the history of a competent cause. The localizing diagnosis is taken up in subsequent chapters, to which the reader is now referred.

Prognosis. The outlook is always most serious. As the paralytic features develop, there is a likelihood of death from interference with respiration by paralysis of the chest-muscles. The intense pain and suffering also serve to exhaust the patient. The first danger being passed, secondary inflammation is likely to terminate the case fatally. Hemorrhage in the cervical region is, of course, more ominous than when situated lower down. If the patient survives the first fortnight, improvement may be confidently expected, and this may practically be complete, though some disability remains, as a rule, and it may be of an extreme degree.

Treatment. At first the most complete rest on the face or side with the spine elevated should be secured. An ice-bag to the back is a valuable measure if persistently and thoroughly used. Venesection to lower the blood-pressure has been used, but will not find many brave enough to employ it. Local wet cups with free flow of blood have also been employed, but are of doubtful value. Ergot may be used. If the diagnosis is fairly certain, the spinal canal should be aseptically opened and the dural sheath also incised. The operation as now done adds nothing to the gravity of the case, and has enabled the surgeon to remove clots with the best results. The secondary meningitis and the sequential palsies are to be treated on their own indications.

CHAPTER II.

INJURIES AND DISEASES OF SPINAL NERVES.

THE spinal nerves, unlike the cranial group, are both motor and sensory. In addition they contain the vasomotor supply, and through them is exerted the trophic influence and control of the spinal centers over the peripheral apparatus. Their injury or disease is, therefore, marked by perversion or abolition of these functions, and gives rise to groups of symptoms anatomically coextensive with the distribution of the particular nerve or nerves involved. We should bear in mind that the fibers making up a nerve-trunk are cellular elements,-prolongations from cell-bodies, of which they form an integral and functionally essential part. When we injure a motor fiber in a nerve-trunk, we injure a motor cell. In other words, we injure the lower neuron. We will first consider nerve injuries and diseases in a general way, and then the particular conditions which pertain to such states in special nerves.

Division of Nerves.-Spinal nerves are frequently divided by incised and bullet wounds, sometimes by crushing accidents, by simple and compound fractures, and rarely by dislocations. Causes acting more slowly may end in the destruction of a nerve, but a neuritis or degeneration is usually, if not always, first induced. After a nerve is divided the peripheral portion degenerates, and the process is called secondary degeneration.

The immediate symptoms are loss of motion, sensation, and muscular reflexes in the distribution of the nerve. Shortly afterward, within forty-eight hours, the muscles

supplied by the injured nerve lose their tonicity and then progressively waste. Vasomotor paralysis appears and trophic disturbances in the cutaneous area of distribution are marked by a thin, shiny skin, with atrophic hairs, nails, and other epithelial structures. There is also a lowered vital resistance to infection, and healing processes are slow and faulty. Even the joints are sometimes affected, and bony growth in the young is retarded. Electrical stimulation through the nerve fails completely. The muscles lose their responsiveness to faradism, and the increased galvanic irritability which at first appears gradually subsides and is finally lost. The electrical changes constituting the reaction of degeneration are more fully described in Part I. In the extremities the unapposed antagonist muscles then draw the joints into fixed, rigid positions. Muscular contractures develop and still further tend to deform the part.

The histological changes that take place in the distal portions of the divided nerve are as follows: The nuclei of the internodal nerve-cells swell, and their protoplasm becomes increased in quantity, but changed in character, as it no longer stains so actively as in health. The nuclei also become segmented, and with the increase in protoplasm encroach upon the myelin and displace it. The nerve-fiber then shows an irregular beading of the myelin, and at the points of greatest constriction the myelin finally separates transversely, and the axis-cylinder is divided at the same time and in the same way. This process takes place uniformly throughout the length of the divided nerve below the

lesion. The segmented myelin becomes more and more aqueous, escapes in part through its sheath, and is absorbed. The nuclei cease proliferation, and the nerve-fiber is left a mere connective-tissue filament, except at irregular intervals, where remaining globules of myelin may distend it.

The segmentation of the myelin in man reaches the point of complete division and consequent rupture of the axis-cylinder at about the end of the third day after nerve-division. At this time electrical conduction or excitability in the nerve is also lost and muscular tonus is destroyed. The entire process of degeneration after nerve-division may be completed within three weeks.

Above the point of division the central stump degenerates for about a third of an inch only, but there is reason to believe that the cell-body is also disturbed (Marinesco).

The muscles supplied by a divided motor nerve are deprived of the trophic influence of the spinal center as soon as division takes place, and the axis-cylinder below the lesion is equally deprived of the trophic support of the cell-body. The sarcode elements waste. The cross striations become less well marked and are closer together; the muscle-fibers become narrowed, cloudy, granular, and sometimes fatty. There is proliferation of the connective-tissue elements of the muscles, which further strangulates the muscle-cells, and eventually a condition of fibrosis or cirrhosis is developed. This has a natural tendency to contract and shorten, and explains the fibrous, tense, cord-like structures and deformities found in such cases of long standing.

The electrical changes that occur in the muscle are also described in Part I. Faradic muscular contractions are lost within a few days, but at first, for about a week, the muscles react to galvanism even more freely than in health; then the galvanic excitability of the muscle is diminished and disappears.

When the ends of a divided nerve are brought together under proper conditions for healing, regeneration may occur in the peripheral portion even when degeneration is complete and of long standing. Bowlby has noted one case of regeneration after fourteen years' division. In nerves freshly divided and at once united, the functions of the nerve are restored in a few days or weeks. After degeneration has been established regeneration is a slow process, requiring from two months to several years, depending upon the condition of the peripheral segment and the surgical features of the given case. The process consists of a growth of the axis-cylinders of the proximal portion into the degenerated part. They become covered with myelin and enveloped in a sheath continuous with that of the central portion. The muscles in turn regenerate, and slight volitional motion returns before electrical responses can be obtained with the usual tests. These appear, as a rule, shortly after voluntary power is manifested, and while it is still very slight. Sensory conduction is usually restored before muscular action. The muscle reflexes are the last to reappear.

It need scarcely be added that the only treatment for a divided nerve is surgical suture. Whenever the distal extremity can be aseptically united to the central end, and in proportion as it is done promptly after