orrhage into the spinal cord gives instantaneous symptoms, immediate paralysis, and may be practically devoid of pain. The rigid form of tetany may present a very close counterfeit, but its long duration, remissions, and amenability to spinal sedatives, the absence of spinal tenderness and shooting pains, the possible history of previous attacks, and the usual irritability from pressure upon the nerve-trunks and arteries should differentiate it. Tetanus may be mistaken for spinal meningitis. The early trismus, the excessive hyperesthesia, the fever of onset, the paroxysms of spasm, and the frequent history of traumatism point the way to diagnosis. Muscular rheumatism and strain present a very superficial resemblance.

Prognosis. The outlook as to life is always serious and is grave in proportion to the acuteness of the onset, to the virulence of the infection, to the implication of the upper portion of the cord, and to the height of temperature. The estimate is also to be guided by the previous condition of health and the age of the patient, children and the aged quickly yielding to the disease. Traumatic and surgical infection is less serious than auto-infection. The possibility of the removal of sources of infection is of some importance as to ultimate results, provided the patient survives the acute stage. The late results, due, for the most part, to permanent changes in the cord, are usually beyond the hope of marked improvement.

Treatment. Complete and absolute quiet is to be insisted upon. The patient should be kept upon the side or face, if it is possible to do so without increasing the cramps. The partial knee-elbow posture over a mound of firm pillows will often be found very comfortable, and at the same time will afford the best opportunity for local applications. These, at first, should be strongly counterirritant, as the thermocautery, blisters, or detergents like leeches, vigorous dry cupping, or wet cups in robust or plethoric individuals. Should myelitis be associated, less active measures are indicated, and the skin must not be broken or highly irritated, owing to the tendency to bedsores. A hot bath and pack at the onset with active catharsis have seemed to do good. Sedatives, especially spinal sedatives, are frequently required to control the spasms and anodynes to relieve the pains. A thorough course of mercurial inunctions over the spine has strong advocates, the quantity used being sufficient to produce slight ptyalism. Owing to the reflex irritability, these rubbings must often be impossible, and the therapeutic value of mercury in the acute stage of non-luetic cases is open to question. Quincke's lumbar puncture has here the same indications as in the cerebrospinal form. Iodid of potassium and ergot are also at this time of little or no value. The ice-bag to the spine is one of the most serviceable measures, but is rarely tolerated long by the patient, and its intermittent application is useless. It should always be tried. As the active stage subsides, light cauterizations with the Paquelin apparatus, mild sinapisms applied for six or eight hours, and the hot-spray douche seem to assist the reparative efforts of nature. Cerebral symptoms usually mean the implication of the brain-coverings, the spinal features become of secondary importance, and the treatment is that of cerebro

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 associated with 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. 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 are induced. 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 the rupture of an aneurysm. In crushing injuries, spinal fractures, and dislocations the cord is almost invariably injured, and hemorrhage, if present, adds very little 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 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 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. Jacobi has also obtained blood by spinal puncture in two cases of injury of the spine. 1 From meningitis the chief distinction is the much more rapid development in hemorrhage 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. Remedies that increase the coagulability of the blood may be exhibited, but ordinarily the flow of blood is of but a few moments' duration, and no time is given for their action. 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 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 motor 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.

1 "Amer. Jour. Med. Sciences," Oct., 1900.

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