a large number of cases in which these anatomical conditions are wanting to explain the sudden onset of this stage. Ordinarily an apoplectic stroke, with or without convulsions, takes place. Usually there are no premonitions or only the vague indications of cerebral mischief which have presented at intervals during the latent period. The apoplectic coma may be punctuated by Jacksonian fits, marked by conjugate deviation of head and eyes and some lateral weakness, and the patient may succumb in a few hours without regaining consciousness. Death, indeed, may be sudden. If the immediate effects of the stroke subside, a hemiplegia with marked rigidity, and often with spasmodic features, is progressively developed. The headache, the fever, and the symptoms of the early stage reappear or become intensified. Nystagmus, pupillary inequalities, and involvement of the ocular muscles appear and death is likely to follow, preceded by delirium and coma.

The localizing symptoms of brain-abscess are rarely prominent. Usually they are quite indefinite or entirely lacking. The location is often in the frontal, temporal, and occipital lobes, or in a cerebellar hemisphere, whence focal symptoms do not arise. As a rule, an abscess of the brain, due to disease of the cranial bones, lies subjacent to the original lesion. In the same way ear disease gives rise to abscess near the petron, but in rare instances the purulent collection has been found at a considerable distance, and even in the opposite half of the brain. Abscess due to embolic process from the heart or lungs is likely to be located in the capsular or Sylvian arteries, and gives rise to early hemiplegic features or disturbances of the motor cortex. The circumscribed headache sometimes furnishes a localizing feature, but it can not be relied upon. Macewen has noted a higher percussion note over the abscess than was yielded by the rest of the head, and Dana has confirmed this symptom in one case. Local tenderness and increased temperature may occasionally be made out. When the abscess is associated with septic sinus thrombosis, we have, in addition, the local superficial evidence of that disease. Even when the sensorimotor zone is invaded, the symptoms may be very slight. Abscesses may, however, yield as definite localizing features as any other encephalic lesion, and these then have the significance and value discussed under the head of Cerebral Localization. Involvement of cranial nerve-trunks, cerebellar symptoms, hemianopsia, Jacksonian fits, aphasias, and other localizing indications should always be carefully sought. Multiple abscesses also lead to symptoms of corresponding diversity.

Diagnosis. The diagnosis of cerebral abscess depends very largely upon the history or presence of trauma or of an infective condition about the head and face or in the thorax. A chronic otorrhea, maxillary abscess, ozena, sinus suppuration, or purulent pulmonary disease, followed by headache, vomiting, delirium, stupor, slow pulse, vacillating temperature, and rigors, means encephalic invasion. These symptoms are common to meningitis and abscess, and the differential diagnosis can not always be made. Any evidence of a circumscribed process, however, favors the idea of abscess, and hence localizing symptoms become very important. The two conditions are often associated and a terminal

suppurative meningitis is common in abscess. In latent periods the differentiation of cerebral abscess from a growth may be impossible; nor is it essential. The terminal stage, with its rapid onset and paralytic features, may readily be confounded with cerebral hemorrhage or softening if it occurs in middle life and is preceded by apparent health. When systemic sepsis is manifested, the purulent character of the encephalic process is less doubtful.

Abscesses resulting from ear disease, bone disease, and disease about and in the facial cavities-in other words, abscesses due to direct invasion —are ordinarily single. Abscesses resulting from pyemic states and from purulent thoracic conditions are usually multiple. Cerebellar abscesses are also usually multiple. The localizing diagnosis is made on the lines already laid down in chapters iii and iv of this part.

Prognosis and Treatment. Suppurative disease within the cranium is always grave. Although a cerebral abscess may encapsulate and lie dormant for years, this can not reasonably be expected to take place, and even when it does, it constitutes a constant menace to life. Encapsulation does not necessarily check suppuration, and eventual rupture or secondary infection is the legitimate sequel. The late results are ordinarily fatal, and latent cerebral abscesses account for a certain proportion of sudden deaths.

The treatment of cerebral abscess should be prophylactic. Chronic suppurations in ear and nose should never be neglected and the utmost precautions should be taken, in the management of all wounds about the head and face, to prevent infection and sepsis. From these largely controllable sources the great majority of brain-abscesses and other endocranial suppurations arise. When the diagnosis is established, there should be immediate recourse to surgery. Of all encephalic diseases abscess promises the best results to surgical measures. Adequate drainage after opening the skull has been followed by brilliant success in numerous cases and in the hands of many operators. All other measures are inadequate.

CHAPTER X.

THE CEREBRAL PALSIES OF CHILDREN.

A NUMBER of varied developmental and acquired cerebral defects result in paralysis in childhood. They involve or destroy within the cranium some portion of the upper motor neuron, and give rise to clinical types that justify a separate description. Their importance and frequency have been recognized only within a few years, but it is now appreciated that in the early years of life cerebral palsies are fully as common as the spinal variety. Etiologically, they may be divided into three groups: (1) Those due to prenatal conditions; (2) those following birth accidents, and (3) those dependent upon disease or trauma after birth. Clinically, we also divide them into those showing unilateral defects, the hemiplegic cases, and those presenting bilateral defects, the diplegic cases.

Etiology. One of the most important prenatal conditions resulting in infantile cerebral palsy is an actual deficiency of brain elements, a true agenesis. This may be marked by convolutional simplicity and a lessened number of cortical cells and pyramidal fibers. In other cases a part or the whole of a hemisphere, or of both hemispheres, may be lacking. Between these gross teratological defects and a condition in which the neuron units have diminished dynamical qualities or a lessened power of endurance, that in early life leads to their atrophic or sclerotic degeneration there is but a difference of degree. The lack of constitutional endurance, of capacity for growth, and of resistive power underlies many brain and cord diseases that present hereditary and familial characteristics. In other instances it furnishes a lowered resistance to toxic influences. In given cases unfinished children, lacking motor elements in the cortical mantles, and children born prematurely, before the pyramidal apparatus has been well established, present various degrees of motor and cerebral defect. The upper motor neuron is well formed only at the ninth intra-uterine month, and not completely developed until the second or third month after birth. Much defect in the upper neuron is always marked by spasticity and impaired motility in the muscles supplied by the lower and terminal motor

neuron.

Rarely direct traumatism has affected the brain of the unborn child, which has presented hemiplegic contractures at birth. In other cases evidence of hemorrhage and softening has been found, and in many instances the probability of a prenatal meningo-encephalitis has been upheld by the presence of localized and diffuse sclerotic changes in the brain of new-born children. Inherited syphilis and other toxic conditions due to illness of the mother have been accused in some of these

cases. Porencephalia is usually due to intrauterine disease of the cerebral vessels.

The conditions attending birth frequently lead to brain-lesions in the child. The great majority of cerebral birth palsies occur in protracted labors, and consequently in primiparæ. A number of them follow precipitate labor and in both are due to violent compression of the fetal head. Comparatively few can be attributed to the use of forceps, and it is exactly in these cases that the labor is likely to have been tedious. Forceps accidents, however, can not be denied or overlooked, and the misuse of these powerful instruments is fraught with serious results to the skull and brain of the child. The facts, however, favor early skilful instrumental interference as compared with tedious labor.

The frequency of hemorrhage into the cerebral and spinal meninges during birth has been put on a sound foundation by the investigations of Litzmann, McNutt, and Spencer. It is found in the great majority of stillborn children and is the common cause of asphyxia of the newborn. Occasionally this blood comes from a ruptured longitudinal sinus, but most frequently from the pial vessels. Punctate and larger hemorrhages within the substance of the brain and cord are frequent. The results of these birth hemorrhages depend upon the quantity and location of the effused blood. Where death does not follow, all degrees of disability are encountered. Palsies follow the involvement of the motor cortex or its pyramidal tracts, but if the frontal lobes are seriously affected, idiocy is a consequence and is a frequent accompaniment of motor disturbance. Similar disturbance of the latent lesion territories of the brain may give rise to insignificant or very obscure symptoms. As a rule, the hemorrhage is basilar in location in vertex presentations and vertical in breech cases. The absorption and organization of these hemorrhages lead to a more or less diffuse sclerosis of the brain-substance that inhibits its growth and diminishes its functional capacity. In other cases in terminal stages large areas of softening and cyst-like formations are found that are indistinguishable from porencephalia. In about one-fourth of these cerebral birth hemorrhages the spinal cord is similarly affected. Some cases of syringomyelia may have this origin.

eases.

The postnatal causes of cerebral palsies in children, according to Osler's list, are hemorrhages, embolism, endo- and peri-arterial changes, encephalitis, and cerebral venous thrombosis. In other words, they are the same as in adults, and hemorrhage is more frequent than thrombosis. The relation of acute infectious diseases to embolism and arteritis only needs to be recalled. Traumatism and tumor formation cause some Of encephalitis much has been said, and Strümpell claimed cortical polio-encephalitis to be the lesion in many of these cases, but the exact pathological process still escapes us owing to the paucity of early post-mortem examinations. It is just as likely that the lesion is primarily vascular. Gowers was the first to insist on the part played by venous thrombosis, and others, among them Osler, have added weight to the contention. This cerebral venous thrombosis is often a part of sinus thrombosis, to which it may hold a primary or secondary

relation. It serves to produce softening, and sclerotic changes in the cortex and palsies follow. As many of these palsies start with convulsions, the question arises whether the convulsion is the cause or effect of the lesion. It may be either. There can be no doubt that the increased arterial tension of the convulsed state may cause rupture of cerebral vessels, but, as a rule, the convulsions are due to the irritant effect of the lesion. Later on epileptic or epileptoid convulsions are very commonly encountered. Sex plays no etiological part. Sex plays no etiological part. Males and females are about equally affected. One-half the postnatal cases in children occur within the first three years of life.

Morbid Anatomy.-The post-mortem findings in these cases furnish various lesions. Sachs gives the following table:

CLASSIFICATION OF INFANTILE CEREBRAL PALSIES.

GROUPS.

MORBID LESION.

I. Paralysis of intra-uterine Large cerebral defects, porencephalia.

onset.

II. Birth palsies.

III. Acquired palsies.

Defective development of pyramidal tracts.

Agenesis corticalis, highest nerve-elements involved.

Meningeal hemorrhage, rarely intracerebral hemorrhage.

Later conditions: Meningo-encephalitis chronica, sclerosis and cysts, partial atrophies.

Hemorrhage, meningeal and rarely cerebral. Thrombosis, from endarteritis, and in marantic conditions.

Embolism.

Later conditions: Atrophy, cysts, and diffuse and lobar sclerosis. Meningitis chronica. Hydrocephalus, seldom the sole cause. Primary encephalitis, the polio-encephalitis corticalis acuta of Strümpell. (?)

The difficulty of deciding the origin of the terminal conditions is very great and it is often impossible. Porencephalia, for instance, may be due to defective development, to embolism, to thrombosis, or to hemorrhage. The initial process of a diffuse sclerosis may be hemorrhagic or inflammatory.

Symptoms. The clinical history of cerebral palsies in children varies in the three sets of cases. In the prenatal cases the condition is congenital, but may not be noticed for some time after birth. In birth palsies the condition is usually noticed shortly after birth or develops within a few weeks. In the later-acquired cases the patients may present an ordinary record up to the onset of the paralytic features. In their final development all present very common attributes and are usually indistinguishable by external examination alone. The great majority of natal and prenatal cases have bilateral palsies. After birth the tendency is to one-sided paralysis and after the age of three it is almost the invariable form. A pure monoplegia is so extremely uncommon as to be almost unknown.