points to the internal capsule and the optic thalamus rather than to the

cortex.

The corpora quadrigemina are seldom singled out by brain-lesions. When involved, adjoining structures almost invariably suffer, so that the resulting symptoms are difficult to analyze. The anterior pair are associated with vision, and apparently with some ocular movements. The pupillary reflex and movements of the eyeballs have been bilaterally impaired in some cases when they were diseased, and nystagmus, enfeebled vision, and blindness have been noted. 1 The posterior pair are thought to be related to hearing and equilibration. When they are diseased, the adjoining portion of the middle cerebellar lobe is usually involved, and probably gives rise to the symptoms mentioned.

The crura cerebri contain the motor tracts on their under portions and the sensory tracts above. Crural lesions, therefore, produce hemiplegia of the face and limbs on the opposite side, marked by hemianesthesia if the sensory paths are at the same time involved. The proximity of the third nerve, as it issues from the inner border of the crus, lays it liable to damage at the same time, and then we also have an ophthalmoplegia. This affects the eye on the same side as the lesion and opposite to the paralyzed limbs,-the Weber syndrome. When the lesion is deep, it gives rise to nuclear disturbance, as described under Diseases of the Cranial Nerves.

The pons Varoli, when diseased, often presents characteristic symptom groups that make the localizing diagnosis comparatively easy. It will be recalled that besides giving passage to the pyramidal tracts, which course downward from the crura to the medulla oblongata, it is traversed by the root-fibers of the fifth, sixth, and seventh pairs of cranial nerves from their nuclear to their apparent origins. The course of the facial fibers and their decussation in the substance of the pons opposite the apparent origin of the fifth pair are described on page 115 and shown in figure 42. If a lesion falls upon the facial fibers before they decussate, and at the same time involve the pyramidal tract, which decussates lower down in the medulla, a paralysis of motion for the face and limbs on the side opposite the lesion ensues. If the lesion occurs below the facial crossing,-namely, in the lower third of the pons,-it will affect the face on the same side and the limbs on the opposite side, producing a crossed or alternating paralysis. Whether or not sensory symptoms are added depends upon the implication of the tegmental fibers, which lie above or behind the motor tracts. When this is the case the motor nucleus of the sixth nerve or its root-fibers is usually implicated at the same time, so that conjugate deviation of the eyes toward the side of the lesion and away from the paralyzed limbs is impossible. In destructive cerebral lesions higher up, it will be recalled, the ocular deviation is toward the lesion and away from the paralyzed limbs. Pontine disease may involve the motor speech-paths, which lie dorsad in the median portions of the pyramidal tracts, and gives rise to articulative disturbance very like motor aphasia. Extension of the lesion dorsad and cephalad may involve the oculomotor centers.

1 Biancone, "Rev. Speriment.," Dec., 1899.

The motor and sensory portions of the fifth cranial nerve-root may be involved separately or together, and trismus may be induced by irritation of the motor nuclei. A lesion which cuts the sensory root-fibers of the fifth induces anesthesia in the face on the same side and crossed paralysis in the limbs through injury to the pyramidal tract. Rigidity, spasm, and choreoid movements in the limbs are sometimes encountered, and convulsions, in acute disease, are common. If the middle cerebellar peduncle is affected, vertigo, vomiting, and tinnitus are usually present, and deafness on the same side may ensue. Irritative lesions of this peduncle produce forced gyratory movements or forced one-sided positions in lying, which may be accompanied by corresponding positions of the head and eyes in the direction to which the turn is made. This may or may not correspond to the side of the lesion.

The medulla oblongata, owing to its small size and the vital importance of its nuclei, is most rarely invaded by acute discase without an immediately fatal termination. Disease of the olivary body may cut off the hypoglossal nerve and at the same time cause a crossed paralysis-the tongue on the same side and the limbs on the opposite. Diseases of this portion of the brain-stem are practically those of the lower cranial nerves and embrace the bulbar palsies already considered in Part II.

The Cerebellum.-According to Luciani, the cerebellum has for its main function the maintenance of sthenic tone in the muscular apparatus. If this be impaired, paresis, ataxia, incoördination, asthenia, tremors, and astasia result. It seems probable that the cerebellum is practically of a uniform functional quality, which is quite evenly represented throughout its entire bulk. One part may take the place of another. Risien Russell 1 and others have shown that the right lobe bears a certain relation to the right side of the body and the left lobe to the left side. Both sides are probably represented in the worm, or middle lobe. It is an experimental and clinical fact that cerebellar lesions of a sudden and extensive character at once produce very marked ataxic and paretic conditions, which may in time entirely pass away. Lesions similar or even greater in extent, but of slow development, may be entirely devoid of symptoms. It is evident that the cerebellum is capable of rearranging its functional relationships if gradually disturbed, and is of great recuperative powers after severe injury. Much confusion has arisen from confounding the symptoms of the secondary involvement of adjoining structures with those purely cerebellar.

We can now say that the right cerebellar hemisphere is in relation with the right side of the body and likewise with the left cerebrum. Mangazzini 2 has shown that injury to the thalamus induces atrophy of the opposite cerebellar half, and we thus have a crossed lesion involving the cerebellum on one side and the cerebrum on the other. With the thalamic lesion the corona radiata and sensorimotor cortex are usually involved.

A lesion in one lateral cerebellar hemisphere, if occurring with suffi1"Brit. Med. Jour.," May 18, 1895. "Neurol. Centralbl.," Aug. 1, 1895.

cient rapidity, as from hemorrhage or quickly developing abscess or tumor, produces sthenic loss on the same side of the body. This becomes manifest in one-sided muscular weakness or readiness of fatigue, in decreased coördination, in a tendency to stagger, and as the side of the lesion is the weaker side, the stagger is more marked in this direction, that is, a patient with right-sided cerebellar disease is inclined to follow his right hand. The reflexes are also unilaterally reduced. At the same time the trunk may deviate to the sound side from the preponderating muscular tone on that side. Weakness of the ocular muscles on the same side as the lesion produces a tendency of the eyes to deviate in the opposite direction, and strong attempts to turn them toward the side of the lesion often develop nystagmic or jerky movements. It seems probable that lesions toward the head of the worm produce a tendency to fall forward, those toward the tail of the worm, a backward falling. These are the paretic manifestations. The cerebellar stagger and the ocular disturbance are often attended by vertigo of a pronounced subjective sort. Very commonly this is greatly intensified if the patient attempts to stand or even to sit up, and may prevent his doing so. In other cases, when the so-called cerebellar gait is well marked, there is no attending vertigo. Vertigo of a similar character may attend a tumor in the frontal region, which at the same time may cause an occipital headache and, according to Williamson,1 in one-fifth of such cases induces bilateral weakness of the reflexes.

Irritative lesions produce another group of symptoms. They are marked by muscular stiffness in the extremity of the same side, by nystagmus, in which the jerk is toward the side of the lesion, and by such an arching of the body with the concavity to the diseased side as tonic excess on the affected side would produce. Emprosthotonos and opisthotonos would perhaps point to the middle lobe or to both lobes. Drummond 2 has also noted convulsions of a tetanoid character on the same side as the lesion, and Ferrier has recorded them in animals subjected to operation. The activity of the lesion dominates the symptoms. They grade off in proportion as the diseased process is slow and may easily reach a vanishing-point in chronic conditions that sometimes are astonishingly extensive.

A third group of symptoms arises from extension of the cerebellar disease to neighboring structures, or from pressure upon them. A onesided cerebellar tumor, for instance, by extension forward above the medullary decussation, presses upon the motor tract from the cerebrum to the cord and gives rise to spastic symptoms on the side opposite the lesion, with increased myotatic irritability and even a tendency to contractures. Pressure upon the floor of the fourth ventricle may affect the nuclei of the cranial nerves and give rise to paralysis of the fifth, sixth, seventh, eighth, ninth, tenth, and twelfth pairs of cranial nerves. eighth or auditory nerve is particularly liable to be affected, and then aural symptoms are added. Tinnitus and vertigo of the Ménière variety may be superinduced, adding greatly to the complexity of the clinical picture. It is needful to investigate the aural condition very critically,

1 "Glasgow Med. Jour.," Nov., 1899.

2 "Lancet," July 28, 1894.

The

as aural vertigo and cerebellar disease are often associated by the extension to the cerebellum of septic processes in the ear, and labyrinthine disease may closely imitate a cerebellar lesion. Irritation in the fourth ventricle may produce polyuria and glycosuria. Obstruction of the Galenic veins produces dropsy of the ventricles, their distention, and all the manifestation of intracranial pressure. Sudden death may follow disturbance of the pneumogastric nuclei. If the middle peduncle-the peduncle to the pons-be affected, forced movements result and forced positions are developed. These seem to be toward the opposite side if the lesion is irritative and toward the same side if destructive. Other clinical manifestations are those common to all intracranial diseases,— namely, headache, vomiting, optic neuritis, and vertigo. Of these an occipital headache is significant and is often associated with a rigidity of the neck and retraction of the head. Friedeberg 1 found this retraction marked in over half of the cases in Aufrecht's clinic. Sensory disturbances are rare. Russell is inclined to think they may be present for a short time immediately after the onset of acute diseases, as hemorrhage, and transient anesthesia is noticed in operated animals. Krauss, 2 from a study of ninety-seven cases of cerebellar disease, enumerates the frequency of symptoms in this order: "Headache, vomiting, optic neuritis, vertigo, ataxia, asthenia, occipital pain and tenderness, inclination to turn toward the side of lesion, convulsions, and such secondary symptoms as nuclear paralysis, polyuria and glycosuria, tremors, and sudden death." Neither the mind nor the sexual desire is necessarily disturbed.

CHAPTER IV.

FURTHER LOCALIZING CONSIDERATIONS.

LESIONS of the brain may be broadly considered as irritative and destructive. From this point of view they respectively produce increased and decreased activity of function. We find the best exposition of these conditions in lesions of the sensorimotor cortex. Given a circumscribed definite lesion, such as a spiculum of bone or a small tumor that rather displaces than destroys the cortical elements in this region, and it is likely to so irritate them that increased activity is manifested in the peripheral area with which they are associated. A limited spasm or convulsion may ensue. If the irritation be too long maintained, necrotic or destructive cortical changes usually follow and are marked by diminished or completely lost peripheral function,-namely, paresis or paralysis. A lesion at first irritative may thus induce spasms in the hand, and after a. time the hand becomes paretic if the progress of the disease reaches a destructive grade. Sudden destruction of the cortical mechanism, as by hemorrhage, causes immediate loss of power.

Were all lesions simply destructive or irritative, difficulty in decipher

1 66 'Berlin. klin. Wochens.," Aug. 19, 1895. 2"N. Y. Med. Jour.," June 1, 1895.

ing them would be greatly reduced, but ordinarily they are combined in varying degree. Around a destructive process a zone of irritation brings new elements of disturbance into the symptom-field which, in turn, may be replaced by evidence of extending destruction. Again, in an area practically paralytic from cortical disease convulsions may occur, perhaps owing to irritation of remaining but inhibited cellular elements or from irritation of the subcortical tracts. In every case, therefore,

it is highly important to know the clinical sequence of irritative and paralytic symptoms in order to determine the point of invasion, the progress of extension, and the limits of the lesion.

B

This brings us to the invasion or extension symptoms. These are transient in the widening convulsive manifestations of cortical epilepsy, and permanent in the slow encroachments of progressive disease. If we consider an irritant or discharging lesion to be located in a given part of the cortex, the disturbance to which it gives rise spreads in concentric and widening circles to the adjoining regions, which are successively upset, and the peripheral display is correspondingly and similarly broadened. The invading march of a Jacksonian fit can be foretold if we know its initial location or storm center. Concentric rings on cortical diagrams enable us to grasp this point firmly. In figure 76, A, a fit starting in the armcenter would next call forth the face and head movements, then those of the trunk, and finally those of the lower extremity. Commencing in the lower extremity, the order would be reversed, as shown in figure 76, C. These sequences are in accordance with clinical facts. convulsive invasion is not one of chance, but is rigidly dominated by the anatomical and functional relations of the cortex. The initial or signal symptom of a cortical fit, therefore, becomes highly significant as pointing to the storm-center, the point of greatest instability and usually the seat of organic disease.

Fig. 76. Schematic figures to show the encroachment of waves of discharge in the cortex, beginning respectively in the arm, face, and leg centers. F, Face; B, arm; J, leg (after

Brissaud).
The order of

Considerations of a similar character sometimes enable us, if we have all the clinical data available, to trace a neoplasm from its origin as it