relating tracts between the two sides of the brain, their destruction would not materially interfere, perhaps, with the independent action of the half-brain.

Lesions involving the optic radiations in the occipital lobes produce hemianopia, and when they cut the radiations from the occipital apex to the angular gyre word-blindness ensues, as described on page 170. Lesions beneath the auditory word-centers likewise produce worddeafness.

The corpora striata can be completely destroyed on both sides without giving rise to motor or sensory disturbance if the internal capsule escapes. Their function is still a matter of speculation. Lesions affecting them, however, almost invariably implicate the capsular tracts.

In this

Fig. 73.-Schematic vertical transverse section of the hemispheres passing through the internal capsule and representing the sensory pathways. G, Left hemisphere; D, right hemisphere; cc, corpus callosum; ci, internal capsule; SG, sensory pathway from left side of cord; SD, sensory pathway from right side of cord. Both sides are brought into intimate relation through the corpus callosum, and the sensory representation is uniformly bilateral (after Brissaud).

locality we encounter the hemorrhagic lesion that is preeminently causative of apoplectic hemiplegia. Whether or not posthemiplegic choreic movements and athetosis are due to disease of the basal ganglia can not be definitely stated.

The optic thalami, when diseased, give rise to no definite symptoms if the lesions are confined to their anterior portions and do not invade the capsule. When the hinder portion of the optic thalamus is involved we are likely to have either a crossed blindness or a double hemianopia, probably from simultaneous injury to the optic tract. Bechterew claims, with much probability, that facial emotional expressions are controlled by the thalamus in some manner. Brissaud, in cases of postparalytic spasmodic crying and laughing, locates the lesion near the knee of the internal capsule. The loss of facial emotional expression at least

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 upward movements of the eyeballs have been impaired in some cases when they were diseased, and blindness or enfeebled vision has been noted. 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 Varolii, 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 114 and shown in figure 40. 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, 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.

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. may or may not correspond to the side of the lesion.

This

The medulla oblongata, owing to its small size and the vital importance of its nuclei, is most rarely invaded by acute disease 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 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 suffi

1"Brit. Med. Jour.," May 18, 1895.

2 Neurol. Centralbl.," Aug. 1, 1895.

cient rapidity, as from hemorrhage or quickly developing abscess or tumor, produces sthenic loss on that side of the body. This becomes manifest in one-sided muscular weakening or readiness of fatigue, in decreased coordination, 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. 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. 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.

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 as tonic excess on the affected side would produce,—namely, a pleurothotonos,-with the concavity to the diseased side. Emprosthotonos and opisthotonos would perhaps point to the middle lobe or to both lobes. Drummond 1 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. It must be ever in mind that 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, as aural vertigo and cerebellar disease are often associated by the extension to the cerebellum of septic processes in the ear, and labyrinthine

1 "Lancet," July 28, 1894.

The

Other

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. 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 the 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

2

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