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TABLE OF DIFFERENTIAL PROBABILITIES IN CEREBRAL HEMORRHAGE AND THROMBOSIS.-(Continued.)

HEMORRHAGE.

THROMBOSIS.

INCITING CONDITIONS.

High arterial tension.

ONSET CONDITIONS.

COURSE.

Excitement, effort, or shock.

No prodromata.

Sudden stroke usual.

Coma marked.

Rectal temperature reduced, and
surface temperature elevated
on the paralyzed side.

Low arterial tension.

Rarely excitement or effort, except in embolism. Sleep favors it.

Prodromata common.

Complete stroke rare.

Coma slight or wanting.

Temperature usually unchanged.

Congested face; respiratory diffi- | Pale face : no respiratory disturbculties.

Pulse slow, full, bounding.

Motor loss usually hemiplegic
and fully developed at once.
General convulsions common.
Rapid improvement in motion.

ance.

Pulse weak, soft, often rapid. Motor loss often monoplegic and inclined to extend.

Limited convulsions common.

Slow motor improvement. Extension of paralysis often observed.

Foot usually gains more rapidly Foot often gains less than hand. than hand.

Anesthesia usually fleeting.

Persistent aphasia exceptional.

Post plegic athetosis, trembling,
and chorea common.
Postplegic convulsions rare.

Spasmodic weeping and laughter

common.

Paresthesia persists.

Persistent aphasia and other cortical symptoms common.

Postplegic athetosis, trembling, and chorea uncommon.

Postplegic convulsions common. Spasmodic weeping and laughter exceptional.

Prognosis. Cerebral softening is an accident following such a wide variety of diseases and conditions which provoke the endarterial process of thrombosis that prognosis can not be generalized. Every case has its own indications. The tendency to immediate death is less than in hemorrhage, but the appearance of pneumonia, or an acute bedsore, or a sudden elevation of temperature, even of moderate degree, indicates a grave complication and a probable fatality. In embolic cases, if it is probable that the embolus is infected, as in infectious endocarditis, diphtheria, and the exanthemata, the outlook is much darkened by the probability of acute infectious encephalitis being set up in the softened area, to be followed by abscess and probably by death. Advanced

years are against the patient. In every case the prognosis should be held in reservation for a week until it is evident that the thrombosis is not spreading and that local infection has not occurred. The temperature is here a valuable guide. Persistent severe convulsions commencing early, perhaps present at the onset, are of grave significance. They point to involvement of the cortex and meninges on the one hand, or of the lateral ventricles on the other. The secondary implication of the meninges or ependyma over the softened area is usually limited, but in infected cases it may lead to a generalized inflammatory process of the utmost gravity. When the first fortnight has passed, the paralytic state may be considered established. Contractures and deformities are thereafter developed, as in hemorrhage. The hemiplegic state presents nothing dissimilar to that following arterial rupture, and has been described in a previous chapter. The condition presented by a given case of softening at the end of the first month is likely to be permanent. This is especially true after middle life. There is also the possibility of epileptoid attacks following at any time, and the persistence of the endarterial disease or its generalized presence constitutes a continual menace. This is particularly true in multiple softenings and in the bilateral forms such as that which furnishes a pseudobulbar palsy.

Treatment. The treatment of cerebral softening to be efficient must antedate the occurrence of thrombosis. In a word, it must be prophylactic. In another word, it must be the treatment of the arterial disease. When the arterial current is cut off we yet have to deal with the basic disease in order to prevent an increase of the thrombus or its repetition and to cause, if possible, its diminution. When called at the onset of the softening in the early hours of the attack, if hemorrhage can be excluded, the treatment consists of maintaining a masterly inactivity. The patient's position should be horizontal, to favor the cerebral circulation; the flagging heart may be encouraged with strychnin; small quantities of nourishment should be administered and the functions of the bowels and bladder supervised. If hemorrhage can not be excluded, the same course is still advisable, but if hemorrhage is diagnosed, the opposite plan of treatment for that condition, already described, should be instituted. Purgation and venesection can not benefit a cerebral territory already exsanguinated. In cases of embolism, cardiac repose is to be encouraged that other particles may not emigrate. Bromid, to control the convulsions, may often be required. The further management of the case is that of good nursing. The arterial state must never escape attention. Its amenability to treatment governs the outlook for the patient and the probability of recurrence. When the paralytic state is established, its management is the same as that laid down in the previous chapter, and for the terminal monoplegia or hemiplegia the indications are likewise identical. The treatment of aphasias and the development of the opposite-sided speech-centers have been described in the chapter on Aphasia.

CHAPTER VIII.

DISEASES OF THE CEREBRAL VEINS AND SINUSES.

Anatomical Considerations.-The blood entering the cranium by the internal carotids and vertebrals after irrigating the encephalon makes its exit mainly by the internal jugular veins. The return circulation from the ventricular portion of the cerebrum and the callosal portion of the hemispheres is by the Gallenic veins and inferior longitudinal sinus, all of which empty into the straight sinus. From the convexity

the pial veins run upward and open into the superior longitudinal sinus

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Fig. 85.-Diagram showing the communications existing between the superior longitudinal and lateral sinuses and the external veins, indicated in the figure by (Leube).

*

in a forward direction against the slow blood-current of this dural channel. Here the circulatory conditions are rendered still more unfavorable by hydrostatic pressure, by the presence of trabeculæ in the sinuses which impede the flow of blood, and by venous retardation during inspiration. The cerebellar veins empty mainly into the lateral sinuses. Into the dural sinuses also empty many veins from the face and scalp. The facial vein communicates with the cavernous sinus through the ophthalmic vein. The veins of the nasal vault open into the anterior extremity of the superior longitudinal sinus. Numerous veins of the scalp along the median line have a similar outlet. Veins from the mastoid process and its cutaneous surface enter the lateral and

petrosal sinuses, and the occipital and posterior auricular veins are connected with the lateral sinus. In addition, many veins of the cranial diploë discharge into the sinuses. Finally, the sinuses connect with the veins of the spinal canal.

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Fig. 86.-Diagram showing the communications existing between the lateral and cavernous sinuses and the external veins, indicated in the figure by * (Leube).

The cerebral veins are subject to the same lesions that influence veins elsewhere, but we are only called upon to consider phlebitis and venous thrombosis. They are usually associated and, practically speaking, severe cerebral symptoms are alone produced by thrombi. Thrombosis may occur in the pial vessels of the convexity and extend into the longitudinal sinus, or, beginning in the sinus, may invade the cortex and give rise to localized softening and focal manifestations. The entire subject may be conveniently described under the head of Sinus Thrombosis.

SINUS THROMBOSIS.

Intracranial sinus thrombosis occurs more frequently even than thrombosis in the pelvic veins, or in those of the lower extremities. It

is favored by the sluggishness of the venous current and the other anatomical peculiarities above indicated. Septic invasion is also extremely liable from the relation of these channels to the cavities of the nose, throat, and ear, and to the frequently traumatized surface of the face, neck, and scalp. It occurs in two forms,-the marantic and the infective.

Marantic sinus thrombosis, or primary thrombosis, is a local condition occurring usually in the superior longitudinal, rarely in the lateral, and very rarely in the cavernous sinus. It occurs in debilitated states, and is most common at the two extremes of life. Exhausting diseases, weakness of the heart, and in general any cachectic state predispose to it. Prolonged illness, as from diarrhea, typhoid fever, pneumonia, phthisis, cancer, malaria, the anemias, etc., often precede it. Under these conditions there is a tendency to fibrin deposit and thrombus formation which, once started, is likely to extend. Should it commence in a cortical vein, or extend from a sinus to the brain-surface, Jacksonian fits may be produced.

Usually on post-mortem examination the thrombus is found to involve several sinuses and their tributary veins. When the entire lumen of a cortical vein is blocked, the drainage of its territory is prevented and localized edema, punctate hemorrhage, and red softening follow. In the same way edema occurs in the superficial parts of the face and head which drain into an occluded sinus. Swelling about the eye and exophthalmos, with retinal thrombosis and epistaxis; swelling about the mastoid, over the vertex or occiput, is produced by the thrombotic closing of the sinuses respectively related to these regions. When the lateral sinus is involved, the thrombus may extend down the internal jugular and be found as a firm, palpable cord in the neck. In marantic thrombosis the clots are firm and non-adherent to the walls of the vein or sinus,—that is, they are not inflammatory. They tend to organize or resorb and do not disintegrate. Reëstablishment of the circulation in the sinus is therefore possible, and usually takes place in long-standing cases, but in cortical veins, if cerebral softening occurs, there is no tendency to circulatory restoration.

The symptoms of marantic thrombosis are those of venous stasis, localized edema, and disturbed brain-function following upon exhausting diseases. As the longitudinal sinus is usually affected there is often epistaxis and disturbance in the leg-centers, indicated by weakness, tremors, paralyses, and spasms in the lower extremities. Convulsions in children are commonly encountered, and may be limited or monoplegic when a cortical vein is invaded. Meningeal irritation often shows itself in rigidities, retracted neck, and vasomotor disturbance.

The diagnosis of marantic thrombosis is usually obscured by the overshadowing picture of the preceding illness, and in those cases where external edema does not point the way it is rarely deciphered during life. There can be little doubt that it furnishes some of the cases of cerebral palsy in childhood. Convulsions coming on late in the history of exhausting illness, especially in children, should direct attention to

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