It may be remarked, in the first place, that the lesions known by this name are not necessarily strictly capillary, but are situated in the very small arteries. The microscope marks the transition from the larger to these smaller embolisms.
More is known about very small embolisms experimentally than clinically, since they have been produced by the injection of small seeds and insoluble particles of various kinds. Embolisms arising from natural causes and deposited in the minutest arteries may have very similar origin to the larger ones already described, but there are also other conditions which give rise to particles which pass through larger arteries without any disturbance, and are arrested in smaller ones. The softening of thrombi is undoubtedly one source. The same thrombus which, if detached en masse, would block the carotid artery, may, if broken up into a number of minute fragments of fibrin and fat, pass into the ultimate distribution of the cerebrals. The same thing may of course happen if the thrombus have already undergone one transportation.
Cases of localized softening are seen where no cause has been found, except perhaps a thrombus in the heart, which has discharged its softened and puriform contents; and it is probable that the connecting links exist in the form of embolisms so minute as to escape ordinary observation.
The consequences of capillary emboli if they block every minute ramification of an arterial branch must be essentially the same as if the branch itself were stopped; but if only a part are thus affected, the resulting anæmia is not so complete, since the zones of capillary congestion surrounding the part the supply of which is cut off may be sufficient entirely to cover it and make more or less complete compensation. The experimental emboli, in the form of tobacco-seed and other insoluble substances, which have been traced into the brain in considerable numbers,often give rise to no distinct lesions in the cases where the immediate effects are recovered from.
Among the other sources, ulcerative endocarditis may be mentioned as of special importance, not from the size but the character of detached emboli, which will give rise, not to simple anæmia, nor, on the other hand, to merely negative results, but to septic changes at the place of lodgment.
Aside from these conditions, which are almost the same on a small scale as we find with the large emboli, we have several peculiar substances formed in the body and floating in the blood which lodge in the capillaries of the brain. These are pigment, fat, lime salts, and white corpuscles. Every one of these, however, is much better known anatomically than clinically.
Pigment scales, flakes, granules, or cells containing them, are formed in the course of severe malarial fever, and deposits consisting of this pigment are found in the spleen, liver, kidneys, heart, lungs, and lymphatic glands, as well as the brain and spinal cord. The brain, when a deposit of pigment has taken place, is of a slaty-grayish or chocolate color, which is marked only in the cortical substance, the white being unaffected. The pigment is found in the capillaries, and, according to Frerichs, fibrinous coagula are often associated. Punctiform hemorrhages in the brain have been seen, as well as meningeal hemorrhages, in connection with this degeneration.
The point at which these masses are formed is still a matter of theory. If the liver, as has been supposed, is one of the places of formation, or if they originate in the blood, it is of course easy to see how they reach the brain. If in the spleen, they must pass through the wide portal capillaries before they are arrested in the narrower ones of the brain.
It is by no means certain, however, that pigment reaches the brain in the form of emboli. It is quite as probable that it is found in many organs which undergo repeated congestions from the local destruction of blood-corpuscles and changes in their pigment. The very general deposition seems to point to a process of this kind rather than to a local origin and a distribution through the blood. The punctiform extravasations which may be found with deposits of pigment are also found without it.
Minute particles of fat have been found in cerebral capillaries, but are much less common here than in the lungs. They may be derived from the decomposition of a thrombus, as described above, or they may come from a fractured bone, when, of course, only particles fine enough to pass through the pulmonary capillaries can reach the brain. This form of embolism has an interest in connection with diabetic coma.
Collections of white corpuscles in considerable number have been observed to form an embolus. These cannot be considered to differ very widely in character from the ordinary fibrinous embolus, which contains white corpuscles. It is, however, not certain that such emboli are deposited during life.
Calcareous masses formed from the decomposition of bone have been seen in cerebral arteries.
About the symptomatology of such emboli little is known. An arrayof minute emboli from the breaking up of a thrombus in the left auricle, carotid, or even aorta, might possibly so block up large numbers of arterial twigs as to give rise to the ordinary symptoms of embolism; but considering the possibility of the re-establishment of circulation, provided a certain proportion of the minutest vessels escape, complete anæmia of a large tract produced in this way must be rare. It is possible that some of the slighter and more transitory attacks of hemiplegia or of more or less vague cerebral symptoms may be referred to a lesion of this kind, the first action of a large number of emboli being to cause an anæmia, which is compensated for much more rapidly and thoroughly than would be the case if a single considerable vessel were obliterated.
Various attempts have been made to connect definite and peculiar diseases with capillary embolisms. Chorea in particular has been said to depend upon a lesion of this kind, but, although cases have been observed where the symptoms and lesion coexisted, yet they are very far from being the rule, or even from constituting a respectable minority of cases. The lesion of chorea in the great majority of cases is not known, although attention has been directed to this theory long enough to have established its truth.
The same may be said of the relationship between pernicious attacks of intermittent and pigment embolism. There is occasional coexistence, but far from invariable. Cerebral symptoms of the same kind and severity occur without as with the pigment deposit. If pigment embolism is the cause of coma, delirium, etc. in pernicious fever, it is difficult to see why such cases can recover so rapidly, and why no symptoms referable to a localized cerebral lesion are observed after the primary unconsciousness.
Even less proof can be adduced as to any connection between leukæmic embolisms and the cerebral symptoms occurring toward the end of severe acute disease.
Calcareous embolism is a pathological curiosity.
DIAGNOSIS.—In the case of multiple capillary embolism it would be impossible, if it were complete, to distinguish it from a blocking of the main branch.
Cerebral symptoms arising in the course of ulcerative endocarditis might be referred, with a high degree of probability, to an embolus, but if they were distinct enough to be referred to a localized lesion, the probability of a single embolus would be much greater than that of a multitude of capillary ones occluding the same vascular territory. The diagnosis of pigment embolism might be a probable, or at any rate a possible, one if in a long-continued case of paludal fever, where the liver and spleen were enlarged and the skin had the slaty hue marking the deposit of pigment, there were decisive cerebral symptoms. It could not, however, be a positive one.
Fatty embolism might be suspected in a case of diabetic coma, though even if the condition were found it would not establish the relation of causation.
PROGNOSIS ANDTREATMENTcan hardly have a definite basis in the absence of all ground for a satisfactory diagnosis, but do not differ essentially from those of the larger occlusions.
It has for centuries been known that coagulation of the blood might take place in the sinuses in a way different from the ordinary post-mortem clots, but this was looked upon rather as an anatomical curiosity than as a fact of practical importance and clinical significance, and it is chiefly among observers of the present century that we find a growing knowledge of the conditions under which it occurs and the symptoms to which it gives rise.
Thrombi in the cerebral sinuses are not essentially different from those formed elsewhere, and the reader is referred to the account given in the article on General Pathology for a history of their formation, growth, appearances, and transformations. For our purposes it is sufficient to recall that they may be white, red, or striated, either partly or wholly obstructing, and that they may become degenerated and partly or wholly washed away. The most important distinction of all, however, is that into two classes, of which the first consists of those which are simply depositions of fibrin in a comparatively healthy vessel, and the second of those which are dependent on a phlebitis.
In order that a thrombus may form it is necessary that there should be, in the first place, a special condition of the walls of the veins—not necessarily, however, inflammation, though this is one of the most frequent and probably the most active form; second, a slackening of the blood-current; and, third, perhaps a peculiar state of the blood, though this latter is not certain. A thrombus tends strongly to grow, and when already formed furnishes a most favorable point for the deposition of more fibrin.
The cerebral veins furnish a very suitable place for the coagulation of the blood for several reasons: they are roomy in proportion to the amount of blood they carry; they are tortuous and abundantly anastomosing, so that the current of blood is almost reversed at some points, and can easily stagnate; the veins of the diploë are held open by their bony walls, and the sinuses by their stiff membranous ones, so that they cannot collapse and thus limit the extension of a thrombus once formed.
The sinuses most frequently affected, though none are free from the liability, are the cavernous, superior longitudinal, and lateral.
The results of thrombosis of the sinuses and veins are not equivalent to those of a similar process in the arteries, and they may be said in a general way to be more diffused, as might be expected from the much greater freedom of anastomosis. Limited softening is rarely a consequence of occlusion even of a considerable number of veins, but it has been observed. A large area of softening of one hemisphere, not involving the temporal and occipital lobes, has been seen with thrombosis of the parietal veins58(the internal capsule and ganglia were not affected).
58Gaz. des Hôp., 1880, 1066.
Passive congestion in the brain, as elsewhere, although apparently entirely incompatible with the normal function, seems to be able to sustain a low form of structural integrity.
Bleeding may take place from the congested veins behind the obstruction, constituting a distinct form of cerebral hemorrhage which does not depend upon an arteritis, although if miliary aneurisms were present theoccurrence of thrombosis would undoubtedly tend to their rupture. The writer, however, is not aware of such a coincidence having been actually observed. Hemorrhages are usually diffuse, composed of or accompanied by a number of small effusions, and situated on or near the surface of the brain or distinctly meningeal. Punctiform hemorrhages are exceedingly common.
Phlebitis of the cerebral veins is very likely to run into meningitis, and the two affections are often so closely united that it is difficult to say which was the first. Œdema is a consequence of venous obstruction in the brain as well as elsewhere, and is seen also around some of the peripheral veins connected with the sinuses.
ETIOLOGY.—Venous thrombosis in the brain depends chiefly on three sets of causes, though it must be admitted that there are a few cases where the origin cannot be distinctly traced and where no previous disease has existed. In the marantic form, occurring chiefly in the very old and in children, as well as in cases of wasting and depressing diseases in adults, a simple thrombosis without inflammation takes place. Two conditions, and sometimes three, are combined here to produce the result—feebleness of the blood-current from a corresponding state of the heart, diseased endothelium of the vessels from defective nutrition, and possibly, where profuse watery discharges have been going on for some time, an increased tendency to coagulation from the inspissation of the blood.
Rilliet and Barthez and Von Dusch59give the following tables of ages at which this form of thrombosis has been observed. The observations of the former were made in a children's hospital, and hence do not affect the question of its frequency in later life. Perhaps the rules of admission may account for the absence of cases under one year of age, of which Von Dusch collected several:
59Sydenham Society's translation.
The special diseases in which thrombosis is most likely to be met with are given by Bouchut as follows. The same remark is to be made about these as about those of Rilliet and Barthez. The table is given as convulsions from thrombosis of sinuses:60
Von Dusch gives a number of cases of the same kind, as do many subsequent writers, but without tabulation. Virchow61reports a case of congenital variola with thrombosis of the sinuses of the dura mater, the superior and inferior cava, and vessels of the cord.
60Gazette des Hôpitaux, 1879.
61Arch., 1859, 367.
It is probable that simple anæmia may, here as elsewhere, either alone or with other debilitating influences, lead to thrombosis. Von Dusch remarks that quickly operating and debilitating influences lead to thrombosis, and gives as an instance a case where a puerperal peritonitis, for the cure (?) of which repeated copious abstractions of blood were made during nine days, was supposed to be the cause. The puerperal condition seems to have a tendency in this direction in a way not always to be explained by the ordinary rules of the transmission of emboli or of phlebitis. Although in those reported by Ducrest62phlebitis of the pelvic veins existed or was suspected, in the first of these five cases the lesion may have been, so far as the description goes, arterial instead of venous thrombosis; and in the second it is possible that the succession of events was uterine phlebitis (with the addition of a large sacral slough), lobular pneumonia surrounded and traversed by veins which were affected with phlebitis, emboli in the arteries of the cortex, and consequent venous thrombosis. In the third, fourth, and fifth the connection between the uterine phlebitis and the inflammation of the cerebral veins (in two cases meningitis) cannot easily be made out, except by the rather vague assumption of a general tendency to phlebitis, which was shown in one by a similar condition in the vein of the arm where the patient was bled. Empyema has been followed by hemiplegia, cerebral softening, and thrombosis of the lateral sinus. The venous thrombosis in such a case may be secondary.
62Archives générales, 1847, p. 1.
Marantic thromboses are more likely to occur upon one side, and that the side upon which the patient habitually lies.
The second class of cases embraces those where a simple obstruction, partial or complete, of the current of the blood gives the starting-point for a thrombus in the veins. Such an obstruction may be formed by an embolus, but in the veins this cannot be considered an important factor, although a portion of a thrombus may be detached and become lodged in a narrower vessel or branch farther along. In this way the propagation of thrombosis for a short distance toward the heart may be accounted for.
A tumor or inflammatory exudation may press upon a vein or intrude into it, but most cases of obstruction-thrombosis are traumatic in origin. Thromboses arising in connection with tubercular meningitis may be looked upon as having both an obstructive and marantic cause. In many wounds of the vertex, gunshot and other, the walls of the superior longitudinal sinus are pressed upon by pieces of bone, and sometimes spiculæ have directly penetrated it. This class of injuries is also likely to cause phlebitis without any actual penetration or compression of the sinus, simply as a result of the inflammation of tissues in the neighborhood. The thrombi formed in these cases are not necessarily completely occluding. Where direct injury to the sinus or in its immediate neighborhood gives rise to phlebitis and consequent thrombosis, we have a condition closely resembling that of the third class, where disease of an inflammatory character in the tissues of the skull, neck, or face sets up a phlebitis and thrombosis which are transmitted to the intracranial veins and sinuses.
The most frequent source of this third form of inflammatory thrombosisis the chronic inflammation of the middle ear with the mastoid cells. The inflammation may be propagated through a carious or necrosed portion of the temporal bone to the petrosal and lateral sinuses, or may, without disease of the bone, be carried by the small veins which open into the sinuses from the petrous and mastoid portion of the temporal in this region. Abscesses in the neck may set up a phlebitis extending up the jugular to the lateral sinuses, to which a meningitis may possibly be added.
Carbuncles about the root of the nose, face, and so far down as the upper lip are very prone to give rise to thrombosis propagated through the ophthalmic vein to the cavernous sinus; and it is probably this risk which gives to carbuncles in this situation their well-known peculiar gravity. The divide or watershed between the regions which drain backward through the cranium and those which are connected with the facial vein below is apparently situated about the level of the mouth, so that a carbuncle of the lower lip is much less dangerous. Billroth, however, gives a case where a carbuncle in this situation was followed rapidly by cerebral symptoms and death, and where a thrombo-phlebitis was not improbable. He mentions another case where a carbuncle upon the side of the head set up an inflammation which travelled along a vein into the cellular tissue of the orbit, and thence through the optic foramen and superior orbital fissure into the skull.
Erysipelas of the scalp apparently causes phlebitis in some cases, and even eczema in the same situation seems to have done so. When the erysipelas is situated about the upper part of the face, the path of transmission is through the ophthalmic vein; but when upon the vertex, it may be propagated through the small veins that penetrate the bone. This result is certainly a rare one in facial erysipelas of the ordinary and superficial kind, which is a notoriously benign disease for one of such apparent severity. It may, however, be more frequent than ordinarily supposed, since cerebral symptoms occasionally appear at a date too late to be accounted for by the fever and too slight to be referred to extensive interference with the cerebral circulation; the lesion to account for which, as they do not cause death, can be only inferred, though it is not unreasonable to suppose it to be a limited thrombosis.
Dowse63describes the case of a robust man who fell on the back of his head, but walked home. After a few days he had a severe headache, chill, and total loss of vision. His temperature rose; he had erysipelas and partial coma, but no convulsions. There was thickening of the scalp, but no fracture of the skull and no adhesions of the membranes. The superior longitudinal lateral sinuses were free from thrombi, though there was a roughness about the latter, as if there had been a fibrinous deposit. The cavernous sinuses were almost completely occluded with adherent fibroid masses, and there was hemorrhage in the anterior lobe. There was some degeneration of the brain-structure, but no disease of the arteries.
63Trans. Clin. Soc., 1876.
Ulcerations in the nasal passages and ozæna have proved starting-points for thrombosis.64
64Med. Times and Gaz., 1878, i. 614.
Thrombosis of the jugular veins and corresponding cavernous sinus, with paralytic symptoms, has been observed in the horse.
The symptoms produced by venous thrombosis, as might be supposed from their varying location and extent, and also from the fact of their being almost invariably connected with other diseases having marked and severe symptoms of their own, are not always easy to pick out from among many others, but they are sometimes very well marked and characteristic. A distinction must obviously be made between the symptoms of simple thrombosis depending on interruption of the cerebral circulation and those of phlebitis, which give rise in addition to febrile phenomena common to phlebitis in any of the large veins.
The symptoms which indicate venous obstruction, without reference to its inflammatory or non-inflammatory character, are of two kinds: first, those dependent upon the disturbance of the functions of the brain; and, secondly, those which depend upon congestion and compression of other structures.
According to the locality and completeness of the obstruction we meet with brain symptoms.
In the marantic thrombosis of children these may be very vague, and consist either in restlessness, followed by somnolence and coma, or, most especially, in convulsions. The convulsions may be partial and involve the face only; they may affect one side only, or, what is more usually the case, be general. There is almost always strabismus. There may be conjugate deviation. This latter phenomenon is said by Bouchut to be of no value in children, as it may take place in either direction, from or toward the lesion, but possibly the distinction between the spastic and paralytic forms was not duly observed by him. The condition of the fontanelles is spoken of as yielding and depressed, with the edges of the bones overlapping. They may, however, become again tense in the course of the disease from exudation or hemorrhage taking place. Paralysis is not so marked as in adults, but may be present.
In adults delirium takes the place of convulsions, due to a disturbance of circulation over a considerable area, rather than to a total suppression in a more limited one. Paralyses are not infrequently met with, either in the form of a hemiplegia or more localized. Hemorrhage will naturally be followed by its usual consequences, according to its location. Headache, often very severe, is among the early symptoms.
It is evident that none of these symptoms can be considered highly characteristic. They can only furnish a certain amount of probability in cases where the general course of the disease has made it likely that thrombosis may take place.
There is another set, however, which, when present, offer the strongest kind of confirmation: these are due to the pressure from the veins themselves.
Œdema about the points at which the intracranial circulation is connected with that of the face and neck may give rise to protrusion of the eyeball, conjunctival ecchymoses, swelling of the upper lip, and even of the upper part of the face, which sometimes becomes slightly cyanosed from the congestion. Epistaxis has been noted. Œdema may be noticed about the mastoid process when the thrombosis is situated in the lateral sinuses, but it would be important in many cases to distinguish this from inflammatory œdema directly due to disease of the bone.
Œdema of the optic disc, as shown by obscuration of its outlines, with large and pale vessels, has been observed by Bouchut.
Veins closely connected with those within the cranium may be thrombosed, and felt as hard cords by the finger. This may occur in the facial veins about the orbit, in those around the mastoid, or in the jugulars. On the other hand, if one cavernous sinus is filled with a coagulum which does not go down into the jugular, this vein will naturally be empty or receive only a small amount of blood from other veins.
When the cavernous sinuses are affected, we are likely to have a set of phenomena due to the pressure of the clot upon the nerves which pass through it—i.e.the third and fourth, part of the fifth and sixth—with filaments of the sympathetic accompanying the carotid artery. Hence dilatation of the pupil, strabismus, or ptosis, and other ocular paralyses may be the symptoms observed.
It is possible that a headache upon the side of the affected sinus may be due to vascular dilatation from paralysis of the sympathetic, or to a direct pressure upon the first branch of the fifth pair.
DIAGNOSIS.—The diagnosis of venous thrombosis may be almost entirely a conjectural one in those cases where the cerebral symptoms are vague or mixed with others peculiar to the causative disease. Where wasting disease has existed, the patient is much emaciated, and profuse discharges have diminished the fluidity of the blood, the rapid supervention of coma with slight spasms or general convulsions will render it highly probably that thrombosis is taking place. Unilateral symptoms would greatly increase this probability, and if any accessible veins about the head, neck, or face could be definitely distinguished as filled with firm coagula, the diagnosis would approach certainty.
In cases of this kind the only condition likely to put on the appearance of thrombosis is the simple inanition or so-called hydro-encephaloid disease, which comes on in exactly the same sort of cases. Localized phenomena must be the chief point of difference. Fortunately, the distinction is practically not an important one.
In wounds of the vertex affecting the longitudinal sinus the question likely to arise where cerebral symptoms supervene is that of thrombosis or abscess. Here the more definite localization is likely to be upon the side of the abscess, although, as is well known, this may remain latent or nearly so for a considerable time, and in general is much more chronic in its course than thrombosis.
The swelling of the external veins, epistaxis, œdema of the lid, protrusion of the eyeball, with œdema of the optic papilla, with only moderate fever, would favor the diagnosis of thrombosis, while optic neuritis, if present, with chills, would render the abscess more probable. Unless the wound were sufficiently severe to fracture a piece of bone into the sinus, or unless the subsequent inflammation were of an unhealthy character, the abscess in a person of middle age and previous good health may be considered the more probable of the two. In the case of Dowse, already mentioned, the diagnosis between abscess and thrombus must have been very difficult, and, as it seems to the writer, would have been more likely to rest upon abscess or meningitis than upon the condition afterward found to exist.
Where inflammatory diseases exist which are known to lead to thrombosis with phlebitis, the practitioner, if on the lookout, can often make a diagnosis with a high degree of probability in its favor. The cerebralsymptoms with the venous swelling, collateral inflammatory œdema in the more immediate neighborhood of the lesion, and slight œdema and congestion at more distant points, and a febrile movement indicating a distinct inflammatory exacerbation, will point very strongly to thrombo-phlebitis.
An absolute distinction between such a condition of the veins and a meningitis arising under exactly the same circumstances may not always be possible, and is the less important since the two affections are likely to coexist and form a part of the same disease.
The localization of the thrombus is to be determined partly by the paralytic symptoms, if such exist, but principally by the situation of the secondary œdema and from the lesion which forms the starting-point. It has been said that the jugular vein of the side on which thrombosis exists is less full; and this point might be of value when the lateral sinus is affected.
PROGNOSIS.—From the character of the lesion itself, as well as from the diseases with which thrombosis is usually connected, it will readily be seen that the prognosis is in general a highly unfavorable one; but it is possibly regarded as too inevitably so, for the reason that a positive diagnosis may be in slighter cases a matter of considerable uncertainty, so that the practitioner, even if attempting to make an accurate anatomical explanation of obscure cerebral symptoms, is as likely to think that he has been mistaken as that his patient has recovered from so serious a disease.
Cases, however, have been reported where the diagnosis seems as clear as it can be made without an autopsy, and recovery has taken place.
A case is reported by Voorman65of a child aged six months who had diarrhœa and vomiting, much prostration, sunken fontanelles, overlapping cranial bones, trembling of the tongue, slight spasm of the right arm and leg, head drawn back, and strabismus. The head afterward increased in size, the temporal vein was swollen and hard, with œdema of the skin in its neighborhood. There was gradual improvement and recovery, though when the patient was four and a half years old its mental development corresponded to that of a child two years younger.
65Centralb. f. d. Med. Wis., 1883.
In another, by Kolb,66a child of seventeen, well nourished, had a purulent discharge from the right ear. Besides headache, delirium, hyperæsthesia, convulsions, and then sleepiness and loss of consciousness, the following symptoms pointed toward thrombosis of the sinuses: Chills, inflammatory swelling over the right mastoid, with fulness of a cutaneous vein passing over it; a purely œdematous swelling in the neighborhood of the internal jugular or temporal fossa, forehead, and both upper eyelids, with exophthalmos on the right side; photophobia, blepharospasm, and cloudy vision; nose-bleed. There was no elevation of temperature, and recovery took place.
66Berl. klin. Woch., Nov. 13, 1876.
A case of thrombo-phlebitis following otitis and terminating in recovery is reported at length by Wreden.67
67Archives of Ophth. and Otol., 1874, lii. (translation).
ThePROGNOSISin any particular case can be based only on the severity of the symptoms and on the character of the preceding disease.
TREATMENT.—The prophylaxis of this affection evidently consists inthe proper treatment of the diseases upon which it depends, and might therefore be made to embrace nearly the whole range of tonic, roborant, antiphlogistic, and antiseptic measures, to say nothing of surgery and obstetrics. The proper nourishment of infants and children, the cutting short, when possible, of their acute diseases, or preventing their debilitating effects, will reduce marantic thrombosis to a minimum. At a later period of life the proper surgical management of carbuncle, abscess in the neck, and of the puerperal condition will tend to avoid this risk.
The most important point of all, however, is undoubtedly the careful treatment of otitis media and early attention to inflammation in the mastoid cells, with incision or trephining as may be necessary.
After a thrombus has formed there is little to be done toward its removal.
It has been claimed68that the preparations of ammonia are capable of diminishing considerably the coagulability of the blood when it is morbidly augmented. Though this cannot be considered proved, yet since the tendency of these salts is also to quicken the blood-current, a trial in a case where other indications are wanting is, to say the least, justifiable.
68Lidell,Am. Journ. Med. Sci., July, 1874, p. 101.
In a case reported by O'Hara,69where the symptoms pointed very strongly toward thrombosis of the cavernous sinuses, recovery took place under mercurials, iodide of potassium, and purgatives. The reporter was inclined to consider the cause of trouble specific.
69N. Y. Med. Record, vol. xvii. p. 617.
Considering the fact that cases with such marked and decisive symptoms as those last recorded have recovered, it is certainly the duty of the physician to prolong the life of his patient to the utmost, that absorption and condensation may go on as long as possible and collateral circulation be developed. Probably most physicians can recall cases of obscure cerebral disease going on to recovery contrary to all expectation, in which thrombosis furnishes an explanation quite as plausible as any other.
is a name which it is yet too early to omit altogether from a systematic work, although in treating of it we have more to do with nomenclature and classification than with pathological anatomy. The phrase may be said to have both an anatomical and a clinical signification, which do not coincide at all points. Clinically and among the laity it is used to express various symptoms and groups of symptoms more or less referable to the brain, some of them connected with one and some with another lesion, and many purely functional—if the word may be used—or at any rate unconnected with any known or definite lesion.
Vertigo, dull headache, sleeplessness, or, on the other hand, drowsiness, failure of memory, failure of power of concentration, of steady application, mental depression, fatigue, and even slight aphasia or actual slight hemiplegia, may any of them be considered symptoms or forerunners of softening of the brain. As nearly as anything, the popular notion of this affection corresponds to general paralysis of the insane or senile dementia, or even mere exhaustion. Many of these symptoms may, of course, be connected with the real softening described as the result of embolism orthrombosis, but it is hardly necessary to say that a symptomatology based on these elements alone is either too vague or else too much like that of diseases already described to be considered useful as a separate clinical grouping.
On the anatomical side softening of the brain has had a definite meaning, and for many years a part of its pathology has been well known. A general softening of the whole brain, such as seems to be the condition supposed when the phrase is used, does not and cannot exist, since a vascular lesion sufficient to cause anæmic necrosis of the whole brain must cause death long before softening would have time to take place. Nearly all the works and reports on softening have been based upon cases such as are now referred to definite lesions of the blood-vessels; and a good idea of the change in nomenclature and pathological views may be obtained by noticing the dates given in the extensive literature of the subject in theIndex Catalogueof the Surgeon-General's library, which are nearly all previous to 1860 or 1865.
Localized softening has already been described under the heads of hemorrhage, embolism, and thrombosis, venous and arterial. Whether it may occur from diseases of the cerebral vessels without actual occlusion is not certain, but, remembering the difficulty of detecting thrombi in minute vessels, and also the fact that it is not a great many years that occlusions have been systematically sought for at autopsies, it is better for the present to assume, in cases where softening is found in the usual form and the usual situations for the results of thrombosis and embolism, that one of these accidents is the cause, even if the actual point of occlusion is not found.
Softening may take place secondarily from tumors in the brain, and the name is also sometimes applied to a local encephalitis, which is an early stage of abscess. When, however, these various forms of disease are removed from the general heading of softening and referred to their proper pathological classes, there is a residuum in which the softening seems to be the primary affection, so far as the brain is concerned, though depending on other constitutional conditions.
In new-born infants softening of the brain, besides the rare cases in which it may be dependent on the same conditions which may cause it in the adult, is observed in two forms, as described by Parrot:70A. White softening in multiple foci, dependent upon fatty degeneration, of which it constitutes the last stage, is found almost exclusively in the centres of the hemispheres.B. Red softening, which affects the same region, but more extensively, and is accompanied by hemorrhage into the lymphatic sheaths with rupture.
70Arch. de Phys., 1873, p. 302.
These two forms may exist with each other, and with other intracranial lesions, such as thrombi of the sinuses and exudation under the arachnoid and around the veins.
Parrot compares this form of softening to that occurring in the other extreme of life, dependent on vascular lesions; but although he supposes the method of production to be unlike in the two cases, it is by no means so certain, either from his conclusions or his cases, that it is always so. In some of his cases the vessels are said not to be abnormal, but in others old thrombi are distinctly mentioned. As secondary consequences maybe observed intracranial dropsy, with perhaps hydrocephalic cranium and degeneration of the pons, bulb, and medulla.
Two cases of red softening of the cerebellum have been reported.71In one of them the pia was adherent, in the other thickened and covered with exudation. The microscopic details are not given nor the state of vessels mentioned. They are probably not strictly analogous to those described by Parrot.
71Jahrbuch. f. Kinderheilkunde, 1877.
The occurrence of granular corpuscles in the brain of the new-born is described by Virchow, and it is thought by him to be pathological and of an irritative character (encephalitis congenita). It is somewhat doubtful if this process is characterized by any distinct symptoms.
TheETIOLOGYis impaired nutrition, deficient or improper feeding, and depressing diseases, frequently tubercle.
TheSYMPTOMSandDIGNOSISof this form of softening are even more obscure than those of venous thrombosis in the same class of cases. Vague cerebral symptoms arising in an infant poorly nourished and suffering from acute disease may be due to this condition, but a positive diagnosis is out of the question. In the two cases of softening of the cerebellum just mentioned, in one, aged five, there was dilatation of the pupil, difficulty of hearing, and vertigo; in the other, aged six, vertigo, inclination to vomit, and clonic spasm of the left facial muscles. Parrot says that in the greater number of patients the encephalopathic troubles observed during life cannot be referred to it (softening), and in no case can it be diagnosticated.
Under these circumstances it is obvious that remarks upon thePROGNOSISandTREATMENTmust be purely works of the imagination.