Case in an infant 5 days old. Not withstanding absence of marked cerebral symptoms, extensive heemorrhage into the brain, no convulsions or even un conseionsness were present. T. M. Rotel' and A. 1I. Wentworth (Boston Med. and Surg. Jour., Aug. 15, '05).
Case of mixed heemorrhage and throm bosis secondary to 'tiara] disease in a ehild 7 years old. Fox (London Lancet, Jan. 27, '94).
While cerebral hmmorrhages often fol low the development of small aneurisms, and embolic lodging in arteries may eau.se the development of aneurisms, aneurism with subsequent cerebral haemorrhage as the result of verrucose endocarditis may also occur. In 3 eases —the patients being 32, 45, and 50 years of age, respectively—fatal cerebral hem orrhage could be ascribed to the lodg ment of a septic embolus, a fresh endo earditis ingrafted on old disease being found, the arteries and the kidneys be ing healthy. Four other illustrative cases mentioned. M. Simmonds (Deut. med. Woch., May 30, 1901).
In traumatic cases the violence is a sufficient explanation. As a rule, the haemorrhage results promptly. But there are now several cases on record showing that several hours or days, even a week or more, may intervene. These are mostly meningeal forms, yet it is cer tain that some are intracerebral. It is these cases of delayed apoplexy that serve to associate the traumatic with the other varieties.
Case of a child of 5, who fell, striking on her head. She became somnolent, answered questions correctly, but hesi tatingly; perfect sensation and muscular eo-ordination. Discoloration of all the palpebral and ocular tissues, with suffi cient cedema to completely close the right eye; left pupil responded readily to light. Trephining, revealed a clot three sixteenths of an inch in thickness and one inch in diameter, which had formed between the dura mater and the parietal bone. This was evacuated and drained and the child recovered. Ruth (Jour. Amer. Med. Assoc.. Fel). 6, '92).
College-student, aged 19, struck in a friendly boxing-bout upon the left jaw, large gloves being used. Death on the sixth day. No external marks of violence. Left found ruptured. No pathological change,* preent in the vessel-walls. Walton (Boston Med. and
Sur g. Jour., Mar. 1, '94).
Nephritis is one of the most certain causes. The arteriosclerosis that de velops may later degenerate, allowinz the vascular tunics to give way. In any case the heightened blood-pressure and perhaps the circulating toxins so weaken the arterial wall that under some sudden stress it breaks.
Syphilitic alterations of the vascular parietes seem at times to be the imme diate cause of their rupture; though this claim needs a better basis than the fact that the patient is a specific or that , antisyphilitic remedies produce a good I effect. Much more certain are the cases where the break results indirectly. In them a former specific arteritis, that may long since have run its course, has left behind it a cicatricial and hence weak ened spot which ever after remains. Like all scar-tissue, this has less resist ance and too often in time yields. This point has been strongly urged by Gow ers. There are also evidently other cases in which softening of this origin makes the intermediary link to vascular rupt ure. In neither of these latter forms can specific treatment well have any value; they differ only etiologically from the creneral run.
of 100 non-fatal personal cases 36 were due to syphilis: they occurred in early life and were often multiple in character. Cerebral ht-emorrhages were rarely repeated. Many eases showed changed vital conditions and personal habits. C. L. Dana (N. Y. Med. Jour., Jan. 5, '95).
Local softening. This may be due to traumatism, embolism, septic infection, syphilis, or whatever other cause. The focus is usually not a large one, and not the cause of any definite symptoms. Even if its presence were known, it is hard to see how anything could be done to remedy it or ward, off this particular sequel. The prevention of the softening must depend on the general management of those affections that lead to it.
Abnormal constitutional blood-condi tions, such as scorbutus, purpura, per nicious anallnia, leucocythremia, and severe infections with haemorrhagic di athesis may act as efficient weakeners of the vessel-parietes. Haemophilia is not known as a cause, however much it might darken a case.