[Learning through case studies--training for home care practice. 3. The family that surrounds the mother suffering from the aftereffects of cerebral hemorrhage].
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More than 1400 necropsies performed on patients with either a nontraumatic cerebral hemorrhage (400 cases) or with dementia over the age of 55 (1010 cases), or both, have been reviewed. There were 15 cases in which a cerebral hemorrhage had occurred together with cerebral amyloid angiopathy all of whom had been demented. Eight of the 15 patients were hypertensive. The 7 non-hypertensives showing only the amyloid change included two cases of "atypical" Alzheimer's disease with acute neurological features, and 5 cases of senile dementia (aged 72 to 78 years) coupled with focal neurological disorders. In the hypertensive patients, aged 67 to 86 years, with a progressive dementing syndrome and acute neurological signs, multiple ball-like hemorrhages (7 cases) and/or cerebral hematomas (3 cases) were associated with a combination of amyloid and hyalinar (hypertensive) angiopathy, often affecting segments of the same pial and cortical vessels. From these data and recent reports on lethal cerebral hemorrhage occurring spontaneously or after neurosurgical procedures in demented old people, cerebral amyloid angiopathy, which is not necessarily associated with systemic amyloidosis or severe (pre)senile cerebral degeneration, may be considered a rare but important cause of cerebral hemorrhage in the aged. The "vascular" type of presenile dementia, occasionally complicated by focal cerebrovascular lesions or bleeds, is considered a variant of Alzheimer's disease. The mechanism leading to formation of cerebral amyloid is unknown.
A series of 247 cases with simple and apparently primitive cerebral hemorrhages selected from the pathological records of Charles Foix laboratory from 1962 to 1977 is reviewed with regard to the accuracy of the premortem diagnosis as a function of the size, the location and the age of the bleeding, the patient's age, the practices of angiography or lumbar puncture and the considered period of death. The clinical diagnosis of cerebral vascular disease was made in 75% of the cases from that serie but the hemorrhagic mechanism was identified only in 50,6% of cases. The diagnosis accuracy was enhanced in large and recent hemorrhages occuring in patients under 70 years old. It seemed better in cerebellar and intermediate locations. It was enhanced in more recent observations (collected since 1974). The practice of cerebral angiography and lumbar puncture rose up (in a somewhat equivalent way) the proportion of accurate diagnoses. The lumbar puncture practice was not associated with a higher rate of cerebral herniae.
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The authors report 6 cases of intracerebral hemorrhages in 6 children, of what appears to be, of primary origin. 3 cases concern children between the ages of 4 and 14 years; the 3 others are situated shortly after birth or during the first months of life. A review of the literature emphasizes the sporadic nature of these cases and the persistance of diagnostic and etiological problems as to the cause of these hemorrhages. In the course of reviewing articles as well as our own personal series, it is evident that the cat scanner has demonstrated its qualifications as a diagnostic tool in the early detection of the lesions, permitting a better adapted treatment, thus improving their prognosis. The prognosis appears to be linked : --to an early diagnosis --to whether or not the hemorrhage is of massive nature or not --to the precise location of the hematoma --to the neurological state of the patient at the time of treatment --to the absence of an associated pathologie (severe prematurity, coagulation pathology). The long distance prognosis in the case of these apparently primary hemorrhages remains uncertain, due to the high rate of recidivism at a later unpredictable date (one month or several years later); to the occurence or not of a hydrocephalus especially in the case of young infants; and frequent sequels affecting superior functions. This long distance prognosis seems, however, to be little affected by the recent acquisitions in diagnostic testing.
Comprehensive ascertainment of all possible new cases of stroke appearing between January 1, 1970 and June 30, 1971, and admitted to three major hospitals in Winnipeg, Manitoba, has been achieved by reviewing the Manitoba Health Services Commission claim reports. The medical records of these cases were reviewed, pertinent data were abstracted, and rigid criteria for diagnosis were followed. Also, data were obtained from death certificates, autopsy reports and long-term hospital records. A total of 606 ascertained cases (410 infarction, 137 hemorrhage, and 59 undetermined type) were matched for age, sex, residence and year of admission with 606 controls from admissions for other than cardiovascular and cerebrovascular disorders. The data were analyzed for elucidating the possible risk factors for infarction (INF) and hemorrhage (HGE). The findings suggested that hypertension was the main risk factor in hemorrhage, whereas in infarction, along with hypertension, other factors such as diabetes, heart enlargement in chest x-ray, ECG abnormalities, and smoking were suggested as risk factors. There was an association also between infarction, on one hand, and the history of receiving anticoagulants, diuretics, and medications for the heart, and the occurrence of myocardial infarction, on the other hand. These features indicate that infarction and ischemic heart disease have similar risk factors. Hemoglobin and hematocrit were higher in infarction cases than in their controls only when measured at stroke admission. No difference was revealed when they were measured prior to stroke. Their association with infraction therefore may be secondary to other factors and of no significance for its risk.
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Evidence of cerebrovascular disease at autopsy was compared in 2 groups of men: 186 long-time residents of Hiroshima, Japan, and 253 men of Japanese ancestry long resident in Honolulu, Hawaii. They were 45 to 71 years-of-age at death. Atherosclerosis of the circle of Willis and its major branches, sclerosis of the intraparenchymal arteries and the frequency of cerebral hemorrhage and cerebral infarct were compared in the 2 populations. The Honolulu subjects had significantly more atherosclerosis of the circle of Willis, but less intraparenchymal artery sclerosis and less cerebral infarction. Cerebral hemorrhage was equally frequent in the 2 cities. It was concluded that cerebral infarction is more frequent in Japanese men in Hiroshima than Honolulu, and that men of Japanese ancestry in Honolulu are spared an appreciable risk of cerebral infarction through decreased frequency of intraparenchymal arterial sclerosis despite higher levels of atherosclerosis of large intracranial arteries.
The incidence of cerebral intraventricular hemorrhage was determined by computed tomography in 100 infants with birth weights less than or equal to 1,500 gm. A comparison of IVH with serum sodium concentrations and the amount of intravenous sodium bicarbonate administered did not reveal a significant relationship. Analysis of the method of infusion of sodium bicarbonate indicated that the rapid infusion of hyperosmolar (M to M/12) sodium bicarbonate is associated with a significantly increased incidence of IVH.
HGH secretion in response to TRH was studied in patients with cerebrovascular disease in order to elucidate an influence of cerebrovascular lesions on the hypothalamus-anterior pituitary function. Blood specimens were obtained before and at the time of 10, 20, 30, 40, 60, 90 and 120 minutes after the intraveneous administration of 200 microgram of TRH in 17 patients with cerebral hemorrhage and in 8 patients with cerebral infarction. With regards to the natural fluctuations of serum HGH caused by cerebrovascular disease, the blood specimens were obrained at the time of 0, 30, 60, 90 and 120 minutes without the administration of TRH in 4 patients with cerebral hemorrhage and in 4 patients with cerebral infarction. Serum HGH was measured using the RIA method and the following results were obtained: 1) An increase in serum HGH was observed in 1 patient with cerebral hemorrhage out of 8 patients with cerebrovascular disease without TRH administration. 2) In 5 out of 17 patients with cerebral hemorrhage, an increase in serum HGH was observed following TRH administration. Three out of these 5 patients were included in the group of non-coma, and 4 out of the 5 patients were female. 3) In 2 out of 8 patients with cerebral infarction, an increase in serum HGH was observed following TRH administration.
A method for induction of subarachnoid hemorrhage (SAH) in a rat model is described. Resolution of the hemorrhage was documented photographically and microscopically at intervals from 1 hr to 8 days. Photographs indicated that most of the hemorrhage was resorbed within 3 days, an observation confirmed microscopically by the amount of red blood cells in the subarachnoid space. Significant cerebral vasospasm was documented within the first 2 days after the induction of hemorrhage with the basilar artery returning to baseline values at an average of 3 days followed by moderate dilatation at 5 to 8 days. The suitability of the rat as an animal model for further investigation of subarachnoid hemorrhage is discussed.