Cause of Death in Ruptured Intracranial Aneurysms

Bebin, José; Currier, Robert D.

doi:10.1001/archinte.1957.00260050099012

Cited by 16 publications

(3 citation statements)

References 21 publications

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“…Massive bleeding into the ventricles usually causes death in less than six hours (Bebin and Currier, 1957). Blood cannot escape rapidly from the ventricles (Symonds, 1924), and great dilatation commonly follows intraventricular bleeding.…”

Section: Resultsmentioning

confidence: 99%

“…Many accounts have been taken from routine necropsy reports and few have included detailed examinations of the brain. Intracerebral bleeding has received most attention, largely since the paper of Richardson and Hyland (1941), but recently ischaemic lesions have been more widely recognized (Robertson, 1949;Wilson, Riggs, and Rupp, 1954;Bebin and Currier, 1957). Robertson (1949) described five instances of ischaemia, and it is noteworthy that three were seen in the 10 cases he observed himself, whereas only two were recorded in more than 80 routine post-mortem reports he reviewed.…”

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confidence: 99%

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Brain Changes in Ruptured Intracranial Aneurysm

Tomlinson¹

1959

J Clin Pathol

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Since the papers of Beadles (1907), Fearnsides (1916), andSymonds (1924), there have been numerous publications on the clinical manifestations, prognosis, and treatment of spontaneous subarachnoid haemorrhage. The pathology of the brain has received less attention. Many accounts have been taken from routine necropsy reports and few have included detailed examinations of the brain. Intracerebral bleeding has received most attention, largely since the paper of Richardson and Hyland (1941), but recently ischaemic lesions have been more widely recognized (Robertson, 1949;Wilson, Riggs, and Rupp, 1954;Bebin and Currier, 1957). Robertson (1949) described five instances of ischaemia, and it is noteworthy that three were seen in the 10 cases he observed himself, whereas only two were recorded in more than 80 routine post-mortem reports he reviewed. The Method of Investigation At necropsy the brain was examined externally only, and the bleeding aneurysm located where this was possible without disturbing the blood lying in the fissures, or between the lobes. After fixation for one to two months in formol-saline, the basal vessels were removed from the specimen. The brain was then cut into numerous slices and the distribution of blood in the sulci and fissures noted; material for histology was taken from many areas of the cerebral cortex, basal ganglia, brain-stem, and cerebellum. Particular attention was paid to any area suggestive of infarction and sufficient sections were taken to map out the area involved.Haematoxylin and eosin staining was used routinely, but Nissl, Mallory's phosphotungstic-acidhaematoxylin, Holzer, myelin, neurofibrillary, and fat stains were used where needed.

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

Brain Changes in Ruptured Intracranial Aneurysm

Tomlinson¹

1959

J Clin Pathol

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“…In 28 of these 57 cases the ventricles had been greatly enlarged by the blood, while in 13 of these 28 cases with enlarged ventricles the fourth ventricle was widely dilated. Bebin and Currier (1957) state that massive bleeding into the ventricles commonly causes death in under six hours. Tomlinson (1959) described infarction around the fourth ventricle as a result of dilatation of this space by blood.…”

Section: Dimensions Of Intracerebral Haematomata Halfmentioning

confidence: 99%

Intracerebral haematoma complicating ruptured cerebral berry aneurysm

Crompton¹

1962

Journal of Neurology, Neurosurgery & Psychiatry

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This paper is an account of the morbid anatomical findings at necropsy in a study of intracerebral haematomata in 103 consecutively examined cases of ruptured cerebral berry aneurysm. In the majority of these cases the site of the ruptured aneurysm had been demonstrated by carotid angiography during life but in a few the aneurysm was only shown at necropsy. It is by studying these lesions at necropsy that information will be gained concerning some of the lesions probably present in patients surviving with a neurological deficit but it must be remembered that the severity and frequency of the lesions in cases coming to necropsy will not necessarily be the same as in these surviving though the nature of the lesions will probably be very similar.As pointed out by Robertson (1949) and again 10 years later by Tomlinson (1959), the factual information to be found in the literature on the intracerebral sequelae of ruptured cerebral aneurysm is very sparse. Many of the conclusions drawn have resulted from impressions gained from a small number of cases rather than from factual observations on a larger series. This paper is primarily concerned with intracerebral haematomata, but figures relating to cerebral infarction and subarachnoid haematomata in the same series will be given for comparison, and also because it is important to avoid giving the impression that intracerebral haematomata are the only complication of the rupture of cerebral berry aneurysms. INCIDENCEOne hundred and three cases of ruptured cerebral aneurysm were examined at necropsy. Sixty-two of them had intracerebral haematomata and 62 had cerebral infarction. This implies definite, large regions of cortical infarction, involving at least onethird of the region of supply of one of the cerebral arteries or ganglionic necrosis at least 5 mm. in diameter. Of those 62 cases with intracerebral haematomata, 32 also showed cerebral infarction. AGE AND SEX DISTRIBUTION Table I shows the age distribution of the 103 cases in decades. These have been separated into subgroups and it can be seen that nearly all the cases over 60 years of age were in women.The age distribution for cases with infarction and cases with intracerebral haematomata is similar to that of the total series, except that infarction is somewhat more common in the older age groups than are haematomata and a large number of these older cases with infarction are in women. The respective incidence of haematomata and infarction in men and women is summarized in Table I, and

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Cerebral Vasospasm and Ruptured Intracranial Aneurysm

Millikan¹

1975

Archives of Neurology

127

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The literature concerning cerebral vasospasm associated with subarachnoid hemorrhage (SAH) due to ruptured intracranial aneurysm contains no definitive study of patients to determine whether there is (1) any clinical picture consistently present coincident with known cerebral vasospasm, (2) any relationship between mortality and known vasospasm, and (3) any relationship between serious brain damage (morbidity) and known vasospasm. To answer these important questions, experience with 198 consecutive acute SAH patients (every patient had a cerebral angiogram demonstrating one or more intracranial aneurysms) was studied. The experience with these 198 consecutive patients led to the conclusions that (1) there is no clinical picture consistently present coincident with known cerebral vasospasm; (2) cerebral vasospasm has no effect on the mortality from SAH due to ruptured aneurysm; and (3) there is no relationship between the frequency and severity of the complications from surgical or conservative treatment and the presence or absence of vasospasm.

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Cause of Death in Ruptured Intracranial Aneurysms

Cited by 16 publications

References 21 publications

Brain Changes in Ruptured Intracranial Aneurysm

Brain Changes in Ruptured Intracranial Aneurysm

Intracerebral haematoma complicating ruptured cerebral berry aneurysm

Cerebral Vasospasm and Ruptured Intracranial Aneurysm

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