The Influence of Adrenocortical Steroids on Severe Cerebrovascular Accidents

Rubinstein, Morton K.

doi:10.1097/00005053-196509000-00005

Cited by 39 publications

(16 citation statements)

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“…288 The treated animals showed more infarction and edema than did the untreated animals. This is attributed to an increase in CBF in nonischemic tissue and a subsequent increase in intracranial pressure.…”

Section: Diureticsmentioning

confidence: 91%

“…Furosemide and acetazolamide inhibit CSF formation and decrease specific activity of sodium in the CSF. 288 Such inhibition may allow faster drainage of the extravasated edema fluid through channels which normally accommodate considerable amounts of bulk CSF flow.…”

Section: Diureticsmentioning

confidence: 99%

“…248 Systemic hypothermia has been shown also to reduce the edema associated with cryogenic lesions in the rhesus monkey, 280 -" ' in the cat, 282 and the dog. 288 - 284 Conversely, raising the body temperature of the rhesus monkey to 104 F for a two-hour period increases this edema by 40%. 288 The authors conclude that in human diseases known or thought to be associated with cerebral edema, fever should be vigorously treated.…”

mentioning

confidence: 99%

“…288 - 284 Conversely, raising the body temperature of the rhesus monkey to 104 F for a two-hour period increases this edema by 40%. 288 The authors conclude that in human diseases known or thought to be associated with cerebral edema, fever should be vigorously treated.…”

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confidence: 99%

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Report of Joint Committee for Stroke Resources. IV. Brain edema in stroke.

Katzman¹,

Clasen²,

Klatzo³

et al. 1977

Stroke

209

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SUMMARY A classification of brain edema is provided as well as an extensive review of the animal models from which we have derived most of the basic information we have about the formation and resolution of edema. The clinical aspects of cerebral edema in stroke are discussed and also modern methods for identifying cerebral edema in the human. Attention is given to computed tomography and enhanced CT and advances in their application to this condition.Treatment of cerebral edema in the stroke patient using glycerol, dextran 40, mannitol, steroids, and other drugs is discussed and the need pointed out for controlled clinical trials of the therapeutic effectiveness of these agents.THE IMPORTANCE of brain swelling in the pathogenesis of stroke assumes growing significance as physicians increase their understanding of cerebrovascular diseases and their attempts to provide treatment. For example, a recent report 1 shows that in 32 of 100 patients who died as the result of cerebral infarction, transtentorial herniation was considered to be the most serious factor contributing to death. In the experience of most clinicians, a "swollen brain" can be demonstrated as well in a substantial number of patients who come to autopsy as a result of cerebral hemorrhage.The study group members appreciate fully the difficulties involved in understanding and interpreting current knowledge of cerebral edema pathogenesis gained from animal experimentation. Nevertheless, the basic information derived from a variety of animal models and reported in detail in the first pages of this report is considered essential to understanding the cerebrovascular events occurring in man. The ultimate objectives are to prevent cerebral edema wherever possible and to treat the condition when it develops, with the expectation of reducing the morbidity and mortality resulting from this complication. Classification of Cerebral EdemaCerebral edema is defined as an increase in brain tissue volume resulting from an increase in its fluid content.2 It must at all times be differentiated from brain engorgement caused by an increase in the volume of blood within a region of the brain 3 and from brain swelling due to intracerebral hemorrhage.• A priori, one might suppose that edema associated with cerebrovascular lesions would be primarily of the vasogenic type, since both overt injury to blood vessels and often a discrete focal brain lesion are present. However, experimentally, the increase in tissue volume and water is found usually to reach a peak prior to the extravasation of protein or of BBB indicators. Clinically, swelling in and around an area of infarction may be present before the radionuclide (RN) scan used to monitor BBB leakage becomes positive. This evidence suggests that brain edema due to focal ischemia begins as a cytotoxic type and is followed by a vasogenic edema. But the pathophysiology of this edema and its pattern of development are sufficiently specific to warrant a separate classification as ischemic brain edema. Biochemical Measures of Exp...

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Section: Diureticsmentioning

confidence: 91%

Section: Diureticsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Report of Joint Committee for Stroke Resources. IV. Brain edema in stroke.

Katzman¹,

Clasen²,

Klatzo³

et al. 1977

Stroke

209

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“…Rubenstein 7 reported on the use of dexamethasone in severe cerebrovascular accidents. Treatment consisted of either a placebo or 1 cc (4 mg) dexamethasone intravenously and 1 cc intramuscularly at the beginning of the study, followed by 1 cc BAUER, TELLEZ intramuscularly every six hours for 72 hours.…”

Section: Additional Abstractmentioning

confidence: 99%

Dexamethasone as Treatment in Cerebrovascular Disease. 2. A Controlled Study in Acute Cerebral Infarction

Bauer

Tellez

1973

Stroke

113

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Steroid Therapy of Brain Edema

1972

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Ischemic brain injury was produced in rats by the intracarotid injection of microspheres. During a 72-hour period of study, large doses of dexamethasone did not favorably affect survival, severity of brain edema, brain electrolyte shifts, or alterations in cerebral red blood cell, albumin, and pertechnetate spaces. The role of steroid therapy in cerebral infarction requires critical clinical appraisal. (27:209-212, 1972) G, riucocorticosteroids have been used in the therapy of cerebral edema since the recognition, in 1945, that adrenal corti¬ cal extract prevented swelling of the cat brain after exposure to air.1 Clinical studies demonstrated the utility of steroids in ede¬ ma due to primary and metastatic brain neoplasm, head trauma, neurosurgical pro¬ cedures, and other causes.2·3 Experimental studies, using various animal models, have largely confirmed a beneficial effect.3Brain edema is a frequent accompaniment of cerebral infarction. This has been demon¬ strated by pathologic studies which suggest that edema is a significant contributory fac¬ tor to the rapidly fatal outcome in patients dying within seven days of acute infarction.4·5 In a retrospective clinical study, Plum showed that brain swelling con¬ tributed to deterioration or death in 22 of 106 patients with acute hemispheric infarcts.6 The use of steroids to treat stroke remains a controversial issue. Initial uncontrolled studies suggested that such therapy might be beneficial.7·8 The results of controlled studies have been discrepant; Rubinstein9 reported favorably, whereas Dyken and White10 found a slightly, but statistically insignificant, higher mortality in the corti¬ sone-treated group. In both groups, rela¬ tively small numbers of patients were studied.Very few experimental studies of this prob¬ lem have been performed, probably due, in part, to the absence of a suitable experimen¬ tal model. Plum and co-workers11 found an adverse effect on mortality following a dose of 0.55 mg/kg of body weight of dexamethasone every 12 hours in rats subjected to hypoxia alone, or unilateral carotid ligation plus hypoxia. Surviving treated animals were unimproved with respect to clinical status, severity of edema and brain electro¬ lyte changes, and altered vascular permea¬ bility to trypan blue. Their results have been criticized because the observations did not extend beyond 24 hours. Pappius and McCann12 demonstrated that studies must be continued for longer periods of time before an effect becomes apparent. The same objec¬ tion applies to the results of Cantu and Ames,13 who found that methylprednisolone, administered 45 minutes to two hours before aortic ligation, did not relieve the cerebro-

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The Influence of Adrenocortical Steroids on Severe Cerebrovascular Accidents

Cited by 39 publications

References 0 publications

Report of Joint Committee for Stroke Resources. IV. Brain edema in stroke.

Report of Joint Committee for Stroke Resources. IV. Brain edema in stroke.

Dexamethasone as Treatment in Cerebrovascular Disease. 2. A Controlled Study in Acute Cerebral Infarction

Steroid Therapy of Brain Edema

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