Howard Morgan

Experimental Study on the Genesis of Cerebral Vasospasm

The cerebral vasospasm produced by blood, fractions of blood, and blood-borne agents administered intracisternally was studied arteriographically to attain a better understanding of the genesis of vasospasm. The results indicate this phenomenon is multifarious in origin, involving a number of spasmogens. Whole blood, platelets, platelet extracts, some isolated components of platelets, plasma, thrombin, histamine, serotonin and prostaglandins F1α, E2 and F2α produced a significant incidence and duration of spasm. Norepinephrine and prostaglandin E1 were inactive. Spasm produced by arachidonic acid and red blood cells was of questionable significance. Compared to whole blood, thrombin usually produced spasm which was more delayed in onset while most other active substances produced a shorter-lived spasm. However, among the pure substances tested, serotonin, prostaglandin E2 and prostaglandin F2α induced spasm in small doses which most nearly resembled that observed with whole blood. The hypothesis that the course of spasm depends upon synthesis of spasmogens by brain and blood is advanced. Prostaglandin synthesis plays a major role in this concept.

Emergency reversal of anticoagulation and antiplatelet therapies in neurosurgical patients

Intracranial hemorrhage (ICH) is a common problem encountered by neurosurgeons. Patient outcomes are influenced by hematoma size, growth, location, and the timing of evacuation, when indicated. Patients may have abnormal coagulation due to pharmacological anticoagulation or coagulopathy due to underlying systemic disease or blood transfusions. Strategies to reestablish the integrity of the clotting cascade and platelet function assume a familiarity with these processes. As patients are increasingly treated with anticoagulants and antiplatelet agents, it is essential that the physicians who care for patients with ICH understand these pathways and recognize how they can be manipulated to restore hemostasis.

Hemorrhagic studies with severe hemodilution in profound hypothermia and cardiac arrest

DURING THE EARLY 1960% profound hypothermia with cardiac arrest gained popularity in neurosurgery as an adjunct to the surgical treatment of intracranial aneurysms. The surgeon had the advantage of a wide operative exposure in a bloodless operative field. The techniques, physiology, and metabolic changes of profound hypothermia were described by several authorities [ 1, 3, 5, 7, 8, 11-141. During the late 1960’s, aneurysm surgery became more refined and these improvements along with the technical, metabolic and hemorrhagic problems encountered with profound hypothermia and cardiac arrest led to the general disuse of this procedure in neurosurgery. Our interests in profound hypothermia with cardiac arrest as an adjunct to the surgical treatment of certain intracranial vascular lesions has continued, and we agree wit’h Sundt and coworkers who recently stated “. . . there are aneurysms presently considered inoperable that might be approached utilizing profound hypothermia . . . [and] . . . it is suggested that the approach, virtually abandoned a

The Measurement of Cerebral Infarction Edema With Sodium 22

Sodium 22 was used to determine quantitatively cerebral infarction edema in cats after occlusion of the middle cerebral artery. A comparison was made of the sodium 22 edema determination with the wet weight-dry weight method of edema determination. There was a high degree of correlation between the two methods. The sodium 22 method of measuring cerebral infarction edema was less time consuming and easier than the wet weight-dry weight method, and served as a reliable means of quantitatively comparing the edema content in the hemispheres of animals with stroke.

Aseptic meningitis due to atheromatous material in the subarachnoid space.

Summary500 mg of sterile pooled human atheromatous material was injected into the cisterna magna of 6 mongrel dogs. Repeated cisternal punctures were done at various intervals until sacrifice from 1 day to 28 days following injection. CSF was obtained for cell count, sugar, protein and analysis in the Technicon 6/60 which measured 14 additional chemical and enzymatic variables. All 6 animals showed a prompt cerebrospinal fluid (CSF) pleocytosis which largely subsided during the first 2 weeks after injection. Increased CSF protein content developed more slowly, but was more prolonged than the pleocytosis. There was a variable decrease in CSF sugar and increase in CSF lactate dehydrogenase, calcium and inorganic phosphorous. Light and electron microscopic studies showed an intense acute inflammatory reaction with marked phagocytosis of the foregin material, probably by arachnoidal cells and moderate edematous changes in the astrocytic processes at the site of injection. During the first 2 weeks after the injection the inflammatory reaction became chronic and the edematous changes in the medulla subsided.