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Evolution of the nervous system, ed. 2
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Surgical Neurology Vol 17 No 1 January 1982
the clinical symptoms associated with it. Transient intraluminal fibroblastic hyperplasia and thrombosis may be present and might explain the rarity of angiographic identification and pathological documentation of the process. Or the pathological changes in the vessels may be large enough to cause symptoms and signs but small enough to escape detection with usual techniques of angiography and of gross and microscopical histopathology [3]. Katsiotis and Taptas [6] reported the very interesting case of a 35-year-old man who had a classic onset of severe headache and whose cerebrospinal fluid was found to be bloody on lumbar puncture. There were no focal neurological signs and he did well until the fifteenth day, when a right internal carotid angiogram revealed a small intravascular carotid filling defect immediately above the superior horizontal limb of the carotid artery. The carotid artery appeared spastic beyond this point. There was delayed filling of the inferior branch of the angular artery, although other arteries filled well. No aneurysm was evident. Three weeks later a left internal carotid angiogram was performed again and the original intravascular carotid filling defect as well as the spasm had disappeared. It was their opinion that a small embolus, the origin of which was a thrombosis at the site of the unidentified aneurysm, explained the focal neurological signs and was the cause of the cerebral infarction. Such intraluminal filling defects are rarely seen and rarely
recorded, and hence this case report. The fact that our patient was noted to have a change in his level of consciousness before angiography tends to militate against the possibility of the procedure causing the embolism. Furthermore, intercurrent embolism secondary to angiography may be eliminated as a possible cause since the defect was observed in a large cerebral vessel. It is also unlikely that the small extraaxial hematoma in the temporal fossa (not seen on CT) and a swollen frontal lobe could explain his sudden deterioration on the tenth postoperative day. It is therefore our belief that this is a rarely documented case of vasospasm with endothelial disruption and thrombosis resulting in distal embolization which may, in fact, be far more common than is generally realized.
References 1. AllcockJM, Drake CL: Ruptured intracranial aneurysm--the role of arterial spasm. J Neurosurg 22:21-29, 1965 2. Alksne J, Green-hootJ: Experimentalcatecholamine-inducedchronic cerebral vasospasm;myonecrosisin vessel wall. J Neurosurg 41:440-445, 1974 3. AlksneJF, Smith RN: Experimentalmodelsof spasm. Clin Neurosurg 24:216-227, 1977 4. Conway L, McDonald L: Structural changes of the intradural arteries following subarachnoid hemorrhage. J Neurosurg 37:715- 723, 1972 5. Heros RC, Zervas NT, Negoro M: Cerebrovasospasm.Surg Neurol 5:354-362, 1976 6. KatsiotisPA, Taptas JN: Embolismand spasmfollowingsubarachnoid hemorrhage. Acta Radiol 7:140-144, 1968
Book Review Evolution of the Nervous System, ed. 2
By Harvey B. Sarnat and Martin G. Netsky, New York, Oxford, Oxford University Press, 1981 504 pp., $23.95 (cloth); $16.95 (paper) Reviewed by Paul C. Bucy, M.D., Editor This is the second edition of this book and it is also available as a paperback publication. This book is an excellent source of information for anyone seeking information regarding the embryology and comparative anatomy of the nervous system. It deserves a place in every medical library.
Surgical Neurology Vol 17 No 1 January 1982
the clinical symptoms associated with it. Transient intraluminal fibroblastic hyperplasia and thrombosis may be present and might explain the rarity of angiographic identification and pathological documentation of the process. Or the pathological changes in the vessels may be large enough to cause symptoms and signs but small enough to escape detection with usual techniques of angiography and of gross and microscopical histopathology [3]. Katsiotis and Taptas [6] reported the very interesting case of a 35-year-old man who had a classic onset of severe headache and whose cerebrospinal fluid was found to be bloody on lumbar puncture. There were no focal neurological signs and he did well until the fifteenth day, when a right internal carotid angiogram revealed a small intravascular carotid filling defect immediately above the superior horizontal limb of the carotid artery. The carotid artery appeared spastic beyond this point. There was delayed filling of the inferior branch of the angular artery, although other arteries filled well. No aneurysm was evident. Three weeks later a left internal carotid angiogram was performed again and the original intravascular carotid filling defect as well as the spasm had disappeared. It was their opinion that a small embolus, the origin of which was a thrombosis at the site of the unidentified aneurysm, explained the focal neurological signs and was the cause of the cerebral infarction. Such intraluminal filling defects are rarely seen and rarely
recorded, and hence this case report. The fact that our patient was noted to have a change in his level of consciousness before angiography tends to militate against the possibility of the procedure causing the embolism. Furthermore, intercurrent embolism secondary to angiography may be eliminated as a possible cause since the defect was observed in a large cerebral vessel. It is also unlikely that the small extraaxial hematoma in the temporal fossa (not seen on CT) and a swollen frontal lobe could explain his sudden deterioration on the tenth postoperative day. It is therefore our belief that this is a rarely documented case of vasospasm with endothelial disruption and thrombosis resulting in distal embolization which may, in fact, be far more common than is generally realized.
References 1. AllcockJM, Drake CL: Ruptured intracranial aneurysm--the role of arterial spasm. J Neurosurg 22:21-29, 1965 2. Alksne J, Green-hootJ: Experimentalcatecholamine-inducedchronic cerebral vasospasm;myonecrosisin vessel wall. J Neurosurg 41:440-445, 1974 3. AlksneJF, Smith RN: Experimentalmodelsof spasm. Clin Neurosurg 24:216-227, 1977 4. Conway L, McDonald L: Structural changes of the intradural arteries following subarachnoid hemorrhage. J Neurosurg 37:715- 723, 1972 5. Heros RC, Zervas NT, Negoro M: Cerebrovasospasm.Surg Neurol 5:354-362, 1976 6. KatsiotisPA, Taptas JN: Embolismand spasmfollowingsubarachnoid hemorrhage. Acta Radiol 7:140-144, 1968
Book Review Evolution of the Nervous System, ed. 2
By Harvey B. Sarnat and Martin G. Netsky, New York, Oxford, Oxford University Press, 1981 504 pp., $23.95 (cloth); $16.95 (paper) Reviewed by Paul C. Bucy, M.D., Editor This is the second edition of this book and it is also available as a paperback publication. This book is an excellent source of information for anyone seeking information regarding the embryology and comparative anatomy of the nervous system. It deserves a place in every medical library.