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Rerupture of intracranial aneurysms
Letters to the Editor
We have reviewed the article written by Dr. Aoki and Dr. Mizutani in the Journal of Neurosurgery and agree that primary subarachnoid hemorrhage in moyamoya is exceedingly rare. We thank the authors for drawing this point to our attention. J O H N W. WALSH, M.D., Ph.D. Lexington, Kentucky
Cerebral Hemorrhage To the Editor: 1 read with interest the article "Moyamoya Disease and Cerebral Hemorrhage" by Hardy and Williams in the May issue o f SURGI('AL N E U R O L O G Y ( S u r g Neurol 1984;2 l:507-10), in which they reported a case of a 54-year-old man with cerebral hemorrhage secondary to "moyamoya disease." As the authors state, it is evident that moyamoya disease causes intraparenchymal hemorrhage as seen in their patient and in cases reported by us as well [1]. However, in regard to the features of the cerebral angiography shown in their case, it is highly doubtful whether this case may belong to moyamoya disease: The right and left common carotid angiograms reveal a long tubular stenosis beginning at the bifurcation of the common carotid artery and extending into the cranial cavity, where it is occluded. Their angiograms do not demonstrate any characteristics of moyamoya disease. Furthermore, on the left vertebral angiogram, nearly normal-appearing internal carotid, middle cerebral, and anterior cerebral arteries are opacified through retrograde flow from the posterior communicating artery; this opacification is sufficient to exclude the diagnosis of moyamoya disease. It is, therefore, hardly acceptable that this case meets the criteria of moyamoya disease [2]. N O B U H I K O AOKI
Tokyo.Japan 1. Aoki N, Mizutani H. Does moyamoya disease cause subarachnoid disease? Review of 54 cases with intracranial hemorrhage confirmed by computerized tomography. J Neurosurg 1984;60:348-53. 2. Guideline for the diagnosis of moyamoya disease: annual report of the Research Committee on the Progressive Occlusive Disease of the Circle of Willis. Tokyo: 1978:1 ~,2.
Reply. We would like to take issue with Dr. Aoki's comments regarding the diagnosis of our patient. There has been considerable discussion regarding the absolute etiology of moyamoya disease. Some authors have considered it to be postviral while others have assumed it to be a primary vasculopathy. Still others have considered the possibility of arteriosclerotic disease [1] as the primary occlusive event in the older population with this pattern. We would agree with Debrun et al [2] on the etiologic nonspecificity of the pattern. Although the Japanese may now
Surg Neurol 1985;23:201-4
203
require proximal occlusion of the anterior cerebral and middle cerebral arteries for inclusion into their syndrome complex, the complex "fibriUar" collaterals arising from deep perforating choroidal, lenticulostriate, and thalamic branches must be explained and have been well defined in moyamoya. These have often been grouped with the moyamoya disease complex. They all share the same clinical syndrome of intracranial occlusive disease with the fine perforating collaterals. Our case fits nicely into this category, and we believe it is only a matter of semantics that Dr. Aoki is pursuing. R. GAYLE WILLIAMS, M.D. ROBERT C. HARDY, M.D. San Antonio. Texas 1. Hinshaw DB, Thompson JR, Hasso AN. Adult arteriosclerotic moya-moya. Radiology 1976; 118:633-6. 2. Debrun G, Sauvegrain J, Aicardi J, et al. Moya-moya, a mmspecific radiological syndrome. Neurology 1975;8:241-4.
Rerupture of Intracranial Aneurysms To the Editor: Concerning the paper "Analysis of 223 Ruptured Intracranial Aneurysms with Special Reference to Rerupture" by N. Ayoagi and I. Hayakawa (Surg Neurol 1984;21:445-52), I have several comments and questions. In the abstract it is stated, "The incidence of rerupture was increased in patients with narrowly localized vasospasm and acute hydrocephalus." These conclusions cannot be made from the data presented. Table 5 (p. 449) suggests that rerupture carries a higher incidence of severe spasm (and higher morbidity and mortality) but does not imply that severe vasospasm leads to higher rate of rerupture. (A problem arises in that no mention is made as to when in the clinical course angiography was performed.) Furthermore, the statement is made (p. 449} that " . . . patients with ruptured aneurysms in whom the perfusion pressure does not change (i.e., little or no vasospasm) are at risk for rerupture." These statements are contradictory to one another. Also. on page 450 it is stated " . . . of patients with a single ruptured aneurysm 19% developed acute hydrocephalus after the hemorrhage compared with 5 4 ~ with rerupture." Again, this does not say that acute hydrocephalus leads to higher rerupture rate? The discussion of rerupture rates (p. 448) is also not clear. Following " . . . of 223 patients, the rerupture rate was 17%, 29%, and 30% for patients with H u n t - H e s s grades 0-1I, Ill, and IV, respectively," the authors go on to suggest " . . . of 46 patients with rerupture, 50%, 33%, and 17% had grades 0-I1, III, and IV, respectively, indicating an inverse relationship between the H u n t - H e s s grade and the incidence of rerupture." This is both artificial and misleading. It simply restates the fact that many more patients in this series were of clinical grades 0 - I I than Ill or IV and has little to do with an "inverse relationship" between true incidence and clinical grade.
204
Surg Neurol 1985;23:201-4
Table 8 (p. 450) lacks any meaningful information. What does 10_< mean? What is the difference between the first column under the heading "Fibrinogen" (i.e., 400 mg/mL) and the second column (i.e., again, 400 mg/mL)? Nothing meaningful is made of "time-course studies" of factors of the coagulating and fibrinolytic system (p. 450 and Table 2) to "suggest their usefulness in predicting the occurrence of vasospasm, infarction, and rerupture," as stated in the abstract. Parenthetically, although antifibrinolytic therapy is mentioned in the discussion, no indication is given as to whether or not patients in this series were so treated. Finally, the concluding paragraph reads "Early operation should be considered in p a t i e n t s . . , of low H u n t - H e s s grade, and accompanied by localized vasospasm and/or acute hydrocephalus." I must emphatically disagree. There is no evidence whatsoever that patients with localized vasospasm should be operated upon early. This statement follows from the erroneous interpretation that localized vasospasm and acute hydrocephalus lead to rerupture, which, as discussed above, is simply not supported by the data presented. It is one thing to suggest an hypothesis; it is quite a different matter to suggest modes of clinical therapy based on improper interpretation of the facts at hand. KEVIN J. KIWAK, M.D. Boston. Massachusetts Reply. Concerning the points raised by Dr. K.J. Kiwak, we respond as follows: 1. Acute hydrocephalus was observed in 30 of 157 patients (19%) with a single rupture and in 22 of 41 patients (54%) with rerupture. This implies that hydrocephalus occurred at a statistically higher rate (X2 = 20.040) in the latter group. In patients with a certain amount of subarachnoid hemorrhage, late vasospasm occurred and changed the severity sequentially. For reasons of simplification, we considered only the cases with a second rupture; angiograms were made 4 - 1 0 days after the occurrence of subarachnoid hemorrhage. Of these patients, nine had no or local spasms, six had severe local spasms, and one patient had severe diffuse spasm. These observations led us to suggest that rerupture occurs at a higher frequency in patients with no or slight vasospasms.
Letters to the Editor
2. Our conclusion is based on the Bernoulli equation. 3. The table headings should read as follows:
F i b r i n o g e n (mg/dL) F D P (/~g/mL)
<400
4 0 0 -< _
4. Coagulation is accelerated at the time of late vasospasms (see references 20, 40, and 41). O n the other hand, fibrinolytic function is also accelerated in patients with multiple infarcts. None of the patients listed in Table 8, in whom fibrinogen and fibrin and fibrinogen degradation products (FDP) values were measured on at least three occassions, had evidence of disseminated intravascular coagulation. Based on these data, we hypothesized that high fibrinogen and FDP values signify the occurrence of multiple intracranial infarctions due to vasospasms and that the decrease in these values signifies the onset of convalescence of the vasospasm and the concomitant danger of rerupture. Prognosis is determined by both the location and the size of the infarct; it was worse in patients who had high FDP values for a prolonged period of time. 5. There is no difference in the static pressure, irrespective of the presence of only localized vasospasms or the normal vascular state (Bernoulli equation). Acute hydrocephalus due to subarachnoid hemorrhage brings about an increase in the perfusion pressure. These facts led us to point to the possibility of rerupture. In general, the H u n t - H e s s grade can be used for timing operations on intracranial aneurysms. Patients with Hunt-Hess grades 0 - I I can be successfully operated upon. Thus we maintain that in order to prevent aneurysmal rerupture, early operation is indicated in patients with a low H u n t - H e s s grade depending on local spasms, acute hydrocephalus and the location of the aneurysm. N O R I O AYOAGI, M.D. ISAO H A Y A K A W A , M.D. Tokyo, Japan
We have reviewed the article written by Dr. Aoki and Dr. Mizutani in the Journal of Neurosurgery and agree that primary subarachnoid hemorrhage in moyamoya is exceedingly rare. We thank the authors for drawing this point to our attention. J O H N W. WALSH, M.D., Ph.D. Lexington, Kentucky
Cerebral Hemorrhage To the Editor: 1 read with interest the article "Moyamoya Disease and Cerebral Hemorrhage" by Hardy and Williams in the May issue o f SURGI('AL N E U R O L O G Y ( S u r g Neurol 1984;2 l:507-10), in which they reported a case of a 54-year-old man with cerebral hemorrhage secondary to "moyamoya disease." As the authors state, it is evident that moyamoya disease causes intraparenchymal hemorrhage as seen in their patient and in cases reported by us as well [1]. However, in regard to the features of the cerebral angiography shown in their case, it is highly doubtful whether this case may belong to moyamoya disease: The right and left common carotid angiograms reveal a long tubular stenosis beginning at the bifurcation of the common carotid artery and extending into the cranial cavity, where it is occluded. Their angiograms do not demonstrate any characteristics of moyamoya disease. Furthermore, on the left vertebral angiogram, nearly normal-appearing internal carotid, middle cerebral, and anterior cerebral arteries are opacified through retrograde flow from the posterior communicating artery; this opacification is sufficient to exclude the diagnosis of moyamoya disease. It is, therefore, hardly acceptable that this case meets the criteria of moyamoya disease [2]. N O B U H I K O AOKI
Tokyo.Japan 1. Aoki N, Mizutani H. Does moyamoya disease cause subarachnoid disease? Review of 54 cases with intracranial hemorrhage confirmed by computerized tomography. J Neurosurg 1984;60:348-53. 2. Guideline for the diagnosis of moyamoya disease: annual report of the Research Committee on the Progressive Occlusive Disease of the Circle of Willis. Tokyo: 1978:1 ~,2.
Reply. We would like to take issue with Dr. Aoki's comments regarding the diagnosis of our patient. There has been considerable discussion regarding the absolute etiology of moyamoya disease. Some authors have considered it to be postviral while others have assumed it to be a primary vasculopathy. Still others have considered the possibility of arteriosclerotic disease [1] as the primary occlusive event in the older population with this pattern. We would agree with Debrun et al [2] on the etiologic nonspecificity of the pattern. Although the Japanese may now
Surg Neurol 1985;23:201-4
203
require proximal occlusion of the anterior cerebral and middle cerebral arteries for inclusion into their syndrome complex, the complex "fibriUar" collaterals arising from deep perforating choroidal, lenticulostriate, and thalamic branches must be explained and have been well defined in moyamoya. These have often been grouped with the moyamoya disease complex. They all share the same clinical syndrome of intracranial occlusive disease with the fine perforating collaterals. Our case fits nicely into this category, and we believe it is only a matter of semantics that Dr. Aoki is pursuing. R. GAYLE WILLIAMS, M.D. ROBERT C. HARDY, M.D. San Antonio. Texas 1. Hinshaw DB, Thompson JR, Hasso AN. Adult arteriosclerotic moya-moya. Radiology 1976; 118:633-6. 2. Debrun G, Sauvegrain J, Aicardi J, et al. Moya-moya, a mmspecific radiological syndrome. Neurology 1975;8:241-4.
Rerupture of Intracranial Aneurysms To the Editor: Concerning the paper "Analysis of 223 Ruptured Intracranial Aneurysms with Special Reference to Rerupture" by N. Ayoagi and I. Hayakawa (Surg Neurol 1984;21:445-52), I have several comments and questions. In the abstract it is stated, "The incidence of rerupture was increased in patients with narrowly localized vasospasm and acute hydrocephalus." These conclusions cannot be made from the data presented. Table 5 (p. 449) suggests that rerupture carries a higher incidence of severe spasm (and higher morbidity and mortality) but does not imply that severe vasospasm leads to higher rate of rerupture. (A problem arises in that no mention is made as to when in the clinical course angiography was performed.) Furthermore, the statement is made (p. 449} that " . . . patients with ruptured aneurysms in whom the perfusion pressure does not change (i.e., little or no vasospasm) are at risk for rerupture." These statements are contradictory to one another. Also. on page 450 it is stated " . . . of patients with a single ruptured aneurysm 19% developed acute hydrocephalus after the hemorrhage compared with 5 4 ~ with rerupture." Again, this does not say that acute hydrocephalus leads to higher rerupture rate? The discussion of rerupture rates (p. 448) is also not clear. Following " . . . of 223 patients, the rerupture rate was 17%, 29%, and 30% for patients with H u n t - H e s s grades 0-1I, Ill, and IV, respectively," the authors go on to suggest " . . . of 46 patients with rerupture, 50%, 33%, and 17% had grades 0-I1, III, and IV, respectively, indicating an inverse relationship between the H u n t - H e s s grade and the incidence of rerupture." This is both artificial and misleading. It simply restates the fact that many more patients in this series were of clinical grades 0 - I I than Ill or IV and has little to do with an "inverse relationship" between true incidence and clinical grade.
204
Surg Neurol 1985;23:201-4
Table 8 (p. 450) lacks any meaningful information. What does 10_< mean? What is the difference between the first column under the heading "Fibrinogen" (i.e., 400 mg/mL) and the second column (i.e., again, 400 mg/mL)? Nothing meaningful is made of "time-course studies" of factors of the coagulating and fibrinolytic system (p. 450 and Table 2) to "suggest their usefulness in predicting the occurrence of vasospasm, infarction, and rerupture," as stated in the abstract. Parenthetically, although antifibrinolytic therapy is mentioned in the discussion, no indication is given as to whether or not patients in this series were so treated. Finally, the concluding paragraph reads "Early operation should be considered in p a t i e n t s . . , of low H u n t - H e s s grade, and accompanied by localized vasospasm and/or acute hydrocephalus." I must emphatically disagree. There is no evidence whatsoever that patients with localized vasospasm should be operated upon early. This statement follows from the erroneous interpretation that localized vasospasm and acute hydrocephalus lead to rerupture, which, as discussed above, is simply not supported by the data presented. It is one thing to suggest an hypothesis; it is quite a different matter to suggest modes of clinical therapy based on improper interpretation of the facts at hand. KEVIN J. KIWAK, M.D. Boston. Massachusetts Reply. Concerning the points raised by Dr. K.J. Kiwak, we respond as follows: 1. Acute hydrocephalus was observed in 30 of 157 patients (19%) with a single rupture and in 22 of 41 patients (54%) with rerupture. This implies that hydrocephalus occurred at a statistically higher rate (X2 = 20.040) in the latter group. In patients with a certain amount of subarachnoid hemorrhage, late vasospasm occurred and changed the severity sequentially. For reasons of simplification, we considered only the cases with a second rupture; angiograms were made 4 - 1 0 days after the occurrence of subarachnoid hemorrhage. Of these patients, nine had no or local spasms, six had severe local spasms, and one patient had severe diffuse spasm. These observations led us to suggest that rerupture occurs at a higher frequency in patients with no or slight vasospasms.
Letters to the Editor
2. Our conclusion is based on the Bernoulli equation. 3. The table headings should read as follows:
F i b r i n o g e n (mg/dL) F D P (/~g/mL)
<400
4 0 0 -< _
4. Coagulation is accelerated at the time of late vasospasms (see references 20, 40, and 41). O n the other hand, fibrinolytic function is also accelerated in patients with multiple infarcts. None of the patients listed in Table 8, in whom fibrinogen and fibrin and fibrinogen degradation products (FDP) values were measured on at least three occassions, had evidence of disseminated intravascular coagulation. Based on these data, we hypothesized that high fibrinogen and FDP values signify the occurrence of multiple intracranial infarctions due to vasospasms and that the decrease in these values signifies the onset of convalescence of the vasospasm and the concomitant danger of rerupture. Prognosis is determined by both the location and the size of the infarct; it was worse in patients who had high FDP values for a prolonged period of time. 5. There is no difference in the static pressure, irrespective of the presence of only localized vasospasms or the normal vascular state (Bernoulli equation). Acute hydrocephalus due to subarachnoid hemorrhage brings about an increase in the perfusion pressure. These facts led us to point to the possibility of rerupture. In general, the H u n t - H e s s grade can be used for timing operations on intracranial aneurysms. Patients with Hunt-Hess grades 0 - I I can be successfully operated upon. Thus we maintain that in order to prevent aneurysmal rerupture, early operation is indicated in patients with a low H u n t - H e s s grade depending on local spasms, acute hydrocephalus and the location of the aneurysm. N O R I O AYOAGI, M.D. ISAO H A Y A K A W A , M.D. Tokyo, Japan