Special articles Uncommon causes of intraventricular hemorrhage Seyed Abbas Taheri*, Mohammad Afzal Wani* * and Janusz Lewko* * * Introduction Summary Since the advent of CT, the facilitated diagnosis of a wide variety of uncommon causes of IVH, in spite of the fact that many cases go unreported, has lead to the shifts in its proportional incidence’-“. Anticoagulant and thrombolytic treatment, blood dyscrasias, tumors, operatively induced bleedings and rare vascular lesions comprise from about 10% of etiologies of IVH’-4. These conditions are never singled out for detailed study and discussion. The introduction of CT has also resulted in changing concepts in the management of ICHs and IVHs. The statement of H.W. Pia who regarded the evacuation of IVHs as useles?, was based mainly on his long standing disappointing experience with hypertensive IVHs in pre-CT era. Considering the experiences which are accumulated during the CT period, this subject appears to deserve a differentiated evaluation. While EVD is proven to be useful in every type of IVHh-X, a prompt evacuation of ICHs and IVHs doesn’t seem to decrease significantly the mortality and morbidity of hypertensive IVH’ and traumatic IVH associated with diffuse brain injury”, but an active neurosurgical approach to the large ICHs and IVHs due to ruptured aneurysms’ and arteriovenous malformations’~“’ appears to be more effective. The advent of CT has lead to discovery of a wide variety of unusual causes of intraventricular hemorrhage (IVH) and hence to the shifts in the proportional incidence of its different etiologies. From 96 patients with IVH, 7 uncommon cases of intracerebral hemorrhage (ICH) associated with IVH, including 2 due to anticoagulation treatment, 1 because of thrombolythic therapy, 1 due to thrombocytopenia, 2 as operative complications and 1 due to metastatic brain tumor are presented. In patients with blood disorders-related IVH the clinical presentation was similar to ‘stroke in evolution’, and the severity of IVH correlated with neurological deficit on admission and outcome of 314. All of the patients were treated with external ventricular drainage (EVD), 1 underwent partial evacuation of ICH in addition. 4 (57%) patients, including 3 with coagulation defect deceased. The peculiar aspects of uncommon causes of IVH are discussed on the basis of a review of the literature. The authors suggest that a standardized differentiated protocol should be adopted for the management of every uncommon type of IVH. An active attitude towards the evacuation of blood disorders-related ICHs and IVHs seems to be justified. Key words: anticoagulation treatment, brain tumor, intracerebral hemorrhage, intraventricular hemorrhage, thrombolytic therapy. * Neurosurgical Dept., Steglitz Medical Center, Free University of Berlin, FRG. * * Shere-Kashmir Soura, Srinagar (Kashmir), India. * * * Klinika Neurochirurgii, Bialystok, Poland. Address for correspondence and reprint requests: Dr. A. Taheri, Arztfiir Neurochirurgie, Institute of Medical Science, Postfach 470704, 1000 Berlin 47, FRG. c‘lin Neuroi Neurosurg 1990, Vol. 92-3 19.5 The purpose of this paper is the presentation of our experience with uncommon causes of IVH, as well as a review of the literature in this matter with peculiar attention to the afore mentioned changing concepts. Table 1: proportional Cases Material and Method The etiologies of 96 cases of IVH who were admitted between Decembre 1979 and Decembre 1987 to the Neurosurgical Department, Klinikum Steglitz of Free University of Berlin, are summarized in Table 1. Among these cases, 4 were proved to be due to blood disorders (2 due to anticoagulant treatment, 1 due to thrombolytic therapy, 1 due to idiopathic thrombocytopenia), 2 were operatively induced and 1 was caused by a metastatic brain tumor. These cases are presented in separate groups in the following. Neurosurgical findings on admission were graded according to Hunt and Hess”, with consideration of proposed WFNS SAH Scale”. The severity of intraventricular hemorrhage (SIVH) was assessed as suggested by Graeb et d3, and modified by Ruscalleda et d4, and Us”, (Table 2). The results are demonstrated in Table 3. Morbidity was assessed at the time of discharge or transferral to other hospitals according to Glasgow Outcome Scale (GOS), suggested by Jennett et UP (Table 3). The method of intensive management of the patients and placement and care of EVD and monitoring of ICP is explained in our previous work6. The occlusion of intraventricular catheter with blood clot occured in 1 patient, needing placement of a new catheter. No patient received antibiotics prophylactically. No patient developed meningitis. 1 patient underwent partial evacuation of ICH and partial excision of a metastatic brain tumor, which was repeated in the day after the operation because of rebleed, without succeed to stop the bleeding. Blood Dyscrasias and Coagulation Disorders Case reports Case 1 A 45year-old man developed left sided hemiparesis within some hours. CT on admission showed a right parietal ICH extending subependymally with rupture into the right lateral ven196 incidence ot etlologtc\ etiology no. hypertension aneurysm trauma AVM blood-disorders operatively induced tumor unknown 33 I6 I1 7 4 3 I 22 $)! oh 1Vfi ( ‘b ) (34.5) (17) (11.5) (7) (4) (2) (I) (23) Table 2: Scoring of Severity of IVH* according to Graeb et aP Lateral Ventricles Score: 1 = trace of blood or mild bleeding 2 = less than half of the ventricle fitled with blood 3 = more than half of the ventricle filled with blood 4 = ventricle filled with blood and expanded (Each lateral ventricle is scored separately) Third and Fourth Ventricles Score: 1 = blood present, ventricle size normal 2 = ventricle filled with blood and expanded Total Score (maximum = 12) Grading of IVH according to Ruscakda et al” score 1 - 3 = score 4 - 6 = score 7 - 9 = score 10 - 12 = _~__ Grade I = mild Grade II = moderate Grade III = severe Grade IV = very severe Our mndikation for pusterior fossu hemorrhage’5 score 1 score 2 score 3 - 6 score 7 - 12 = = = = Grade Grade Grade Grade I = mild II = moderate III = severe IV = very severe * IVH: intraventricular hemorrhage tricle inducing IVH which scored 6 point on the SIVH Scale (moderate IVH). Idiopathic thrombocytopenia (Platelets = 18OOO/cc)was established and treated successfully. Placement of EVD lead to improvement of neurological situation and the patient was transferred with moderate disability for further rehabilitation within 46 days. Table 3: Relation of Severity of Intraventricular Hemorrhage (IVH) to the Neurological Deficit on Admission and to the Outcome of 7 Patients*. No. Neurological deficit* * Severity of IVH See Table 1 Outcome of patients* * * IVH due to blood disorders ._ 1 2 3 4 II IV IV IV II II IV IV Case 4 II V V V operatively induced IVH 5 6 I III II III cle, inducing a severe IVH (SIVH for posterior fossa bleedings = 4 scores), and moderate dilatation of lateral ventricles. EVD didn’t improve the situation. The intraventricular catheter was occluded with coagulated blood and therefore had to be replaced. She deceased within 4 days. II II IVH due to brain tumor * More than 1 Grade difference is considered as non-correlating [standard deviation (SD) = fl Grade]. In the GOS Grades IV and V have the same value. * * According to Hunt and Hess’with consideration of proposed SAH Scale of WFNS”. * * * Glasgow Outcome Scale’? Grade I : normal or mild disability Grade II : moderate disability Grade III : major disability Grade IV : vegetative state Grade V : dead Case 2 A 57-year-old woman developed left sided hemiparesis and became comatose within 12 hours, while she was being treated with Phenprocoumon (Marcumar) because of thrombosis of deep iliac veins. The result of Quick Test amounted 10% on admission. CT demonstrated a massive right temporal ICH associated with a severe IVH (7 scores). The patient deceased within 1 week in spite of appropriate treatment of coagulation defect and placement of EVD. Case 3 A 45-year-old woman developed headache and vomitting and became gradually within 24 hours unconscious during treatment with Marcumar and Aspirin because of foot deep vein postthrombotic syndrom. Quick Test on admission amounted 30%. CT revealed a left intracerebellar hemorrhage with rupture into the 4th ventri- A 66-year-old man developed signs of increased ICP and became unconscious within some hours while he was being treated with Streptokinase infusion because of a deep foot vein thrombosis. CT demonstrated a right intracerebellar hematoma with rupture into the 4th ventricle, inducing a severe IVH (5 scores). In spite of insertion of EVD the situation deteriorated. The repeated CT on the day after admission revealed a brain stem infarction. The patient died within 4 days. Discussion The incidence of intracranial hemorrhage due to bleeding disorders is constantly increasing”. Intracerebral bleedings, ranging from multiple microhemorrhages to large hematomas, which sometimes lead to IVH, are frequent complications or terminal events in leukemias (about 50%), lymphomas, blood marrow depression and coagulation defects, including polycytemia, hemophilia, thrombocytopenia, and thrombocytopathieslx. The most of IVHs go unreported. We found only 1 case of IVH due to hemophilia2 and 1 due to leukemia” in the literature. The most striking change in the proportional incidence of intracranial bleeding, however, is the increase in the rate of hemorrhages due to coagulation defect (iatrogenic hemorrhage), as a consequence of widespread use of anticoagulants. Wintzen et al found that the risk of intracerebral hemorrhage was more than ten times higher for anticoagulated patients over 50 years of age than for similarity aged untreated individuals in the general population2”. Moskopp et al reported a twelve fold increased risk of intracranial and intraspinal hemorrhage during anticoagulation therapy”. We found 21 (5%) cases of IVH due to coagulation disorders among 430 IVHs reported in extensive series in Eighties ’ -.‘J.‘~.‘~ (Table 4). This is higher than our own incidence of about 2%. 197 Figure 1: Anticoaguiation-related intracerebral hemorrhage with rupture into the left lateral ventricle inducing severe intraventricular hemorrhage (case 2) (scoring: left ventricle = 3, right ventricle = 1, third ventricle = 1, forth ventricle = 2, total = 7). A considerable number of intracranial hemorrhages in anticoagulated patients is said to develop either among alcoholics or during alcoholic intoxication”. Kase et al found hypertension in 67% of their patients with anticoagulantrelated intracerebral hemorrhages’“. Winzen et al, reporting hypertension to be present in 80% of their 166 patients suffering from this condition, considered it as the most important predisposing factor in iatrogenic hemorrhages’“. Non of our patients was hypertensive. The most consistent risk factor for hemorrhage in anticoagulated patients is the prolongation of @. As Winzen et al reported, in most cases of hemorrhagic stroke during anticoagulation treatment, there is only a slight shift in the median PT towards a higher intensity. Nevertheless, the risk of bleeding rises with increasing intensity of anticoagulatior?“. Forfar concluded that less serious bleedings occur more 198 often without excessive prolongation of PT, and prolongation of PT beyond the therapeutic level causes more commonly major hemorrhages. Hence, keeping the intensity of PT within therapeutic limits protects only against life-threatening bleedings 24. The severe decrease in results of Quick-Test in our patients (case 2-3), reflecting a very low PT, was associated with extensive fatal hemorrhages. The gradual development of neurological deficits in our patients, similar to the picture sometimes called ‘stroke in evolution’ is a common clinical picture in anticoagulant-related ICHs. It may reflect the slow speed of bleeding from small vessels in this condition. This is in agreement with explanation of Kase et aPi. Cerebellum is accounted for a disproportionately high number of anticoagulant-related hemorrhages (37.5%) by Kase et aP3. They reviewed the literature and found a frequency of Table 4: proportional incidence of uncommon causes of intraventricular Name of the Author No. (%) of IVHs due to blood disorders _-_ Sganzerla” Little’ Graeb’j Ruscalleda’J Stendel’ Steudel? hemorrhage (IVH) No. (%) of IVHs due to brain tumors .~. -~ _.. 1 (1%) 2 (3.5%) 3 (4.5%) 5 (6%) 7 (6.5%) 4 (6.5%) 2 (3.5%) 1 (1.5%) 4 (4.5%) 4 (6.5%) Total no. of cases 80 54 68 78 90 60 .~_~ Total Taheri 22 (5%) 4 (4%) 11 (2.5%) l(l%) Total 26 (5%) 12 (2%) 23% for cerebellar hemorrhages in other series. The incidence of intracerebellar hemorrhage of other etiologies is about 5lo%*‘. 2 of our 4 patients (cases 3 and 4), had an intracerebellar hemorrhage with rupture into the 4th ventricle. The mechanism of this appearant predilection of anticoagulation-related hemorrhages for the cerebellum remains speculative. Fibrinolytic agents are receiving increasingly wide therapeutic application for dissolution of thrombi of central and peripheral arteries, as well as peripheral deep venous thrombosis*‘. The incidence of intracerebral hemorrhages during or following intravenous or intra-arterial infusion of Streptokinase or Urokinase in the abscence of demonstrable cerebrovascular disease is estimated to be less than 1%26. The hemorrhages are usually small and don’t result in functional deterioration*‘. To our knowledge, a severe lethal ICI-I with rupture into the ventricles, as in our case, is not reported yet. In 3/4 patients in this group, the severity of IVH correlated with neurological deficits on admission and outcome. This correlation, which is present also in hypertensive ICHs with ventricular rupture, as we have shown in our previous workh, is not an epiphenomenon but related in a direct way to the basic pathophysiological mechanisms, and can be considered as a reliable prognostic indicator. The morality of anticoagulant-related intracerebral hemorrhages is higher than most other etiologies. It is estimated to be about 65%*‘. The neurosurgical management of IVH due to coagulation disorders differs from other forms of 430 96 ~___~ .~ 526 IVH only in the necessity of appropriate treatment of coagulation disorders before operation2,3,27.Following the suggestion of Pias, we didn’t evacuate the IVHs in our patients. 3/4 patients of this group deceased. Stendal et al, however, reported a survival rate of up to 5/7 cases of IVH due to coagulation disorders?. Their report doesn’t provide data about the neurosurgical management of their patients. Seeler et al stressed that ‘wait and watch’ attitude doesn’t improve the results of management of hemophiliac patients with intracranial bleedings and progressive neurological deficitsz8. With regard to this statement and to our disappointing results we are keen to revise our passive attitude and suggest that evacuation of blood-disordersrelated ICHs and IVHs may improve the outcome, especially in young patients and when the EVD doesn’t stop the clinical deterioration. Operatively induced IVH Case reports Case 5 A 49-year-old man underwent stereotactic biopsy of a right thalamic lesion which was suspected to be a low grade glioma. He became stuporous and developed a severe left sided hemiparesis on the day after operation. CT revealed an ICH involving the right basal ganglia with grade 2 IVH (SIVH = 5 scores). EVD lead to improvement and he was transferred within 46 days in GOS grade II. Histological examination revealed brain infarction. 199 Case 6 A 45year-old female became after total extirpation of a large left olfactory groove meningioma stuporous and developed a decompression intracerebral bleeding left frontotemporal, which ruptured into the lateral ventricles and induced a severe IVH (SIVH = 9 scores). The level of consciousness improved after EVD, and she was transferred in grade II on GOS. Discussion The presence of blood in the ventricular system after operative approach to the intraventricular and periventricular structures should be considered as a complication when it acquires space occupying character or disturbs CSF dynamics. The fact that EVD may overcome even a severe postoperative IVH (case 6), is suggesting that IVH per se is not necessarily a grave complication. The incidence of severe intracerebral bleeding following stereotactic brain biopsy is very low, and that of fatal hemorrhages is about o,1%29. We were not able to find any report about the frequency and prognosis of IVH following streotactical or open neurosurgical interventions. Tumor induced IVH Case report Case 7 A 47-year-old female was admitted because of apoplectiform development of stupor and left sided hemiparesis. CT showed an ICH in a heterogenous tumor mass in deep right parietal gray matter, and a moderate IVH (6 scores). The ICH was evacuated and the tumor, which was histologically proved to be a metastatic bronchial carcinoma, was partially excised. Despite EVD the level of conscioussness deteriorated further up to Grade IV. CT demonstrated rebleed in the tumor cavity and increase in severity of IVH (9 scores). Second operation couldn’t avoid the worsening of the neurological state and she died within 9 days after admission. Discussion 3-10% of intracerebral 200 hemorrhages in clinical series are due to tumors--‘-“‘--“. An unknown number of bleedings originates from or rupture into the ventricles. More than one third (h/l 5) cd intracranial hemorrhages caused by metastatic tumors reported by Mandybur were associated with IVHj3. 2% of IVHs reported in large series (including ours) are caused by neoplasms’“~X.13,14) (Table 4). The incidence of gross intracerebral bleeding in primary cerebral neoplasm is reported to be about 1.3%“. Hemorrhage is more common in glioblastomas and oligodendrogliomas. Gilber et al reported a case of IVH induced by an ependymoma34. Choroid plexus papilloma is a very rare etiology of IVH35”6. Intracerebral bleeding from a benign cerebral neoplasm is rare and usually attributed to angiomatous tumor vessels3”. Askenasy et al reported 2 cases of intraventricular meningiomas presented as SAH. They believed that the enlarged tortuous feeding arteries have been responsible for the bleeding 37. A true IVH from intraventricular meningiomas has not been reported. Hemangiopericytoma is reported to induce intracerebra1 hemorrhage 3”. In the posterior fossa hemangioblastoma has a known tendency to bleed with possibility of rupture into the 4th ventricle. Little et al maintained that brain hemorrhage from metastatic and primary intracranial tumors are of equal frequency”‘. Mandybur, however, found gross hemorrhage in 14% of metastatic brain tumors, namely beyond ten fold higher than primary tumors. Referring to the literature, he reveals that the order of frequency of tumors most prone to develop hemorrhages is metastatic choriocarcinoma, melanoma and bronchogenic carcinoma.“’ The most frequently associated neoplasm should be probably bronchogenic carcinoma3’. Madow et al reported a massive IVH from a small metastatic nodule of hypernephroma3”. High vascularisation of tumors is a predisposing factor for bleeding. Pathological ‘huge, disorderly, fistulous veslses’ are responsible for higher frequency of intracranial bleeding in malignant tumors39. According to Mandybur the factors promoting the hemorrhage tendency in metastatic tumors seem to include speed of vascular invasion, growth, vascularisation, hemorrhagic infarction, edema, necrosis, localisation and possibly fibrinolysis”“. Little et al found elevated blood pressure in 8/13 patients with tumor induced intracranial hemorrhages and suggest that hypertension might be an important contributing factor in this condition”“. The clinical signs appeared in an apoplectic form in our case. Repeated partial excision of the metastatic tumor was not able to stop the bleeding. This experience suggest that the neurosurgeon should prepare himself for a radical excision of the underlying lesion, when he is going to evacuate a tumor induced ICH, as it is usual in the evacuation of AVM-induced bleedings. Other uncommon etiologies of IVH Various uncommon vascular lesions may lead to IVH: Arteriolosclerosis: or as it is called in cerebral pathology hyalinosis of small vessels of brain, is mostly correlated to hypertension. However, this condition may induce ICH and IVH in absence of any evidence of elevated blood pressure. In 7/70 cases of massive arteriolosclerotic striatal hemorrhages of Zulch, there were no history of hypertension3’. The ultimate diagnosis has to be made on the basis of post-mortem examination. Old age (over 60 years) and the presence of clinical signs of general small vessel disease (coronary heart disease, changes of retinal vessels) may contribute to the establishment of the clinical diagnosis. Moyamoya disease: Hayashi et al reported 8 cases of intracerebral hemorrhage associated with IVH due to Moyamoya, found among 105 cases of IVH because of cerebrovascular disease in Japan’. Sporadic cases are reported from other parts of the world4”. rhage in this condition41. Cerebral amyloid angiopathy (CAA): This disorder is characterized by deposits of amyloid in the media and intima of the arteries and arterioles of brain and meninges4?. Vinters et al found some degree of CAA in 36% of all aged brains (over 60 years) with a higher proportion of patients affected in each successive decade of life, most frequently in parietal and occipital gray matter43. CAA is demonstrated in up to 89% of brains with Alzheimer’s disease4”. It may result in intracerebral hemorrhage, most commonly in lobar areas, predominantly in parietooccipital areas, also in non-demented individuals4’,44. From 21 patients with CAA-related ICH, only 5 patients were known as demented before bleeding4?.M. 2 of bleedings reported by Kalayan-Raman et al occured in striatum including 1 with associated rupture into the lateral ventricle42-44.CAA is a pathological diagnosis, but an important clinical consideration in the elderly, especially if the hemorrhage occurs in a peripheral location and superimposes a history of dementia. Arteritis: Theoretically all kinds of arteritis may be included as potential etiologies of IVH. Among the infective types of arteritis those due to septic emboli4’ and luetic arteritis’, and among the non-infective cases those due to collagen disease, especially panarteritis nodosa have a predilection to intracerebral bleeding”. We didn’t find any report about IVH caused by arteritis in the literature. References LITTLE JR, BLOMQUIST GA, ETHIER K. Intraventricular hemorrhage in adults. Surg Neural STENDEL Mycotic aneurysms: Little et al reported 3 cases of IVH caused by mycotic aneurysms of middle cerebral artery resulted from subacute bacterial endocarditis (2 cases) and infected prosthetic mitral valves’. It is worth mentioning that mycotic aneurysms underline only a fraction (about lo-15%) of intracranial hemorrhages in infective endocarditis. Septic arteritis is encountered responsible for the majority of bleedings occuring in acute phase of endocarditis. Anticoagulation contribute also to intracranial hemor- treatment WJ, SCHNEIDER E, BECKER (of intraventricular 1971; 8:143-9, 1971. H. CT Scan and hemorrhage). In: Pia HW, Langmaid C. Zierski J (eds.), Spontaneous Intracerebral Hematomas, Berlin, Heidelberg. New York, Springer Verlag, 1980: 331-3. STEL:DELWI,SCHNEIDERE,BECKER H. Management and prognosis of intraventricular hemorrhage. In: Marguth F. Brock M, Kazner E, Klinger M, Schmiedek P: Neurovascular Surgery, Specialized Neurosurgical Techniques. Berlin, Heidelberg, New York, Springer Verlag. 1979: 81-8. LUYENDIJK w. Intracerebral hematoma. In: Vinken RT. Bruyn GW (eds.), Handbook of Clinical Neurology, Holland Publishing Company, Stockholm, 1972: 660-71. PIAHW.Location, Indication and Prognosis (of intraventricular hemorrhage). In. Pia HW. Langmaid C, Zierski 201 J (eds.), Spontaneous lntracerebral Hematomas, Berlin, Heidelberg. New York, Springer Verlag. 1080: 329 31. TAHERI A, WANI MA, LEWKO I. External ventricular drainage and passive vs active neurosurgical intervention in the management of hypertensive intracerebral hemorrhage with rupture into the ventricles. J Neurosurg. Anesthes. 1989, 1:233-40. HAYASHIM,HANDAY,KoBAYASHlH,KAWANoH.NOZAhI JI.Management of intraventricular hemorrhage in patients with hemorrhagic cerebrovascular diseases. Br J Neurosurgery, 1988; 2:23-32. SGANZERLAEP,RAMPINIPM.GAINISM,GARAN'IAG.ZAVANONE M, VILLANI RM. Intraventricular hemorrhage: Role of early ventricular drainage. J Neurosurg Sci 1984: 28:61-5. TAHERIA,TRITTMACHERS,WANIMA,LEWKOJ. Traumatic intraventricular hemorrhage, a new classification. In: Bhatia R, Bhatia S (eds.), Book of Abstracts of 9th International Congress of Neurological Surgery, New Delhi. India, 1989, 336. TAHERI A, WANI MA, LEWKO J. IIItraVeIItriCUlBT hemorrhage due to ruptured AVM. Zbl Neurochir (in press). HUNT WE, HESS RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg 1968; 28:14-20. WORLDFEDERATIONOFNEUROSURGICALSOCIETIETIES. Resolution I, Proposed W.F.N.S. SAH Scale. Neurochirurgia, 1988; 31:133. GRAEB DA, ROBERTSON WD, LA POINTE JS,NUGENT RA, HARRISON PHD. Computed tomographic diagnosis of intraventricular hemorrhage. Etiology and prognosis. Neurorad, 1982; 143:91-6. RUSCALLEDA J,PEIRO A. Prognostic in intraparanchymatous hematoma with ventricular hemorrhage. Neurorad 1986; 28:34-7. TAHERI A, BROCK M. External ventricular drainage in the management of hypertensive intracerebral hemorrhage with rupture into the ventricles. In: Hoff JT, Betz AL: Intracranial Pressure VII, Berlin, Heidelberg, New York, Springer Verlag, 1988, 741-4. JENNETT B, BOND H. Assessment of outcome after severe brain damage. Lancet 1975; l&30-4. ZULCH KJ. Neuropathology of intracranial hemorrhage. Prog Brain Res 1968; 30:151-65. JELLINGER K. Pathology and aetiology of ICH. In: Pia HW, Langmaid C, Zierksi J (eds.). Spontaneous Intracerebral Hematomas, Berlin. Heidelberg, New York, Springer Verlag, 1980: 13-29. MCCALLUMJE,DOLORESLO,DOLCERN,BOEHNKEM. CT Scan in intraventricular hemorrhage: Correlation of clinical findings with computerized tomographic scans of the brain. Neurosurgery, 1978, 3:22-5. W!NTZ_ENAR,DEJONGE H,LOELIGEREA,BOTSTAM. The risk of intracerebral hemorrhage during oral anticoagulant treatment: a population study. Ann Neurol 1984; 16:553-8. MOSKOPP D, BRASSEL F, RIES F. IntTaCTanielle und intraspinale Blutungen unter Behandlung mit Cumarin Derivaten. Katamnese von 63 Faellen zwischen 1978 und 1986. Klin Wochen Sch, 1987; 65:781-90. IIZUKA J. Anticoagulants and ICH. In: Pia HW, Langmaid C, Zierski J (eds.), Spontaneous Intracerebral Hematomas, Berlin, Heidelberg, New York, Springer Verlag, 1980: 40-l. KASECS,KENTROBINSON R,STEINRW,DANADEWI'I-TL, HIER DB, HARP DL, POWELL WILLIAMS I, CAPLAN LR, MOHR JP. Anticoagulant-Related intracerebral hemor- 202 rhage. Neurology 1985; 35:943-X. FORFAR JC‘. A 7-year analysis of hemorrhage m patients on long-term anticoagulant treatment. Br He;irt J. 1970: 42: 128-32. DEL ZOPPO GJ, ZEUMEK H, HARKER LA. I’hrombolytic Therapy in stroke: Possibilities and hazards. Stroke. 1986: 17:5Yh-607. ALDRICIi MS, SHERMAN SA. GKEENBERG 115.ccrebrovascular complications of Streptokinase infusion. JAMA. 1985; 253: 1777-9. LoEw r, JAksctm F. Surgical treatment (of intraventricular hemorrhage). In: Pia HW. Langmaid C, Zierski J (eds.), Spontaneous Intracerebral Hematomas, Berlin, Heidelberg, New York, Springer Verlag, 1980: 326-8. SEELER RA, IMANA RB. Intracranial hemorrhages in patients with hemophilia, J Neurosurg, 1973, 39:181-5. MIJNDINGER F.Streotaktische intrakranielle Bestrahlung von Tumoren mit Radioisotopen (Curie-Therapie). In: Dietz H, Umbach W, Wtillenweber R (eds.): Klinische Neurochirurgie, Band II, Stuttgart, New York, Georg Thieme Verlag, 1984, 519-65. t_rrrLE JR, DIAL B, BELANGFR G, c.4nPENrta Y. Brain hemorrhage from intracranial tumor. Stroke, 1979: 10:283-8. SCOTTM. Spontaneous intracerebral hematoma caused by cerebral neoplasms. Report of eight verified cases. J neurosurg, 1975; 42:338-42. TSEMNETZIS SA. Surgical management of intracerebral hematomas. Neurosurgery, 1985; 16:562-72. MANDYBUR TI.Intracranial hemorrhage caused by metastatic tumors. Neurology, 1977; 27: 650-5. TOFFOL GJ, BILLER J, ADAMS JR HP. Nontraumatic intracerebral hemorrhage in young adults. Arch Neurol, 1987,44:483-485. BUTLER AB,PARTAIN RA,NETSKY MG. Primary iBtTaVeIItricularhemorrhage,amild and remediable form. Neurology, 1972; 22:675-87. MATSUSHIMAM,YAMAMOTOT,MOTOMOCHlM,ANDOK. Papilloma and venous angioma of choroid plexus causing primary intraventricular hemorrhage. Report of two cases. J Neurosurg; 1973; 39666-70. ASKENASYHM,BEHORAMAD. Subarachnoidhemorrhage in meningiomas of lateral ventricle. Neurology (Minneap), 1960; 10:484-9. MADOW L, ALPERS BJ.Cerebral vascular complications of metastatic carcinoma. J Neuropathol Exp Neurol 1952; 11:137-48. ZULCH KJ. Stroke. In: Pia HW, Langmaid C, Zierski J (eds.), Spontaneous Intracerebral Hematomas, Berlin, Heidelberg, New York, Springer Verlag, 1980: 1-12. DAKBYDG,DONNANGA.SALINGMA,WALSHKW,BLADIN PF. Primary intraventricular hemorrhage: Clinical and neurophysiological findings in a prospective stroke series. Neurology, 1988, 38:68-75. HART RG,KAGAN-HALLETK.JOERNSSE. Mechanismsof intracranial hemorrhage in infective endocarditis. Stroke, 1987; 18:1048-54. KALYAN-RAMAN UP, KALYAN-RAMAN K. Cerebral amyloid angiopathy causing intracranial hemorrhage. Ann Neurol 1984; 16:321-9. VINTERS HV, GILBERT JJ.Cerebral amyloid angiopathy: Incidence and complications in the aging brain. II. The distribution of amyloid vascular changes, Stroke.1983; 14:924-8. GILBERT JJ,VINTERS HV. Cerebral amyloid angiopathy: Incidence and complications in the aging brain. 1. Cerebral hemorrhage. Stroke, 1983; 14:915-23.