Development of microsurgical techniques has made neurosurgical operation safe and accurate. However operation on AVMs on the motor cortex is still controversial because of postoperative neurological deficit. One milimater of brain around the AVM was reported to be nonfunctional. Two out of patients with AVMs on the motor cortex were operated on under MEP (motorevoked potential) monitoring. Case 1: A 37 year old male was admitted with convulsions. CT and angiogram showed a moderately large AVM on the left motor cortex. Surgical excision was scheduled under MEP monitoring. The AVM was just on the motor cortex. MEP was taken from the gyrus below the AVM. The AVM was nicely removed without bleeding or extra brain damage. The threshold of MEP was the same or slightly better after removal of the AVM. Post-operatively, the patient developed hemiparesis, especially in the legs, which recovered 2 months after the operation. Case 2: A 22 year old female was admitted with convulsions. CT and angiogram showed on AVM on the right motor cortex. Surgical excision was done following a chart which was drawn from the angiogram. Post-operatively, the patient developed left hand palsy, which recovered a month after the operation. These operative techniques and course of recovering post-operative neurological deficit were reported.

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The authors reported a co-operative study of 212 patients with an intracranial arteriovenous malformation (AVM). 123 cases initially bled, 12 cases had an ischemic attack (focal neurological deficits) and 48 patients were admitted with convulsive episodes. The 24 AVMs were incidentally diagnosed by CT scan and/or DSA examinations in patients with head injury or headache.
On the basis of size of the nidus, the AVMs were subdivided into 3 groups, small (3cm>), medium (3-6cm) and large (6cm<). The small group had the tendency to bleed and the large group tended to have convulsive or ischemic attacks.
154 cases were treated surgically and 52 were conservatively. Total removal of the AVM was performed in 140 cases and the postoperative mortality was 1.3%. On the other hand, subtotal removal of the AVM and/or clipping of the feeding arteries was performed in 14 cases, and of these 5 died from rebleeding. The conservatively treated group was followed up for 1 to 28 years (mean followup time 8.3 years). The mortality rate was 7.7%, which was rather lower than previous reports. But in these conservatively treated cases, 19 patients had re-attack and 8 of these patients had recurrence of bleeding within 10 years.

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In a retrospective study of 40 patients with a cerebral arteriovenous malformation, we examined the clinical courses, angiographical findings, and operative results. We divided the patients clinically according to their initial symptoms, that is, bleeding, convulsion and other. Furthermore, patients were divided into two groups, those who consulted a doctor early (less than 6 months from onset), and those who consulted a doctor late (more than 6 months from onset). Twenty-six out of 40 cases are in the late group and the others fall in the early group. Mean intervals from initial symptoms until visiting hospitals in the late group are 10.7 years. Overall results (including surgically treated patients) are slightly better in the early group than in the late group.
In particular, we analyzed the late consulting group and conservatively treated cases (total 28 cases) for the purpose of defining the natural history of the arteriovenous malformations. The results are as follows: 1) Mortality was 3.6%(1/28). One patient with a huge AVM in the left cerebral hemisphere died because of bleeding from the AVM. 2) Morbidity was 35.7%(10/28). Five cases initially ruptured and 5 cases were unruptured. 3) Risk of bleeding is 25%(8/28). Five cases initially ruptured and 3 were unruptured. Two out of 8 cases had localized deep-seated or posterior fossa. Two out of 8 had small AVMs. 4) Mean follow-up period was 12 years.
In our examination, the results of natural history is relatively good. But, in the late consulting group, because of recurrent hemorrhages and frequent convulsive seizures, progressive worsening of neurological symptoms are frequently observed. For that reason, results for the late consulting group are slightly poorer than those for the early group. We have to give careful consideration to those facts in deciding whether to operate.

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The risk of bleeding and rebleeding from cerebral arteriovenous malformation (AVM) was analysed in 142 cases. Life table analysis was used for the assessment, and surgical cases in preoperative period were also included for the analysis, in addition to non-surgical cases. The follow-up period ranged from one month to 29 years with a mean of 4 years.
The age of the patients at onset ranged from 6 to 69 years, and averaged 29 years. Seventy percent of the patients were males. As an initial symptom, intracranial bleeding was noted in 105 cases and other symptoms in 37 cases. The rate of bleeding as an initial symptom was significantly higher in patients with a small AVM (within 5cm3) than larger ones (p<0.01).
During the follow-up period, 26 patients had rebleeding and 6 patients with initially unruptured AVM had bleeding. Mortality in cases with single bleeding was 3%, double 14%, and triple 28%.
Cumulative probability of bleeding for all patients after the onset was 9%in the first year, and 22%in the fifth year. The probability of rebleeding was 13%in the first year and 30%in the fifth year, while the risk of bleeding with an initially unruptured AVM was 3%in the first year and 7%in the fifth year. There was no correlation between the cumulative probability of rebleeding in five years and age at the onset or location or volume of AVM.

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The case records of sixty-seven patients who were treated conservatively for a cerebral arteriovenous malformation (AVM), were reviewed to analyse the natural history. We divided the 67 patients into three groups. Group A: 35 patients who had initial symptoms of hemorrhage, Group B: 6 patients who had detected unruptured AVM following intracranial hemorrhage, and Group C: 26 patients who had no episode of hemorrhage during a follow-up period. The follow-up period was an average of 9.5 years.
Prognosis of patients treated conservatively depends mainly upon the presence or absence of intracranial hemorrhage. The overall mortality rate of the 67 patients treated conservatively was 10.6%and the morbidity rate was 16.7%. Forty-one patients had episodes of hemorrhage (Group A and B), and the mortality rate at the first bleeding was 4.9%. Twenty-five of the 39 survivors had excellent prognoses, 7 minimal disability, 1 partially disability, 1 was totally disabled and 5 died of rebleeding. Thus the average rebleeding rate was 5.9%per year, mortality rate 17.9%and morbidity rate 22%. In thirty-two patients who had detected unruptured AVMs (Group B and C), the incidence of hemorrhage was 1.7%per year with mortality rate 3.1%and morbidity rate 12.9%. On the other hand, no patient died among the 26 patients who had no episode of hemorrhage (Group C).

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362 cases of intracranial AVM were presented to analyze the incidence of intracranial bleeding after onset. Of these, 91 patients were treated conservatively, and then long time follow-up study was done on 80 patients until death or until May 1989 (mean follow-up time 9.9 years).
The incidence of bleeding among these 80 cases was analyzed according to age at onset, location and size of AVM, and initial symptoms. Only the initial symptoms were significantly related to the risk of bleeding after onset. The average yearly risk of re-bleeding in the hemorrhage onset group was 2.8%, and the same risk of first bleeding in the non-hemorrhage onset group was 1.2%.This finding is useful in deciding the treatment where a difficult operation is predicted.

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During the past 20 years, we have treated 187 patients with cerebral arteriovenous malformations (AVMs). Among these patients, 134 were treated surgically and the remaining 53 were managed non-surgically. We analyzed the long-term results of 47 patients who were treated nonsurgically for AVMs to clarify the natural course of AVMs. The duration of the follow-up ranged from 1 year to 21 years (mean 7 years). In the follow-up period, neurological deterioration was found to be infrequent. As to the incidence of bleeding, there were 9 cases including 6 cases involving rebleeding (bleeding rate 19%) and 4 cases involving fatel bleeding. The risk of fatal bleeding is high in cases with large and deep-seated lesions. On follow-up angiography, the size of the AVMs were unchanged in the majority of cases, with the exception of 2, in which there were slight regressions. Particularly in another 2 cases a newly formed aneurysm was discovered in the follow-up angiography, emphasizing the fact that serious follow-up angiography is required in cases of non-surgically treated AVM. Consequently, the bleeding AVM should be treated surgically, even though the long-term follow-up results were not much worse than those of the surgically treated AVMs. The indication for surgery should be determined on careful consideration.

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We have reviewed 37 non-surgical cases of arteriovenous malformation (AVM), and analyzed several factors affecting bleeding and outcome. The risk of re-bleeding was higher in the cases with bleeding than in the cases without bleeding. Deep-seated AVM's seemed to have a somewhat greater tendency to bleed than those located superficially. Bleeding and location of the nidus seemed to be responsible for the mortality. The outlook for a patients with an infra-tentorial AVM was worse than for a supratentorial AVM. The outlook for a patients with a deep-seated AVM was worse than for a superficially located AVM. Spetzler grade of the AVM was not significantly related to the outcome of the non-surgical cases.

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During the years 1974-1988, sixty-three cases of arteriovenous malformation (AVM) in children and adolescents were experienced. Fifty-three patients (84.1%) had hemorrhage (intracerebral hematoma and/or intraventricular hemorrhage), and 2 of them died from the first hemorrhage. Ten patients had nonhemorrhagic symptoms, such as epilepsy and cerebral steal syndrome. Three fourths of the patients with hemorrhagic presentation had small AVMs (less than 2 cm in diameter).
Forty cases (63.5%) were treated with surgery and total excision of AVMs could be accomplished in 32 (80.0% of surgical cases). Eight cases had incomplete surgery (feeder clipping or partial resection of the nidus) and 21 cases were followed without surgery. Of these 29 cases, 10 cases (34.5%) experienced later hemorrhages during the mean follow-up period of 6.0 years. There was no difference in incidence and interval of later hemorrhages between cases with hemorrhagic and nonhemorrhagic presentation.
Outcome was poor in cases of recurrent hemorrhages and also poor in young patients developing cerebral steal syndrome with large AVM.
Optimal management consists of total excision of AVMs. There were, however, approximately 30-40% of patients for whom no surgery was indicated. It is important to recognize the natural history of these non-surgical cases. To improve overall mortality and morbidity of AVMs in children, non-surgical cases should be properly treated by any other means such as radiosurgery or embolization.

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We examined the natural history of 35 patients with arteriovenous malformations (AVMs) who were treated non-surgically and of 5 who underwent feeder-clipping. The bleeding rate was 4.0% and mortality rate was 0.91% per year with a mean follow-up period of 9.4 years in non-surgically treated group. The bleeding rate was 6.2% and mortality rate was 3.1% per year with a mean follow-up period of 6.5 years in feeder-clipped AVM group. Clipping of feeding arteries for AVM was thought to have no beneficial effect in preventing bleeding from AVMs. AVMs with a history of bleeding tended to rebleed more frequently than those without. Deeply seated AVMs also have a tendency to bleed more frequently than superficially seated AVMs.

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Subcortical hemorrhage is observed in about 10%of intracerebral hemorrhage. Various causes of hemorrhage other than hypertensive should be taken into account. In this report, we identified that the relationship between the cause of subcortical hemorrhage and the angiographical findings. During the past four years, we experienced 41 subcortical hemorrhages. The average age was 59.6 years. Thirty-three angiogram were studied among 41 subcortical hemorrhages. Three patients (8%) showed arteriovenous malformation and one (3%) patient showed a small angiomatous malformation (SAM). The other 33 patients (89%) showed normal angiogram.
Removal of subcortical hemorrhage was performed in 26 cases. Three (11%) operative specimen showed arteriovenous malformation, five (19%) showed SAM, one (4%) demonstrated venous angioma and the others 17 (66%) revealed no vascular malformation. The pathology of angiographicaly positive cases showed the same diagnosis as diagnosed before the operation. Angiography of five cases (19%), which showed vascullar malformation after the operation, demonstrated negative angiography.
In all cases that were diagnosed by angiography as arteriovenous malformation, surgery proved the diagnosis to have been correct. One SAM demonstrated by angiography also proved to be SAM by surgical specimen.
Four of angiographycally occult vascular malformations proved to be SAM and one proved to be venous angioma on histological evaluation. 19% of operated cases revealed angiographycally occult vascular malformation. Unlike other reports, we did not experience rebleeding of subcortical hemorrhage in this series.
Various causes of angiographically occult vascular malformation such as SAM, cavernous angioma, venous angioma, thrombosed AVM, amyloid angiopathy and the capacity of the instrument has been reported.
But there is still a problem of the mortal history of small angiomatous malformations and subcortical hemorrhage. The indications for surgical treatment of intracerebral hemorrhage has not been determined yet.
Due to the sampling problem inherent in biopsy material, there was the possibility of operative false negative cases. But we are of the opinion that radical extirpation of the wall cavity should not be performed in the operation.
We recommend the minimum extirpation of the wall cavity and the total removal of the vascular malformation.
Intensive enlarged stereotaxic cerebral angiography should be performed on patients with subcortical hemorrhage and surgical removal of the vascular malformation and hematoma should be considered to prevent rebleeding from the vascular malformation.

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In our series of 30 operative cases of subcortical hemorrhages, 23 were considered spontaneous, since causes for the hemorrhages were not identified preoperatively. In 13 cases (56.5%) of these 23, small angiomatous malformations (SAM) were verified as sources of the bleeding. They were recognized as small hemorrhagic nodules or small vascular meshworks in the walls of the hematoma cavities. Histologically, 11 were arteriovenous malformations and 2 cavernous angiomas. From this result, we stress the significance of SAM as a cause of spontaneous hematoma and the importance of a meticulous search for and subsequent biopsy of a suspected lesion intraoperatively.
We analyzed these 13 cases with SAM, which included 8 males and 5 females ranging from 15 to 77 years of age; 4 were older than 60. Angiographically, no case showed any abnormal vascularity. In contrast with previous reports, most cases in our series showed rapidly progressive courses resulting in emergent operations. This seemed attributable to our criteria for operative investigation of spontaneous hematomas. It is suggested that SAM can be one of the important causes of severe intracerebral hemorrhages. On the other hand, in patients with hematomas who are treated nonoperatively, the presence of SAM can not be ruled out. When a follow-up CT scan suggests the presence of SAM and it is accessible, surgery should be considered.

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A total of 259 patients with arteriovenous malformation (AVM) who had undergone cerebral angiography were evaluated in this study. The patients were divided into two groups, those with cryptic AVM and those with larger AVM. Age distributions, onset patterns, initial symptoms and symptoms on admission were compared. Group I was for cases of angiographic nidus ?1.0 cm. Group II consisted of cases in which angiographic early venous filling was the only abnormal finding, and diagnosed AVM histopathologically. In Group III, there was no angiographic abnormal finding, and the diagnosis of AVM was obtained from excised specimens histopathologically, and so-called “angiographically occult AVM.” Group I, II, and III included cryptic AVM. Group IV was the control group: the nidus of AVM was larger (>1.0 cm).
There were 72 cases in Group I (27.8%), 13 cases in Group II (5.0%), 22 cases in Group III (8.5%), and 152 cases in Group IV (58.7%). There was a total of 107 cases of cryptic AVM in Groups I, II, and III. This was 41.3% of the total cases of AVM.
Results were as follows: 1) Average age of patients with cryptic AVM was 37.4 years, compared with 35.5 years for patients with larger AVM. Age distribution of patients with cryptic AVM ranged from the teens through the 30s. For patients with larger AVM, age distribution peaked in the 30s.
2) Onset patterns of cryptic AVM were analyzed by studying the existence of hemorrhage on CT scan. In Group I, hemorrhage was the cause of AVM in 56 cases (87.5%), and in all cases in Group II and III the AVM was triggered by hemorrhage. Hemorrhage was the cause of cryptic AVM in 89 cases (91.8%), while patients with symotoms other than hemorrhage, such as convulsions, accounted for a slight 8.2% of cryptic AVM. However, in Group IV, hemorrhage was the cause of larger AVM in 88 cases (65.2%), while 47 cases (34.8%) had no hemorrhage.
In the 177 cases of all hemorrhagic AVM, cryptic AVM accounted for 50.3%.
3) Headache was the most common initial symptom (44.9%) of patients with cryptic AVM. But convulsions was as few as 10.3%. With larger AVM, convulsions were characteristic in 23.7%. It is interesting that cryptic AVM, on admission, disturbance of consciousness about doubled, to 27.2%.
To conclude, over 90% of cases of cryptic AVM had an onset pattern with hemorrhage. This figure would be higher than in cases of larger AVM.

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CT guided stereotactic evacuation is recently favored in selected cases of intracerebral hematoma, because of the less invasive nature. However risk of recurrent bleeding remains unresolved with this procedure. We report two cases of angiographically occult AVM, which presented the typical appearance of hypertensive hematoma. They were treated by stereotaxy but craniotomy was emergently needed because of rebleeding. Histological examination revealed partially thrombosed AVMs in both cases. In our consecutive series of 76 stereotactic hematoma evacuations, we found 3 cases of rebleeding. We stress that careful observation should be done after stereotactic evacuation of a hematoma.

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The diagnostic advantages and disadvantages of conventional computerized tomography (CT), prolonged high dose delayed CT (PHDD-CT) and MRI are mainly discussed in 22 histologically verified cases of angiographically occult vascular malformations (AOVMs). The abnormal enhancement effect by conventional enhanced-CT (CE-CT) and PHDD-CT were demonstrated in 4 (22%) of 18 cases and in 11 (79%) of 14 cases. Contrast enhancement effect of PHDD-CT was more evident than that of CE-CT in all cases. In 4 cases, the lesions were more clearly delineated in PHDD-CT, In 7 cases, only PHDD-CT could demonstrate the lesions. The advantage of PHDD-CT was that it has a strong enhancement effect for AOVMs, On the other hand, in three cases with small hemorrhage and with enhancement effect, it was difficult to differentiate normal granulation from AOVM because PHDD-CT was performed early at one or two months after the onset. The disadvantages of PHDD-CT suggested that a long follow-up was needed until granulation completely disappeared in order to differentiate granulation from AOVM. In two of the three cases, which were difficult to define as AOVMs by PHDD-CT, MRI clearly demonstrated nidus as signal void and hemorrhage as high signal on T₁-weighted and T₂-weighted images. Signal void showing nidus of AOVMs was demonstrated in 2 (28%) of 7 cases by MRI. In the other two cases, MRI clearly demonstrated repeated hemorrhage which strongly suggested hemorrhage from AOVMs. The advantage of MRI is that it is capable of delineating nidus and various stage of hemorrhage. On the other hand, 4 cases of AOVMs were not defined as nidus in MRI. One disadvantage of MRI is that it is not able to demonstrate nidus with remarkably reduced flow. One other disadvantage of MRI is its inability to differentiate hyposignal or signal void secondary to calcification from these caused by flowing blood of nidus. A further disadvantage of MRI is that it is inappropriate for diagnosing residual AOVM after surgery because it strongly receives operative influence for a long time. Because it is not easy to demonstrate AOVM, in order to diagnose it, CT with PHDD-CT and MRI should be performed as much as possible taking into consideration the advantages, disadvantages and clinical course.

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The authors reviewed 23 cases of angiographically occult cerebrovascular malformations (AOCVM's) operated on in our institute during the past 13 years and investigated their clinicopathological characteristics. There were 18 arteriovenous malformations (AVM's) and 5 cavernous angiomas (CA's). Ages of patients ranged from 7 to 69 years (mean, 45 years). There were 8 men and 15 women. Fourteen of the 18 AVM cases presented intraparenchymatous hemorrhage: 11 in the cerebral hemisphere, 2 in the cerebellum and 1 in the medulla. In the remaining 4 cases, epilepsy was the initial symptom. Angiographically occult AVM's constituted 24.8% of all AVM's (73 cases) operated on during the same period. All 5 CA's presented with intraparenchymatous hemorrhage: 4 in the cerebral hemisphere and 1 in the cerebellum. Among the causes of intraparenchymatous hemorrhage, AOCVM constituted about 19% of the 80 cases with lobar intracerebral hemorrhage and 20% of the 15 cases with cerebellar hemorrhage operated on during the same period. Five of the 19 AOCVM cases presenting with intraparenchymatous hemorrhage had previous bleeding episodes. In all 4 cases presenting with epilepsy, hemosiderin deposits indicating the presence of old hemorrhage were found histologically. In one case with AVM, hemorrhage recurred 3 year after the initial operation. Histological examination of the specimen taken at the first operation showed only cavernous vessels whereas examination of the specimen removed at the second operation using a serial sectioning technique revealed it to be an AVM.
In conclusion: 1) All patients who are strongly suspected of harboring AOCVM's on CT and/or MRI should be treated surgically so as to prevent recurrent hemorrhages and to confirm the pathology. 2) In cases of intraparenchymatous hemorrhage, the hematoma wall should be searched thoroughly using a surgical microscope to find any vascular nodule [6]. 3) Incomplete removal of an AOCVM might cause recurrent hemorrhage. 4) The removed tissues should be examined histologically using the serial sectioning technique [11] to obtain a precise pathological diagnosis.
The operative technique using a surgical microscope to find a bleeding cause in cases of intraparenchymatous hemorrhage is described and the operative indication for lobar intracerebral hemorrhage is discussed.

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We have experienced ten cases of angiographically occult cerebral angiomas (AOA).
The mean age of the patients was 26 years old. There was no sex difference in the prevalence. Symptoms consisted of convulsion in seven cases, and headache, hemianopsia and motor weakness in each case.
CT showed high density lesions in nine cases. One patient has a punctate calcified mass, and positive contrast enhancements were seen in five patients. MRI was performed in three cases. MRI was useful in detecting subacute and chronic hematoma which revealed high signal intensity in T1 and T2-weighted-image and hemosiderin with low signal intensity in T2 image. All angiomas were extirpated by open surgery. There were two transient neurological deficits and one permanent deficit (homonymous hemianopsia). The angiomas consisted of five arteriovenous malformations, four cavernous angiomas and one unclassified angioma. Histological examinations showed acute or old hemorrhage with hemosiderin deposition in all specimens. AOAs cause macroscopic and subclinical hemorrhages. It is important to differentiate AOA from brain tumor because these lesions sometimes appear similar in CT and MRI.
Therefore, surgically accessible AOAs should be extirpated by meticulous microsurgical technique.

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