Changes of cerebral blood flow (CBF), low perfusion areas (LPA) and redistribution phenomenon (RD), in which operations were performed within 24 hours after the onset of SAH, were examined using N-isopropyl-p-[¹²³I] iodoamphetamine (IMP) SPECT in 16 cases.
CBF patterns changed remarkably during the acute, subacute and chronic stages. In the acute stage, CBF of the affected side decreased due to vasospasm and operative procedures, and large LPAs were seen in many cases. However, good RD was recognized in most cases. In the subacute stage, CBF of the affected side increased and LPA decreased in size and number. In the chronic stage, CBF of the affected side decreased again, and in some cases transhemispheric diaschisis was seen.
In eight cases the absolute values of CBF were also measured. These values showed almost the same changes described above in each stage. Cases with remarkably low CBF and large LPA without RD in the acute stage showed poor prognosis.

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Auditory brainstem evoked potentials (BAEPs) reflect activities of the brainstem auditory pathway and its surrounding structures. It is said that BAEPs are reliable indicators of the prognosis of patients with severe brain damage. We studied the relationship between initial BAEP findings, particularly interpeak latencies of waves I to V and waves III to V, and mortality resulting from severe subarachnoid hemorrhage.
BAEPs were sequentially recorded in 76 cases of severe subarachnoid hemorrhage (Hunt & Kosnik grade IV, V) during the first few days after onset.
BAEPs were graded into four groups based on initial findings. Group A: waves I to V were all recorded (41 cases). Group B: waves IV & V were absent (3 cases). Group C: either wave I or waves I & II only were recorded (12 cases). Group D: all waves absent. Prognosis in Groups B & C was poor, with only one patient surviving in a vegetable state. There were no survivors in Group D.
The relationship between interpeak latencies (I-V ipl, III-V ipl) and prognosis in Group A is discussed in this paper. In cases where severe subarachnoid hemorrhage resulted in death, there was significant prolongation of I-V ipl and III-V ipl over the mean latency of 20 normal subjects plus 2SD. The difference in initial BAEP findings between the dead and survivors was significant (p<0.001). We reasoned that severe subarachnoid hemorrhage cases received primary brainstem damage and secondary brainstem damage due to increased intracranial pressure associated with acute cerebral swelling. We therefore concluded that poor prognosis could be predicted based on initial BAEP findings.
On the other hand, in acute hydrocephalus cases latencies were recovered by ventricular drainage. Continuous BAEP monitoring was therefore considered to be useful for predicting the effect of ventricular drainage in acute hydrocephalus.
BAEP monitoring appears to be a useful clinical indicator of prognosis of severe subarachnoid hemorrhage. Prolonged interpeak latencies of over mean plus 2SD can indicate poor prognosis in severe subarachnoid hemorrhage.

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The problematic points in the management of severe cases of subarachnoid hemorrhage admitted within 24 hours after onset were studied based on laboratory findings obtained during the first 14 days hospitalization. The present study covered 106 cases classified as Hunt and Hess grades 4 and 5 (Group A) and 203 cases classified as Hunt and Hess grades 1-3, which were used as controls (Group B).
First, blood pressure (BP), white blood cell count (WBC), serum sodium (Na), serum potassium (K), blood glucose (BG), GOT, GPT, LDH, CPK and CPK-MB (%), and ECG (heart rate (HR), QTc time, ST changes, giant T wave, inverted T wave and U wave) obtained on admission were examined. A significant difference (p<0.01) was observed between Group A and Group B in WBC, Na, K, BG, GOT, and LDH. WBC (normal: 9,000/mm³ or less) was elevated in both groups with the mean in Group A being 13,100/mm³ and that in Group B being 11,600/mm³. The number of cases in Group A with Na and K values found to be lower than normal was significantly greater than that in Group B (p<0.01). The mean blood glucose level was significantly elevated in Group A (p<0.01) with the mean value being 214.4mg/dl in Group A and 150.3mg/dl in Group B. Almost all of the serum enzyme levels were within the normal limits in both groups. Abnormal ECG findings were observed in 79 out of 81 cases in Group A and in 170 out 192 cases in Group B. In particular, the incidence of such abnormal ECG findings as tachycardia, arrhythmia, prolongation of QTc time, ST changes, and inverted T wave was significantly elevated in Group A.
Next, a study was made on the changes from day 0 to day 14 in BP, HR, body temperature (BT), Na and K. An increasing tendency was observed in Group A for HR and BT to deviate from the normal limits during the course. There were many cases in Group A where Na and K levels declined.
An elevated incidence of abnormal laboratory findigs was observed during the acute stage of subarachnoid hemorrhage with the incidence being significantly elevated in severe cases when compared to light cases. These fingings indicate that subarachnoid hemorrhage during the acute stage should be managed as a systemic disease.

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A coagulation-fibrinolytic study was performed on 98 patients with subarachnoid hemorrhage, with reference to severity of subarachnoid hemorrhage and symptomatic vasospasm (S-VS). They were classified in a Grade I & II group (40 patients), a Grade III & IV group (37 patients), and a Grade V group (21 patients) according to their neurological grade (Hunt & Kosnik) at the time of admission.
APTT on the day of onset was shortened in all groups, but particularly so in the III & IV and V groups. Fibrinogen levels were slightly lower in the V group than in the other groups on the day of onset. These levels increased with time in almost all patients. In S-VS cases of the I & II group, the following increase of fibrinogen levels was more remarkable than in cases without S-VS. FDP concentrations were abnormally high in 14%of the I & II group, 42%of the III & IV group, and 56%of V group on the day of onset. The number of cases showing an abnormally high level of FDP increased with time in the III & IV and the V group. Levels of both AT III and prekallikrein were low in the V group on the day of onset. In most cases with S-VS of the I & II and the III & IV groups, AT III levels decreased with time. Platelet counts on the day of onset were within an almost normal range in all groups. They decreased with time and showed the lowest level on Day 4.
On the basis of these data, it seems that the activation of an intrinsic pathway of coagulation is reflected by the severity of subarachnoid hemorrhage, being most enhanced in the V group.
The decrease of AT III level seemed to play an important role in S-VS.

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Twenty-one adult patients who had suffered from subarachnoid hemorrhage (SAH) and subsequent cardiopulmonary arrest were analyzed from the viewpoint of the possibility of functional reversibility and genesis of cardiac catastrophy. The patients included 10 men and 11 women, with a mean age of 50 (range 21 to 76 years). All patients reached our hospital within one hour of the onset of symptoms. Families of two patients reported an apparent history of sudden and severe headache. The mean duration of resuscitation was about eight minutes, and 11 patients showed restoration of respiratory effort and reconstriction of pupils. CT scan showed only severe subarachnoid hemorrhage in fourteen cases. Marked ventricular hemorrhage with acute hydrocephalus was seen in four cases; intracerebral or intrasylvian hematoma were encountered in three cases. Follow-up CT scan in most instances disclosed remarkable cerebral swelling and edema due to hypoxia, but in patients who had operatively decompressed developed less hypoxic edema in comparison with cases who were treated medically. Angiography was performed in 14 cases but two of them had already shown so-called'non-filling', despite the fact that they were studied within a few hours after the onset. The location of the aneurysms was not critical; 11 out of 12 were located in the anterior half of the circle of Willis. Intracranial pressure (ICP) was continuously monitored in five cases. In three conservative cases, the ICP values were very high from the start, showing 50-60 mmHg. Their cerebral perfusion pressures rapidly decreased within a couple of days and finally fell to zero. Two operative cases had much less drastic ICP. In one patient the rise of ICP was completely controlled within six days. Auditory brainstem response (ABR) was monitored in 15 cases. In all instances ABR record showed great deterioration; only the 1st and/or 2nd wave could be identified in nine cases, and the 3rd wave like shape could be detected in six cases at abnormally long latent times. Prognosis of all cases was awfully poor; 17 cases (81%) were brain dead within a week, and 95%had died within a month. Only one patient who had been operated on during the acute stage survived for five months under successful control of ICP, but she was in a vegetable-like state.<Conclusion> The most probable cause of sudden cardiac arrest after SAH can be transient critical arrhythmias. SAH cases whose cardiac function has ceased on admission are candidates for intensive care for the time being, whether they suit or not, but their initial brainstem damage is really severe. If they are treated aggressively, their final outcome depends on the duration of the cardiopulmonary arrest which caused the cerebral hypoxia.

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Nine cases of coma (Japan Coma Scale=JCS 200-300) which occurred after aneurysmal intracranial hemorrhage was discussed from the viewpoint of the possibility of recovery.
1) The control of blood pressure and ventilation were the most important points.
2) Abnormal pupille and decerebrate posture were indications of early death, but the latter condition could be remedied by decreasing the intracranial pressure.
3) CT scan showed a thick hematoma in all basal cisterns and a casting hematoma of the ventricle, especially in the prepontine cistern and the IVth ventricle. This may have caused the poor prognosis. There was a hydrocephalus in all cases.
4) The auditory brainstem response and the EEG were useful monitors in forcast the prognosis. A prolonged interval of the I-V wave in ABR may indicate the possibility of recovery.
5) Patients who received ventilation by intratracheal intubation, control of blood pressure and decrease of intracranial hypertension through ventricular drainage and barbiturate therapy, as early as possible after hemorrhage, recovered and responded to commands. But two such cases out of the nine, who were given active treatment, were totally dependent after three months.

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The authors studied the clinical features and computerized tomographies of 92 patients with ruptured intracranial aneurysms who were admitted to our hospital within eight hours after the last attack and died within 21 days without direct intracranial surgery. Seven cases (8%) were of Grade I and II on admission (Hunt & Kosnik grading), seven cases (8%) of Grade III, 19 cases (21%) of Grade IV, and 59 cases (64%) of Grade V. Thirteen cases of Grade V were dead on arrival (DOA).
Thirteen out of 14 cases of Grade I-III succumbed because of rebleeding. Six out of 19 cases of Grade IV and two out of 46 cases of Grade V had an uphill course, and died from subsequent rebleeding. Overall, rebleeding occurred after admission in 12 cases of Grade IV and eight cases of Grade V. Rebleeding was especially frequent within 24 hours after admission (63%). Rebleeding occurred before admission in 17 out of 78 cases of Grade IV, V, and DOA.
Another cause of death was the direct effect of subarachnoid hemorrhage in 58 out of 78 cases of Grade IV, V, and DOA.
The initial CT findings of those who died without having uphill course were classified into four types (S, H, V, H + V). The total number of hematoma type (H, V, H + V) amounted to six out of 13 cases of Grade IV (46%), 33 out of 44 cases of Grade V (75%), four out of 14 cases of DOA (31%). Distortion of brain stem or obliteration of mesencephalic cistern were seen in 23% of Grade IV, 48% of Grade V, and 15% of DOA.
Pupillary abnormality and abnormal motor response were recognized in almost all cases of H and H + V type in Grade V.

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The severity of ruptured intracranial aneurysms may be determined by the volume of subarachnoid hemorrhage, the volume of intracerebral hematoma, the presence of intraventricular hemorrhage, or an acute hydrocephalus on the CT scan. But in some cases, brain swelling seemed to be the only determinant factor of severity.
We have experienced 32 such cases among 515 patients with ruptured intracranial aneurysm who were admitted within 72 hours of attack (6.0%). Five cases had previous convulsions (group 1), and 15 cases had preceding hypoxia and/or hypotension episodes (group 2). But in the remaining 13 cases, we could not find such a preceding episode (group 3).
In group 1, clinical grade on admission varied from 3b to 5, and blood pressure varied from 118/80mmHg to 190/100 mmHg. Outcomes of this group were one GR, two SD and three death.
Because brain swelling in this group may be a reversible brain edema caused by a convulsion, a delayed operation must be employed.
In group 2, the clinical grade on admission of all patients was five, and blood pressure varied from zero to 210/110 mmHg. The outcomes of this group were miserable (death: 13, PVS: 1).
Since brain swelling in this group is a manifestation of hypoxic brain damage, there is no indication for an operation.
In group 3, 12 of 13 cases had marked hypertension and the average MABP was 130mmHg. Regional cerebral blood flow measurement by means of Xe inhalation was performed in two cases whose CT scan showed hemispheric swelling, and hyperperfusions of the swelling side were noted. In three cases autopsies were performed, and marked brain swelling, dilated small vessels and diapedesis of erythrocytes were found.
We speculate that acute brain swelling of unknown etiology may be brought about by disautoregulation caused by SAH concomitant with persistent hypertension.
It must be stressed that lowering of blood pressure in the acute phase of a ruptured intracranial aneurysm is very important not only for preventing rebleeding but also for impeding the development of brain swelling.

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In this paper, twenty-four patients with acute neurogenic pulmonary edema (NPE) following subarachnoid hemorrhage (SAH) are presented, and clinical features are discussed. Among the 503 patients admitted for SAH during a seven year period, 24 cases (4.8%) involved NPE associated with SAH. Seventeen (70.8%) of these were admitted within 60 minutes after the onset of SAH. Fourteen patients were in Hunt & Hess SAH Grade V and ten in Grade IV. The hemodynamic study using the Swan-Ganz catheterization method noted an increase in pulmonary capillary wedge pressure and mean pulmonary arterial pressure in three patients. Seventeen patients (70.8%) were treated by assisted ventilation with positive end-expiratory pressure within three days. However, thirteen (76.5%) of these 17 patients died from increased intracranial pressure due to severe SAH. The remaining four patients underwent surgery for intracranial aneurysm. Two of those recovered well but two had severe disabilities.
This result implies that acute pulmonary edema associated with severe SAH can be successfully treated with assisted ventilation. However, the direct surgical treatment of intracranial aneurysm has a high incidence of morbidity and mortality because of a high preoperative SAH grade.

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Four cases of subarachnoid hemorrhage complicated with neurogenic pulmonary edema were reported. The Hunt and Kosnik gradings on admission were III in one case and IV in three cases. Chest X-ray films on admission demonstrated a typical pattern of pulmonary edema in all cases. CT showed a diffuse subarachnoid clot in each case: one was complicated with a large hematoma in the temporal lobe, and two with acute hydrocephalus. Angiography disclosed an intracranial aneurysm in three cases: one on the AComA, one on the VA-PICA junction and one on the MCA. Angiograms on the other patient showed no aneurysm. Blood gas analysis demonstrated severe hypoxemia in each case. ECG demonstrated nonspecific ST-T changes in two cases. Blood gas analysis, CVP measurement, chest roentgenography and ECG recording were serially performed. In one case, hemodynamic changes were observed by a Swan-Ganz catheter. Artificial ventilation with PEEP was applied in three cases, while only oxygen was given through a face mask in one case. The pulmonary edema improved under such respiratory care within one to five days in each case. ECG abnormalities noted at the time of admission in two cases disappeared in a few days. CVP measurement showed no significant rise in pressure in three cases. In the other, CVP was not measured. Pulmonary arterial and capillary wedge pressures measured 18 hours after subarachnoid hemorrhage in one case were normal, 30/10mmHg and 7mmHg, respectively and they remained normal thereafter. Two patients underwent an aneurysm surgery in the chronic stage, and one patient with an intracerebral hematoma did in the acute stage. The other patient with subarachnoid hemorrhage of unknown etiology underwent a ventricular drainage for acute hydrocephalus on the day of admission. The patient with an intracerebral hematoma developed a mild motor aphasia, but the other three patients had no neurological complications.
Neurogenic pulmonary edema itself generally responds promptly to treatment. Thus, aneurysm surgery in the acute stage is not necessarily taboo if appropriate respiratory and cardiovascular management is given. The outlook for patients with a ruptured aneurysm complicated with neurogenic pulmonary edema primarily depends on the severity of the subarachnoid hemorrhage. Therefore, early operation may be performed in good grade patients to prevent rebleeding. It may also be recommended in poor grade patients in whom an intracerebral hematoma or acute hydrocephalus is responsible for the poor neurological condition because the control of increased intracranial pressure due to an accompanying intracerebral hematoma or acute hydrocephalus might ameliorate the neurogenic pulmonary edema itself.

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Prognostic factors on severe cases of ruptured aneurysm admitted within one hour after onset between 1983 and 1987 were evaluated.
Forty-two ruptured aneurysm having consciousness disturbance more than 30 points in Japan coma scale (JCS), 91% of which was more than 100 points (JCS), involved 16 MCA aneurysm, 14 A Com aneurysm, 9 IC aneurysm and three vertebro-basilar aneurysm. Hemorrhages caused by a ruptured aneurysm were classified as massive subarachnoid hemorrhage (SAH) (26 cases), intracerebral hematoma (ICH) or subdural hematoma (SDH) (14 cases) and intraventricular hemorrhage (IVH) (two cases).
The most severe cases of ruptured aneurysm started with sudden consciousness disturbance as the initial symptom. There were two types of clinical course of massive subarachnoid hemorrhages. One was that consciousness disturbance improved within several hours; two to three hours after admission in 14 cases. The other was no improvement, but rather respiratory arrest leading to death in 12 cases. Only one patient lived out of 25 with severely ruptured aneurysm and showing no reaction to light and no oculocephalic reflex on admission, whereas 12 of 17 patients with two brain stem reactions lived.
The CT findings of the deaths caused by subarachnoid hemorrhage demonstrated massive hemorrhage in diffuse subarachnoid space with thick hemorrhage in the basal cistern around the brain stem combined with intraventricular hemorrhage into the third and fourth ventricle due to the reflex of blood. Also huge intracerebral hematoma of more than 6cm in diameter and diffuse intraventricular hemorrhage caused by ventricular rupture were recognized on the CT scan in the deaths caused by ruptured aneurysm.
Operations were performed on 19 of 42 patients with ruptured aneurysms. Eleven patients (58%) survived of whom eight recovered well and three had mild deficit on GOS. On patients with severe SAH caused by ruptured aneurysm, operation was performed within two days after onset as soon as consciousness level improved to 2-10 points (JCS). Three of 14 subarachnoid hemorrhage patients recovering from severe consciousness disturbance died of rerupture of the aneurysm in the early stage before operation. The main causes of death after operation for a ruptured aneurysm were vasospasm in subarachnoid hemorrhage and herniation due to huge intracerebral hematoma.

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The purpose of this study is to investigate the management and application of appropriate surgical treatment for patients admitted to hospital during the acute stage of severe ruptured intracranial aneurysms. There were 204 patients, in which the onset of stroke due to subarachnoid hemorrhage was clearly recognized. These were classified into three groups, according to the time of admission. Group A consisted of 133 patients admitted to hospital within three hours after onset of symptoms Group B consisted of 39 patients admitted between 3 and 24 hours Group C consisted of 32 patients admitted from 1 to 14 days after onset. The percentage of severe cases categorized as grade IV to V on admission was: A group (52%), B group (37%) and C group (19%). The percentage of cases which progressed to a severe condition, from I to III, was: A group (19%), B group (4%) and C group (12%). These results were rather high, the main cause of which was recurrent hemorrhage occurring more frequently within six hours. The percentage of recurrent hemorrhage was: A group (21%), B group (10%) and C group (9%). The frequency of direct operation was 78%, 79% and 84% respectively for groups A, B and C. The percentage of cases belonging to grade IV to V, as observed at the time of surgery, was: A group (49%), which was high compared with B group (29%) and C group (22%). The favourable surgical outcome for severe cases was grade IV (50%), and grade V (10%), and the clinical features are as follows: under 60 years of age; the middle cerebral artery aneurysms; in the Group 2 classification of Fisher or with intracerebral hematoma shown on CT; for grade V patients surgery could be performed within 12 hours. In severe cases vasospasm was not prevented by surgery at the most acute stage within 12 hours. Thus, in order to obtain a better overall result for ruptured aneurysms, we considered it appropriate to conduct radical, curative surgery and management of the patients overall condition for even severe cases if they did not have the complications of irreversible cerebral injury with the clinical features mentioned above, because there is as yet no other means available to prevent recurrent rupture of the aneurysm.

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The effect of intracerebral hematoma (ICH) on the clinical manifestations and prognosis was studied in 486 consecutive cases with ruptured aneurysm at the acute stage. Grade III and IV cases were investigated with special interest because the indication of early surgery for these groups is thought to be still in controversy. Conclusions obtained from this study are as follows: 1) The poorer the grade from II to V on admission, the higher the incidence of ICH is.
2) ICH is rarely seen in cases with aneurysms in the vertebro-basilar system. In the anterior circulation, middle and anterior cerebral artery aneurysms are more often accompanied with ICH than those on the internal carotid and anterior communicating arteries.
3) At grade III and IV, cases with major neurological deficit (ND) such as hemiparesis or aphasia more frequently have ICH. Prognosis evaluated on the Glasgow outcome scale, however, is not worse in cases with ND or ICH than those without these seemingly harmful factors provided that they are managed properly.
4) Incidence of symptomatic vasospasm is less frequent in cases with ICH than those without it, and the differce between these two groups is statistically significant at Grade IV.

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We have treated 25 cases of ruptured intracranial aneurysms with intracerebral hematoma. There were nine male and 16 female patients, and the mean age was 51 years old. The ruptured aneurysms were located in the middle cerebral artery (MCA) in nine cases, the anterior communicating artery and the distal anterior cerebral artery (ACA) in 14 cases, and the internal carotid artery in two cases. Five of 25 patients died of rebleeding in the preoperative period. Fourteen of 18 patients who were surgically treated were operated on within three days after admission. Preoperatively, one patient was classified as Hunt and Kosnik Grade I, two as Grade II, 12 as Grade III and three as Grade IV. Grade I and II patients had a favorable outcome. Half of Grade III patients had a favorable outcome. However, the other half had an unfavorable outcome mainly due to postoperative symptomatic vasospasm. All Grade IV patients had MCA aneurysms, and had an unfavorable outcome, partly because of delay of surgery or intraoperative complications. In MCA aneurysms. the mass effect of intracerebral hematoma was thought to affect the prognosis; therefore, earlier operation might have improved the outcome of the patients. On the other hand, in ACA aneurysms. a poor outcome was thought to be due to symptomatic vasospasm, not to the presence of hematoma. The extent and gravity of subarachnoid hemorrhage had a great influence on the prognosis in cases where intracerebral hematoma was in ruptured aneurysms without hematoma. In ruptured aneurysms with intracerebral hematoma, especially in MCA aneurysms, early surgery including evacuation of the hematoma might improve the morbidity and mortality of patients.

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Eighty-two seriously ill patients with ruptured cerebral aneurysms were studied to elucidate the efficacy of surgery and the factors influencing their outcome. All appeared moribund, in semicoma or deep coma, pupils unilaterally or bilaterally dilated and fixed, decerebrate posture, and markedly abnormal respiratory pattern when the operative indication was considered.
Coputerized tomography (CT) scan was taken of all patients on admission and just after subsequent attacks. CT findings were divided into the following three groups: (1)“Hematoma type”having massive intracerebral or subdural hematoma, (2)“Ventricle type”having intraventricular casting hematoma, so called“Hematocephalus”, (3)“Severe SAH type”having dense SAH.
Forty-nine cases were operated on directly. The outcome of these cases was as follows: 7 (14%) fully recovered with no neurological deficits, 11 (22%) were moderately severely disabled with mild neurological deficits, 15 (13%) were severely disabled, 9 (18%) were vegetative and 7 (14%) died.
An attempt to define a therapeutic principle for seriously ill patients with ruptured cerebral aneurysms was made by investigating the efficacy of surgery and the factors influencing outcome, such as CT findings, pre-operative conditions just after administration of 600-900ml of Mannitol, symptomatic vasospasms, complications and so on.
From this study, the following conclusions were“Hematoma type”and Severe SAH type”cases could be cured if the pre-operative symptoms were improved by injection of 20% Mannitol and if the operation could be performed within six hours from the last attack of SAH, while most of the“Ventricle type”patients lapsed into poor condition without direct surgical removal of the intraventricular hematoma. Also, symptomatic vasospasm, other serious complications and surgical troubles such as pre-mature rupture, venous injury and brain contusion secondary to excessive brain retraction contributed to poor outcome.

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We examined 40 patients with ruptured middle cerebral aneurysms showing local symptoms in the brain as well as disturbance of consciousness. The overall mortality of those 40 cases was 27.5%. This was much lower than the mortality of 44.4% for cases with ruptured aneurysms of Hunt and Kosnik Grade IV which we also observed at approximately the sane time.
The 40 cases consisted of 29 patients who survived (Group S) and 11 patients who died (Group D). A comparison between the two groups revealed that Group D had a higher rate of signs of cerebral herniation, with cases showing signs of bilateral herniation all ending in death. The CT scan of the groups revealed SAH and midline shifts to a great extent in Group D but no significant differences in the largest diameters of hematoma between Groups S and D. There were more cases of severe delayed ischemic neurological deficit (DIND) in Group D. An examination of the nine cases with signs of unilateral herniation (five cases of survival and four cases of death) showed that all the patients who survived underwent operation within 12 hours of the attack. This suggested the necessity of rapid treatment for these serious cases. The 29 survival cases were composed of 23 cases which could take care of themselves and six cases which, at least partially, required the assistance of others. Five of these six cases had hematoma of the left hemisphere.
It has suggested that possibility of improvement in functional prognosis would depend on the management of the intra Sylvian hematoma extending into the rear part of the Sylvian fissure.

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A middle cerebral artery aneurysm (MCAn) is apt to be regarded as comparatively easily accessible and the parent artery more capable of being secured compared with aneurysms in other sites. Unexpectedly, however, activity of daily living (ADL) in such MCAn are not seldom unfavorable. Influences of various factors on postoperative outcome of 122 well-documented cases, out of a total of 151 cases of MCAn, are discussed in this paper.
There were 52 male and 70 female patients (1: 1.35). The following study was made on a group with good outcome (G) showing an ADL of 1, 2, and 3 and a group with poor outcome (P) showing an ADL of 4, 5, and 6. Group G and P included 92 cases (75.4%) and 30 cases (24.6%) and averaged 50.3 and 56.8 years, respectively, indicating a correlation between age outcome (p<0.01). There is no significant correlation between sex on number of aneurysms and the outcome. As for the shape of the aneurysm, major axis, major axis/neck and major axis/minor axis were 8.47, 1.68, and 1.35 for Group G and 8.78, 1.79, and 1.41 for Group P, indicating a correlation not only between aneurysmal shape and the prognosis (p<0.05) but also between preoperative grading (p<0.05) and the prognosis. Repetition rate of subarachnoidal hemorrhage (SAH) was 1.29 for Group G and 1.66 for Group P, in 50% of which a plurality of SAH was observed (p<0.05). The preoperative grade and the SAH grade (5 stages) were 1.86 and 2.79 for Group G and 3.33 and 3.86 for Group P, indicating a close correlation between each of these two parameters and the outcome (p<0.000001). There was also a correlation between the SAH-Ope interval and the outcome (p<0.01); early operation was included predominantly in Group P. As for preoperative findings, premature rupture occurred in 11 of 92 cases (12%) in Group G and in seven of 30 cases (23%) in Group P, i. e. abuot twice the Group G rate, and both the quantity and the color of CSF outflow from the chiasmal cistern showed close correlation with spasm (p<0.01), onset of hydrocephalus (p<0.01) and the outcome (p<0.001). Moreover, spasm and hydrocephalus grade itself also showed close correlation with the outcome (p<0.000001). Hematoma grade (5 stages) was 1.45 for Group G and 2.82 for Group P, being regarded as one of the most influential factors on the outcome (p<0.000001). Blood pressure was also an important factor in hemodynamic stress; all of blood pressure grade (5 stages), BP max, BP min, BP fluctuation showed correlations not only with preoperative grade (p<0.001) and prognosis (p<0.0001) but also with SAH frequency, number of aneurysms, and major axis/neck ratio.
Multiple factors were thought to be involved in the prognosis; with the complex interrelations of these factors having a great influence on the outcome.

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