Regional cerebral blood flows (rCBF) in the cortex, thalamus and midbrain of the dogs were measured by H₂ clearance method and compared before and during CO₂ inhalation. The responsiveness of rCBF to CO₂ was studied on the PaCO₂-rCBF curves obtained from the control group and denervated groups with phenoxybenzamine (POB), atropine or 6-hydroxydopamine (6-OHDA). The mean increase of cerebrospinal fluid pressure (CSF-P) per unit increase in PaCO₂ was also calculated in each group for the PaCO₂ range below 65 mmHg. Findings were as follows :
1) PaCO₂-rCBF curves obtained from the thalamus and midbrain exhibited both concave function before administration of POB or Atropine, but changed to be linear function after POB or Atropine.
2) PaCO₂-rCBF curves obtained from the cortex were all linear function, and did not change significantly after POB or Atropine.
3) The values of ΔCSF-P/Δ PaCO₂ were considered to indicate the rate of increase in the volume of total cerebral vascular bed.
4) ΔCSF-P/ΔPaCO₂ remarkably decreased in the group with POB, but increased in the group with Atropine. In the group with 6-OHDA, howerver, the change in ΔCSF/-P/ΔPaCO₂ was not clear.
With these results, it was thought that the role of neurogenic factors is to maintain vascular tone in thalamus and midbrain areas when CO₂ effected these vessels as a vasodilator. In cortical circulation, however, the role of neurogenic factor was found to be insignificant, probably because cortical vessels were less innervated than thalamic and mesencephalic vessels.

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Recently aspiration therapy for intracerebral hematoma through a burr hole has been reported with good result. Althrough in many literatures stereotactic devices are used to determine the location of the tip of the needle, we report the simplified method of CT guided manual insertion of the needle.
The location of a burr hole is settled on the CT film by two mesurements, ie distance from orbito-meatal line and the midline of forehead to hematoma.
This technique would shorten operation time and be available even for the aged of high risk. Operative timing should be set in the subacute stage when hematoma becomes liquefied without danger of rebleeding by aspiration.
This method had been applied in ten cases of putaminal haemorrage. Four cases improved disturbance of consciousness and another four cases gradually recovered hemiparesis in a week after the operation.
Our protocal for treatment of putaminal haemorrage is as in the followings. If hematoma is larger than 6 cm in the largest diameter and pupils are not fully dilated, removal of hematoma by craniotomy is immidiately performed. If hematoma is larger than 3 cm and a patient exhibits hemiplegia, craniotomy is also planned. If moter deficid is mild or moderate, conservative treatment is recommended. When neurological signs do not improve after more than one week of conservative treatment, aspiration of hematoma is a choice of treatment.

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To demonstrate patterns of vulnerability differences in hindbrain neurons at early stages of ischemia without recirculation periods, immunohistochemical study with antiserum to tubulin was performed on the brains of Mongolian gerbils obtained 10 min to 6 hours after occlusion of the basilar artery. The occlusion of this vessel in this animal has been demonstrated to produce moderate degree of ischemia in the cerebellum, brain stem and a part of thalamus. In terms of immunohistochemical changes in cytoplasmic tubulin, various types of selective vulnerability were observed in the hindbrain structures. Firstly, vulnerability was different among different neural structures; the vestibular nucleus was involved within 10 min after vascular occlusion and the cerebellar cortex between 30 min and 2 hours. The deeper portions of the cerebellar folia were affected more readily than the superficial portions. These regional differences in vulnerability may be related to the different threshold of the individual structure or to the different amount of residual blood flow. Secondly, vulnerability was different among different types of neurons even within the same neural tissue; large neurons in the vestibular nucleus were more susceptive than small neurons and all the large cells did not respond in the same manner. In addition to the conventional morphological typing of neurons, the chemical typing based on the neurotransmitter differences may provide some, but limited, value in evaluating vulnerability differences among certain types of neurons. Thirdly, vulnerability was different among different portions even within a single neuron; the dendrites of the cerebellar Purkinje cells lost tubulin immunoreactivity faster than the perikarya. Thus, the dendrites may be an early target of ischemic insult at least in some limited situations.
The present investigation demonstrated various types of selective vulnerability in the gerbil hindbrain structures. Although many of the causative factors responsible for the selectivity are currently only speculative or totaly unclear, this kind of immunohistochemical study is expected to provide an important clue for understanding the complex pathophysiology of ischemia in these important portions of the nervous system.

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Thirty-three adult autopsy brains with ruptured cerebral saccular aneurysm mainly in the acute stage with intraventricular hemorrhage were examined to clarify the correlations between the ruptures and the route of intraventricular hemorrhage. Thirteen cases (or more than one third) showed an intraventricular hemorrhage due to a back flow from the subarachnoid space through the apertura lateralis et medialis of the fourth ventricle without a ventricular rupture, while the other 20 cases had a ventricular rupture. Of 13 cases with a cast hematoma in the all ventricles, twelve revealed a ventricular rupture. No correlations were found between the amounts of subarachnoid and intraventricular hemorrhages. Most of the brains only showed findings of mild transtentorial herniation. The weight of the brains showed a 5 to 10% increase compared to the normal mean value of the adult brain. Volumetry revealed that the mean volume of the whole brain including that of a cast hematoma of the total ventricles was 993.2 cm³, while the mean volume of intraventricular cast hematoma was 78.3 cm³ (7.9% to the total brain volume). The ratio of the cast hematoma to the total brain volume was considered to be about double the normal volume ratio of the ventricles to the total brain volume. The above results indicate that the ventricular system can be a kind of refuge for the subarachnoid high pressure and in such cases the brain may be subjected to a fairly high pressure from both outside and inside in spite of the presense of mild transtentorial herniation.

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Stereotactic evacuation for hypertensive intracerebral hematomas has been carried out for basal ganglionic and thalamic (supratentorial) hematomas since 1978 in our clinic. We also operated the pontine and cerebellar (infratentorial) hematomas by Komai's CT stereotactic apparatus for the first time in 1982. Six patients of pontine hemorrhage and seven patiens of cerebellar hemorrhage whose ages were from 44 to 60 (49.8 in average) years old in the pons and from 45 to 75 (61 in average) years old in the cerebellum were operated by the stereotactic method with plasminogen activator (urokinase). Its operative method and results are discussed.
These patients were operated by the stereotactic method under local anesthesia at from the 6th hour to the 36th day after the ictus. The estimated volumes of hematomas were from 3 to 8 ml in the pontine and from 7.9 to 20 ml in cerebellar hemorrhages. Evacuated rates of the hematomas (evacuated volume/estimated volume) were 73.3% in average in the pons and 88.4% in average in the cerebellum, and the rates were not always reffered to the operative timings. It was found that level of consciousness, eye signs, motor paresis, cerebellar signs, and signs of increased intracanial pressure improved immediately after the opeartion of stereotactic evacuation. Then, these good operative results and non-invasive manoeuver of stereotactic method indicate that this treatment is accepable for pontine and cerebellar hemorrhages.
We conclude that the surgical indication of stereotactic evacuation for pontine hemorrhage remains in unilateral type on CT and not in massive type, and the indication for cerebellar hemorrhage remains in all cases with neurological syndrome.

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Among the 611 cases of subarachnoid hemorrhage (SAH) experienced in our clinic during a period from April 1978 to June 1983, the etiology was not defined in 26 cases in spite of four vessel study which were performed more than twice.
The follow-up studies on such 26 cases were performed 5 to 67 months later from the onset by means of questionnaire. The follow-up study was completed 25 out of 26 cases and episodes of recurrent SAH was not recognized in any of the 25 cases.
Also follow-up cerebral angiography was done on 10 cases 8 to 44 months later in which SAH had been found on CT scan. And in only one case, an anterior cerebral artery aneurysm was found.
These results suggest that the prognosis of the cases with SAH of unknown etiology is very good when the diagnosis is made strictly. However, careful observation for more than a year including differential diagnosis follow-up angiography is strongly recommended in such cases, especially when CT scan obviously demonstrates SAH.

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Recently percutaneous transluminal angioplasty (PTA) has been refined for dilating peripheral stenotic arteries, after Gruntzig's dilating balloon catheter was developed for treating coronary artery stenosis. However, few successful cases of carotid artery treatment have been reported due to difficulties in application as well as the fear of complications, such as distal embolization.
This paper describes successful dilation of bilateral carotid arteries using PTA. The patient treated was a 46 year old male, who was suffered from TIA, primarily amaurosis fugax for 2 years. His attacks disappeared by administering aspirin, 300 mg/day. Two years after the last TIA, minor chest pains started to occur. After an extensive examination it was revealed that the patient had coronary arteriosclerosis, diabetes mellitus and hyperlipidemia (type IV). Carotid angiography showed severe stenosis in both carotid arteries at bifurcation. The patient refused to have a carotid endarterectomy, and after discussion, the patient select to be treated by PTA.
First, a 260 cm-long exchange guide wire was selectively positioned in the internal carotid artery using a conventional catheter. Then a 7 French Grüntzig balloon dilating catheter was introduced transfemorally over the guide wire. After this procedure, the balloon was inflated with a diluted constrast material for 3040 sec and then the collapsed balloon catheter was withdrawn. Carotid angiogram showed disappearance of the stenosis. This technique was performed to the bilateral carotid arteries without any problems or complications.
No TIA occurred since then, and there was no recurrence of stenosis in the dilated portion according to the last carotid angiogram which was performed 2 years after the PTA.
Clinical application of PTA for stenotic carotid arteries has not been clearly defined. However, in severe cases such as the one described, PTA should be considered as a choice of therapy. Further study is needed to justify this approach.

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The changes of blood coagulation function after subarachnoid hemorrhage (SAH), produced by cisternal injection of autogenous arterial blood in 38 mongrel dogs, was evaluated to make clear a cause of ischmic symptoms on cerebral vasospasm after SAH. Blood samplings and vertebral angiographies were carried out before SAH and every 1-3 days during 8 days after SAH. Diffuse vasospasm, which had a peak at 4 days after SAH, was confirmed by vertebral angiography in this experimental model. Intravascular factors, that were erythrocyte, hemoglobin, hematocrit, deformability of erythrocyte, activated all blood coagulation time, PT, APTT, fibrinogen, platelet aggregation, were measured on every blood sampling. Increase of fibrinogen, which had a peak at 1-4 days after SAH, and increase of platelet aggregation, which did not decrease during experiment, were observed. No characteristic changes were observed in other intravascular factors. These results indicate that the acceleration of blood coagulation function is prepared after SAH. Reliable standered values of these intravascular factors in the dog were also obtained in this study.

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Clinical significance of multimodality evoked potentials (MEPs) was studied in 27 patients with hypertensive intracerebral hemorrhage mainly treated by surgical evacuation. MEPs were consisted of auditory evoked brainstem response (ABR), cortical somatosensory evoked potential (SEP) and visual evoked potential (VEP) and serial changes of MEPs were observed for 14 days after onset by grading the abnormality on MEPs into 4 categories according to the modified classification of Greenberg's MEP grading. Intracranial pressure (ICP) from the extradural space was also recorded in 10 selected patients. The neurological status and CT finding were evaluated according to the classifications presented by the committee of the conference of surgical treatment of stroke (1978). The outcome was divided as good, partial disability, total disability and dead according to ADL at 3 months after onset.
An abnormality on MEPs was most significant in SEP in all patients throughout and was well correlated with functional recovery of the patients. Neurological grading was also nearly well correlated with the grade of MEPs. Significant degree of abnormality was noted in VEP and ABR as well as SEP in patients with poor outcome although there was little changes on ABR in good and partially disabled patients. MEPs were improved within 7 days after onset regardless of the difference of the treatments in the patients with good outcome. The dysfunction of the internal capsule was considered as reversible in these patients. On the other hand, transient deterioration of MEPs within 7 days or delays in improvement of MEPs over 7 days after onset was noted in the patients with poor outcome. Elevation of ICP more than 20 mmHg was recorded in association with deterioration on ABR in the patients with severe neurological signs on admission.
The present results indicated that MEPs were useful indices for the assessment of global as well as focal brain dysfunction including brainstem in the patients of hypertensive intracerebral hemorrhage and the rapid recovery on SEP suggested the reversibility of function of the internal capsule. The prediction of the outcome was also possible by the serial recording of MEPs for 7 to 14 days after onset.

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A rare case with localized small midbrain hemorrhage which was caused by rupture of arteriovenous malformation (AVM) was reported.
A 46 year-old right handed man was admitted because of sudden onset of occipital discomfort followed by diplopia and drowsiness. On admission (7 days after the onset) he was still drowsy, and neurological examination revealed incomplete Horner sign on the right, trochlear palsy, mild hypoglossal palsy of the central type, mild hemiparesis and disturbance of superficial sensation on the left side. Brain CT scan showed a small high density area localized in the right tectum and tegmentum of the midbrain. Vertebral angiography demonstrated abnormal stains in the dorsolateral aspect of the quadrigeminal segment of the right superior cerebellar artery, which were thought to be a nidus of AVM. An abnormal vein draining from the nidus to the basal vein of Rosenthal via the posterior mesencephalic vein was also seen in the early arterial phase, although the feeding artery was not demonstrated in the films.
These findings suggest that the localized midbrain hemorrhage of the present case was caused by rupture of the small AVM in the brain stem. There are only a few reports in which the AVM of the midbrain causing a localized hemorrhage was demonstrated by cerebral angiography.

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Chemical mediators for shear-induced platelet activation which might contribute to thrombogenesis in cerebral arteries, particularly in their parts of bifurcations or stenoses, were investigated by using a new in vitro platelet-sensitive technique, Filter Bleeding Time (FBT). FBT is based on progressive decrease of flow rate of citrated blood through a disk filter of woven Dacron under controlled pressure (150 mmHg) as platelet aggregates occlude the filter.
FBT was prolonged from 2.0± 1.0 (x ± SD) to 10.4 ± 2.7 min (p<0.002) by a monoclonal antiplatelet antibody (HP1-1D), which is specific for platelet membrane antigens, presumably glycoproteins IIb and IIa. FBT was prolonged from 2.7 ± 1.8 to 6.2 ± 1.8 min (p<0.007) by the combination of CP and CPK, which remove plasma ADP, with ATP, which inhibits the effects of ADP on platelets. Thromboxane synthetase inhibitors (TXI), UK-37, 248 and UK-38, 485 did not affect platelet aggregation to ADP. Platelet aggregation to arachidonate was inhibited by UK-38, 485 in 3 of 6 subjects, designated “responders”. In neither responders nor non-responders FBT was prolonged by this agent. TXI had, however, a synergistic effect on FBT when added with CP/CPK/ATP.
Plasma oxyhemoglobin (Hb) increased from 5 ± 2 to 555 ± 52 mg/dl (p<0.001) in human subjects and from 11 ± 6 to 496 ± 435 mg/dl (p<0.04) in canine subjects during passage of blood through the filter. FBT was correlated with the increase of plasma Hb during FBT in canine subjects (r= -0.87). Platelet lysis during FBT was measured by increase of ¹¹¹Indium-tropolone in platelet-poor plasma. Plasma ¹¹¹Indium increased from 2.8 ± 1.5 to 5.1 ± 1.3% (p<0.003) during FBT. This shear-induced platelet lysis was inhibited by HP1-1D but not by UK-37, 248. The results above indicate that thromboxane A₂ plays a minor role and ADP plays a central role in shear activation of platelets. It should be considered that ADP is liberated not only from dense granules released from platelets but also from ruptured cytoplasms of erythrocytes and platelets.

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One hundred cerebrovascular recurrent cases among 660 patients admitted to our hospital during the past three years were found by clinical manifestations and CT scan findings. In one hundred recurrent cases, 73 cases were both initial stroke and recurrence of cerebral thrombosis, and 17 cases were both initial stroke and recurrence of cerebral hemorrhage. Other ten cases were different recurrences from initial stroke, namely 6 cases were recurrences of cerebral hemorrhage after initial stroke of cerebral thrombosis, and 4 cases were recurrences of cerebral thrombosis after initial stroke of cerebral hemorrhage.
In cerebral thrombosis, the recurrences occurred in the ipsilateral cerebral hemisphere as many as in the contralateral cerebral hemisphere. However, in cerebral hemorrhage the recurrent site was almost always the cotralateral cerebral hemisphere.
The third of the recurrences of cerebral thrombosis had only one reattack and all the recurrences of cerebral hemorrhage had only one rebleeding.
Within the first year, the recurrences were found in 37% of cerebral thrombosis, and in 49% of cerebral hemorrhage.
Seven cases of 23 cases (30%), which the recurrences were cerebral hemorrhage, died or were in vegetable within one month after the first reattack, suggesting poor prognosis.

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