In general, infarctions of the basal ganglia are present in about 40% of all cerebral infarctions. Most basal ganglia infarctions are lacunar, typically caused by thrombosis of the small penetrating arteries, but some are due to embolism or thrombosis of the main trunks of the internal carotid and/or middle cerebral arteries. Differential diagnosis based on the pathogenesis of infarction is important clinically to assess the patient's prognosis and select the correct surgical treatment.
In order to clarify the characteristics of each type of infarction, 5 of 105 patients with internal carotid artery occlusion and 52 of 246 patients with middle cerebral artery occlusion, who had deep cerebral infarctions in the basal ganglia and internal capsule, were examined based on CT, clinical manifestations, cerebral blood flow (CBF) and computed mapping of the EEG (CME).
The results were as follows :
1) Based on CT, the 57 patients were divided into three groups according to the size of the low density area (LDA) on a slice of 5 cm ±1 cm over the orbitomeatal line (OM line). The group with less than 1.5 cm as the longest diameter of LDA consisted of 17 patients, while 13 patients with LDA between 1.6 and 2.5 cm and 27 patients with LDA of more than 2.6 cm were present. Round or oval shaped LDA were mainly located in lenticular nucleus or internal capsule, partially in the head of the caudate nucleus. 88% of them were associated with LDA on the centrum semiovale, which was considered to be a border-zone infarction.
2) As for clinical manifestations, severe motor disturbances were present in 60% of upper extremity (U/E) and 32% of lower extremity (L/E). Comparable motor disturbances in both the U/E and L/E were seen in 68%. In spite of no apparent cortical change on CT, patients with aphasia were present. Hemianopsia was seen in 16 patients and minimal disturbance of consciousness in 18. Pure motor hemiplegia was demonstrated in about 1/3 of all cases.
3) Regional CBF, detected in 19 patients by ¹³³Xenon intra-arterial injection, revealed diffuse ischemia in 12 patients and focal ischemia in 3.
4) Examining 35 times with CME in 18 patients, abnormal findings of high-voltage foci of slow components and/or an asymmetrical distribution of alpha activity were present 29 times in all patients.
It is concluded that cerebral infarction of the basal ganglia due to main trunk obstruction has been more or less associated with diminution of blood flow in the cortical area.

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A resumption of blood flow after transient cerebral ischemia often causes a severe cerebral edema leading to a further deterioration of neuronal function. Even the flow recovery as early as 3-6 hours after the onset of focal ischemia seems to bring about a remarkable post-ischemic cerebral edema in adults. Little is, however, known whether the flow recovery in juvenile cerebral ischemia also causes a similar post-ischemic cerebral edema. The present study was undertaken to clarify the susceptibility of juvenile brain to the post-ischemic cerebral edema.
The experiments were performed in 123 adult gerbils with more than 24 weeks of age and 141 juvenile gerbils with 5-6 weeks of age. In both groups, the right common carotid artery was clipped, and the following measurements were undertaken in the animals showing ischemic symptoms. 1) The cerebral water content was measured after 6 hour-ischemia, 9-hour-ischemia and 6-hour-ischemia followed by 3-hour-reperfusion. 2) The regional cerebral blood flow (rCBF) was repeatedly measured in the reperfusion groups. 3) A permeability of blood brain barrier (BBB) was examined in the reperfusion groups using the Evans blue (EB).
Both in the adults and the juveniles, severe cerebral edema was developed after 6-hour-ischemia as well as 9-hourischemia. The degree of edema in two groups was the same. In the adults, the reperfusion after 6-hour-ischemia caused a marked deterioration of edema. On the other hand, in the juveniles, the reperfusion tended to improve the edema. The degree of rCBF reduction during the carotid occlusion did not differ significantly between two groups. However, a flow recovery after the reperfusion was greater in the juveniles than in the adults. After the reperfusion, a remarkable BBB disruption was seen in the adults, whilst no BBB disruption was observed in the juveniles.
The present study suggests that the juvenile brain may be less susceptible to the development of post-ischemic cerebral edema compared to the adult brain. It is generally considered that a sudden flow resumption after transient ischemia may increase the hydrostatic pressure in ischemic area and may thereby produce post-ischemic cerebral edema. In our experiments, the flow recovery in the juveniles was greater than that in the adults, nevertheless, no deterioration of edema occurred in the former. It should be noted that after the reperfusion, BBB was maintained intact in the juveniles but was disrupted in the adults. Lower susceptibility of juvenile brain to the post-ischemic cerebral edema may be attributable to the higher tolerance of BBB to ischemic insults.

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Regional cerebral blood flow (rCBF) was measured during chronic stage (later than 1 month after onset) in 43 cases with embolic and in 43 cases with thrombotic cerebral artery occlusion, using ¹³³Xe inhalation technique. All cases had unilateral supratentorial ischemic events. Diagnostic criteria of embolic and thrombotic cerebral artery occlusion have been reported elsewhere (Jpn Circ 48 : 50, 1984). Presumed cerebral thrombosis in regions of perforating arteries was excluded from the study, because of the difference of size of occluded artery. Functional outcome of embolic group, determined from the stand-point of walking ability, was not much different from that of thrombotic group, i.e., 31 out of 43 embolic cases and 32 out of 43 thrombotic cases were able to walk at the time of measurements (two months after the onset).
In embolic group, mean rCBF of the affected hemisphere was 39.4 ± 9.5 (ISI) and that of the unaffected hemisphere was 43.2 ± 9.9. In thrombotic group, mean rCBF of the affected and the unaffected hemisphere were 39.1 ± 9.7 and 43.1 ± 9.3, respectively. In either group, mean rCBF of the affected side was significantly lower than that of the unaffected side (p<0.001). There were no significant differences in mean rCBF between embolic and thrombotic group not only in the unaffected but affected sides. However, the mean Infarct-Index (ratio of the largest hypodense area to the hemispheric square measure in CT films) was larger in embolic group than in thrombotic group (p<0.05).
In either group, mean rCBF in ambulatory cases was significantly higher than that in non-ambulatory cases. When mean rCBF of ambulatory cases in embolic and thrombotic groups were compared, there was no significant difference in flow values between embolic and thrombotic group.
When mean rCBF in each case was plotted against age (y.o.), a significant negative correlation was obtained in either hemisphere in both groups. Correlation coefficients were -0.58 (p<0.001) in the unaffected side and -0.53 (p<0.001) in the affected side of embolic group, and -0.47 (p<0.01) in unaffected side and -0.36 (p<0.02) in the affected side of thrombotic group.
A significant negative correlation was obtained between mean rCBF and Infarct-Indices in either hemisphere of embolic group (affected side : p<0.001, unaffected side : p<0.01), but it was seen only in the affected hemisphere in thrombotic group (p<0.05).
All cases were divided into three subtypes by the distribution of rCBF over each hemisphere, i.e. diffuse ischemic, focal ischemic and focal hyperemic pattern. Forty-one percent of embolic cases were classified as focal ischemic pattern, and thirty-two percent as diffuse ischemic pattern. In contrast, diffuse ischemic pattern was more frequently observed than focal ischemic pattern in thrombotic group (49% and 37%, respectively).
It is concluded that functional outcome is well reflected with mean rCBF in both ambolic and thrombotic group, and that mean rCBF in embolic group appears to be a good indicator of the size of ischemic lesion. In thrombotic group, however, correlation of mCBF with the size of ischemic lesion is not so good as in embolic group. In the latter, there might be areas of hypoperfusion that are not detected by CT as a hypodense area.

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Prognostic factors for survival and neurological recovery are assessed in 35 patients with hypertensive cerebral subcortical hemorrhage. The average age of patients is 63 years, ranging from 46 to 89. Nineteen are male and 16 female. There are 3 deaths; 2 treated conservatively (7.7%), and 1 treated surgically (9%). The overall mortality is 8.6%, which is markedly lower than the mortality reported in other series. Twenty-two of 35 patients are treated conservatively and 13 are treated surgically. Twenty-five of 35 patients had a history of hypertension (71%). Hemorrhage is located in the temporal lobe in 15 (43%), the frontal lobe in 8 (23%), the occipital lobe in 7 (20%), and the parietal lobe in 5 (14%). Twenty hemorrhages are in the right hemisphere and 15 in the left. In the present study we evaluated various factors contributory to the outcome of cerebral subcortical hemorrhage, such as the size and location of the hematoma, presence of the signs of transtentorial herniation on CT, neurological grading on admission, and treatment. And we assessed the correlation between the activity of daily life (ADL) and these factors. In the present study relatively good results for both survival and ADL have been obtained in conservatively treated patients with hypertensive cerebral subcortical hemorrhage, and we emphasize that surgical evacuation of hematoma is unnecessary in most of the patients and should be restricted only to a small groups in which a large hematoma causes rapid neurological deterioration with imminent danger of transtentorial herniation.

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We reviewed the surgical treatment in six patients with cerebral aneurysms associated with cerebral arteriovenous malformation (AVM) in a series of 35 consecutive cases with AVM. All patients were males with an average age of 55 years. All aneurysms were located either in the main feeding arteries of the AVM or in the arteries of the circle of Willis which were hemodynamically related to AVM, suggesting that the marked increase in blood flow of the feeding arteries plays an important role in developing aneurysms.
One of 6 patients who presented with generalized seizure underwent surgery for both the aneurysm and the AVM in one stage and recovered completely. The remaining 5 patients presented with intracranial hemorrhage resulting from ruptured aneurysms, in these patients, computerized tomography could demonstrate the site at which intracranial hemorrhage had occurred. The early operation for ruptured aneurysms was performed in 2 patients, one recovered completely, but the other, in whom 2 aneurysms in the anterior part of the circle of Willis were obliterated successfully, died 13 days after operation from the rebleeding of the remaining non-obliterated basilar aneurysm. The delayed operation for ruptured aneurysms was intended for 3 patients because their preoperative conditions were poor, but only ventricular drainage was performed in 2 patients. These three patients developed rebleeding from ruptured aneurysms within 2 weeks after admission and died ultimately, although obliteration of the aneurysm was performed in only one patient after rebleeding.
Thus, it is emphasized that surgery for ruptured aneurysms should be performed as early as possible with or without an excision of the AVM in patients with cerebral aneurysms associated with cerebral AVM, when intracranial hemorrhage is caused by rupture of the aneurysm.

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In attempt to elucidate the factors which promote cerebral and systemic embolization in idiopathic atrial fibrillation, cardiac pathophysiology was studied in patients with cerebral embolism due to atrial fibrillation (af), by using two-dimensional echocardiographic technique. Difference in clinical features of cerebral embolism between patients with persistent af and with paroxysmal af was also investigated.
Left atrial diameter (LAD) and left ventricular dimension were measured by echocardiography, and end-diastolic volume (LVEDV) and ejection fraction (EF) as a parameter of left ventricular function were calculated from the results of above measurements.
The embolic group was consisted of 20 patients with chronic persistent af and 10 patients with paroxysmal af. One hundred and six patients without having systemic embolization were used as controls, of whom 68 were with persistent and 38 were with paroxysmal af.
There were no significant differences in LAD, LVEDV and EF between embolic and control groups. Differences were found only in LAD and EF between patients with persistent af and paroxysmal af of the control group; i.e. larger LAD and lower EF in persistent af than in paroxysmal of of the controls. Besides, intracardiac thrombus was not detected by echocardiography in the embolic group.
From the results of the present study, it was suggested that left atrial enlargement and hypofunction of the left ventricle did not necessarily promote systemic embolization in patients with idiopathic af, and it appeared to be difficult to obtain a cue for embolization from the echocardiographic findings.
With regard to the preceding ischemic episodes in the embolic group, 50% of those with persistent af had experienced previous ischemic cerebral events including TIA, and 20% of the embolic patients with paroxysmal af had the history. Thus, it is necessary to provide a preventive measure against further ischemic stroke, when the patient with idiopathic af having a history of ischemic episodes is encountered.

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Lactate accumulates in the brain tissue during ischemia due to anaerobic glycolysis and produces lactic acidosis. It is suggested that lactic acidosis is an important causative factor for ischemic cell damage. In complete or severe incomplete cerebral ischemia, concentrations of cerebral tissue lactate are influenced by levels of blood glucose.
This study explores the influence of levels of blood glucose in the cerebral ischemic rats on postischemic recovery of the tissue energy metabolism and EEG, on the neuropathology, and on the accumulation of free fatty acids in brain tissue during ischemia.
Severe incomplete cerebral ischemia was induced by four-vessel occlusion and reducing the systolic arterial pressure to 100 mmHg and recirculation was started by release of bilateral carotid artery clamping and restoration of arterial blood pressue to preischemic level. The EEG was continuously recorded from gold-coated screws inserted bilaterally in the parietal bones with the tips in extradural position, against a reference inserted prefrontal bone. The brains were frozen in situ with liquid nitrogen and then chiselled out during irrigation with liquid nitrogen.
Concentrations of ATP and free fatty acids in brain tissue were determined with high performance liquid chromatography. Immediately after the end of 120 minutes of recirculation period, the brains were removed and fixed in formalin and stained by hematoxylin-eosin and luxol fast blue methods to observe ischemic changes.
Experimental animals were divided into 3 groups according to their preischemic blood glucose levels as follows. Group 1 animals were normoglycemic controls (blood glucose levels 116-196 mg/dl, mean 149 mg/dl). Group 2 animals were injected 0.5 ml of 50% glucose solution before ischemia (blood glucose levels 316-430 mg/dl, mean 373 mg/dl). Group 3 animals were injected 2 ml of 50% glucose solution before ischemia (blood glucose levels 684-954 mg/dl, mean 788 mg/dl).
After four-vessel occlusion associated with mild hypotension, the EEG became isolectric within 10-20 seconds in all experimental animals. Following 30 minutes of ischemia, a spontaneous EEG returned after 17-35 minutes of recirculation in group 1 animals and after 40-63 minutes in group 2 animals. At the end of the 120 minutes recirculation periods, the EEG activity in group 1 animals showed better recovery than in group 2. Group 3 animals did not recover any significant EEG activity or showed only a burst suppression pattern.
At 120 minutes of recirculation, concentrations of ATP in the brain were 2.195 ± 0.062 μmol/g in group 1 animals, 1.877 ± 0.016μmol/g in group 2 and 1.501 ± 0.080 μmol/g in group 3. Ischemic neuronal change, such as shrinkage and dark staining of the cytoplasm and perineuronal edema, was more remarkable in hyperglycemic animals than in normoglycemic animals.
The results demonstrated that hyperglycemia before severe incomplete cerebral ischemia had a deleterious effect on postischemic recovery of EEG activity and brain energy metabolism and markedly augmented morphologic brain damage.
Possible mechanisms by which hyperglycemia before ischemia took a deleterious effect on postischemic recovery were discussed.

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A 41 year-old hypertensive male was admitted because of progressing left hemiparesis and dysarthria. CT demonstrated hyperdense mass with partial contast enhancement, extending from the level of lower pons to that of suprasellar cistern. Reconstructed imaging of CT showed a huge mass lesion, in which a wide curvilinear hyperdensity was demonstrated by contrast enhancement. Cerebral angiography revealed markedly elongated and dilated basilar and carotid arteries. From these findings, the prepontine hyperdense mass lesion was diagnosed as megadolichobasilar anomaly with marked wall thickening. Findings of abdominal aortic angiography and abdominal CT suggested the presence of marked atherosclerosis and abdominal aortic aneurysm with mural thrombi. Six months after initial admission, neurological symptoms gradually deteriorated and CT showed dilatation of the 3rd and lateral ventricles, suggesting the development of hydrocephalus due to compression of the aqueduct by the megadolichobasilar anomaly. Magnetic resonance imaging at this time demonstrated more details of the lesion and the deformity of the brain stem, which was not detected by conventional CT.
Megadolichobasilar anomaly is known as an enlarged, dilated and tortuous basilar artery, and is reported to be often complicated with megadolichocarotid anomaly and other anomalies of cerebral vasculature. Complications of vascular anomalies other than intracranial vasculature, such as aortic aneurysm, have also been repoted. After the introduction of CT, demonstration of a long, wide, curvilinear structure with abnormal density in the prepontine region has been reported to be diagnostic for the megadolichobasilar anomaly, leaving little room for differential diagnosis. For more accurate diagnosis and recognition of this anomaly, however, cerebral angiography is still essential and important, and systemic investigation should be performed.
There are many controversies in the pathogenesis of megadolichobasilar anomaly. This patient has had hypertension for 10 years, which probably due to chronic nephritis. He had no definite findings for angitis, but had abdominal aortic aneurysm with mural thrombi. From these findings, atherosclerosis of large vessels may have played one of the roles in the pathogenesis of this anomaly in the present case.

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Noradrenergic innervation of cerebral arteries has been histochemically and electromicroscopically established.However, the direct evaluation of its function and significance has never been attempted.
Recently we succeeded in demonstrating the action potentials directly from the cerebral arterial walls of cats. Discharges of the action potentials increased during induced hypotension and decreased during induced hypertension respectively. These responses of action potentials were abolished by the intravenous administration of a ganglion blocking agent (hexamethonium bromide) and they were also inhibited in the chronic cats with superior cervical ganglionectomy.
The purpose of the present study is to evaluate the role of the noradrenergic nerve terminal in the action potentials of pial arteries.
Fifteen adult cats were anesthetized with 1.0% α-chloralose and 10% urethane followed by artificial respiration. Rectal temperature was kept at between 37 and 38°C.
The action potentials from the pial arteries were simultaneously recorded with blood pressure and respiration by means of fine bipolar platinum electrodes, high sensitive preamplifiers, band-pass filters, and a data analyzing computer. The mass discharges of the action potentials were analyzed by using the program of pulse density variation.
Biosynthesis of noradrenaline was inhibited by intracarotid injection of fusaric acid, an inhibitor of dopamine-β-hydroxylase, through a catheter placed in the lingual artery.
Following the intracarotid infusion of fusaric acid, the discharges decreased markedly in all 15 cats at the doses from 3 to 15 mg/kg.
Next, the effect of fusaric acid on the responses of the action potentials to changes in cerebral perfusion pressure was investigated. The normal responses were maintained in the cats injected with smaller doses (<4 mg/kg) of the agent. On the other hand, in the cases with higher doses (>8 mg/kg) the responses of the discharges to the alteration of blood pressure were suppressed with the passage of time.
Since fusaric acid inhibits the noradrenaline biosynthesis in the noradrenergic nerve terminal, it can be concluded that the action potentials from the surface of pial arterial walls have a close relation to the noradrenergic system, especially to the noradrenergic nerve terminal.

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Changes in morphology, regional cerebral blood flow (rCBF), local cerebral glucose utilization (LCGU) and spontaneous neuronal activity (SNA) were observed following 5-minute forebrain ischemia produced by bilateral common carotid arteries (CCA) occlusion in Mongolian gerbils. Neurons in the cortex (CorN) showed no pathological changes during the observed periods, while neurons in the hippocampus CA1 subfield (CA1N) showed delayed neuronal death until 3 days following ischemic insult. rCBF revealed homogeneous forebrain ischemia during CCA occlusion, then reactive hyperemia was noted immediately after recirculation. Post-ischemic hypoperfusion was noticed at 10 minutes after recirculation, thereafter rCBF recovered gradually. LCGU showed heterogeneous activity following ischemia. Most conspicuously, LCGU in the hippocampus showed hyperactivity during 24 hours of recirculation, then followed by CA1 subfield hypoactivity at 48 hours of recirculation. SNA disappeared within about 20 seconds after the ischemic onset, and recovered gradually from 10 minutes after recirculation in both CorN and CA1N. CorN persisted their function in the normal frequencies during post-ischemic periods, however, CA1N showed noticiable hyperactivity during 7-24 hours of recirculation, then followed by functional death at 48 hours of recirculation. With those data obtained, pathophysiology of selective vulnerable neurons were reviewed and the cause of “ischemic cell death” was discussed.

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It is very uncommon that aortitis syndrome involves intracranial arteries of muscular type. The authors experienced such a very rare case of aortitis syndrome which accompanied occlusion of the bilateral middle cerebral arteries on angiogram. A 24 year-old woman was admitted to our hospital with chief complaints of cough, palpitation, chest pain and lumbago. At admission ESR was increased and CRP was positive. Angiography showed occlusion of the left pulmomary and the left renal arteries with stenosis of the abdominal descending aorta and the right renal artery. She was diagnosed as aortitis syndrome and treated mainly with administration of adrenal corticosteroids. Two years later she experienced TIA of three times consisting of dysarthria and motor weakness, and the first TIA was on the right limbs and the other ones on the left. The internal carotid angiograms at the second admission demonstrated occlusion of main trunk of the bilateral middle cerebral arteries.
The occlusion of the arteries was most likely due to extension of arteritis from the following reasons; 1) ESR was accelerated and CRP was positive at the time of occurrence of TIAs, suggesting aggravation of inflammatory process. 2) In addition of bilateral middle cerebral arteries occlusion, irregularity or slight stenosis of the vessel was extensively noted in the intracranial arteries, suggesting progression of inflammatory process into the intracranial arteries. 3) No embolic source was verified in the bilateral common and internal carotid arteries and heart. 4) Arteriosclerotic process is less likely from her age.
It is presumed that reports of the intracranial arteries involvement will be increased with spread clinical application of digital subtraction angiography.

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