The effects of various antihypertensive agents in relation to cerebral circulation and cerebral vessels were widely reviewed throughout the literature. The changes of cerebral blood flow (CBF), cerebral metabolism and CBF autoregulaiton were also discussed under the acute or chronic administration of antihypertensive agents in human being and experimental animals as well.
Antihypertensive agents include diuretics, methyldopa, clonidine, reserpine, alpha-blockers, beta-blockers, vasodilators, calcium antagonists and angiotensin converting enzyme inhibitors, which habe been widely used for hypertensives with or without stroke.
Acute effects : A bolus or continuous injection, or a single oral administration of vasodilators, calcium antagonists and reserpine increases CBF regardless of the blood pressure alteration. In contrast, both clonidine and beta-blockers decrease CBF by direct vasoconstriction or by decreasing cerebral metabolism. CBF remains unchanged or slightly increases by administration of alpha-blockers and angiotensin converting enxyme (ACE) inhibitors. No documents have been reported about the acute effect of diuretics and methyldopa. The lower limit of CBF autoregulation is shifted to lower levels by the administration of alpha-blockers, vasodilators and ACE inhibitors. Beta-blockers have no effects on autoregulatory range, while calcium antagonists affect little or or slightly raise the lower limit to a upper level.
Chronic effects : Long-term administration of antihypertensive agents has different influence on CBF compared with acute administration. In hypertensive patients without stroke, most of agents do not change CBF, but some agents rather increase. In hypertensive patients with stroke CBF is increased by methyldopa and ACE inhibitors, but unchanged by alpha-blockers.
Each antihypertensive agent has different inherent effects on cerebral circulaiton. Therefore we must know the pharmacological action of the drugs on brain itself or cerebral circulation, when we treat the hypertensive patients, especially in the cases who have a history of stroke.

View full abstract

Using a model of focal, reversible cerebral ischemia, the effects of blood-reflow on brain edema and mortality for the 1st one week of the experiment were investigated. Flow was ceased in the middle cerebral artery by a simple occluding device which was withdrawn to get reflow after various duration of ischemia. Water content of the brain did not increase when reflow was given after one hour-ischemia in the territory of middle cerebral artery, but increased after two or longer ischemia. And mortality went on increasing in parallel with duration, that is, from 0% at one hour of ischemia to 22% at two, 70% at three, 75% at four and 100% at six within one week experiment. Especially in the case of six hour-ischemia, all animals died within four hours after recirculation due to acute post-ischemic brain edema. Small hemorrhagic foci were found histologically in ischemic regions.

View full abstract

The contrast enhancement of cerebro-vascular diseases on CT are thought to be due to the increase of the cerebral blood volume (CBV) and/or the disruption of the blood brain barrier (BBB). However, it is difficult to differentiate these two conditions only by contrast enhanced CT. We employed dynamic CT (DCT) to analyse these lesions with respect to the patterns of time-density curve and peak height (PH) of the curve upon the theoretical basis that flattening of the latter part of the time-density curve reflected the degree of BBB disruption and PH reflected the CBV. In all cases of hypertensive intracerebral hemorrhage (11 cases), the contrast enhanced lesion around the hematoma showed marked BBB disruption according to the results of DCT. In 11 cases of cerebral infarction, patterns of BBB disruption and CBV varied at the contrast enhanced lesions according to the result of DCT. However, all contrast enhanced lesions with increased PH were associated with hemorrhagic infarction. Thus, the precise analysis of DCT provides appropriate therapeutic schedules by predicting the occurrence of hemorrhagic infarciton.

View full abstract

A case of a posterior fossa dural arteriovenous malformation (AVM) associated with an intracerebellar hemorrhage is reported.
The patient, 62 year-old-man fell into a comatous state after suddenly occurred headache on August 26, 1985. As his past history, he experienced an intracerebellar hemorrhage in 1981, and he recovered completely with the conservative treatment at another hospital. He had never had symptoms of dural arteriovenous malformation and hypertension.
On admission he was comatous (Glasgow coma scale=3), and neurological examination revealed absent ciliospinal and oculocephalic reflexes and ataxic breathing.
An emergent CT scan demonstrated a large intracerebellar hematoma, and a saccular high density area was enhanced in the right cerebello-pontine angle (Fig. 2 & 3). Right carotid angiography (DSA) showed a transverse sigmoid dural AVM, which was fed by markedly dilated and tortuous tentorial artery with a large vascular sac (Fig. 4 & 5). Furthermore, the veins of cerebellum appeared in the arterial phase. Continuous ventricular drainage was performed, but no improvement was obtained in his brain stem response. He is now in the vegetative state.
The main symptoms of posterior fossa dural AVM are intracranial bruit, headache, choked disk and so on. And intracerebellar hemorrhage is very rare, for only two cases have been reported (Table 1).
The causes of intracerebellar hemorrhage of dural AVM are not well known. We discuss the causes in this paper, and we suspect that intracerebellar veins may be rupture by increased intracerebellar venous pressure under the presence of dural AVM in this case.
We recommend the examinations with enhanced CT and angiography in a case of non-hypertensive intracerebellar hemorrhage.

View full abstract

The phenomenon of decreased blood flow and metabolism in contralateral cerebellum following supratentorial lesions has been termed crossed cerebellar diaschisis (CCD) by Baron et al. Many factors including the location and size of the lesion, the presence of motor paralysis, and the time after onset have been considered to be important in the development of CCD. In order to elucidate what factors contribute to the development of CCD, 43 patients suffering from a unilateral supratentorial disorder were studied using a single photon emission computerized tomography with ¹²³I-iodoamphetamine. The phenomenon of CCD was here defined as significant contralateral cerebellar hypoperfusion.
CCD was observed in not only cerebral infarction (58.1% of patients) and cerebral hemorrhage (66.7%), but also brain tumor (50.0%) and chronic subdural hematoma (25.0%). Therefore, the localized and acute brain lesion was not necessarily essential for the development of CCD. Analysis by a quantification theory (Type 2) in 31 patients with cerebral infarction showed that the location and size of the lesion appeared to greatly contribute to CCD rather than the presence of motor paralysis and the time after onset. CCD was present more frequent and prominent in the patients with either extensive multilobar infarction or relatively larger deep infarction. Serial studies showed transient phenomena in smaller deep infarctions, but this phenomena tended to persist for a long time in larger infarctions suggesting transneuronal degeneration of the corticopontocerebellar pathway.
It is likely that the pathophysiological mechanism of this phenomenon consists of reversible diaschisis and irreversible degeneration depending on the location and size of the lesion.

View full abstract

The hemodynamics supplied by the extracranial-intracranial bypass was evaluated by the use of the transcranial doppler flowmetry (TCD). 23 extracranial-intracranial bypass surgeries (EC-IC bypass) were performed in 19 patients. The deepest site reached by the blood flow via the bypass in the direction opposite to the normal blood flow of the middle cerebral artery (MCA) was defined watershed. The watershed was identified in MCA at a depth of 4050 mm in 62% of the patients. The velocity of the blood through the bypass was 2140 cm/sec in 68% of the patients, and that of MCA on the deeper side of the watershed was 2160 cm/sec in 77%. No correlation was observed among the depth of the wateshed, the blood velocity via the bypass, the blood velocity of MCA on the deeper side of the watershed and the interval between EC-IC bypass and TCD examination. It is hoped that clinical significance of watershed by TCD will be evaluated in detail.

View full abstract

Eleven cases with Chilaiditi's syndrome were found in 2588 stroke patients who were hospitalized in Reimeikyo Rehabilitation Hospital for 13 years from (Jan.) 1975 to (Mar.) 1987. The average age of 7 males and 4 females was 66.4 years old. The incidence of Chilaiditi's syndrome was 0.43%. That is higher percentage than that in mass chest roentgen examinations. All cases which were recognized by regular chest roentgen examination showed no specific symptom. The organ found between the liver and the diaphragm was the colon in all cases. Hemiplegias were found in all cases and high grade damage of brain funciton were guessed from the CT scan and EEG. The 24.2 average months passed from the onset of stroke to the discovery of the syndrome.

View full abstract

A case of an aneurysm arising at the anterior cerebral artery and associated with the accessory middle cerebral artery was reported.
A 54-year-old female was admitted to our hospital with complaints of headache, nausea, vomiting and consciousness disturbance. CT scan showed a high-density area in the basal cistern and Sylvian fissure.
Left carotid angiogram revealed saccular aneurysm at the horizontal portion of the left anterior cerebral artery (A₁) and accessory middle cerebral artery originating from the A₁-A₂ junction.
An operation was performed 20 days after admission. The neck of the aneurysm was clipped. Postoperative course was uneventful.
The relationship between the genesis of aneurysms and the accessory middle cerebral artery was discussed. From the location of these aneurysms associated with the accessory middle cerebral artery, we suggested that acquired etiological factors were involved.

View full abstract

During the past 4 years, we experienced 222 cases of the hypertensive putaminal hemorrhage. A comparative clinical assessment of the surgical group of 146 cases and the non-surgical group of 76 cases has been performed. The stastistical analysis of our cases led to the following conclusions.
1) According to neurological grading of putaminal hemorrhage, the cases of grade I had no necessity of surgery and the outcome in grade V was so poor that there was no indication for surgery. On the other hand, in grade IV, surgical treatment showed a better result of mortality than non-surgical treatment.
2) The surgical procedure had better results in mortality even if in the fulminant cases in which there were an eye signs such as negative oculocephalic reflex at admission.
3) From results of CT findings, the influencing factors of the poor outcome were suggested that the hematoma size was larger than 4 cm, the shift of III ventricle more than 6 mm, and the upper and lower extension of putaminal hematoma more than 4 cm. Especially, the cases associated with ventricle rupture were resulted in the poor outcome.
4) There was no correlation between the mortality and neurological dominancy of cerebral hemisphere, but from the aspect of morbidity, the cases of non-dominant side hemorrhage had better results than those of dominant side hemorrhage in both surgical and non-surgical groups.
5) Generally, there was no advantage of early operation. But the per-acute operation should be carried out in the cases in which consciousness level was taking downhill course within a few hours after onset.
6) No significant differences of the functional recovery of extremities between two groups could be found, because the functional recovery of extremities was satisfactory in the cases with mild hemiparesis. On the other hand, the functional recovery in the cases with severe hemiplegia was a little more favoured in surgical group, comparing to non-surgical group.

View full abstract

A poorly controlled diabetic woman of 36-year-old who had right upper limb monoparesis 14 days ago, developed right hemiparesis and motor aphasia soon after fluorescein retinal angiography (FAG).
Brain CT revealed small low density area in the left frontal lobe, while positron emission CT demonstrated larger area of the reduced cerebral blood flow and decreasd cerebral oxygen utilization.
Right hemiparesis stepwisely deteriorated with motor aphasia and became complete 12 days after FAG. Thereafter, hemiparesis began to improve and on 67th hospital day she was discharged on walk.
Although cerebral thrombosis is uncommon complication of FAG, the mechanism of FAG induced cerebral ischemia in this case was discussed.

View full abstract

The purpose of the present study was to evaluate the role of vagus in the action potentials of pial arteries reported in our previous studies.
Twelve adult cats were anesthetized with a-chloralose and urethane followed by an artificial respiration. Rectal temperature was maintained between 37 and 38°C. The action potentials from the pial arteries were recorded by using fine bipolar platinum electrodes, high sensitivity preamplifiers, band-pass filters and a data analyzing computer.
In seven cats, mass discharges of the action potentials were accumulated during the stimulation of the rostral end of the vagus, which was unilaterally severed at the proximal portion of the ganglion nodosum. Five out of the seven cats showed a marked decrease of the action potentials after the intravenous administration of tetrodotoxin (20-30 μg/kg), which is a potent inhibitor of the axonal propagation of nervous action potentials.
The effect of vagotomy on the responses of the action potentials to changes in cerebral perfusion pressure was investigated in the other 5 cats. The mass discharges of the action potentials were analyzed by the use of a program of pulse density variation. Induced hypotension by hemorrhage resulted in a significant increase (174 ± 79%) of the frequencies of the discharges before section of the vagus, but the increase became less remarkable (62 ± 59%) after the vagotomy. Induced hypertension by infusion of the blood significantly decreased the discharges (-57 ± 31%) before the vagotomy, but the change was minimum (-2 ± 36%) after the vagotomy.
The above data suggest that the vagus plays a significant role in the action potentials derived from the pial arterial walls.

View full abstract

The purpose of this study was to evaluate the change of S-adeosyl-L-methionine (SAM), S-adenosyl-L-homocystein (SAH), adenosine in gerbil brain during progression of cerebral ischemia using high performance liquid chromatography (HPLC). Cerebral ischemia was induced in gerbils by the bilateral ligation of the carotid arteries for 10 min. The effect of cerebral energy metabolism was also examined after intraperitoneally administrated with SAM at dose of 250 mg/kg. SAM, SAH and adenosine were assayed by cation-exchange HPLC system (SP-2SW column), and adenine nucleotides (ATP, ADP and AMP) were assayed by anion-exchange HPLC system (DEAE-2SW column).
1) The endogenous SAM level in gerbil brain was 85 ± 4.2 nmol per g of dry weight (mean ± SEM).
2) 30 min after intraperitoneal administration of SAM, SAM level in gerbil brain significantly increased up to 107 ± 8.1 nmol per g of dry weight (p<0.05), without concomitant increase of SAH level.
3) Cerebral ischemia caused decrease of SAM level in gebil brain (p<0.05). That of SAM treated group decreased more rapid than the untreated group (p<0.05).
4) The decrease of cerebral ADP level and energy charge were supressed in the SAM treated group in comparison with the untreated group, while no difference in the decrease of cerebral ATP level.
These findings demonstrate that extrinsic SAM increases the cerebral SAM level in the gerbil brain and can effect the ADP and energy charge in the ischemic gerbil brain during the acute phase.

View full abstract

We developed a method for long-term culture of microvascular endothelial cells derived from mongolial gerbil brain, and investigated their biological properties in vitro. Microvessels were isolated from mongolial gerbil brain by combination of the enzymatic treatment, filtration and centrifugation, and seeded onto a gelatin coated dish. A morphologically homogeneous cell plaque was removed two to three weeks after the seeding, and the obtained cells were subcultured. The cultured cells grew as monolayers of flat polygonal cells, and sometimes formed cellular cords. The cultured cells were carried more than 20 passages without morphological change, and have retained an endothelial specific marker, Factor VIII-related antigen even in late passages. Histochemical activity of alkaline phosphatase was present in almost all cells as an intense diffuse and granular staining in primary culture. The activity slowly disappeared as the cells proliferate, and almost completely disappeared after fifth passage. Activity of γ-glutamyl transpeptidase was demonstrated only in the cells at the center of the cell plaque sorrounded by non-reactive cells in primary culture. There was no activity in the cells after the second passage. The membrane specific enzyme for cerebral microvessel seemed to disappear when the cells migrate or proliferate from the microvessel isolates.

View full abstract

This paper describes a patient (57-year old female) in which subarachnoid hemorrhage occurred due to the rupture of an aneurysm at the juncion of the right internal carotid artery and the posterior communicating artery 8 weeks after the onset of herpes zoster in the first branch region of the right trigeminal nerve. Only two cases of post-herpetic cerebral aneurysm have been reported in the literature. However, since the formation and rupture of an aneurysm is likely to be attributable to angiitis caused by a herpes zoster virus infection, careful clinical observation is required in patients with herpes zoster.

View full abstract