The non-invasive 133-Xenon intravenous (IV) injection method for measuring regional cerebral blood flow (rCBF) has many advantages compared to the 133-Xenon inhalation method. In order to evaluate the possibility of clinical application of this IV injection method, normal regional and mean hemispheric values of rCBF were determined in this study.
The rCBF data were obtained on 27 normal Japanese right-handed volunteers with an age range of 18 to 81 years (mean age 43).
The subjects were requested to relax, keeping the eyes closed but without falling asleep. End-tidal 133-Xenon curves were used for correction of recirculation. The blood flow of the fast compartment (gray matter) of the brain was calculated, as well as the initial slope index (ISI) and the relative weight and the fractional flow of the fast compartment. CBF values thus obtained were compared to those obtained by the 133-Xenon inhalation method previously reported by us.
The mean gray matter flow values for the right hemisphere was 90.3±17.5 ml/100 g brain/min (mean±S.D.) and that for the left was 90.0±17.8.
The mean value of ISI for the right hemisphere was 75.1±17.0 and that for the left was 74.6±17.0. There was no significant difference of blood flow between the hemispheres. These values were higher than those obtained by the inhalation method. The reason for this difference is discussed.
The rCBF values were the highest frontally and the lowest parietooccipitally in both hemispheres, which is in good agreement with the results obtained by the other non-invasive methods and the intracarotid injection method.
It is concluded that the 133-Xenon intravenous injection method, which has many advantages compared with the inhalation method, is applicable for rCBF measurements in man.

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It is still a matter of dispute whether the cervical sympathetic nervous system plays an important role in cerebral blood flow (CBF) autoregulation. The purpose of the present study is to investigate quantitatively whether the cervival sympathetic pre- or postganglionic nerve participates more effectively in CBF autoregulation.
Thirty-nine monkeys were anesthetized with α-chloralose and urethane, kept at 37.5±0.5°C of body temperature and 34.6±3.7 mmHg of PaCO₂. Cervical sympathetic nerves and internal carotid arteries were isolated using microsurgical technique. Internal carotid blood flow (ICBF) was measured by an electromagnetic flowmeter and changes in mean arterial blood pressure (ΔMABP) were induced by exsanguination and reinfusion of the blood. CBF autoregulation was analyzed by dysautoregulation index (D.I.=ΔICBF/ΔMABP, ml/min/mmHg).
Results : 1) Following the preganglionectomy, the D.I. showed a tendency to increase from 0.10±0.16 ml/min/mmHg to 0.20±0.15 during induced mild hypotension (ΔMABP<20 mmHg). 2) After the postganglionectomy, the D.I. increased significantly from 0.05±0.04 ml/min/mmHg to 0.12±0.10 (p<0.02) during induced moderate hypotension (ΔMABP≥20 mmHg). 3) No significant changes in D.I. were observed in cases of mild or moderate alteration in blood pressure during reinfusion of the blood.
The above data suggest that the cervical sympathetic postganglionic nerve regulates more specificially the tone of the cerebrovascular vessels during induced hypotension.

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Central nervous disorders in the vibration syndrome (VS) due to cerebrovascular anomaly are discussed.
Incidence and mortality of cerebrovascular disorders and prevalence of transient ischemic attacks, examined between patients with VS and age-matched controls at rural communities in Tottori Prefecture during a period between 1976 and 1981, showed no significant differences.
Cases of VS with Raynaud's phenomenon were attacked by vertebrobasilar insufficiency mainly characterized by sudden onset lasting 5 min or less and often by recurrent dizziness and unbalanced gait. Incidence of the insufficiency was significantly higher than controls aged 40 to 49 (p<0.01). Furthermore, severe cases of VS presented significantly higher incidence of abnormal rotation in the closed-eye 50 stepping test. These facts suggest that there might be subclinical balance disturbance due to insufficiency of cerebral circulation in the vertebrobasilar area.

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A case of a right middle cerebral arterial occlusion, with moyamoya phenomenon, showing a subependymal hemorrhage was reported.
A healthy 17-year-old man complained a pulsative frontal headache, nausea, and vomiting when playing baseball. Three days later he had stiff neck and was admitted to our hospital on Sept. 18, 1982.
On admission, he was drowsy and showed no involuntary movements, paresis and sensory disturbances. Sluggish light reflex was present, and a lumbar puncture yielded a xanthochromic spinal fluid under the initial pressure of 200mmH₂O. ACT scan obtained on the third day of admission showed a subependymal hemorrhage.
The right internal carotid angiography revealed the occlusion of right middle cerebral artery at the M₁ portion, with moyamoya phenomenon and the transdural anastomosis was present.
The left internal carotid angiography revealed no moyamoya phenomenon, sclerosis, or occlusion. The right vertebral angiography revealed no arterial stenosis or occlusion, but leptomeningeal anastomosis of the posterior pericallosal artery was present.
On the 18th day of admission, there was perfect recovery of consciousness, light reflex, and neck stiffness without complication. There was no change in findings observed in angiography, one year after discharge.
This case demonstrated only an unilateral, middle cerebral arterial occlusion in the M₁ portion associated with moyamoya phenomenon on angiograpy. This findings does not fully satisfy the criteria of moyamoya disease, so this case may be one of moyamoya-like disease. However, the angiographic findings in this case has the same characteristic finding of idiopathic middle cerebral arterial occlusion, reported recently.
A long term follow up is necessary in order to make an exact diagnosis in this case. It may be emphasized that, one must be careful to make the diagnosis of moyamoya disease, especially when moyamoya phenomenon was associated with unilateral middle cerebral arterial occlusion.

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Two stroke patients (case 1 : 50 yrs. female and case 2 : 57 yrs. male) showed weakness and pyramidal signs on one side combined with a cerebellar-like ataxia on the same side. Computed tomography (CT) revealed a small hemorrhage in most posterior of basis in the contralateral pons. Recovery was satisfactory within six weeks. This is an uncommon presentation of pontine hemorrhage and adds to the known causes of ataxic hemiparesis (AH).
Another patient (case 3 : 59 yrs. female) experienced the sudden onset of a hemiparesis. The leg was more affected than the arm. No sensory deficit was found. CT showed a small hemorrhage in most anterior of basis pontis. Recovery was satisfactory within ten weeks. This is also an uncommon presentation of pontine hemorrhage and adds to the known causes of pure motor hemiplegia (PMH).
These patients were studied the physiological examinations such as EEG, blink reflex (BR), auditory evoked response (ABR) and somatosensory evoked potential (SEP) in the acute and the recovery stage. EEGs were normal in all three cases. BRs in all three cases were abnormal in the acute stage and were normal in the recovery stage. ABR in case 2 was abnormal in the acute stage and returned to normal in the recovery stage. SEPs in case 1 and 2 were ab-normal but in case 3 was normal in the acute stage. The abnormal SEPs returned to normal in the recovery stage.
These data implies that a small hemorrhage does not have directory an effect on the BR, ABR and SEP. The abnormalities of physiological examinations are transient under the pressure and/or edema of the hemorrhage.

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We studied temporal change of somatosensory potentials in 24 patients with circumscribed thalamic hemorrhage. Initial clinical signs of these patients included mild ocular disturbances (anisocoria and/or conjugated deviation), contralateral hemiplegia and contralateral all modality sensory loss. With recovery these severe symptoms were replaced by dysesthesia, paresthesia and ataxia.
High density area gradually blurred and finally disappeared leaving no detectable lesion by CT scan.
On the contrary, SEP components which had initially disappeared reappeared gradually as clinical symptoms improved. P15 component was present in the majority of cases even at the onset of severe hemorrhage (79%). But, N20 and P23 were present only in exceptional cases with small lesions (21% and 16% respectively). P15-N20-P23 components recovered in this order. Patterns of recovery among these components were different. P15 component was seen both at the onset and at the follow up time (89%), but N20/P23 complex was not seen at the onset and seen at the follow up time (72% and 67% respectively).
Thus, SEP can serve as an effective method for the evaluation of the clinical course even after the lesion becomes silent radiologically.
Comparison of intact SEP and recovered SEP revealed selective prolongation of the interpeak latency between N20 and P23 in recovered SEP (p<0.01). Further, comparison of onset-SEP and follow up-SEP revealed (1) persistence of P15, (2) recovery of N20 with normal latency and (3) recovery of P23 with markedly prolonged latency. This N20/P23 dissociation in the later stage of thalamic hemorrhage has not been reported.
Exact origin of each component of SEP following median nerve stimulation remains controversial. Our results support the theory that P15 originates below the thalamus, N20 originates in the thalamus and P23 originates in the thalamocortical fibers or in the primary sensory cortex.

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A 69-year-old right-handed female was admitted to the hospital on Nov. 27, 1982, because of the disturbance of standing and gait. She had suffered from right hemiparesis in 1980, and the small infarction in the thalamic region had been pointed out by CT. But she had almost recoverd. On November 24, 1982, she suddenly fell and then she could not walk. On admission, her consciousness was alert. Her blood pressure was 160/110, pulse rate was 90/min with irregular rhythm (atrial fibrillation).
Neurological examinations revealed mild left hemiparesis and clumsiness of the right hand but no apparent cerebellar ataxia. She could not keep standing position and fell to back straightly. She could not step forward even by supporting her hands. But her voluntary movements of legs on the bed were almost skillful!. She could write letters by the right hand but apraxic agraphia was observed in her left hand writing. No sensory disturbances inclusing position sense were noted.
CT scan revealed the lesion in the anterior half of the right corpus callosum and involved a small part of the cinglate gyrus. On the 3rd hospital day, she could sit and stand. On the 4th hospital day, she was able to walk by assistance. The 14th days after the admission, she could walk by herself, but small steppage gait was observed.
This case shows that the corpus callosum may play a some kind of role in walking.

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The effect of sympathetic stimulation on resting cerebral blood flow (CBF) is still somewhat controversial, although the adrenergic innervation of both pial and intraparenchymal arteries was confirmed histochemically. Harper assumed that the neurogenic constriction of extraparenchymal vessels might be countervailed by the metabolic dilation of intraparenchymal vessels.
To test his hypothesis, the responses of both pial and intraparenchymal vessels to the sympathetic stimulation were investigated in 9 cats by means of a new method. This method consists of the videocamera system already established and the photoelectric system to estimate local cerebral blood volume (CBV). Two cranial windows were placed in the unilateral parietal skull of the cats at the distance of 3 mm. The brain surface under one cranial window was lighted by an optical fiber derived from a halogen lamp. The same illumination was utilized for simultaneous measurements of both pial vessel diameters and CBV. A silicon photodiode was attached to another window to measure the intensity of scattering light through the brain tissue, which mainly reflected changes in blood volume of the intraparenchymal vessels (arteriolescapillariesvenules). This method permits atraumatic simultaneous analysis of both superficial and deep cerebral circulation. The ipsilateral superior cervical ganglion was stimulated electrically (3-8V, 300μsec, 100Hz) for 5 minutes.
Initially, both pial and intraparenchymal vessels constricted and reached their maximum constriction at 79±14 seconds in intraparenchymal vessels, at 130±30 seconds in pial veins and at 179±37 seconds in pial arteries. The maximum constriction of intraparenchymal vessels occured earlier than that of pial arteries (p<0.05). The maximum constriction rates of pial arteries and veins were 10.7±3.0% and 6.3±2.3% respectively without significant statistical difference. The pial arteries remained constricted throughout the stimulation, however, the intraparenchymal vessels started to dilate at 79±14 seconds. The dilation continued to exceed the control level at 238±39 seconds even during the stimulation.
In conclusion, the sympathetic vasoconstriction occured in both pial and intraparenchymal vessels. The compensatory metabolic dilation of intraparenchymal vessels was delayed 4 minutes after the initiation of the stimulation.

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The clinical course and findings on cerebral angiograms and computed tomography (CT) were investigated in 11 cases which died immediately after cerebral infarctions in territories of the internal carotid artery system. When pale infarctions presented high density areas on CT during their clinical course, they were classified as hemorrhagic infarctions. Accordingly, there were 8 cases of pale infarctions and 3 cases of hemorrhagic infarctions.
At first, the clinical course, angiographical findings and CT findings were examined in the 8 cases of pale infarctions. Severe conscious disturbance and hemiplegia emerged immediately after the onset. Angiographically, occlusions in the extra- and intracranial internal carotid artery were found. On the CT, low density areas were found in territories supplied by 2 or more main arteries including a middle cerebral artery. Moreover a midline shift of over 10 mm was seen in the early stage. The duration from onset to death was 4.9 days on the average.
On the other hand, in the 3 cases of hemorrhagic infarctions, the neurological conditions on admission were not so severe as those of pale infarctions, but over a period of time the conditions suddenly deteriorated. The low density areas didn't usually range over a wide area; In fact, two cases had lesions only in the territory of the middle cerebral artery. The duration from onset to death was 9.6 days on the averrage.

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Induced hypertension was done for 9 patients with vasospasm after ruptured aneurysm. Dopamine for 6 patients and Angiotension II for 3 patients were used for hypertension when the clinical sign of the vasospasm appeared. Cerebral blood flow (by Argon inhalation method) and cardiac function (by Swan-Ganz catheter and thermodilution method) were examined before and after the drug infusion. In one case Xe-CT CBF study was performed and this study showed marked increase of CBF at the part of vasospasm in relation to the increase of blood pressure.
At the hypertensive state, the increase of total cerebral blood flow and improvement of clinical signs were found. As the cause of increased cerebral blood flow at the hypertensive state, local disruption of autoregulation shown in Xe-CT CBF study was suggested, although direct actions of these drugs to cerebral vessels could not be denied.
At the point of cardiac function Dopamine increased cardiac output in relation to its dose. An increase of the blood pressure was not found at the dose of 8μg/kg/min but found at 20μg/kg/min. Angiotensin II decreased cardiac output and increased total vascular resistance and blood pressure in relation to its dose. Angiotensin II should be used carefully especially for patients with heart disease because of its vasoconstrictive action.

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The authors applied oxygenation at high pressure (OHP) to 49 patients who developed mental signs lasting more than approximately two weeks following direct operation of cerebral aneurysms. Aneurysms of 30 cases were located at the anterior communicating and the anterior cerebral arteries (AC group), while the aneurysms of 19 cases were at the other arteries (non-AC group). Twenty six cases were operated on within two weeks after the attack of subarachnoid hemorrhage and the other 23 cases underwent direct operation later than two weeks after the attack. OHP was performed one hour per a day under conditions of exposure to oxygen pressure of two atmospheres.
The results obtained are as follows.
1) 47% in AC group and 63% in non-AC group took excellent or moderate recovery by OHP.
2) Loss of spontaneity and disorientation were signs which were improved satisfactorily by OHP, while akinetic mutism and Korsakoff's syndrome were hard-to-cure signs even by OHP.
3) Excellent or moderate recovery was noted more frequently in patients who underwent OHP within one month following clipping of aneurysms.
4) On the follow-up studies, no or slight residue of mental signs were 78% in the patients who were treated by OHP and 60% in the patients without OHP. In addition, marked residue or dead patients was 5% in the patients treated by OHP, and 24% in the patients without OHP. The patients with moderate and marked neurological deficits took better outcome by OHP than without OHP.

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