Angioarchitecture was investigated by using scanning electron microscopy of microcorrosion casts in 12 hydrocephalic rats and 5 normal control rats to observe changes in the vascular bed of the cerebral mantle in hydrocephalus.
Hydrocephalus was induced by infusion of kaolin into the cisterna magna using puncture through the occipital bone. After injecting polyester resin into the brain vessels from the aortic arch, the head was cut into serial sagittal sections close to the midline to observe the ventricle size. Among the hydrocephalic rats, two showed advanced ventricular size and 10 moderate. Brain tissue, dura mater, cranium and muscle were corroded together to prevent destruction of the microvascular casts. Reduction in the number and caliber of the capillaries in the white matter was the most remarkable change in the hydrocephalic rats. This change increased in proportion to the severity of hydrocephalus. Similar changes were observed in the basal ganglia. Changes in the cortical capillaries were mild, but cortical “palisade” patterns disappeared in some hydrocephalic cases. The crossing and pressing phenomena of the white matter vessels were characteristic, and not seen in the control rats.
Three dimentional consideration of the angioarchitecture by using microvascular casts in rat hydrocephalus is discussed, compared with the m icroan gio graphic techniques.

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Spheroids of rat glioma clone-6 cells having a central necrosis were used to determine the effect of combined treatment of x-rays and 1-(4-amino 2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU), where the optimum time intervals and doses in the combination were analyzed.
The treatment with ACNU 2 to 6 hours prior to x-ray irradiation was most effective for cells in both monolayers and in spheroids. The dose survival curves with x-ray irradiation indicated that the hypoxic cell fraction in spheroids disappeared with a prior treatment by ACNU. The enhancement ratio in spheroids was thus larger for larger x-ray doses, and was always larger than that in monolayer cells. The survival curves versus concentration of ACNU indicated that the enhancement ratio in spheroids was more than 1.2 in all concentrations with the combined x-ray irradiation, and exceeded that in monolayer cells with a surviving fraction of less than 0.4.

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The existence of the opioid-mediated pain inhibiting system has been well demonstrated. Facilitation of this system by administration of analgesic drugs, such as morphine or by electrical stimulation provides relief of excess pain but not of deafferented pain (thalamic or suprathalamic pain or phantom limb pain). This experiment clearly demonstrates that the suppressive effect of this opioidmediated system is exerted only on the nociceptive neurons in the subnucleus caudalis of the spinal trigeminal nucleus (STNcd), but not on the sustained neuronal hyperactivity provoked by the deafferentation of the peripheral trigeminal nerve.
Preliminary studies using 16 adult cats ascertained STNcd located from obex to 2 mm caudally, and an electrophysiological study elicited nociceptive neurons distributed 3-4 mm lateral to the midline. Gasserian ganglion of the left side was totally coagulated through a subtemporal extradural approach, and it was found that a definitive neuronal hyperactivity could be observed from about 10 days after the denervation.
The experiment was performed using another 13 adult cats, which were unilaterally (left side) denervated. The longest survival period of the cats was 63 days after the denervation. Forty-three neurons were identified in the STNcd of the intact (non-denervated) side, the majority of which (40 neurons) being wide dynamic range neurons. Twenty-two neurons were identified in the STNcd of the denervated side, 12 of which (55%) showing sustained high amplitude firings with no correlation to noxious stimuli (denervation hyperactivity). Such spontaneously remarkable hyperactive neurons were never detected in neurons in the intact side. Intraventricular injection of morphine or enkephalinamide, or electrical stimulation of periaqueductal gray apparently and significantly suppressed the nociceptive neuronal firing of the intact side. By contrast denervation hyperactivity was not affected.
These results are compatible with the clinical experience that only excess pain but not deafferented pain is relieved by various procedures to facilitate the opioid-mediated system. From these experimental confirmations, it can be postulated that there is a close relationship between the deafferentation hyperactivity provoked in this experiment and the so-called “deafferented pain”.

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The authors previously reported on local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) in rats 1 hour after the occlusion of the left middle cerebral artery. It was found that LCGU was decreased in the ipsilateral cerebral cortex and the lateral striatum, where the LCBF was also reduced. On the other hand, LCGU was increased in the ipsilateral medial striatum, olfactory tubercle, globus pallidus, subthalamic nucleus, and lateral habenula, which are the “non-ischemic” regions and closely connected with the dopaminergic neurons. In the present work, catecholamines and their metabolites were measured using the same ischemic model rats. The results were compared with the changes in LCGU and LCBF in the various cerebral regions. Noradrenaline concentration was reduced mainly in the “ischemic” regions, such as the ipsilateral cerebral cortex and lateral striatum, and there was an increase in the “non-ischemic” lateral thalamic nucleus. On the other hand, dopamine (DA) was increased bilaterally in the regions closely connected with dopaminergic neurons. However, 3, 4-dihydroxyphenylacetic acid and homovanillic acid were increased only in the ipsilateral regions and a small decrease was found in the contralateral striatum. These changes in DA and its metabolites indicate that DA metabolism was increased ipsilaterally in both the “ischemic” and “non-ischemic” regions but it was probably inhibited on the contralateral side. Since DA agonist, apomorphine, has been reported to increase energy metabolism (LCGU) mainly in the regions closely connected with the dopaminergic neurons, the results of the present work suggest that the ischemia in the ipsilateral cortex and lateral striatum caused an increase in DA neuron activity, which may be the cause of the increased LCGU in the ipsilateral “non-ischemic” dopamine rich regions, whereas the decrease in LCGU, inspite of the increased DA metabolism in the ipsilateral cortex and lateral striatum, were probably due to the direct effects of ischemia (the depletion of glucose supply). The contralateral change in DA was thought to be a biochemical diaschisis, which was mediated neuronally via a crossed nigrostriatal pathway.

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Previously the authors have studied local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) in rats 1 hour after the occlusion of the left middle cerebral artery. It was found that LCGU was decreased in the ipsilateral cerebral cortex and the lateral striatum, where LCBF was also reduced. On the other hand, LCGU was increased in the ipsilateral medial striatum, olfactory tubercle, globus pallidus, subthalamic nucleus, and lateral habenula. They have also investigated changes in catecholamine metabolism in these regions and found very close relationship between LCGU, LCBF, and dopamine metabolism. In the present work, changes in serotonin metabolism were investigated measuring tryptophan (TRP), serotonin (5-hydroxytryptamine, 5-HT), and its metabolite, 5-hydroxy-indoleacetic acid (5-HIAA) in certain regions of the cerebral cortex, basal ganglia, and brain stem using the same ischemic model rats. The results were compared with the changes in LCGU and LCBF. The concentration of TRP was significantly increased in the “ischemic” regions, such as the ipsilateral cerebral cortex and lateral striatum. On the other hand, 5-HT was significantly decreased not only in the “ischemic” regions but also in the “nonischemic” regions such as the globus pallidus. There was a tendency for 5-HT to decrease in the ipsilateral substantia nigra and raphe nuclei. 5-HIAA showed no significant change in the “ischemic” regions but was significantly increased in the globus pallidus and raphe nuclei and had a tendency to increase in the substantia nigra. There was no significant change in any of these parameters in the regions of the contralateral side. The changes in 5-HT metabolism in the “ischemic” regions, such as the ipsilateral cortex and lateral striatum indicate that the synthesis of 5-HT was reduced, but its release was unchanged. Increase in 5-HT metabolism in the “nonischemic” regions, such as the globus pallidus, substantia nigra, and raphe nuclei indicates a presence of neuronally-mediated biochemical diaschisis.

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Auditory evoked brain-stem responses (ABRs) reflect activities of the auditory pathway in the brain-stem and by inference activities of the structures surrounding the auditory pathway. It is said that ABR is a reliable diagnostic tool for predicting the outcome of patients with primary or secondary brain-stem injuries as a result of head trauma, cerebrovascular disorders, and others. However, the evaluation of ABRs has depended mostly on the delay of the fifth wave, and such parameters as intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP), were not considered.
The authors have made a new automatic and serial monitoring system of ABRs, which is composed of an audio-stimulator, a stimulus-controller, an amplifier, a signal processor, and a X-Y recorder. The stimulus-controller enables to monitor ABRs automatically and serially. The clinical study consisted of 17 patients with severe brain damage, including 10 head injuries, five cerebrovascular disorders and others. Following findings were observed. 1) The fifth wave delayed synchronously with a decrease in CPP in critical brain failure. 2) In some cases, decreases in the amplitude of the waves except the fifth wave were exaggerated during trans-tentorial herniation. For better use of the new monitoring system, the ABR-ICP-MAP correlative arrays are being made up, in which ICP, MAP, and other vital signs are evaluated at a glance, which makes it easy to recognize the status of the brain failure and to decide on the appropriate therapy.

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Both brainstem auditory evoked responses (BAER) and short latency somatosensory evoked responses (SSER) were recorded to detect brainstem damage in 40 cases (group III), and the results were compared with those in the other two groups; one group (group I) consisted of 64 cases in which BAER was recorded at emergency admission and the other group (group II) consisted of 40 cases in which BAER was repeatedly recorded for several days after emergency admission. All of them suffered from severe head injury having a Glasgow Coma Scale of less than 7.
As authors previously reported, that even a single recording of BAER was able to estimate the severity of primary or secondary brainstem damage, better than by the use of neurological findings or computed tomography findings such as deformation of the cistern around the brainstem. Its accuracy of predicting the outcome or recovery from the unconscious state was less than 85%, as shown by the results in group I. The accuracy became 92%, if BAER was repeatedly recorded until 2 weeks after injury, as shown by the results observed in group II. In group III, monitoring of both BAER and SSER at emergency admission and subsequent 2 to 4 days estimated brainstem lesion of all levels including the cervical spinal cord more accurately and the abnormalities of both responses predicted poor recovery from unconsious state following severe head injury (accuracy 99%).
It is concluded that the analysis of the multi-modality brainstem evoked responses (BAER and SSER) is the most useful method for predicting the outcome from a severe head injury.

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Computerized tomography (CT) features of ruptured cerebral arteriovenous malformations (AVM) were analyzed in 21 cases, whose CT scans were taken within 7 days after the attack. High density areas were seen in all cases, and distributed in 14 cases (66.7%) of the subcortical region, 3 (14.3%) of the basal ganglia, 2 (9.5%) of the corpus callosum, and 2 (9.5%) of the cerebellum.
In 12 out of 21 cases (57.1 %), high density areas were combined in the ventricular system. High density areas were also seen in one case, either in the ambient cistern or in the Sylvian fissure, respectively. High density area was never seen in the basal cistern, such as in cases with ruptured intracranial aneurysms.
From these CT features of the ruptured cerebral AVM, it should be classified in the intracerebral hemorrhage rather than the subarachnoid hemorrhage group.

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The body temperature, computed tomography (CT) findings, and vasospasm were observed in 40 patients affected by subarachnoid hemorrhage due to ruptured aneurysms. Thirteen patients (32.5%) had moderate fever between 37.5°C and 39°C or over 39°C beginning day 4 to 6 and lasting an average of 8.5 days. Delayed fever was observed with a greater statistical significance in the male patients, patients with consciousness disturbance on admission, and patients with intraventricular blood shown on CT within 24 hours after subarachnoid hemorrhage. Urinary catecholamines of 16 patients were measured by high-speed liquid chromatography. In the patients with intraventricular blood and fever, catecholamine values, especially noradrenaline, were markedly elevated. It is suggested that the delayed fever is not a simple meningeal sign but a sign of modulated fever control mechanism of the hypothalamus damaged by intraventricular bleeding.

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A case of the intracranial hemorrhage due to the congenital factor XIII deficiency was experienced. The patient was a 27-year-old female, who had been diagnosed as congenital factor XIII deficiency at the age of 18. She presented acute consciousness disturbance and the left hemiplegia which was caused by a subcortical hemorrhage in the right frontal lobe. Removal of the hematoma through craniotomy was successfully carried out under a total of 1, 500 units of factor XIII concentrate derived from human placenta, was followed by complete recovery without rebleeding or delay in wound-healing.
Clinical features of the congenital factor XIII deficiency with intracranial hemorrhage were discussed with analysis of 27 cases including this case. Whenever a patient with intracranial hemorrhage is encountered, especially in case with a past history such as umbilical bleeding, posttraumatic hematoma, and defective wound-healing, congenital factor XIII deficiency must be borne in mind. Although intracranial hemorrhage is the most fatal complication with deficiency of coagulation factor XIII, the surgical treatment may be safe under replacement therapy of factor XIII concentrate derived from human placenta.

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A rare case of an intrasellar epidermoid cyst with ophthalmologic and endocrinological disorders is reported.
A 54-year-old male complained of decreased visual acuity and visual field defects. On admission, bitemporal hemianopsia and panhypopituitarism were revealed. Computed tomography (CT) demonstrated a homogeneous low density area in the sellar region. The margin of the low density area was slightly enhanced. The low density area was clearly distinguished from the cerebrospinal fluid space in the metrizamide CT cisternography. The mass lesion was totally removed by the transsphenoidal approach. Histological examination of the surgical specimen showed that the cyst wall consisted of stratified squamous epithelium with keratinization and confirmed the diagnosis of epidermoid cyst.

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A case with hydrocephalus subsequent to neonatal intraventricular and intracerebral hemorrhages is reported. The hydrocephalus in this case was diagnosed to be obstructive due to subarachnoid hemorrhage. However, one lateral ventricle, in which intracerebral hemorrhage occurred, dilated predominantly compared with that in the contralateral hemisphere.
Hydrocephalus which occurs in the brain suffering from destructive changes due to some other causes than hydrocephalus, such as in this case, should be named “destruction hydrocephalus” as a new entity, and be discriminated from one which shows dilated ventricles simply due to increased intraventricular pressure. In this hydrocephalus, dilatation of the ventricle occurs irregularly and relatively in short periods, causing secondary cerebral destruction. Therefore, ventriculostomy to prevent progression of cerebral damage is required as soon as possible.

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