To determine the ultracytochemical localization of alkaline and acid phosphatase activities of normal rat choroidal epithelium, the lead citrate method after Mayahara, for the former and the Gomori's method for the latter were used.
The electron dense reaction products of alkaline phosphatase activity are found only along the basal plasmalemma and in the wall of capillary endothelium in the choroid plexus. The activity of acid phosphatase is limited to the lysosomes and the inner cisternae of the Golgi lamellae.
The possible function of these two enzymes was briefly discussed.

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Localization of carbonic anhydrase (CAHase) activity was studied electron microscopically on rat choroid plexus epithelial cells.
The ultracytochemical localization of CAHase activity was found in the microvilli and in the basal infoldings of the choroidal epithelial cells using Yokota's technique (1969). The carbonic anhydrase helps the formation of H⁺ and HCO₃^- from CO₂. Intracellular H⁺ exchanges with extracellular sodium ion through the basal infoldings. The HCO₃^- moves into the cerebrospinal fluid through the plasmalemma of the microvilli.

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Experimental cerebral infarction has been produced in dogs by clipping the middle cerebral artery and lowering the systemic blood pressure to 50mmHg for one hour. In this study, changes in microvasculatures in or near the ischemic area of the experimental animals were examined with light and electron microscope. All the dogs were sacrificed 24 hours after restoration of blood pressure. They were devided into three groups: the clip was permanently placed (Group 1); the clip was removed at the time of sacrifice (Group 2); and the clip was removed 4 hours after restoration (Group 3).
Hemorrhage from venules at the boundary zone between the gray and white matters was the common and conspicuous finding in all groups. Venules showed severe ischemic damages including disruption of the limiting membrane of the swollen perivascular glial processes. The enlarged perivascular space was filled with erythrocytes. The capillaries of this boundary zone were occluded by erythrocytes and by the endothelial swelling, but were not ruptured.
In the ischemic cortex, capillaries of Group 1 and 2 were packed with erythrocytes and platelets, but were not broken down. In the third group, on the other hand, hemorrhage from necrotic capillaries was one of the characteristic findings; Endothelial flattening and discontinuity and destruction of the basement membrane were observed under electronmicroscope. Marked brain edema was also seen.
These results indicated that changes in the fine structure of the microvasculature in the area of focal cerebral ischemia varies according to the location of the area and the degree of ischemia.

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It is well known that the intracranial pulse wave amplitude increases with rising intracranial pressure (ICP). However, little is known about how the form of the pulse wave changes with variation in ICP. One or two peaks were observed in the descending slope of the pulse wave, synchronous with the heart beat in dogs. As ICP increased, the amplitude as well as the peak of the pulse wave became more prominent and the shape finally became monotonous. These changes can be used as a diagnostic tool to assess the intracranial volume-pressure relationships. In dogs where the vasotonicity was strengthened by a hypertensive drug (noradrenalin), alteration of the pulse wave occurred with ICP elevation. However, when the systemic blood pressure was elevated by inflation of an aortic balloon, ICP elevation resulted in the monotonous form of the pulse wave. On the contrary, when the vasotonicity was weakened by a hypotensive drug (regitine), the form of the pulse wave became monotonous. However, exsanguination did not change the form of the wave under ICP elevation.
These results suggest that the cerebrovascular tone contributes to the form of the pulse wave under increased ICP.

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The effect of stimulation of peripheral and supraspinal sensory system on the activities of raphe-spinal neurons were studied extracellularly in chloralose-anesthetized cats. Among 300 raphe neurons recorded from the brainstem of cats, a total of 74 raphe-spinal neurons were activated antidromically by stimulation of the cervical dorsolateral funiculus. The mean conduction velocity of these neurons, calculated from the stimulation-recording distance and latencies, was 25.4 m/sec.
These raphe-spinal neurons were found to originate in the caudal raphe nuclei, i.e., 56 in raphe magnus, 14 in raphe obscurus, 3 in raphe pallidus and 1 in raphe pontis. All of them were shown to respond to innocuous and/or noxious peripheral mechanical stimuli, all with broad receptive fields. Single pulse periaqueductal gray (PAG) stimulation evoked driven firing with the spike per stimulus ratio ranging from 1 to 4 and latencies ranging from 5 to 15 msec in 57 (95%) of 60 units examined. Driven firing was followed by inhibition with a period ranging from 100 to 200 msec. Repetitive PAG stimulation at 20 Hz induced powerful facilitation of firing. The facilitation persisted for several minutes after termination of the stimulation when the repetitive stimulation was continued for 5 to 30 sec.
Single pulse VPL or VPM stimulation evoked driven firing with the spike per stimulus ratio ranging from 1 to 4 and latencies ranging from 10 to 20 msec in 58 (97%) of 60 units tested. Long lasting powerful facilitation was also provoked in those units by repetitive stimulation at 20 Hz for 5 to 30 sec. This facilitation was not affected by removal of the bilateral sensorimotor area.
PAG-induced facilitation was apparently and reversibly avoided by the administration of naloxone (0.1-0.3 mg/kg, i.v.) in 7 (70%) of 10 units investigated. On the other hand, the administration of naloxone (0.3 mg/kg, i.v.) was found not to affect VPL-induced facilitation of firing in any of ten units examined.
Effects of sustained repetitive stimulation of the thalamic relay nucleus on activities of raphe-spinal neurons were studied in 17 units. After sustained stimulation for 3 hours, facilitation of firing by the thalamic relay nucleus stimulation was shown to completely disappear. Facilitatory response to single pulse thalamic relay nucleus stimulation was also found to be reduced. Nevertheless, facilitation of firing induced by single pulse or repetitive PAG stimulation was apparently unchanged.
These results suggest that both thalamic relay nucleus stimulation and PAG stimulation for pain-relief may activate a final common path, i.e., raphe-spinal neurons, which then inhibit spinal neurons sensitive to pain, as a part of the mechanism of pain-suppression. Although the thalamic relay nucleus-induced facilitation of raphe-spinal neurons was shown to be as powerful as that of PAG, it did not appear to relate to the opiate mechanism, unlike that of PAG.

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It has been reported that stimulation of the midbrain periaqueductal gray (PAG) is effective for relief of intractable pain. However, this procedure appears to have some disadvantages; i.e., technical difficulty of inserting electrodes exactly, side effects such as abnormal occular movement, and limitation of candidates because of the poor effect on pain in those with morphine-tolerance. Previously the authors reported that stimulation of the thalamic relay nucleus as well as of PAG produced long lasting, profound excitation of raphe-spinal neurons which then inhibit nociceptive dorsal horn neurons. Furthermore, naloxone (which is a specific antagonist of morphine-like substances) was shown to avoid the excitation induced by PAG stimulation, but not that by induced thalamic relay nucleus stimulation. Based on these findings, attempts were made to treat intractable pain with morphine-tolerance by stimulation of thalamic relay nucleus. Prevention of stimulation-tolerance was attempted by administration of monoamine precusors, i.e., l-DOPA and l-tryptophan, on the basis of the experimental observation reported previously. Chronic implantation of a stimulating electrode in the thalamic relay nucleus was performed in five cases which suffered from cancer pain (2 cases), thalamic pain (1 case), and paraplegic pain (2 cases). All of these cases enjoyed excellent relief of pain at least during the initial period. Only one case, which suffered from paraplegic pain developed stimulation-tolerance. Experiences in the other four cases suggested that administration of l-DOPA prevent the stimulation-tolerance. On the other hand, there was no evidence that administration of l-tryptophan interfered with progress of stimulation-tolerance. There were no operative complications and no side effects with this stimulating treatment.
In summary, stimulation of the thalamic relay nucleus, which is more safe and acurate when electrode insertion using electrophysiological monitoring is done during operation, is effective in relief of intractable pain, even with morphine-tolerance. Administration of l-DOPA seems to prevent stimulation-tolerance.

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The effect of hemodynamic stress on the development of cerebral aneurysms was evaluated in cases of intracranial aneurysm coexistent with arteriovenous malformation (AVM) of the brain. Three such cases were presented, in which 5 aneurysms were noted on the feeding arteries to the AVM. The findings strongly indicated the importance of hemodynamic stress on aneurysm formation.
The first patient, a 39-year-old male, had 3 aneurysms on the anterior cerebral artery feeding the left frontal AVM. Although two of these aneurysms received no surgical treatment, they almost disappeared several months after excision of the AVM. The second patient, a 54-year-old female, had a huge left fronto-parietal AVM and an aneurysm of the cavernous portion of the dilated internal carotid artery. No surgical treatment was performed. The third patient, a 25-year-old male, had a deep-seated AVM fed by the right anterior choroidal artery, the lenticulostriate artery, and the insular branches of the middle cerebral artery. Although no aneurysm was noted in the first angiogram taken immediately after an attack of subarachnoid hemorrhage, a small aneurysm appeared on the lenticulostriate artery in the second angiogram taken 8 days after the attack. The aneurysm gradually reduced in size during the following several weeks, and he was discharged with no neurological deficit. Twenty-one months after the first attack, he suffered a second apoplectic attack of intracerebral hematoma and received surgical evacuation of the hematoma. The aneurysm was histologically found to be a false one. These facts further explain the association of these two different kinds of lesions.
Seventy-five previously reported cases of intracranial aneurysm with AVM were reviewed and the effect of hemodynamic stress on aneurysm formation was evaluated. These findings also strongly indicated that the hemodynamic stress due to the presence of the AVM seems to have played an important role in the development of aneurysms in these cases.

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Two cases of severe chronic subdural hematomas of infants who were treated by “the lowering of the superior sagittal sinus (LSSS)” are reported.
Case 1, an 8-month old boy, who had received a head trauma one month prior to admission was proved to have thick bilateral subdural hematomas and moderate ventricular dilatation by CT scans. He had subdural taps, two trephinations, and irrigations followed by external drainage. But the subdural hematomas remained and brain atrophy progressed. Cerebral angiography revealed the presence of thick, avascular areas over the cerebral hemispheres and stretching of the cortical bridging veins going into the superior sagittal sinus. Four months after the injury, bilateral large craniotomies, evacuation of hematomas, and lowering of the superior sagittal sinus were performed. He is now 20 months old. He has regained visual acuity, can walk with assistance by hand, and can speak simple words as well.
Case 2, an 11-month old girl who had started infantile spasm at 7 months of age was found to have thick chronic subdural hematomas and remarkable brain atrophy. She was refered to our clinic at one year of age for the indication of subduro-peritoneostomy. CT scans disclosed enormously increased subdural hematoma in the left side. Bilateral large craniotomies, removal of hematomas and LSSS were performed. She is now 18 months old. She can watch and handle toys in the sitting position.
It has been reported that one fourth to one fifth of infants with chronic subdural hematomas or fluid collection develop brain atrophy and severe psychomotor retardation, even with treatment by subduroperitoneal shunts. For those patients who do not respond to conventional treatments, LSSS is indicated to deminish the craniocerebral disproportion and to improve the venous return of cerebral hemispheres.

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A case of tuberculous brain abscess diagnosed from the macroscopic, histological and bacteriological aspects is presented.
A 39-year-old man was initially admitted to a sanatorium in June, 1977 for the treatment of lung tuberculosis with associated diabetes mellitus. He developed fever, headache and convulsion in April, 1978. Brain CT scan revealed a mass in the cerebrum. Neurological examination demonstrated mental confusion with memory disturbance and disorientation with urinary and fecal incontinence. He had mild right hemiparesis with a positive Babinski sign. There was no meningeal sign. Repeated brain CT scans showed a low density area surrounded by enhanced ring blush in the left frontal lobe and displacement of left lateral ventricle to the right. A presumtive diagnosis of tuberculous brain abscess was made.
External drainage yielded 60 ml of purulent material. Acid-fast bacillus stains of the puss were positive and the culture proved M. tuberculosis. A left frontotemporal craniotomy was then performed and the abscess was excised en bloc. Histological examination of the capsule wall demonstrated an internal necrotic zone with polymorphnuclear leukocytes. The necrotic area was surrounded by granular reaction, rich in epitheloid cells, some of which showed giant cells of the Langhans type. Outside this zone, there was a fibrous tissue wall with a large number of immature vessels and collection of mononuclear cells. Postoperative recovery was uneventful. At the time of discharge, he showed no evidence of any neurological defects.
Tuberculous brain abscess have rarely been reported unlike the more common tuberculoma, even before the introduction of antituberculous chemotheraphy. Diagnostic criteria of tuberculous brain abscess should be based only on macroscopic and bacteriological aspects.

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Two rare cases of traumatic aneurysm involving intracranial carotid arteries are reported.
A 58-year-old man was admitted, with the chief complaint of visual disturbance. The patient had been treated with radiation under the diagnosis of pituitary tumor 7 years prior to admission. A CT scan demonstrated a pituitary tumor with suprasellar extension. Bilateral carotid angiograms demonstrated lateral displacement of the proximal supraclinoid carotid arteries. There was no medial displacement of the cavernous portion of the internal carotid artery. A right fronto-temporal craniotomy was performed. During intracapsular removal of the tumor, massive bleeding from the left medial wall of the sella which was considered to be from the left internal carotid artery, suddenly occurred. The hemorrhage was controlled by packing with oxycell. On the third postoperative day, the patient complained of double vision. A left carotid angiography demonstrated a multilobed false aneurysm in the cavernous portion of the left internal carotid artery. The aneurysm was then successfully treated by trapping of extra-and intracranial carotid ligation. The patient was discharged with left visual disturbance and left opthalmoplegia.
A 22-year-old man was rendered unconscious by a blow to the face and admitted semicomatose, with fixed and dilated pupil on the right side. An emergency CT scan demonstrated massive subarachnoid hemorrhage in the basal cisterns and clots in the right frontal lobe as well as in the lateral ventricles. External decompression and ventricular drainage were performed. A postoperative carotid angiography on the right demonstrated a irregular narrowing of the supraclinoid carotid artery. After the operation, the neurological status improved with intensive medical treatment. Two weeks later, however, the patient suddenly became comatose with decerebrate rigidity. A right carotid angiography demonstrated a bilobed aneurysm of the supraclinoid portion and marked narrowing of C₂ portion of the internal carotid artery. An emergency operation for radical treatment of the false aneurysm was performed after the third episode of bleeding. The previous craniotomy was reopened and massive subarachnoid hemorrhage around the right internal carotid artery was removed following evacuation of frontal intracerebral hematoma. The aneurysm involved both the C₁ portion of internal carotid artery and carotid bifurcation. During the dissection, the aneurysm ruptured and bled profusely. The hemorrhage was controlled by ligation of the right internal carotid artery at the neck, and the dome of the aneurysm was coated with a muscle piece. Postoperatively, the patient remained in a persistent vegetative state. In this report, possible mechanisms causing these false aneurysms are described.

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