Large-sized infarctions of the cerebral hemisphere (LSICH) were experimentally induced in 20 dogs by injecting two silicone cylinders through the right cervical internal carotid artery. The LSICH models were perfused with heparinized saline and fixed with 1.5% glutaraldehyde solution through the contralateral carotid artery 7 days after the embolization. Mercox® was then injected manually. The brains were immediately removed, and specimens were obtained from the basal ganglia and the ectosylvian gyrus. Regenerated microvessels were observed within the necrosis in the basal ganglia. The regenerated microvessels had an irregular, “bead-like” surface, and formed anastomosed networks. The regenerated capillaries had double basement membranes and endothelia with abundant ribosome and increased pinocytotic vesicles. It is suggested that the regenerated capillaries had immature blood-brain barriers of increased permeability. It is thought that the brain functions of this area are reversible. The microvessels within the vasogenic edema in the corticomedullary junctional area of the ectosylvian gyrus had smooth surfaces, and formed normal capillary networks, but their perivascular spaces were dilated with edematous fluids.

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The effect of stable xenon on the regional cerebral blood flow (rCBF) was studied in 12 adult cats. Xenon in concentrations 17%, 33%, 50%, and 60% was mixed with oxygen, and inhaled by a semi-closed rebreathing system. Cortical rCBF was continuously measured by a heat clearance probe which had been calibrated using the hydrogen clearance method. Cortical rCBF decreased to 96%, 92%, 88%, and 88% of the control after inhalation of 17%, 33%, 50%, and 60% xenon, respectively, and these decreases in rCBFs were statistically significant (p<0.01, Student's paired t-test) under the high concentrations of xenon of 33% or more. No significant changes were seen in arterial carbon dioxide tension and the mean arterial blood pressure during xenon inhalation, whereas diffuse electroencephalographic slowing was observed during 50% xenon inhalation. The mechanism of the decrease of rCBF by xenon gas remains to be solved. The direct effect of xenon on rCBF should be considered when high concentrations of xenon are used for stable xenon-enhanced computed tomography.

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Hemorrhagic infarction is a rare condition after vasospasm in patients with aneurysmal subarachnoid hemorrhage (SAH). Induced hypertensive therapy is being performed recently for patients with vasospasm, but this treatment risks inducing hemorrhagic infarction. It is important to study hemorrhagic infarction after vasospasm, in order to treat patients more safely with induced hypertensive therapy. 221 patients whose first computed tomographic (CT) scanning was examined within 2 weeks after SAH were investigated for this study. Symptomatic vasospasm was seen in 99 (45%), cerebral infarction in 37 (17%), and hemorrhagic infarction in 13 (6%). Hemorrhagic infarction usually occurred from day 20 to 30 after the aneurysmal rupture, and this stage corresponded with the remission stage of the vasospasm. On the CT scan, the hemorrhagic infarction was revealed as leaky hemorrhage in the low density area previously recognized in 11 cases, and massive hemorrhage with mass effect was seen in 2 cases. These findings suggest that hemorrhagic infarction after vasospasm may sometimes be fatal. The autoregulation of the cerebral blood flow in patients with vasospasm was normal or of the hypertensive type in the remission stage of vasospasm, when hemorrhagic infarction usually appeared. This finding shows that induced hypertensive therapy is ineffective in this stage. Induced hypertensive therapy, therefore, should be stopped by this stage because this treatment is not only ineffective but also has a risk of aggravating hemorrhagic infarction.

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A sensitive biochemical marker for acute brain damage is important in assessing the severity of head injuries. Acute brain damage is followed by increased creatine phosphokinase (CPK) activity in the serum. The present study was undertaken to examine whether the measurement of serum levels of brain type isoenzyme (CPK-BB) and heart type isoenzyme (CPK-MB) is valuable in assessing and evaluating the clinical status of patients with acute head injuries. Fifty-seven patients with acute head injuries were studied. Fourty-four patients were male and thirteen patients were female with ages ranging from 2 to 69 years. All patients were diagnosed by computed tomography (CT) scan within three hours after head injury. Serial blood samples were drawn during the first 7 days after head injury. The Glasgow Coma Scale (GCS) for all patients was recorded on admission. Clinical outcome was assessed at the time of discharge according to the Glasgow Outcome Scale. The “good” group consisted of patients with good recovery or moderate disability. The “poor” group consisted of patients with severe disability and persistent vegetative state. The maximal serum levels of CPK-BB and CPK-MB occurred in most patients on the first day of trauma. There was a highly significant correlation between the serum levels of CPK-BB and GCS (p<0.001), whereas there was little correlation between serum levels of CPK-MB and GCS. The peak levels of CPK-BB in the “poor” and “dead” groups were significantly higher than those in the “good” group (p<0.01). Particular correlation between CT findings and serum levels of CPK-BB was found. Cases with serum levels of CPK-BB higher than 10 IU/l were associated with cerebral contusions. The major factors in the increase of serum levels of CPK-BB were associated with the severity of cerebral contusions and particular sites of the brain injuries. New lesions in serial CT scans didn't seem to be a factor in raising serum levels of CPK-BB. Serum levels of CPK-BB did not correlate with intracranial pressure. Measurement of serum levels of CPK-BB may offer useful information for making a prognosis. It seems to be a sensitive index of acute brain damage and a reliable marker of cerebral contusions.

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Fifty-eight cases of traumatic intracerebral hematoma were investigated by sequential computed tomography (CT) to clarify the time when the hematoma appeared and was completed after head trauma, and to determine if the term “delayed traumatic intracerebral hematoma (DTICH)” should be used for hematoma in the acute stage. They were classified into two groups, A and B. In Group A, 49 cases, initial CT was performed within 3 hours after head trauma, and in Group B, 9 cases, it was performed more than 3 hours after head trauma. Among the 49 cases of Group A, 19 were cases of non-delayed traumatic intracerebral hematoma (N-DTICH) in which the hematomas were found by the initial CT. Emergency surgery was performed on 6 cases out of the 19. In 9 cases out of the remaining 13, the hematoma increased in size within 24 hours and their outcome was worse compared with the outcome of 4 cases of non-enlarged hematoma. The cases of DTICH in which the hematomas were found by the follow-up CT numbered 30. In these 30 DTICH cases, those in which the initial CT finding was normal were 7 and their outcome was good. However, 10 cases of DTICH appeared several hours following removal of extracerebral hematomas, and their outcome was poor, with death in 6 cases. The appearance times of the hematomas were investigated using the sequential CT of the 49 cases in Group A. Twenty-two cases of hematoma were found within 3 hours, 18 were found 3 to 12 hours, and 7 were found 12 to 24 hours following head trauma. The completion time of the hematomas was investigated by sequential CT in 43 cases of Group A and all 9 cases of Group B. The hematomas were already completed within 6 hours after trauma in 13 cases out of the 52. The other 14 cases of hematoma were completed 6 to 12 hours after trauma, and the remaining 21 except 2 were completed 12 to 24 hours after trauma. It could be said that the hematomas appeared and completed their growth within 24 hours after head trauma in 96% of the cases.
It may be postulated that almost all traumatic intracerebral hematomas appear relatively early after trauma and gradually change their size and shape with the lapse of time, and complete their growth around 24 hours from the occurrence of head trauma. Therefore, the term “DTICH” should not be used for the delayed type of hematoma which appears during the acute stage, especially 24 hours following head trauma.

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Ten neuronal tumors of the central nervous system (CNS) were studied using the peroxidaseantiperoxidase method of Sternberger, in regard to their immunohist, chemical reactivity to dynorphin (DYN), β-endorphin (END), corticotropin-releasing factor (CRF), somatostatin (SMT), neurophysin (NPY), vasopressin (VSP), and oxytocin (OXY). They are considered some of the representative neuropeptides normally associated with hypothalamic neurons. Seven of the tumors were located in the frontal, temporal or parietal lobes, two in the hypothalamo-pituitary region, and one in the pineal gland. Histologically, the tumors examined contained well-differentiated neuronal cells and ranged in diagnosis from gangliocytoma and ganglioglioma to ganglioneuroblastoma. Among these tumors, two hypothalamo-pituitary gangliocytomas, one frontal ganglidglioma, one temporal and one parietal ganglioneuroblastoma showed positive reactions for two or more of the neuropeptides in the cytoplasms and/or in the processes of neoplastic neuronal cells. Reactivity with DYN was found in three tumors, with END in two, with CRF in three, with SMT in three, with NPY in two, with VSP in three and with OXY in four. These results indicate that these neuronal neoplasms of the CNS are polyclonal tumors without topographic recapitulation of normal neurosecretion, and may have originated in dysgenetic focus of multipotential neuroblasts.

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The operative benefits and goals in the treatment of craniosynostosis were considered mainly from the cosmetic standpoint before the 1960s. In the last 25 years, two major clinically critical points have been added to the consideration of an operative method. One is the associated increased intracranial pressure (ICP) and the other is the newly recognized pathophysiology of associated premature closure of skull base sutures. Thus, classical linear craniectomy, which used to be the only accepted operative method for craniosynostosis, has been reconsidered with its unsuccessful and unsatisfactory results both for cosmetic and decompressive purposes.
Twenty-five cases were analyzed in the light of operative procedures and discussed with the results of pre and postoperative ICP monitoring in treatments for craniosynostosis. Only 13 out of 25 children were treated before 1 year of age. Simple suture closure was seen in 13 patients, namely, six sagittal, four coronal, and three metopic. Multiple involvements were seen in the other 12 patients, namely, five Crouzon's disease, two Apert's syndrome, one cloverleaf skull, and four other multiple cranial suture closures. The signs and symptoms and radiological evidence of increased ICP with or without continuous ICP monitoring were checked in all cases. All children over 2 years of age or with multiple suture involvements revealed the evidence of increased ICP before the operation. All six patients over 3 years of age had one or more symptoms of decreased visual acuity, headaches, psychomotor developmental delay, or convulsion. Pre and postoperative pressure monitoring confirmed satisfactory improvement in ICP in advanced elderly cases treated with bilateral wide flap operations or in infantile craniofacial dysostosis, plagiocephaly, or trigonocephaly treated with lateral canthal advancement with radical forehead remodeling. This study strongly emphasizes that ICP is an extremely important factor in considering operative procedure for craniosynostosis.

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Three cases of acute subdural hematoma without head injury but attributable to surgically verified bleeding from a cortical artery are presented. Case 1: A 46-year-old male complained of a headache. Neurological examination revealed no abnormality. A subdural hematoma was found on computed tomography. Case 2: A 49-year-old male developed a consciousness disturbance. Removal of a hematoma was performed leaving mild confusion. Case 3: A 68-year-old female was admitted because of acute onset of confusion. An emergency operation was performed but profound hypotension occurred. Confusion persisted and the patient died from a complication. The previous reports on acute subdural hematoma caused by rupture of a cortical artery consisted of 17 cases with preceding trivial head trauma and 34 without. In most of the cases without head injury, the initial symptom was a headache mimicking that of subarachnoid hemorrhage which was followed by consciousness disturbance. Tearing of a cortical artery adhering to the dura mater by a trivial trauma or rapid head movement is proposed as a causative mechanism of the hematoma. In chronic subdural hematomas, only a negligible or no preceding head injury is often demonstrated. It is suggested, therefore, that a hemorrhage of the artery may cause an acute subdural hematoma if massive, and may also cause chronic subdural hematoma when it is minimal and subsequent bleeding from the hematoma membrane in the organizing process takes place.

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Two cases of chronic subdural hematoma after craniotomy, removal of the hematoma, dural plasty using lyophilized human cadaver dura mater, and external decompression for acute traumatic intracranial hematoma are reported. One of these was acute subdural hematoma and the other acute epidural hematoma. The pathophysiology of the chronic subdural hematoma in these two cases was considered to be: collection of a mixture of cerebrospinal fluid and blood in the subdural space caused by torn arachnoid at head injury or craniotomy, and unbalanced volume between the brain and subdural space caused by excessive dural plasty and intracranial hypotension due to external decompression. Opening and irrigation of the hematoma cavity were sufficient treatment at cranioplasty.

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Cardiac myxoma is a slowly growing benign intracavitary neoplasm most frequently occurring in the left atrium. Embolization from this friable, supposedly benign tumor may cause a variety of neurologic symptoms and signs. A case of left atrial myxoma with cerebral infarction and a monstrous aneurysm of the left middle cerebral artery is reported.
A 54-year-old woman was admitted because of fever, right hemiparesis, and dysphasia. M-mode and cross-sectional echocardiograms revealed a large mass in the left atrial cavity. Successful surgical removal of the tumor was accomplished by open heart surgery. This patient was transferred to the department of neurology and left carotid angiography was done, and a monstrous aneurysm of the left middle cerebral artery was found. She was therefore transferred to the department of neurosurgery. The neck of this monstrous aneurysm was partially clipped and the residual parts were encased with many small gauzes, and the aneurysm was partially cut for pathological examination, but no infiltration of the myxomatous tissue was seen. Sequential computed tomography showed the growing process of this aneurysm.

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A cerebral aneurysmal case associated with persistent trigeminal artery and occlusion of the subclavian artery is reported. The patient was a 58-year-old female who had an episode of dizziness, headache, and consciousness disturbance in 1980. Another sudden attack of dizziness and unconsciousness occurred in November, 1982. At admission her consciousness was almost clear, and she complained severe headache. Neurological findings were normal, except for nuchal rigidity. The pulse in the left radial artery was irregular and that in the right radial artery was not palpable. Cerebral angiography showed right persistent trigeminal artery and a saccular aneurysm of the right internal carotid artery at the posterior communicating branch. Right frontotemporal craniotomy and neck clipping of the aneurysm were performed. Occlusion of the right subclavian artery was demonstrated by brachiocephalic angiography.
The authors have collected reports of 33 cerebral aneurysmal cases associated with persistent trigeminal artery. No cases of cerebral aneurysm associated with both persistent trigeminal artery and occlusion of the subclavian artery were found.

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A case of aortitis syndrome associated with a ruptured anterior communicating artery aneurysm and hypertensive intracerebral hemorrhage is reported. The patient was a 48-year-old woman who had been suffering from aortitis syndrome for the past 6 years. She was admitted with severe headache. Computed tomography (CT) scan and cerebral angiography revealed a ruptured anterior communicating artery aneurysm. Neck clipping of the aneurysm was successfully performed. However, 5 weeks after the operation she became unconscious and right hemiparesis was noted. CT scan showed intracerebral hemorrhage in the left putaminal region and an emergency operation was performed.
In the literature there were only nine cases of aortitis syndrome associated with cerebral aneurysms. These aneurysms developed frequently in the vertebro-basilar system and in the anterior communicating artery. From the standpoint of pathogenesis, development of these aneurysms was closely related to the hemodynamic stress caused by altered hemodynamics and vascular degeneration resulting from long-term hypertension. It should be remembered that some of the patients suffering from aortitis syndrome might develop cerebral aneurysms, and it is very important to control blood pressure strictly.

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A 57-year-old male developed sudden severe headache and nausea with right retroocular pain. On admission bruit could not be heard and neurological examination revealed mild nuchal stiffness. Computed tomography scan showed marked subarachnoid hemorrhage with a small intracerebral hematoma in the right temporal lobe. Right and left carotid angiograms showed a dural arteriovenous malformation (dAVM) in the right olfactory groove fed by bilateral anterior and posterior ethmoidal arteries. The right olfactory vein was a drainer with a vascular sac draining into the sinuses. Bifrontal craniotomy was performed. Removal of the nidus was abandoned due to its deeply seated location in the olfactory groove, so coagulation of the nidus and clipping of the drainer were performed. On postoperative carotid angiograms the dAVM was not visualized any more. The patient showed no neurological deficit.
From 21 dAVMs of the anterior cranial fossa, the following features can be seen: 1) dominance in male (75%), 2) frequent intracranial hemorrhage (86%), 3) drainage to the pial vein (90%), and 4) associated vascular sac (90%). All these features could be seen in this patient. The associated vascular sac originating from the dilated pial vein as a drainer in this case was thought to be the source of the hemorrhage, for its location was the same as the small hematoma. A blockade of cortical drainage would be effective to protect against intracranial hemorrhage.

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Idiopathic brain stone (Averback, 1977), or intracranial pathologically calcified lesion with unknown etiology, is very rare. A case of idiopathic brain stone in the cerebellum is reported. The patient, a 28-year-old female, was admitted because of sudden onset of severe vertigo and nausea. Plain computed tomography scan revealed a spotty high density area at the right dentate nucleus of the cerebellum which was not enhanced by contrast media. Vertebral angiography did not show any stain or abnormal vasculatures even with a prolonged injection method. Surgery was performed with the aide of sector scanning ultrasonography. The surgical specimen showed scattered calcium deposits without any vascular or neoplastic component.

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Arachnoid cysts are found wherever the arachnoid membrane exists. Therefore, arachnoid cysts tend to occur extracerebrally. A case of an intraventricular arachnoid cyst in a 37-year-old female is reported. The cyst was found in the left lateral ventricle and arose from the choroid plexus. The cyst wall, histologically, consisted of the arachnoid cell lining. Light microscope examination showed the hypocellular membrane without glial tissue. Electron microscope examination showed that the cyst lining cells adhered by an interdigitation with desmosome and the cells had no microvilli. These findings were compatible with the features of an arachnoid cyst.

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