The role of vasospasms in the pathogenesis of cerebral infarction following rupture of the intracranial aneurysms has not been well determined. To clarify the importance of vasospasms, 135 cases of ruptured intracranial aneurysms without fatal attack or intracerebral hematoma which were admitted within two weeks after the last episode of subarachnoid hemorrhage were studied. Analysis was carried out mainly by cerebral angiography, computed tomography (CT), and periodic clinical checks.
Vasospasms were identified in 92 cases (68%) of all of those studied by angiography. Cerebral infarction due to vasospasms was revealed in 29 cases (21%) by CT. In the CT scans, the ischemic region shown as low density area appeared 9±3 days after the onset, contrast enhancement became positive after 17±5 days and in six cases, the low density area turned into a high density area (hemorrhagic infarction) 26±5 days after the onset. The area of cerebral infarction, which was more complicated than that ofinfarction due to occlusion of a cerebral artery, depended upon severity and distribution of the vasospasm. For simplification, patterns of infarction were classified into four types. These were (1) main trunk area type … 69%, (2) branch area type … 10%, (3) white matter dominant type … 14% and perforator area type … 7%. In CT scans, cerebral infarctions due to vasospasm were shown mainly in the cortex and the white matter and rarely in the basal ganglionic region perfused by perforating arteries. Hemorrhagic infarction occurred in six cases (21%) among the 29 cases with cerebral infarction due to vasospasms. In the six patients with hemorrhagic infarction, the low density area turned into a high density area after relaxation of the vasospasm with angiographical findings of hyperemia. Distribution of the hemorrhagic infarction in CT was cortical (gyrus type) in five cases and subcortical in one case (subcortical type).
From these reults, it was concluded that there really is a process of cerebral infarction following vasospasms (subarachnoid hemorrhage→vasospasm→cerebral ischemia→infarction). Cerebral infarction following vasospasm is one of the important factors determining prognosis.

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Correlations among plain CT findings, clinical severity at the time of onset and subsequent development of the cerebral infarction due to vasospasms were studied retrospectively in the 32 cases with subarachnoid hemorrhages secondary to the initial rupture of cerebral aneurysms. It was found that the clinical severity was well correlated with the CT findings indicating the amount of blood in the subarachnoid space. Furthermore, it was possible to correlate the subsequent occurrence of cerebral infarctions with sequential CT findings. Persistent high density areas with Hounsfield numbers of over 60 showed good correlation with subsequent development of the cerebral infarction.

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Normal pressure hydrocephalus (NPH) often complicates after the rupture of intracranial aneurysms (NPH developed in 17.4% of our series). To clarify the pathophysiology and indication of shunting, intracranial pressure (ICP), cerebral blood flow (CBF) and radio nuclide cisternography were studied in patients who developed hydrocephalus after subarachnoid hemorrhage (SAH).
Patients developing hydrocephalus after SAH were divided into three stages, i.e., the acute stage (within one week after SAH), pre-NPH state and NPH state. Pre-NPH and NPH state patients had enlarged ventricles and periventricular lucency on CT scans and delayd absorption of CSF and/or complete block of the subarachnoid space with ventricular filling on cisternography. The ICP base-line in continuous ICP recordings was at a level of less than 15 mmHg in NPH patients, and at a level of more than 15 mmHg in pre-NPH state patients. ICP curves in the acute stage of patients who were drowsy after SAH showed pressure variations superimposed on an increased ICP base-line. The pressure variations were recurring increases in ICP in the range of 20 ?? 40 mmHg and resembled the B and C-waves of Lundberg. ICP curves in pre-NPH and NPH state patients showed plateau waves or B-waves. The plateau waves seen in these patients usually ranged between 30 ?? 50 mmHg and lasted for 5 ?? 10 minutes, i.e., the waves were smaller and briefer than those seen with increased intracranial pressuer from brain tumors. A few NPH patients showed a continuously low and flat ICP curve. ICP in these patients were recorded more than six months after SAH.
Changes in CBF were analysed. Mean values of 42.9 ml/ 100 gr/min were obtained in acute stage patients. Pre-NPH and NPH state patients showed flows of 35.1 and 28.7 ml/100 gr/min, respectively. Marked reduction in CBF (23.8 ml/ 100 gr/min) was found in NPH patients with the low and flat ICP pattern. Thus, CBF was markedly reduced in patients with NPH in spite of the lowered ICP.
The shunting procedure brought about remarkable recovery in pre-NPH and NPH state patients who showed pressure waves in continuous ICP recordings and a CBF of over 25 ml/ 100 gr/min.

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Aldolase isozyme patterns of brain tumors and the normal brain were investigated using 7.5% polyacryl-amidgel disc-electrophoresis.
Normal human brain tissue, obtained from surgery and autopsies contained aldolase A4, C4 and also three A-C hybrid sets, A₃C, A₂C₂, AC₃. Most gliomas such as astrocytomas, a ependymoma, glioblastomas and medulloblastomas showed the same pattern as that of the normal brain, but one glioblastoma showed only aldolase A₄ and A₃C hybrid. In meningiomas which seem to originate from mesodermal tissue, aldolase A₄ and A₃C hybrid were detected. In some meningiomas, however, the A₃C hybrid alone was found. Sarcomas and a chemodectoma showed the A₃C hybrid only. In acoustic neurinomas, pituitary adenomas and metastatic tumors from lung cancer, aldolase A₄ and A₃C hybrid were detected but aldolase C and other hybrids were always absent.
From these results, it was considered that the aldolase isozyme pattern was useful for identifying the genetic origin of brain tumors, especially when histological diagnosis was inconclusive.

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During two and a half years since the introduction of a CT scanner in February, 1977, 38 patients with traumatic subdural hygroma (SD hygroma) and 42 patients with chronic subdural hematoma (chronic SDH) were experienced.
Clinical symptoms and CT findings in SD hygromas were studied. Intensity of the head injury and appearance of the clinical symptoms in both conditions were compared, and the possibility of the development of chronic SDH from SD hygromas was studied. Clinical symptoms, such as headache and decreased spontaneity, occurred more often in patients with SD hygroma after head injury. Surgical treatment was necessary for patients who had disturbances of consciousness and an increased intracranial pressure (five cases). However, most patients improved with conservative therapy (33 cases). Bilateral SD hygromas were seen more frequently in older patients (over 60 years old). Low density areas in the CT decreased or disappeared in 23 out of 38 SD hygroma patients. In nine patients, the low density area remained as it was. In two patients, low density changed to high density and then disappeared. In four patients SD hygroma changed to chronic SDH 50, 70, 71, 72 days after the head injury respectively. Initial unconsciousness and skull fracture were more severe in SD hygroma than in chronic SDH. A long term asymptomatic state was observed in chronic SDH, but nine out of 42 chronic SDH patients had clinical symptoms from a few days after head injury.
From the clinical features, it seemed that SD hygroma was an entity distinct from chronic SDH. However, it was also thought that SD hygroma was a factor in the development of chronic SDH.

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The F-wave is a small muscle potential which follows the direct M-wave on supramaximal stimulation of a mixed nerve. Many authors have convincingly demonstrated that the F-wave travels at first from the stimulating point via motor fibers to the spinal cord and activates the anterior horn cell antidromically, which results in the delayed muscle potential. The F-wave changes can thus reveal the lesions of proximal nerve segments which are not accessible to conventional nerve conduction studies. The present study was undertaken in search for possible changes of the F-wave parameters in spinal root compression syndromes. In patients with unilateral cervical or lumbosacral root compression syndromes, F-waves were elicited in the corresponding myotomes. As compared to the intact sides, the minimum-latency of the F-waves was significantly delayed (P<0.05) in the presence of S1, L5 and C8/Th1 root compression syndromes. On the other hand, the delay of the minimum-latency of the F-wave recorded from the thenar muscles by the stimulation of median nerves did not statistically correlate with C7/C8 syndromes, probably because multisegmental innervations to the thenar muscles may be more distinct than to other muscles. Furthermore, the limits of the minimum-latency differences in normal subjects were calculated at the 5% level. Using these limits, the false positive rate may be 5%, and the false negative rate may range from 12.5% (Ulnar N. F-wave) to 36.9% (Tibial N. F-wave).

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A case of causalgia treated by the PISCES spinal cord stimulation system (produced by Medtronic, U.S.A.) was reported. The patient was a 48-year-old man who sustained partial damage to the right median nevre about seven years ago during an open brachial angiography in another hospital as a preoperative examinatior for a ruptured mycotic aneurysm in the left occipital region. The mycotic aneurysm was successfully treatec leaving right homonymous hemianopsia. However, he suffered from weakness in flexion of the fingers and spo. ntaneous severe pain in the distribution of the median nerve since that time. Motor functions had recovered almos to normal after median nerve neurolysis on several occasions, but the disagreeable pain remained unchanged.
He obtained an excellent immediate effect from percutaneously inserted spinal cord electrical stimulation Since this system in not widely used in Japan, the method and our experience in this case were described in detai and the literature was reviewed. In conclusion, intractable chronic pain with hyperpathia seems to be one of the most favorable candidates for this mode of treatment. This stimulation method is easy to perform and should be applied before considering other more destructive procedures for pain relief.

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It is generally accepted that intracerebellar hemorrhages account for ten per cent of all intracerebral hemorrhage, but reports of intracerebellar hemorrhages in children under fifteen years of age are rare. Two cases of intracerebellar hemorrhage in children were experienced.
Case 1-A two-year-old boy was admitted because of vomiting and ataxia which appeared two days after a minimal head trauma. A CT scan showed a cerebellar hemorrhage. After a gradual recovery another hemorrhage attack occurred six days after admission and he again started vomiting and became drowsy. Removal of the hematoma was carried out. The histological examination of the wall showed an angiomatous malformation. Case 2-A thirteen-year-old girl had occipital pain for two months prior to admission. A CT scan showed a low density area in the cerebellum. Then she suddenly developed a severe headache and drowsiness and was admitted as an emergency case. Another CT scan showed that the low density area observed in the initial examination was replaced by high density, suggesting a hemorrhage into the cystic tumor. She had a coma, tetraplegia and respiratory arrest after a ventriculo-peritoneal shunt was established. Removal of the hematoma was carried out fifteen hours after the onset. Histologically, no tumor tissue was found, and the cystic wall showed vascular proliferation and mild gliosis. The hemorrhage may have been due to a cystic astrocytoma or hemangioblastoma. The postoperative courses were excellent in both cases.
Operative results in children, in the acute phase were good with satisfactory functional recovery in all reported cases. This suggests that surgery in children should be positively indicated, even if serious neurological findings are present.

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A 38-year-old female with delayed development of a traumatic intracerebellar hematoma which was demonstrated on serial CT scans, associated with a supratentorial cerebral contusion was reported. The patient fell and struck the occiput. She became confused and agitated, with mild anisocoria (R>L) and peripheral paralysis of the right facial nerve. Swelling and laceration were present over the right occiput. There was bloody cerebrospinal otorrhea on the right. X-ray films of the skull revealed a right temporo-occipital linear fracture, a right occipital linear fracture extending across the transverse sinus and separation of the right lambdoid suture. An initial CT scan showed a faint high density area in the cerebellar vermis suggesting a hemorrhage in addition to cerebral contusion of the right temporal lobe and a tentorial injury. The level of consciousness progressively improved within several hours with treatment including corticosteroid and hypertonic solution. CT scans performed 36 hours following the injury revealed a newly formed hematoma in the right cerebellar hemisphere and enlarged hemorrhagic foci in the right temporal lobe with perifocal edema. Ten days after the injury, she gradually became semicomatose. Marked anisocoria and bilateral spasticity followed by respiratory arrest developed when a perifocal low density area around the intracerebellar hematoma was demonstrated by CT scans. Emergency posterior fossa craniectomy was then performed. On opening of the dura mater which showed a 2 cm long laceration 20 ml of solid hematoma was extruded from an underlying cortical laceration. Debridement of the contused cerebellar hemisphere was also performed. On the first postoperative day, the level of consciousness progressively improved. However, she became semicomatose again on the second postoperative day. A postoperative CT scan performed on the second day revealed marked swelling of the cerebellum in addition to supratentorial brain edema at the site of the cerebral contusion. Despite intensive management with hypertonic solutions she died of secondary brain stem compression due to the cerebellar swelling on the 6th postoperative day. The present case suggested that a contusional hematoma of the cerebellum should be removed as soon as possible when it shows a mass effect in CT scans even if clinical signs and symptoms show improvement.

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