Intradermal tumors derived from three rat neurogenic tumor cell lines were treated by magnetic induction hyperthermia involving a ferromagnetic implant with a low Curie temperature. A single session of hyperthermia (1 hour at 45°C) against the T₉ tumor was apparently effective: almost all of the tumors disappeared. However, hyperthermia had no obvious effects on the other two tumors, even after repeated treatments at weekly intervals. Histological study of T₉ intradermal tumors following hyperthermia showed marked loss of cells and diffuse edema as well as venous dilatation and bleeding by day 0, granulocytic infiltration by day 4, and massive lymphocytic infiltration by day 8. On the 14th day extensive necrosis and lymphocytic infiltration were observed within the tumor. At this point most of the tumors had shrunk considerably. Cultured T₉ tumor cells subjected to water bath hyperthermia for 1 hour at 46°C and then injected intradermally into rats failed to develop into tumors. Weekly injections of such T₉ cells produced no recognizable immunity in the rats, as proven by the growth of tumors in subsequent challenges with untreated T₉ tumor cells. However, treating the T₉ tumor cells by hyperthermia for 1 hour at 42°C before injection produced apparent immunity in the rats, although one half of the immunizing injections resulted in the development of small intradermal tumors.
The results indicate an immunogenic activity in heat-treated tumor cells. The involvement of immunological factors in the regression of intradermal neurogenic tumors following hyperthermia was demonstrated.

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Progress has been made in hyperthermia research, but the thermal microenvironment of human brain tumors has received little attention. In six patients with brain tumors located in the cortex or subcortex, the thermal variations of the cortical surface in both the steady and dynamic states were scanned by infrared thermography, which is essentially a noninvasive technique. Hypothermal area was observed on the surfaces of cystic and necrotic lesions, which were delineated with intraoperative sonography. Recovery of surface temperature after thermal loading was delayed in these hypothermal areas. Blood flow in brain tumors, which was estimated by means of the new imageprocessing technique of thermography, was lower than that in surrounding normal tissue. Knowledge of the differences in thermal microenvironments and blood flow patterns between tumor and normal tissue will provide a theoretical framework for the use of regional hyperthermia in the management of brain tumors.

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Serial examinations by nuclear magnetic resonance-computed tomography were carried out in 35 head-injured patients aged 7 to 77 years. The injuries were classified as cerebral contusion (nine cases), acute epidural hematoma (eight cases), acute cerebral swelling (two cases), and chronic subdural hematoma (16 cases). The results of 92 measurements were divided into two groups: acute stage (within 3 days of injury) and chronic stage (2 weeks or longer after injury). The spinlattice relaxation times (T₁) of brain tissue adjacent to chronic subdural hematoma were evaluated pre and postoperatively. A Fonar QED 80-alpha system was used for magnetic resonance imaging and measurement of focal T₁. The T₁ values at the region of interest were measured 3 to 5 times by the field focusing technique (468 gauss in the focused spot), and the mean value was used for evaluation. The standard T₁ values obtained from healthy subjects were 290±41 msec in the cerebral cortex and 230±34 msec in the white matter.
Prolongation of T₁ in perifocal brain gradually shortened over time and normalized in the chronic stage. The degree of contusional edema may have been reflected in alterations in T₁. In contrast, parenchymal injury resulted in a progressive T₁ elevation, which far exceeded 500 msec in the chronic stage. Such time courses of T₁ may indicate irreversible tissue damage. There were no noticeable changes in tissue T₁ over time in patients with acute diffuse cerebral swelling or those who underwent evacuation of acute epidural or chronic subdural hematomas. The underlying pathophysiology in such situations seems to be not brain edema but cerebral hyperemia. In the presence of ischemia, the T₁ value was prolonged in the early stage, reflecting progression of ischemic edema. Remarkable prolongation of T₁—up to 1, 000 msec in the chronic stage—appears to be attributable to post-traumatic degeneration of brain tissue.

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To clarify the pathogenesis of hyponatremia in the acute phase of severe cerebrovascular disease, the authors studied 119 patients who had been too ill to eat by mouth for at least 2 weeks. In 38 patients the serum sodium (Na) level fell below 130 mEq/l. In these 38 patients, the serum Na, potassium (K), and creatinine (Cr) levels and osmolarity, blood urea nitrogen (BUN), and hematocrit, and urinary Na, K, and Cr were measured daily for 2 consecutive weeks. The balance of water, Na, and K, Cr clearance, free water clearance, and excreted fraction of filtered Na were calculated. Body weight and plasma levels of such hormones as antidiuretic hormone (ADH), aldosterone, and cortisol were measured. Ten of the 38 patients with hyponatremia were dehydrated, which is incompatible with the syndrome of inappropriate secretion of ADH (SIADH). The remaining 28 patients fulfilled the criteria for SIADH. Subsequently, special attention was directed to the serum K level in the hyponatremic stage. (The serum K level should be lowered due to the dilution mechanism in SIADH.) Based on the results, these 28 patients were divided into two groups: Group A (17 patients) had elevated serum K levels in the hyponatremic stage and Group B (11 patients) had no elevation of serum K. In Group B, changes in ADH, BUN, and body weight, which are characteristic of SIADH, were observed, but no such changes were noted in Group A. In Group A the K balance showed a tendency for K out>K in and an increased serum K level despite profuse urinary excretion of K. These findings indicate an increased K level and hyponatremia due to extracellular K outflow and intracellular Na inflow, respectively, suggesting an Na-K pump disorder. The mechanism of hyponatremia in the acute phase of cerebrovascular disease may involve not only dehydration and SIADH but also “sick” cells responding to the apparent Na-K pump disorder.
The group who tended to become dehydrated appeared to require a hypertonic Na solution to compensate for the loss of Na. Patients with SIADH were not considered to require water restriction, since they recovered spontaneously in a short period of time. Those with sick cells, a condition that is dependent on the underlying disease, were considered to require nutritional and glucose/insulin/K therapy to recover from the disease.

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Digital subtraction angiography with intravenous injection of contrast medium was used to assess 10 patients with ischemic disease. The time-density curve (TDC) was evaluated for its usefulness in analyzing brain blood circulation (dynamics). Such other parameters as peak time (PT), mean transit time (MTT), and mode of transit time (MOTT) were also assessed. Particular attention was paid to high convexity, watershed, and perforator areas of the middle cerebral artery, which are regions of interest in the bilateral hemispheres. The dynamics of blood circulation demonstrated by this method were compared with those demonstrated by single photon emission computed tomography (SPECT).
In patients with carotid artery stenosis, the TDC at the convexity area on the affected side showed both a gentle upward slope and a slow downward slope, and all parameters (PT, MTT, MOTT) were prolonged. After endarterectomy, the delay in all parameters decreased and the laterality of the TDC diminished. In patients with middle cerebral artery occlusion, the TDC at the convexity area on the affected side showed delay of attenuation, and all parameters were prolonged. After superficial temporal artery-middle cerebral artery anastomosis, the peak on the operated side was higher than that on the unaffected side and prolongation of MTT and MOTT on the affected side was decreased. In cases of moyamoya disease, none of the parameters could be calculated because the TDC showed no downward slope. In all of the evaluable cases, TDC data were superior to SPECT determinations in detecting laterality of the circulation. These results indicate that this method accurately demonstrates laterality of circulation time and volume as well as the degree of collateral circulation. The TDC and other parameters appear useful in determining whether or not surgery is indicated and in estimating the postoperative circulation in patients with ischemic disease.

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Although conventional anastomosis of the superficial temporal artery (STA) to the cortical branch of the middle cerebral artery (MCA) is a common procedure in many parts of the world, postoperative angiography shows that, in terms of MCA branch filling, the results are not as good as might be expected. In an attempt to achieve good perfusion of the branches of the MCA, the authors anastomosed the STA and MCA in the sylvian fissure just distal to the trifurcation (STApMCA anastomosis) in 11 patients between March, 1983 and June, 1985. Ten had ischemic cerebrovascular lesions and one had a saccular aneurysm at the cavernous portion of the internal carotid artery. Postoperative quality of life was excellent in seven cases and good in four. On angiograms obtained 1 month after surgery, visualization of the MCA was excellent in seven cases, good in one, and poor in two; an occlusion persisted in one.
One advantage of this procedure is the immediate restoration of flow into the MCA tree via a larger caliber anastomosis than is possible with a standard cortical bypass. In addition, postoperative angiography allows better visualization of the MCA tree than is achievable with conventional STA-MCA anastomosis. The disadvantages are that one of the main branches of the MCA must be temporarily occluded, new instruments must be prepared for the anastomosis in the sylvian fissure, and the anastomosis must be performed deep in the sylvian fissure. None the less, STA-pMCA anastomosis is a satisfactory alternative in cases of transient ischemic attack, reversible ischemic neurological deficits, and minor completed stroke caused by occlusion or stenosis of the internal carotid artery.

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Clinical features of 70 elderly patients (over age 65) with ruptured intracranial aneurysms were compared with those of 70 middle-aged patients (45 to 55 years old) with similar clinical grades. Postoperative complications were particularly noted. There were more females and a higher incidence of internal carotid artery aneurysms in the elderly than in the middle-aged group. Contrary to expectation, the frequency of rebleeding was 45% among the elderly patients who received conservative therapy. The mortality rate among elderly patients who underwent surgery was 12.5%, whereas it was 1.5% in the middle-aged group. The cause of poor outcome in the elderly group was cerebral infarction after severe vasospasm, although the incidence of symptomatic vasospasm was almost the same in both groups. Hyponatremia, gastrointestinal bleeding, and electrocardiographic abnormalities were more prevalent in the elderly group. Although intensive postoperative care may be required, an aggressive approach to treating ruptured intracranial aneurysms in the elderly is recommended.

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B-mode real-time ultrasonography using linear and sector scanning probes of 5 or 7.5 MHz was applied during 17 operations for the following spinal cord lesions: five syringomyelias, one arachnoid cyst, eight intramedullary tumors (three benign astrocytomas, three hemangioblastomas, one ependymoma, and one subependymoma), one intradural extramedullary tumor (neurinoma), and two lipomas with spina bifida. Preoperative computed tomography (CT) scan was performed with a Somatom II scanner. Following laminectomy the wound was filled with a sterile solution and scanning was performed through this “water path” before the dura was opened. Five of eight intramedullary tumors (one benign astrocytoma, one subependymoma, two hemangioblastomas, and one ependymoma) were enhanced on CT, whereas three (two benign astrocytomas and one hemangioblastoma) were not enhanced. Three lesions (two hemangioblastomas and one ependymoma) were hyperechoic on intraoperative spinal sonography (IOSS), while five (three benign astrocytomas, one subependymoma, and one hemangioblastoma) were isoechoic. One intradural extramedullary tumor (neurinoma) was enhanced on CT and hyperechoic on IOSS. Two lipomas showed low density on CT but were hyperechoic on IOSS. Ten of 13 syrinxes or cysts (five syringomyelias, one arachnoid cyst, one benign astrocytoma, one subependymoma, one hemangioblastoma, and one ependymoma) were identified with CT, but three (one benign astrocytoma and two hemangioblastomas) were not defined. Twelve of these 13 lesions were anechoic on IOSS, and multiple cysts were detected. One cyst that was identified with IOSS had not been identified preoperatively. Masses and cysts were visualized more clearly with the 7.5 MHz transducer than with the 5 MHz transducer. However, one very small lesion was not detected, and the probe is large. Therefore, a transducer of higher frequency should be developed for the spinal cord. IOSS is noninvasive and demonstrates the precise size and location of the lesion in real time, so the lesion can be approached with minimum damage to the spinal cord. This technique is extremely useful and should be applied in all surgery for spinal cord lesions.

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Most chronic subdural hematomas (CSH) are caused by trauma, but they sometimes occur nontraumatically or after surgery for nontraumatic intracranial disease. During the past 5 years, the author encountered 10 cases of postoperative CSH. They included five of 101 patients who had undergone extra-intracranial anastomosis (5.0%), four of 177 who had received ventriculoperitoneal shunts (2.3%), and one of 233 who had undergone aneurysmal repair (0.4%). Computerized tomographic, operative, and pathological findings were the same as in traumatic CSH. Four cases were resolved by surgery and two by blocking of the shunt system; four patients recovered without therapy. CSH appears to develop under specific conditions, namely, cerebrospinal fluid or a mixture of blood and cerebrospinal fluid remain in the subdural space for a long interval. Cerebral compliance may play an important role in the aggravation of nontraumatic CSH.

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The authors encountered three cases of intracerebral hematoma (ICH) occurring early after surgery for chronic subdural fluid collection. A 54-year-old male complained of speech disturbance and facial weakness 22 hours after irrigation of a chronic subdural hematoma (CSH). Computed tomography scan showed an ICH beneath the previously removed CSH. His neurological deficit disappeared with conservative treatment. A 73-year-old male developed expressive aphasia 14 hours after surgery for chronic subdural hygroma. The patient was treated conservatively and the aphasia was still present 1 year after the ictus. A 3-month-old boy developed a left ICH and had a generalized convulsion 60 hours after irrigation of bilateral CSH. With conservative treatment there was no neurological deficit 1.5 months after the episode. Almost all of the reported ICH appeared in the subcortex just beneath a previously evacuated collection of subdural fluid. The symptoms were rapid deterioration of consciousness and focal neurological deficits developing soon after surgery. One possible mechanism of ICH is diapedesis through increased permeability of parenchymal blood vessels due to the sudden increase in cerebral blood flow after longstanding extracerebral fluid collection. The prognosis of this complication is poor. Therefore, subdural fluid should be removed slowly to avoid sudden decompression.

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The authors report three cases of subdural hematoma of acute onset in association with the rupture of intracranial aneurysms. Although all were in critical condition, two patients recovered after emergency surgery, which entailed removal of the hematoma and aneurysmal neck clipping. Acute subdural hematoma most often results from the tearing of bridging and cortical veins. Much less frequently, subdural bleeding may be secondary to the rupture of an intracranial aneurysm. In these instances, the subdural clot may be massive and immediately life-threatening. Currently, computed tomography (CT) is the examination of choice for the diagnosis of acute subdural hematoma. However, CT does not reliably depict blood vessels and so is of little value in ruling out such vascular abnormalities as aneurysms. The dilemma is whether or not to perform angiography prior to surgery in the presence of dire neurological signs. The authors conclude that, if the patient's condition allows, angiography should be performed, for the following reasons: 1) rebleeding from the aneurysm can be adequately controlled; 2) in skillful hands, angiography can be accomplished within the time required for other preoperative examinations; and 3) the aneurysm can be treated after evacuation of the hematoma, thereby such complications as vasospasm can be adequately managed.

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Two patients with germ cell tumors of the basal ganglia and the thalamus are described. A 10year-old boy developed left hemiparesis and precocious puberty. Computed tomography (CT) of the brain revealed a small lesion in the right basal ganglia, which appeared to be rapidly growing. Elevation of human chorionic gonadotropin (HCG) in both serum and cerebrospinal fluid was compatible with germ cell tumor. A craniotomy was performed and the tumor was partially removed. Histological examination verified a mixed-type germ cell tumor composed of embryonal carcinoma, choriocarcinoma, and germinoma. An 11-year-old boy complained of right hemiparesis, and a CT scan showed a well-enhanced, cystic tumor in the left thalamic region. The tumor was partially resected and was diagnosed histologically as germinoma. A high level of HCG was found in the contents of the cyst. HCG and alpha-fetoprotein, which are so-called tumor markers, decreased over the course of treatment in both cases, and seemed to be indicators of the effectiveness of treatment. However, the authors feel that the differential diagnosis of germ cell tumors cannot be based solely on the level of these tumor markers. The characteristic features of germ cell tumors of the basal ganglia and thalamus are discussed.

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A 65-year-old woman had a 2 months' history of speech and gait disturbance. A precontrast computed tomography scan revealed a low-density mass in the left temporal region, which was irregularly enhanced after administration of contrast medium. A left carotid angiogram showed a shift of the middle cerebral arteries, but neither tumor staining nor feeding from the external carotid artery were observed. The extracerebral tumor in the left temporal region was removed, and the histological diagnosis was microcystic meningioma. Light microscopy revealed abundant microcysts throughout the tumor tissue, and electron microscopy disclosed that the microcysts were located in the extracellular spaces and not in the cytoplasm. It is possible that the microcysts simulate the formation of the subarachnoid space of the normal pia-arachnoid membrane and that, through their aggregation, the microcysts might form the macrocyst of the cystic meningioma.

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A 15-year-old boy underwent radiation therapy for a pineal tumor. He appeared to enjoy complete clinical recovery, follow-up computed tomography (CT) scans showed no evidence of residual tumor. Surgery was not performed. The tentative diagnosis of pineal germinoma was based on the tumor response to radiation therapy. However, 5 years later, the patient visited the hospital with a complaint of left knee pain. Myelography disclosed scattered spinal tumors below the Th₁₂ level, and laminectomy and biopsy showed the tumors to be pineoblastoma. Thus, it is likely that the initial pineal tumor was not germinoma but pineoblastoma and, in fact, on re-evaluation of the earlier CT scan, the characteristic features of pineoblastoma were evident. It has been well accepted among neurosurgeons that, for pineal tumors, radiation therapy is the treatment of first choice, unless the neuroradiological findings suggest a radiation-resistant tumor, such as teratoma. Both pineal germinoma and primitive neuroectodermal tumor (medulloblastoma, neuroblastoma, and pineoblastoma) are sensitive to radiation therapy. On the other hand, it is well known that, whereas pineal germinoma is relatively benign, pineoblastoma is not. It may be advisable for neurosurgeons to adopt a more aggressive approach to pineal tumors, including biopsy and histological diagnosis prior to treatment planning.

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An atypical, walnut-sized parietal mass was identified in a 9-day-old male. The pregnancy and delivery had been normal. A plain skull X-ray obtained on admission showed a small defect beneath the mass and excessively split sutures, which indicated very high intracranial pressure. A computed tomography (CT) scan revealed a triangular-shaped, low-density area in the falx, extending to the quadrigeminal cistern. Magnetic resonance imaging (MRI) demonstrated a peculiar intracranial extension from the skull defect to the cistern via an intrafalcial sinus-like tract. After excision, it was confirmed by metrizamide CT cisternography that the sinus-like tract was a cerebrospinal cavity. The histological diagnosis was myxofibroma. It was speculated that the mass might have arisen from primitive mesenchymal cells. MRI should be the first diagnostic procedure performed in cases of midline anomalous lesions.

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