Early neurophysiological changes and pathological findings were studied following experimental cerebral concussion in rabbits. The animals were lightly anesthetized and subjected to occipital trauma with a pendulum impactor. Experimental concussion was defined as fulfillment of at least two of the three following criteria: apnea for more than 10 seconds, absence of the light reflex for more than 10 seconds, and bradycardia or tachycardia (less than 50% or more than 10% of the preimpact rate, respectively). There were 13 cases of lethal concussion, 16 of nonlethal concussion, and 15 of nonconcussion. The resultant head acceleration ranged from 250 to 1660 G and its duration was 0.8 to 5.5 msec. During the first 30 seconds after impact, electroencephalographic activity showed little change even in cases of lethal concussion, but slowed over the next several minutes due to respiratory suppression. The duration of apnea in cases of nonconcussion was under 9 seconds and, in cases of nonlethal concussion, averaged 21 seconds. Five of the rabbits with lethal concussion were apneic throughout the observation period, and the remaining eight exhibited apnea for an average of 46 seconds after impact. The light reflex was absent for less than 9 seconds in nonconcussion cases and for an average of 71 seconds in cases of nonlethal concussion. One animal with lethal concussion exhibited absence of the light reflex throughout, and the remaining 12 animals for an average of 39 seconds. Bradycardia was seen in 15 cases of nonlethal and two cases of lethal concussion. Six rabbits with lethal concussion had tachycardia. Two animals without concussion showed bradycardia and the remainder showed no change. In cases of nonconcussion there was little hemorrhagic change in the brainstem and upper cervical region. In nonlethal concussion, gross hemorrhagic change was observed in the pons in 25% of cases, in the medulla in 56%, and in the cervical cord in 19%. For lethal concussion the rates were 75%, 83%, and 75%, respectively. Among rabbits with fatal concussion, microscopic parenchymal perivascular hemorrhage was seen in 56% in the pons and in 78% in the medulla, but was not observed in the brainstem of rabbits with nonlethal or nonconcussion. Brainstem pathological changes were well correlated with the severity of concussion. Hemorrhagic changes were seen in the cerebrum in 47% of animals and in the cerebellum in 72%, and there was no correlation with the severity of injury. The authors conclude that the lesion responsible for concussion was in the brainstem and that cerebral contusion and respiratory disturbance modified the primary brainstem damage.

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Lesions in the frontal base have been conventionally approached extra and intradurally through a bilateral frontal craniotomy. However, when the lesion is large or deeply situated, wider retraction of the bilateral frontal lobes is required to obtain a sufficient operative field. The authors describe a new operative approach to dumbbell-shaped tumors in the frontal base, consisting of en bloc osteotomy of the bilateral orbital roofs and frontal sinus. This procedure, which is a modification of the transbasal approach described by Derome, is termed the “extensive transbasal approach.” Successful applications of this procedure in three patients with frontal base tumors, two with frontal base fractures, one with a frontal arteriovenous malformation, and one with a frontal sinus mucocele are described. Also, the advantages of this approach over other, conventional operative approaches are discussed.

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In the acute neurosurgical setting, nonketotic hyperosmolar hyperglycemic coma (NHC) is thought to be caused by cerebral dehydration therapy and administration of steroids, glycerol, or mannitol. The mortality of this complication is reportedly very high, and is due to acute renal and/ or cardiac failure. The authors evaluated the effect of low-dose dopamine (LDD; 1 to 5μg/kg/min) administration in 10 patients with this syndrome. LDD was given to five patients. In these cases, hypovolemia was treated under central venous pressure monitoring with an iso-osmolar hyponatremic lactate solution given in a volume greater than the urine output. After the hypovolemia was corrected, the fluid was administered in a volume equal to the urine output until the serum osmolarity was normalized. In the five patients not given LDD, a large quantity of hypotonic solution was rapidly administered. In all patients treated with LDD, the urinary sodium increased and the urinary output stabilized. Consequently, the excess urea-nitrogen and serum sodium were quite easily washed out. The total net intake volume for the normalization of serum osmolarity was small and the duration of treatment was much shorter than that of patients not treated with LDD. The LDD regimen was not associated with complications, such as aggravation of cerebral edema, renal failure, or cardiac failure. On the other hand, three of the five patients not given LDD died of acute renal and/or cardiac failure without normalization of laboratory data. It is emphasized that this therapy, which results in β-effect of catecholamine, sodium diuresis, and increased renal blood flow, is a practical means of managing acute neurosurgical cases complicated by NHC.

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The authors examined numerous clinical features in 15 patients in whom brain metastases from lung cancer recurred after total or subtotal removal. The incidence of recurrence after initial removal of brain nodules was 46.9% (15 of 32 cases). There was no significant correlation between the incidence of recurrence and the histology of the lung cancer, the site of brain nodules, or age. Recurrent brain nodules were the cause of or contributed to death in 60% of recurrent cases. Recurrence was within 3 months of initial removal of brain nodules in 10 of the 15 patients. Brain metastasis recurred only at the initial site in 11 cases (73.3%). Three patients developed carcinomatous meningitis and one had multiple metastases in addition to recurrence or regrowth at the original site. The primary lung cancer was relatively stable at the time of recurrence of brain nodules in 60% of the patients.
Tumor removal and radiotherapy are highly recommended for prevention of early recurrence following initial removal of brain metastases. Removal of metastatic tumor is advised in the event of recurrence after 1 year from initial surgery, since the outcome after second surgery tends to be fair. However, tumor removal and radiotherapy are sometimes capable of inducing recurrence of brain nodules. Therefore, it is hoped that more effective cancer chemotherapy will be developed in the near future.

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Two cases of olfactory neuroblastoma with intracranial extension are described. The radiological features, including those of magnetic resonance (MR) imaging, are emphasized. On plain X-rays, the nasal cavity, ethmoid, sphenoid, and/or frontal sinuses were opacified. Erosion of the bony confines of the sinuses and orbit was seen in Case 1, but no bony destruction was observed in Case 2 despite intracranial tumor invasion via the seemingly intact cribriform plate. Angiography showed tumor staining in the ethmoid sinus, and in Case 1 tumor vessels were also found in the base of the frontal lobe. Computed tomography (CT) disclosed a large, soft, enhanced tissue mass occupying the nasal cavity and paranasal sinuses and extending into the anterior cranial fossa. In Case 1, MR images (0.5 Tesla) with a short spin echo sequence (repetition time [TR], 600 msec; echo time [TE], 26 msec) and a long spin echo sequence (TR, 2100; TE, 30, 60, 90) were obtained. T₁weighted images delineated the tumor accurately in relation to the normal architecture. T₂weighted images revealed widespread brain edema, with the tumor recognizable as a mass of low signal intensity within the high-intensity region of brain edema. The CT and MR imaging findings are by no means specific to olfactory neuroblastoma. However, both modalities, particularly MR imaging, are of special value in demonstrating the precise extent of the tumor in three dimensions.

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A case of pituitary apoplexy causing pituitary hemorrhage with extension into the third ventricle is reported. The patient was a 73-year-old, obese female admitted with sudden onset of vomiting and impaired consciousness. Neurological examination revealed that she was stuporous, with marked neck stiffness and a dilated left pupil. A plain skull X-ray showed sellar enlargement and destruction of the dorsum sellae. Computed tomography demonstrated a high-density area in the third and lateral ventricles and a round, high-density mass in the suprasellar cistern. The patient died the next day. Autopsy revealed a large tumor in the sellar and suprasellar areas. The tumor and the hematoma within it compressed the floor of the third ventricle and passed through the lamina terminalis and the hypothalamic region. Histological examination disclosed a basophilic adenoma. The pituitary hemorrhage appeared to be the result of ischemia and necrosis within the pituitary adenoma caused by its acute expansion. The extension of the hematoma into the third ventricle was attributable to the large size of the tumor and its close adhesion to the floor of the third ventricle.

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A 15-year-old boy suddenly developed a headache, followed by progressive weakness of the right extremities. A computed tomographic scan obtained on admission showed a low-density area in the left putamen extending to the internal capsule. No neurological deficits were observed other than slight dysarthria and right hemiparesis. Left carotid angiography showed the characteristic “string of beads” deformity of fibromuscular dysplasia (FMD) extracranially and complete occlusion of the internal carotid artery at the C₂ portion. The right carotid artery and both vertebral arteries were normal. Anastomosis of the left superficial temporal and middle cerebral arteries was performed 1 month after the onset. The patient recovered quickly from the hemiplegia and was discharged with no neurological deficits. Angiograms obtained 3 months later showed not only patency of the bypass, but also recanalization of the intracranial internal carotid artery. Cervicocephalic FMD mainly affects middle-aged women, and is uncommon in children; only nine childhood cases have been reported. This disorder may play an important role in the genesis of strokes among children.

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A 76-year-old female struck her head in the parietal region and noticed a soft scalp mass. Approximately 3 months later, the mass was enlarged and she was evaluated at a local hospital. Although the tentative diagnosis was old subcutaneous hematoma, incision of the scalp revealed not hematoma but rather a tissue and bony defect. On admission to the authors' institution, she was found to have a round, smooth, subcutaneous mass in the upper left parietal region. The tumor was about 5 cm in diameter and 4 cm in height, and was soft, nonpainful, and pulsatile. Plain X-rays revealed an osteolytic lesion in the left parietal bone. Computed tomography demonstrated a highdensity lesion corresponding to the bony defect, which was homogeneously enhanced by contrast material. Left external carotid angiography showed the mass to be vascular, its main feeder being the middle meningeal artery. It was concluded that the tumor originated from the diploe. The tumor was subtotally removed, and histopathological examination showed it to be a plasmacytoma. Laboratory tests, including protein electrophoresis, disclosed hypergammaglobulinemia with Mspikes. Immunoelectrophoresis demonstrated a serum paraprotein of immunoglobulin G kappa specificity.
Multiple myeloma diffusely involving bone is well known, but a soft mass alone with a bony defect in the cranial vault is very rare. The clinical features and treatment of silent, solitary masses associated with multiple myeloma are discussed.

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A 56-year-old male with a 11-month history of late-onset epilepsy was hospitalized because of status epilepticus. The physical examination and laboratory data were normal. Neurological examination revealed weakness of the right leg. Coronal computed tomography showed a mass of slightly high density in the bilateral parietal convexity, with homogeneous enhancement by contrast medium. Magnetic resonance imaging disclosed an en-plaque epidural tumor in the parietal region along the superior sagittal sinus, which was normointense on T₁-and T₂-weighted images. Conventional and digital subtraction angiography showed an avascular mass between the superior sagittal sinus and the inner table of the skull at the parietal region. The mass was thought to be situated in the parietal epidural space. On surgery, however, the tumor was found to be located mainly in the dura and subdural space. The histological diagnosis was malignant lymphoma of the B cell type. Ga-scintigraphy, physical examination, and bone marrow and peripheral blood examinations disclosed no systemic abnormalities. Therefore, the tumor was interpreted as a primary intracranial malignant lymphoma. Reports of primary intracranial malignant lymphoma have been increasing, but most have been located in the cerebrum. The dural-subdural location in this case is evidently rare.

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A 63-year-old female was admitted with a 5-day history of left hemiparesis. Computed tomography showed an enhanced mass with perifocal edema in the right frontal parasagittal region and an irregular-shaped, high-density mass anterior to the tumor. Right carotid angiography disclosed the prominent middle meningeal artery (MMA) to be the main feeding vessel of the tumor. In the venous phase, the superior sagittal sinus (SSS) was obstructed and a dilated middle meningeal vein (MMV) drained downward to the sphenoparietal sinus. Left carotid angiography demonstrated similar findings. There was a filling defect in the lumen of the MMV due to the MMA running within the vein. At surgery, careful manipulation was required, as the venous blood in the left MMV drained not only from the tumor but also from the anterior half of the SSS. The left MMA was found to run through the cavity of the dilated MMV. The SSS was invaded by tumor. There was an old hematoma cavity containing xanthochromic fluid in the brain parenchyma adjacent to the tumor. Histological examination showed meningothelial meningioma. The postoperative course was uneventful, although the right MMV was opacified on carotid angiography. It was suspected that obstruction of the SSS by tumor invasion had caused dilatation of the bilateral MMV and peritumoral hemorrhage due to disturbance of the venous drainage.

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A 39-year-old male experienced unilateral right hearing loss and tinnitus for 7 years and was hospitalized after he suddenly developed severe headache, vertigo, and right facial paralysis. Computed tomography (CT) showed a round, high-density area in the right cerebellopontine angle. Magnetic resonance (MR) imaging demonstrated a crescent-shaped region of high signal intensity, representing hemorrhage, in the superior aspect of the tumor, surrounded by edema. The right internal auditory canal was enlarged. Four-vessel angiography disclosed neither an aneurysm nor an arteriovenous malformation. A right suboccipital craniectomy revealed an encapsulated mass 3 cm in diameter in the right cerebellopontine angle. The tumor was totally removed. Histological examination revealed a typical neurinoma composed of Antoni type A and B cells. After undergoing anastomosis of the right hypoglossal and facial nerves, the patient was discharged in good condition. In this case MR imaging demonstrated intratumoral hemorrhage (which is rare in cases of acoustic neurinoma) and the surrounding tissue more clearly than did CT scanning.

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A 68-year-old male was hospitalized because of headache, nausea, and disturbance of consciousness. Neurological examination on admission disclosed somnolence, disorientation, marked neck stiffness, papilledema, and quadriparesis. Computed tomography (CT) scanning demonstrated a round mass with marked contrast enhancement in the right sylvian fissure and small contrast-enhanced masses in the interpeduncular, quadrigeminal and ambient cisterns. CT also showed marked peritumoral edema, a midline shift, and hydrocephalus. The patient's consciousness level and respiration deteriorated 3 days after admission and a craniotomy was performed. The tumor, which was well demarcated, firmly attached to the sphenoidal ridge, and grossly appeared to be a meningioma, was totally removed. Histologically, the tumor had two well defined components, glioblastoma and fibrosarcoma. The patient underwent ventriculoperitoneal shunting, chemotherapy, and radiotherapy after surgery, but the primary tumor soon recurred, with scalp metastasis, and he died 5 months postoperatively. Autopsy revealed metastases to the liver, spleen, and spinal cord. The histogenesis of this mixed tumor and the mechanism of extracranial metastasis are discussed, and the literature is reviewed.

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A 58-year-old male presented with painful right ophthalmoplegia and was diagnosed as having Tolosa-Hunt syndrome. High-dose oral administration of a corticosteroid provided significant pain relief, but total ophthalmoplegia persisted. Computed tomography (CT) showed a tumor-like mass in the bilateral cavernous sinus. Angiography revealed occlusion of the right internal carotid artery. According to the literature, about 70% of cases of Tolosa-Hunt syndrome are caused by parasellar neoplasms. A transcranial biopsy of the patient's lesion revealed a nonspecific granulomatous process in the wall of the right cavernous sinus. He was again placed on high-dose corticosteroid therapy and within 1 week the right visual acuity improved slightly. The corticosteroid dose was gradually tapered over 3 months. After 2 months of therapy, the external ocular movement had almost fully recovered, although the light reflex was absent and the CT findings did not change.

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A solitary hemangioblastoma of the optic nerve was found in a 36-year-old male with a distinct family history of intracranial hemangioblastoma. The patient was admitted with complaints of visual loss and exophthalmos of the right eye. X-rays showed enlargement of the right optic canal. Right carotid angiography revealed a hypervascular tumor in the orbital apex, supplied by the ophthalmic artery. Computed tomography disclosed a pear-shaped, isodense mass with moderate contrast enhancement in the orbital apex. The right optic nerve was enlarged along its entire course and was involved with the apical mass. Surgery via the right frontal extradural approach disclosed a solid, vascular tumor involving the optic nerve at the apex of the orbit. Histological examination showed the tumor to be a characteristic hemangioblastoma. Over 90% of intracranial hemangioblastomas are located in the posterior fossa. Supratentorial hemangioblastomas, especially those arising in the optic nerve, are extremely rare. In addition, optic nerve hemangioblastomas are frequently familial and are associated with infratentorial hemangioblastomas, angiomatosis retinae, and cysts of the abdominal viscera.

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