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Technical advances in accessing the lateral cranial base have permitted disease in this area previously deemed inoperable to be resected. The procedures required to effect an oncologically adequate resection are often long and accompanied by the potential for serious, even life-threatening, complications. Although it has been demonstrated that such disease can be extirpated, the question of whether such heroic surgery improves long-term survival remains unanswered. We retrospectively reviewed the records of 25 patients who underwent a combination of frontotemporal craniotomy with other, more conventional, anterolateral procedures (eg, infratemporal fossa approach, maxillectomy, orbitectomy, mandibulopharyngectomy) to resect stage IV malignant disease of the lateral to midcranial base between 1983 and 1990. Perioperative deaths occurred in 2 patients, 1 patient died of unrelated causes free of disease, and 2 patients were lost to follow-up, leaving 20 patients with a minimum 5-year evaluation. Five (25%) of the 20 patients we monitored were free of disease. Of those patients in whom recurrent disease developed, local control was achieved in about 50%; however in 80% of those with recurrence, metastatic disease developed. Surgical treatment of selected stage IV malignant disease of the lateral to midcranial base appears to have provided long-term disease-free survival to 25% of patients in this series who would otherwise have had little hope of survival.

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Two cases of neurosarcoidosis in the pituitary gland are presented with a review of past cases from the literature. Previous reported cases have always shown changes on the ondocrine exis clinically. These two cases, however, were endocrinologically normal prior to surgery. The evaluation of neurosarcoid in the pituitary, clinically and radiographically, is discussed.

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OBJECTIVE: To evaluate lipomas of the internal auditory canal (IAC) and cerebellopontine angle (CPA). STUDY DESIGN: Retrospective review. METHODS: Review of a multi-institutional series of 17 lipomas of the IAC/CPA, combined with a Medline review of the 67 cases reported in the world literature. RESULTS: This series of 17 IAC/CPA lipomas is the largest reported series to date, bringing the total number of documented cases to 84. There appears to be a nearly 2:1 male to female predominance. Sixty percent were left-sided lesions, and three were bilateral. Hearing loss, dizziness, and tinnitus were the most common presenting symptoms. Surgical resection was performed in 52 (62%) of these lesions; however, total tumor removal was accomplished in only 17 (33%), which is most likely because of the fact that these tumors tend to have a poorly defined matrix and a dense adherence to neurovascular structures. Sixty-eight percent of patients experienced a new deficit postoperatively, 11% were unchanged, and only 19% improved with no new deficit. Only one documented case of tumor growth was identified; however, the reported follow-up was short (average, less than 3 years). CONCLUSION: With the magnetic resonance imaging techniques now available, lipomas can be reliably differentiated from other masses within the CPA and IAC, so histopathologic diagnosis is rarely necessary. Because of the potential for significant morbidity with resection of these lesions, we believe that conservative follow-up is the best treatment option for patients with these rare lesions. Surgery is indicated only when significant progressive or disabling symptoms are present.

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PURPOSE: To assess the accuracy of MR imaging in predicting dural, venous sinus, and perineural invasion by skull base tumors. METHODS: The preoperative MR images of 22 patients who had resection of skull base neoplasms were evaluated for the following characteristics: dural enhancement, pial enhancement, local perineural invasion by adjacent tumor, and venous sinus invasion by tumor. The greatest width of dural enhancement was measured, and the character of dural enhancement was noted. The pathologic and surgical reports were reviewed retrospectively with specific attention to dural, venous, and local perineural invasion. RESULTS: Of the 22 patients studied, dural invasion by tumor was confirmed in eight patients, vascular invasion in six patients, and perineural invasion in four patients. The sensitivity of dural enhancement in predicting invasion was 88%, the specificity 50%, and the accuracy 64%. When enhancement and focal nodularity were present, the sensitivity remained at 88%; however, specificity was 100% and accuracy 95%. If the dural enhancement was more than 5 mm thick, sensitivity, specificity, and accuracy were 75%, 100%, and 91%, respectively. Predicting tumor invasion of the dura by the presence of pial enhancement was 50% sensitive and 100% specific. Venous sinus/jugular vein invasion was predicted with 100% sensitivity, 94% specificity, and 95% accuracy. Local perineural invasion was predicted with 100% sensitivity, 50% specificity, and 59% accuracy. CONCLUSIONS: The presence of pial enhancement, focal dural nodules, or dural thickening of more than 5 mm is highly accurate in predicting the presence of neoplastic dural invasion. Linear enhancement of dura does not imply dural infiltration by tumor. Venous invasion by tumor can be predicted accurately with preoperative MR imaging.

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Brain injury is the leading cause of death among individuals under the age of 45 years in the United States and Europe. Recently, the neuropathologic classification of posttraumatic brain damage has provided insight into the specific mechanisms underlying traumatically induced neuronal damage and death. Studies regarding the biomechanics of brain trauma have also provided great insight into the pathophysiologic mechanisms underlying specific patterns of posttraumatic cellular death. Based upon recent clinical evaluations and biomechanical studies, laboratory models of human brain injury have been developed that faithfully reproduce a number of important features of clinical brain trauma. Biomechanical models have been used to study both the acute sequelae of brain injury and the role of neurochemical alterations in contributing to the development of secondary or delayed cellular death and damage. This report reviews and integrates the laboratory investigations linking experimental models of brain injury to clinical diagnosis and treatment.

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PURPOSE: To determine the value of magnetic resonance (MR) imaging in predicting resectability of head and neck neoplasms around the carotid arteries. MATERIALS AND METHODS: Forty-nine patients (28 male patients and 21 female patients aged 17-79 years; mean, 57.3 years) with head and neck masses and clinical evidence of carotid wall invasion underwent MR imaging. T1-weighted, T2-weighted, and gadolinium-enhanced T1-weighted images were analyzed to determine circumferential involvement of 53 arteries by tumor. RESULTS: More than 270 degrees of circumferential involvement was considered suggestive of unresectability of the malignant neoplasm; 270 degrees or less was considered lack of invasion. The sensitivity of MR imaging for determination of unresectable disease was 100% (12 of 12 cases), specificity was 88% (36 of 41), and accuracy was 91% (48 of 53). Accuracy was 100% for squamous cell carcinoma (n = 29). CONCLUSION: Tumor that encompasses more than 270 degrees of the carotid artery probably cannot be removed from the artery. Tumor that involves 270 degrees or less of the artery can be removed.

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Intracranial meningiomas are known to infiltrate surrounding structures such as the calvaria and dural sinuses, and the brain itself. The issue of whether meningiomas invade major intracranial arteries is of clinical importance, particularly in the case of meningiomas of the cavernous sinus. If a meningioma has not invaded the carotid artery wall, complete tumor removal may be accomplished with careful dissection from the carotid artery; however, if the tumor has infiltrated the wall of the carotid artery, complete removal may require sacrifice of the artery. To determine whether cavernous sinus meningiomas invade the carotid artery, the authors retrospectively reviewed the histopathology of 19 consecutively treated individuals whose carotid artery was sacrificed during removal of a meningioma involving the cavernous sinus. Patients were selected for carotid artery resection based on preoperative magnetic resonance imaging studies demonstrating complete encasement of the artery. Reconstruction of the carotid artery was planned depending on the results of preoperative balloon test occlusion with blood flow determinations. None of the 19 patients had pathological evidence of malignant tumor. Eight individuals (42%) were found to have infiltration of the carotid artery by meningioma. In five cases, focal involvement of the adventitia of the carotid artery wall was noted and, in three, the vessel was infiltrated up to the tunica muscularis. In no case was the tunica muscularis invaded by tumor. Thus, meningiomas of the cavernous sinus do infiltrate the internal carotid artery and, in order to completely resect these lesions and effect a surgical cure, it may be necessary to sacrifice the carotid artery with or without reconstruction.

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Traumatically induced hippocampal damage is a frequent sequela of fatal human head injury and is traditionally considered to be the result of decreased cerebral perfusion secondary to raised intracranial pressure (ICP). However, in previous studies employing an experimental model of acceleration head injury, hippocampal lesions have been observed in the absence of high ICP. To further elucidate the role of raised ICP in the production of posttraumatic hippocampal neuronal damage, 14 cases of fatal human nonmissile head injury, in which the measured ICP was less than 20 mm Hg, were subjected to light microscopic evaluation for the frequency and anatomic distribution of hippocampal damage. The mean maximal ICP of the 14 patients was 17.6 mm Hg. Detailed light microscopic evaluation revealed hippocampal lesions in 12 of the 14 cases studied (86%). These lesions were typically bilateral foci of selective neuronal loss in the CA1 subfield of the hippocampus. The nature and distribution of hippocampal lesions were similar to those previously reported both in fatal human head injury associated with elevated ICP and in experimental acceleration head injury without raised ICP. These results provide further evidence that the occurrence of hippocampal neuronal loss following head injury is not exclusively dependent on elevated ICP. Other mechanisms, such as pathologic excitation of neurons, may be involved.

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The hippocampus is known to be frequently involved in head injury. In adults, such hippocampal lesions frequently include regions of selective neuronal necrosis. The present report examines the frequency and distribution of hippocampal damage in 37 cases of fatal head injury in children. Damage to the hippocampus was noted in 27 of 37 cases (73%). Lesions were often focal areas of selective neuronal necrosis located in the CA-1 subfield. Other subfields of the hippocampus were involved to lesser degrees. The frequency and distribution of hippocampal damage in fatal childhood head injury is similar to that reported for fatal head injuries of all ages. Pathological evidence of high intracranial pressure and/or hypoxic brain damage in other anatomical locations was present in the majority of cases. Clinical seizures prior to death occurred in 22% of the cases studied. However, these factors could not account for all cases of hippocampal damage in the present report. Thus, the hippocampus is frequently damaged in fatal head injury in children. The mechanisms involved in the production of such damage may involve hypoxia, raised intracranial pressure and altered cerebral perfusion. However, other, yet to be elucidated, mechanisms may be involved.

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The hippocampus has been known to be involved in fatal non-missile human head injury, although detailed histopathology of this lesion has yet to be described. This report documents the frequency and distribution of hippocampal damage in a consecutive series of 112 fatal human non-missile head injuries. Damage to the hippocampus was noted in 94 cases (84%). Lesions always involved the CA1 subfield and were bilateral in 70 cases. Other subfields of the hippocampus were involved less frequently. Lesions were focal in the majority of cases (58%). Pathological evidence of high intracranial pressure was present in 86% of the cases. Hypoxic brain damage in other regions of the brain was present in 74% of cases. Thus, the hippocampus is frequently damaged in fatal non-missile human head injury. The pattern of this damage is similar to that observed in experimental head injury. Hypoxia and high intracranial pressure are likely to contribute to the occurrence of human traumatic hippocampal damage but other mechanisms, such as excitotoxicity, are likely to be operative.

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Traumatically induced subtotal hippocampal neuronal loss traditionally has been considered a consequence of intracranial hypertension and impaired cerebral perfusion. We have examined the frequency and distribution of hippocampal lesions in an acceleration model of brain injury in 54 anesthetized nonhuman primates undergoing physiologic monitoring and subjected postinjury to comprehensive neuropathologic examination. Hippocampal lesions occurred in 32/54 animals (59%). These lesions always involved the CA-1 hippocampal subfield and were bilateral in 24 animals. Hippocampal involvement was not associated with marked elevation of intracranial pressure or depression of cerebral perfusion pressure. These lesions occurred in the absence of involvement of other brain regions considered selectively vulnerable to hypoxic insults. Hippocampal damage occurred in 46% of animals with mild injury characterized by brief periods of unconsciousness and no residual neurologic deficit. Ninety-four percent of animals with severe injuries and prolonged posttraumatic coma had hippocampal involvement. Traumatically induced selective neuronal necrosis of the hippocampus is a specific lesion not explained by the conventional mechanistic theories of head injury. An alternative hypothesis, such as excitotoxicity involving glutamate or other neurotransmitters, may account for the lesions demonstrated in this study.

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