Pituitary aspergillosis in a kidney transplant recipient and review of the literature.

Pituitary aspergillosis is a very rare disease, documented in only 12 cases. Although seen in both immunocompetent and immunocompromised patients, serious invasive sequelae, such as meningoencephalitis and death, have been noted in immunocompromised patients. Immunocompromised patients are susceptible and require complex multidisciplinary care to contain the spread of infection and maximize outcomes. This is the first case report, to our knowledge, of pituitary aspergillosis in the setting of an organ transplant. A 68-year-old woman presented with cephalgia, left temporal hemianopsia, and ptosis. Non-contrast magnetic resonance imaging of the head revealed a sellar mass, which was believed to be a benign pituitary adenoma. She underwent trans-sphenoidal resection, and subsequent histopathologic examination showed aspergillosis. She was subsequently started on voriconazole. On postoperative day 3, she developed a left anterior cerebral artery ischemic stroke, likely from Aspergillus angioinvasion and occlusion. Her mental status declined further and she died when care was withdrawn.

Neurosurgery at the University of Pennsylvania Medical Center.

The University of Pennsylvania Medical School was the nation's first medical school, and its Department of Neurosurgery is one of the nation's oldest. The history of the Department of Neurosurgery at Penn is recounted, beginning with the pioneer surgeon Charles Harrison Frazier. The evolution of the current department, its contemporary status, and its residency program are described.

Magnetization transfer imaging of traumatic brain injury.

Magnetization transfer imaging (MTI) has been shown to be sensitive for the detection of white matter abnormalities in entities such as multiple sclerosis, progressive multifocal leukoencephalopathy, and wallerian degeneration. Our hypothesis was that MTI would detect traumatic white matter abnormalities (TWMA) and provide information additional to that obtainable with routine spin- and gradient-echo imaging. We hypothesized that the presence of TWMA defined by MTI would correlate with outcome following TBI. Twenty-eight victims of head trauma and 15 normal controls underwent magnetic resonance imaging including MTI. Magnetization transfer ratios (MTR) were calculated for areas of shearing injury and for normal-appearing white matter (NAWM) in locations frequently subject to diffuse axonal injury. Abnormal MTRs were detected in NAWM in eight patients. All eight had persistent neurologic deficits, including cognitive deficits, aphasia, and extremity weakness. Seven of the 28 patients had no abnormal findings on neurologic exam at discharge, transfer, or follow-up. None of these patients had an abnormal MTR in NAWM. In the remaining 13 patients, who had persistent neurologic deficits, no regions of abnormal MTR were detected in NAWM. MTI is a sensitive method for the detection of TWMA. Detection of abnormal MTR in NAWM that is prone to axonal injury may predict a poor patient outcome. The presence of normal MTR in NAWM in these areas does not necessarily confer a good outcome, however.

Endoscopically assisted anterior cranial skull base resection of sinonasal tumors.

The traditional approach to sinonasal tumors involving the base of skull has been the anterior craniofacial resection. Endoscopic techniques have created the potential to approach the intranasal aspect of skull base lesions without external incisions and still develop an en bloc resection when removed. We report our initial experience with skull base neoplasms in which the otolaryngic portion of the standard resection was accomplished instead through an endoscopic approach. The nature of lesions favorable for this approach and associated technical issues are discussed. Although we do not consider this approach a replacement for the traditional anterior craniofacial resection, it is an important adjunct in the skull base surgeon's armamentarium.

Characterization of white matter lesions in multiple sclerosis and traumatic brain injury as revealed by magnetization transfer contour plots.

BACKGROUND AND PURPOSE: Magnetization transfer imaging provides information about the structural integrity of macromolecular substances, such as myelin. Our objective was to use this imaging technique and contour plotting to characterize and to define the extent of white matter lesions in multiple sclerosis and traumatic brain injury. METHODS: Magnetization transfer imaging was performed of 30 multiple sclerosis plaques and 10 traumatic white matter lesions. Magnetization transfer ratios (MTRs) were calculated for the lesions, for the normal- or abnormal-appearing surrounding white matter, and for remote normal-appearing white matter. MTR contour plots were constructed about these lesions. RESULTS: The contour plot appearance of MS plaques differed from that of traumatic white matter lesions. There was a gradual increase in MTR values at points at increasing distances from the center of the MS plaques; this was true for those lesions with and without surrounding T2 signal abnormality (halos). In contrast, there was an abrupt transition in MTR values between traumatic lesions and normal-appearing surrounding white matter. Additionally, the size of the MTR abnormality exceeded the size of the T2 signal abnormality for the MS plaques. CONCLUSION: MTR contour plots permit characterization and border definition of white matter lesions. Analysis of the contour plots suggests that MS is a centrifugal process with the lowest MTR within the center of the lesion. In contrast, traumatic white matter injuries are discrete lesions with abrupt transitions between the abnormal lesion and normal brain.

Treatment of malignant neoplasms of the lateral cranial base with the combined frontotemporal-anterolateral approach: five-year follow-up.

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.

Unusual presentations of middle fossa encephaloceles: report of two cases.

Basal encephaloceles are rare occurrences with occult and often varied presentations. Frequently, the need for surgical treatment is not clear to the patient or the physician, leading to potentially fatal complications. We report the case of a 44-year-old woman with an 8-year history of nonspecific complaints who presented to us with trigeminal neuralgia. Also, an unsual case is presented of a 60-year-old man with bilateral middle fossa encephaloceles who suffered acutely from widespread pneumocephalus acting as a mess lesion. Both are cases of nontraomatic middle fossa encephaloceles, which are of perficular interest due to the age of the patients, their atypical presentations, and the asseciated complications.

Neurosarcoidosis presenting in the pituitary gland with normal endocrine studies.

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.

Lipomas of the internal auditory canal and cerebellopontine angle.

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.

Brainstem origins of the n18 component of the somatosensory evoked response.

Proposed generator sites for the N18 component of the somatosensory evoked potential (SEP) range in location from the medulla to the thalamus. Additional knowledge regarding the generators of the N18 will be important in interpreting the results of intra-operative monitoring during skull base surgery and providing the surgeon more specific information. The goal of this study was to use both intracranial electrical recording and the effects of acute brainstem ischemia in humans to further define the generators of N18. Monopolar electrodes were used to record SEP (after median nerve stimulation) from the brainstem surface in eight patients undergoing posterior fossa surgical procedures. Recordings were made from various locations, from the cervico-medullary junction to the level of the aqueduct of Sylvius. As the electrode moved rostrally on the brainstem surface, the difference in latencies between the scalp N18 potential and the electrode potential approached zero, suggesting an upper pontine-lower midbrain origin of the N18 potential. These findings were supported by the lack of change in the N18 potentials of ten patients with basilar tip aneurysms who experienced marked changes of their N20/P22 potentials during temporary occlusion of the distal basilar artery.

Use of preoperative MR to predict dural, perineural, and venous sinus invasion of skull base tumors.

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.

Neuropathological sequelae of traumatic brain injury: relationship to neurochemical and biomechanical mechanisms.

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.

Carotid artery invasion by head and neck masses: prediction with MR imaging.

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.

Infiltration of the carotid artery by cavernous sinus meningioma.

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.

Hippocampal pathology in fatal human head injury without high intracranial pressure.

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.

Hippocampal damage in fatal paediatric head injury.

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.

Hippocampal pathology in fatal non-missile human head injury.

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.

Selective vulnerability of hippocampal neurons in acceleration-induced experimental head injury.

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.

Cerebral venous oxygen content as a measure of brain energy metabolism with increased intracranial pressure and hyperventilation.

In order to test the hypothesis that the cerebral arteriovenous oxygen difference (AVDO2) and venous oxygen content (VO2) could be used to monitor brain energy metabolism in the setting of increased intracranial pressure (ICP). 12 cats were studied with 31P-magnetic resonance spectroscopy. six cats were subjected to intracranial hypertension by cisternal infusion of saline. Energy failure occurred at an average AVDO2 of 8.4 +/- 3.2 vol% (+/- standard deviation) (range 4.7 to 14.7 vol%). The VO2 at the point of metabolic failure averaged 1.45 +/- 0.6 vol% and extended over a narrower range (1.0 to 2.9 vol%). In an additional six cats, ICP was raised to the threshold of metabolic failure and hyperventilation was then instituted (pCO2 10 to 18 torr). Five of the six cats experienced a drop in VO2 with hyperventilation. In two of these animals, hyperventilation resulted in a VO2 of 1.1 vol% or less and in metabolic failure as evidenced by a fall in phosphocreatine. It is concluded that a VO2 of less than 2 vol% is correlated with brain ischemia and that the safety of hyperventilation in the setting of increased ICP can be monitored by the use of VO2.