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Background: Since the emergence of neurosurgery as a distinct specialty ∼100 years ago in Canada, it took >40 years for Canadian women to enter the field in the province of Quebec, and longer in the other provinces., Methods: We provide a historical overview of Canadian women in neurosurgery, from the early pioneers to the modern-day leaders and innovators in the field. We also define the current participation of women in Canadian neurosurgery. Chain-referral sampling, historical books, interviews, personal communications, and online resources were used as data sources., Results: Our historical review highlights the exceptional journey and unique experiences of female neurosurgeons, describes their achievements, and identifies career obstacles and enabling factors. We also incorporate comments from Canadian female neurosurgeons, both retired and in active practice, addressing gender inequities in the field, and provide advice and encouragement to the new generations to come. Despite the achievements of these female trailblazers, women represent a small proportion of the Canadian neurosurgery trainees and the active workforce, in stark contrast to the increasing number of women in medical school., Conclusions: To the best of our knowledge, this study represents the first historical overview of female women neurosurgeons in Canada. Providing a historical context will help us to better understand the important role of women in modern neurosurgery, identify persistent gender issues in the field, and provide a vision for aspiring female neurosurgeons., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Hypercalcemia was identified in a canine patient with a benign vaginal leiomyoma. Subsequent diagnostic workup did not reveal hypercalcemia of malignancy. Surgical resection of the leiomyoma resulted in a conversion to normocalcemic status. Although rare, hypercalcemia of benignancy should be considered in a patient in which hypercalcemia is identified via clinical pathology.

Background and Purpose: The development of a delayed epidural hematoma as a result of decompressive craniectomy represents an urgent and potentially lethal complication in traumatic brain injury. The goal of this study was to determine the incidence of delayed epidural hematoma and whether patterns of skull fractures on the preoperative CT scan could predict risk of a delayed epidural hematoma., Materials and Methods: We retrospectively evaluated medical records and imaging studies for patients with acute traumatic brain injury who underwent a decompressive craniectomy during a 9-year period. We compared patterns of skull fractures contralateral to the side of the craniectomy with the occurrence of a postoperative delayed epidural hematoma., Results: In a series of 203 patients undergoing decompressive craniectomy for acute traumatic brain injury, the incidence of a delayed epidural hematoma complication was 6% (12 of 203). All 12 patients who developed a delayed epidural hematoma had a contralateral calvarial fracture on preoperative CT at the site where the delayed epidural hematoma subsequently formed. A contralateral calvarial fracture has perfect sensitivity (100%) for subsequent development of delayed epidural hematoma in our study population. Moreover, a contralateral calvarial fracture involving 2 or more bone plates had an especially high diagnostic odds ratio of 41 for delayed epidural hematoma., Conclusions: Recognition of skull fracture patterns associated with delayed epidural hematoma following decompressive craniectomy may reduce morbidity and mortality by prompting early postoperative intervention in high-risk situations., (© 2014 by American Journal of Neuroradiology.)

A two-year-old female poodle with abdominal distention was diagnosed with concurrent enteric duplication cyst and lymphangiomatosis. Both lesions were shown as cystic structures, but some characteristic features of enteric duplication cyst were identified including a thick cyst wall and shared blood supply with the duodenum. Although it was challenging to discriminate between the types of cyst based on diagnostic imaging, this report describes the characteristics of each type of lesion using several different imaging modalities., (© 2014 British Small Animal Veterinary Association.)

Cerebral edema plays a central role in the pathophysiology of many diseases of the central nervous system (CNS) including ischemia, trauma, tumors, inflammation, and metabolic disturbances. The formation of cerebral edema results in an increase in tissue water content and brain swelling which, if unchecked, can lead to elevated intracranial pressure (ICP), reduced cerebral blood flow, and ultimately cerebral herniation and death. Despite the clinical significance of cerebral edema, the mechanism of brain water transport and edema formation remain poorly understood. As a result, current therapeutic tools for managing cerebral edema have changed little in the past 90 years. "Malignant ischemic stroke" is characterized by high mortality (80%) and represents a major clinical problem in cerebrovascular disease. Widespread ischemic injury in these patients causes progressive cerebral edema, increased ICP, and rapid clinical decline. In response to these observations, a series of recent studies have begun to target cerebral edema in the management of large ischemic strokes. During cerebral edema formation, the glial water channel aquaporin-4 (AQP4) has been show to facilitate astrocyte swelling ("cytotoxic swelling"). AQP4 has also been seen to be responsible for the reabsorption of extracellular edema fluid ("vasogenic edema"). In the present review, the role of AQP4 in the development of cerebral edema is discussed with emphasis on its contribution to ischemic edema. We also examine the potential of AQP4 as a therapeutic target in edema associated with stroke.

A Mycobacterium avium subspecies paratuberculosis (MAP) vaccine that reduced the incidence of clinical disease or reduced fecal shedding of MAP would aid control of Johne's disease (JD). The objective of the present study was to evaluate the efficacy of four MAP vaccine combinations, including cell-wall competent (CWC) alum adjuvant, CWC-QS21 adjuvant, cell-wall deficient (CWD) alum adjuvant and CWD-QS21 adjuvant vaccines. Eighty baby goats were vaccinated at 1 and 4 weeks of age with one of these vaccines or a sham control vaccine consisting of alum adjuvant. Kids were challenged orally with approximately 6.0x10(9) organisms in four divided doses of 1.5x10(9) organisms using a goat isolate of MAP. Vaccinated challenged and challenged control groups had 10 and 6 kids per group, respectively. Half of the kids within each group were necropsied at either 6 or 9 months post-challenge. Gross and microscopic lesions and relative number of acid-fast bacilli were evaluated and scored at necropsy. Results indicated all challenged kids had some lesions compatible with JD suggesting none of the vaccines prevented infection. Three vaccines (CWC-alum, CWC-QS21 and CWD-QS21) reduced lesion scores by 46-51% at 9 months. CWD-alum vaccine resulted in a more severe (+33.5%) lesion score than sham-vaccinated challenged control. Lesion scores were greater at 9 months than at 6 months post-challenge in the sham-vaccinated challenged group and CWD-alum vaccinated group, while lesion scores were generally stable with remaining vaccines. Mean fecal CFU/g were significantly different across time from challenge to 9-month necropsy (p=0.043) and the CWC-QS21 vaccine group had a marked reduction in fecal CFU/g at all time points post-challenge. A reduction in MAP CFU/g was also detected in necropsy tissues from kids given the CWC-alum, CWC-QS21 and CWD-QS21 vaccines, and increased CFU/g were detected in tissues from kids given the CWD-alum vaccine. Immunological tests evaluated included, humoral response evaluation by AGID, ELISA and Western blot, and cell mediated response by comparative PPD skin testing (M. avium, Old Johnin, M. bovis and Lot 2 Johnin PPD's), and production of MAP induced gamma-interferon. Vaccination also resulted in false-positive PPD skin test reactions for M. avium PPD, Old Johnin PPD and gamma-interferon tests. When a 2-mm cutoff above normal skin thickness was used to define positive skin test reactions, false-positive reactions for M. bovis were detected in only 2 of 32 kids given a vaccine with QS21 adjuvant.

Angiogenesis is a critical component of stroke, head injury, cerebral vascular malformation development, and brain tumor growth. An understanding of the mechanisms of adult cerebral angiogenesis is fundamental to therapeutic vessel modulation for these diseases. To study angiogenesis in the central nervous system, we injected an adenoviral vector engineered to express vascular endothelial growth factor (VEGF-A164) into adult murine striatum. Vector-infected astrocytes expressed VEGF-A164 resulting in vascular permeability, hemorrhage, and the formation of greatly enlarged "mother" vessels. Subsequently, endothelial cells and pericytes lining mother vessels proliferated and assembled into glomeruloid bodies, complex cellular arrays interspersed by small vessel lumens. As VEGF-A164 expression declined, glomeruloid bodies involuted through apoptotic processes to engender numerous small daughter vessels. Characterized by modestly enlarged lumens with prominent pericyte coverage, daughter vessels were distributed with a density greater than normal cerebral vessels. Daughter vessels remained stable and patent to 16 months and represented the final stage of VEGF-A-induced cerebral angiogenesis. Together, these findings provide a mechanistic understanding of angiogenesis in cerebral disease processes. Furthermore, the long-term stability of daughter vessels in the absence of exogenous VEGF-A164 expression suggests that VEGF-A may enable therapeutic angiogenesis in brain.

Neurological signs characterized by marked progressive weakness and convulsions culminating in death were observed in 3 goats over a 24-h period. Affected animals were in a group of 5 goats confined toa fenced paddock: a domestic goose within the paddock was also found dead. Present in the same paddock, but unaffected, were 2 other goats and an adult cow. Five days prior to the animals' deaths, the owner had trimmed the surrounding brush and had thrown the cuttings into the enclosure. Post mortem examination of 2 of the dead goats and the goose revealed reduced muscle mass and fat stores, serous atrophy of adipose tissue, and reduced gastrointestinal contents, which included numerous leaves identified as Carolina jessamine (Gelsemium sempervirens). Histologic lesions included mild diffuse neuronal degeneration and cerebellar Purkinje cell loss in all animals with mild multifocal vacuolation of brainstem and cerebral white matter in 1 goat, and myofiber atrophy with perimyseal fibrosis in the goose. Preexisting malnutrition and lack of adequate alternative forages likely resulted in ingestion of Carolina jessamine and subsequent toxicosis. To our knowledge, this is the first reported case of Carolina jessamine toxicosis in goats and geese.

Objective: Micro-arteriovenous malformations (AVMs) represent approximately 8 to 10% of surgically treated brain AVMs. We examined the clinical presentations, radiological features, principles of surgical resection, and factors affecting outcomes for micro-AVM lesions., Methods: Twelve patients with micro-AVMs that had been treated by surgical resection were retrospectively analyzed. The mean follow-up monitoring period was 35 months (range, 2-76 mo). Outcomes, as assessed in follow-up visits and telephone interviews (using a questionnaire), were classified according to the Glasgow Outcome Scale., Results: All 12 patients presented with intracranial hemorrhage, which was intraparenchymal and superficially situated in 10 patients (83%) and intraventricular in 2 patients (17%). Hemorrhages were large (mean volume, 23 ml3; range, 1-58 ml3) and were associated with neurological deficits for 10 of 12 patients (83%). The identification of an arterialized draining vein during surgery and stereotactic angiography greatly facilitated surgical localization of the lesions. One patient (8%) developed a mild permanent deficit as a result of surgery. Although Glasgow Outcome Scale scores were excellent for all except one patient, nine patients (75%) experienced long-term neurological problems., Conclusion: Micro-AVMs typically present with large hemorrhages and are associated with significant neurological deficits. If a superficial clot is present, surgical resection of the lesion is strongly advocated. The ultimate clinical outcomes are determined primarily by deficits present after the initial hemorrhaging episodes.

Stab wounds to the spinal cord are relatively uncommon in North America, but even rarer is the presentation of such an injury in a delayed fashion. We report a case of a 31-year-old male who presented with neurologic deficit 4 weeks after a stab wound injury to the spine. Because of worsening neurologic deficit, the retained knife fragment was operatively removed, and the patient had an uneventful recovery. The management of such an injury is discussed, with a review of the literature.

Microarteriovenous malformations (micro-AVMs) are a subgroup of brain AVM with a nidus diameter of less than 1 cm. Although many micro-AVMs may appear angiographically occult on cursory review, careful analysis will often reveal a subtle diagnostic feature. Micro-AVMs present with intracranial hemorrhages that are generally large and associated with significant neurologic impairment. An awareness of these lesions as a possible source of hemorrhage in a young person is critical. In general, micro-AVMs are eminently resectable lesions and patient outcome is determined primarily by the hemorrhage that brings them to medical attention.

Objective and Importance: This case study provided us with the opportunity to explore the histopathological effects of Guglielmi detachable coil (GDC) therapy on the aneurysm orifice and parent vessel-aneurysm neck interface. This type of study is important to the understanding of the mechanisms of obliteration of aneurysms by GDCs., Clinical Presentation: The patient presented with a Hunt and Hess Grade III subarachnoid hemorrhage that occurred secondary to the rupture of a small anterior communicating artery aneurysm., Intervention: The aneurysm was successfully coiled without complication, but the patient died 36 hours later. We examined the gross and microscopic pathological findings of this GDC-treated anterior communicating artery aneurysm 36 hours after coiling. A discrete membrane composed of fibrin had formed completely across the aneurysm orifice, excluding the aneurysm sac from the circulation. This membrane was contiguous with the parent vessel., Conclusion: This case represents one of the first examples in humans of the formation of a membrane over the aneurysm orifice after GDC therapy. The formation of this membrane, shown to be composed of fibrin, was found at 36 hours after coiling, which is the earliest time frame at which membrane formation has been noted in either humans or animal models. This fibrin membrane may function both as a scaffold for subsequent endothelialization across the aneurysm neck as well as to isolate the aneurysm from the parent circulation, permitting thrombus within the aneurysm sac to mature to an endovascular scar. The factors contributing to the formation of this membrane and its clinical implications are discussed.

Background: Acute and chronic brain injury are common sequelae of high-dose focused radiation, as in radiosurgery and brachytherapy. Development of protectors of radiation injury, which would work in brain but not in tumor, would help enhance the therapeutic ratio of focused-radiation therapy., Methods: Radiation protection by a clinically available 21-aminosteroid, Tirilazad, was studied in a rat brain brachytherapy model, both in tumor and non-tumor bearing animals. For the tumor model, 9L Glioma/SF line cells were implanted stereotactically into the right frontal lobe of F-344 rats and grew to a sphere of 5.0-mm diameter after 12 days. Animals received a standard brachytherapy dose of 80 Gy to a 5.5-mm radius volume administered by a high-activity removable iodine-125 seed. Radiation damage was evaluated 24 hours after removal of the seeds in all animals and again at 3 months in non-tumor-bearing animals, by T1-weighted gadolinium-enhanced and T2-weighted magnetic resonance imaging (MRI) on a 1.5-T unit. Treated animals received Tirilazad 5 mg/kg intravenously 15 minutes prior to implant, 1 hour after implant, every 6 hours for the duration of the implant, and for 24 hours after removal of the seed. Control animals were administered vehicle only., Results: In both non-tumor-bearing and tumor-bearing rats, no difference in the volume of lesions on enhanced T1 or T2 MRI was seen between the Tirilazad-treated and control groups. In the non-tumor-bearing rats, volume of both T1 enhanced and T2 MRI lesions was significantly reduced at 3 months compared to the values at 24 hours., Conclusions: In the present model, Tirilazad failed to reduce the volume of radiation brain injury from brachytherapy as seen on MRI, studied acutely in tumor-bearing and non-tumor-bearing animals and also at 3 months in non-tumor-bearing rats.