Canadian Women in Neurosurgery: From Early Pioneers to World Leaders.

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.

ACR Appropriateness Criteria® Penetrating Neck Injury.

In patients with penetrating neck injuries with clinical soft injury signs, and patients with hard signs of injury who do not require immediate surgery, CT angiography of the neck is the preferred imaging procedure to evaluate extent of injury. Other modalities, such as radiography and fluoroscopy, catheter-based angiography, ultrasound, and MR angiography have their place in the evaluation of the patient, depending on the specific clinical situation and question at hand. The ACR Appropriateness Criteria are evidence-based guidelines for specific clinical conditions that are reviewed annually by a multidisciplinary expert panel. The guideline development and revision include an extensive analysis of current medical literature from peer-reviewed journals and the application of well-established methodologies (RAND/UCLA Appropriateness Method and Grading of Recommendations Assessment, Development, and Evaluation or GRADE) to rate the appropriateness of imaging and treatment procedures for specific clinical scenarios. In those instances where evidence is lacking or equivocal, expert opinion may supplement the available evidence to recommend imaging or treatment.

Treatment of traumatic acute posterior fossa subdural hematoma: report of four cases with systematic review and management algorithm.

BACKGROUND: Traumatic posterior fossa subdural hematomas (SDHs) are rare lesions. Despite improvements in intensive care and surgical management of traumatic brain injuries over the last decades, the outcome for posterior fossa subdural hematomas remains poor. METHODS: We conduct a retrospective study over a 2-year period of patients sustaining traumatic brain injury and posterior fossa SDH. Additionally, a systematic review of case series published to date was performed. RESULTS: The incidence of posterior fossa SDH was 0,01% (4/326). All patients in this current series had poor prognosis. Three out of four exhibited ischemic/edema lesions in postoperative CT scans leading to fourth ventricle effacement and persistent brainstem compression. Our literature review retrieved 57 patients from only seven case series. Unfavorable outcomes were seen in 63% of patients. CONCLUSIONS: Our data and data from the literature do not provide sufficient evidence to establish an optimal treatment strategy for posterior fossa SDH. However, based on lessons learned with these four cases, together with results from review of the literature, we propose an algorithm for the management of this rare condition.

Bilateral cervical spinal dural arteriovenous fistulas with intracranial venous drainage mimicking a foramen magnum dural arteriovenous fistula.

We describe a unique case of bilateral cervical spinal dural arteriovenous fistulas mimicking an intracranial dural arteriovenous fistula near the foramen magnum. We review its detection via MRI and digital subtraction angiography and subsequent management through surgical intervention. Pitfalls in diagnostic angiography are discussed with reference to accurate location of the fistula site. The venous anastomotic connections of the posterior midline spinal vein to the medial posterior medullary vein, posterior fossa bridging veins, and dural venous sinuses of the skull base are discussed with reference to problem-solving in this complex case. The mechanism of myelopathy through venous hypertension produced by spinal dural fistulas is also emphasized.

Delayed acute spinal cord injury following intracranial gunshot trauma: case report.

The authors report the case of a patient who presented with a hoarse voice and left hemiparesis following a gunshot injury with trajectory entering the left scapula, traversing the suboccipital bone, and coming to rest in the right lateral medullary cistern. Following recovery from the hemiparesis, abrupt quadriparesis occurred coincident with fall of the bullet into the anterior spinal canal. The bullet was retrieved following a C-2 and C-3 laminectomy, and postoperative MR imaging confirmed signal change in the cord at the level where the bullet had lodged. The patient then made a good neurological recovery. Bullets can fall from the posterior fossa with sufficient momentum to cause an acute spinal cord injury. Consideration for craniotomy and bullet retrieval should be given to large bullets lying in the CSF spaces of the posterior fossa as they pose risk for acute spinal cord injury.

Marked reduction in wound complication rates following decompressive hemicraniectomy with an improved operative closure technique.

Although decompressive hemicraniectomy with dural expansion and bone flap removal is a potentially life-saving procedure, concerns remain regarding the morbidity associated with this approach. We and others have noted the high rate of wound complications resulting from this technique, often associated with cerebrospinal fluid (CSF) absorption problems. Here, we present our experience with an improved technique for wound closure after unilateral decompressive hemicraniectomy with a wide cruciate durotomy. Data for all patients who underwent a decompressive hemicraniectomy at our institution from October 2005 to October 2009 were gathered prospectively. Starting in mid 2008, we adopted an alternate approach to operative wound closure, which involved skin closure with a running Monocryl absorbable stitch, and prolonged subgaleal drainage. We compared the rates of wound complication using this approach with those obtained with earlier conventional closure techniques. Over a 1year period, we dramatically reduced the rate of wound complications in patients undergoing hemicraniectomy at our hospital using this new (Monocryl technique, 0% (n=29) compared to other techniques, 35% (n=98), chi-squared [χ(2)] p<0.001). Patients closed using our new technique experienced markedly reduced rates of wound infection (p<0.01), and CSF leak (p<0.05), compared to other, more standard, techniques. Thus, attention to closure of hemicraniectomy wounds can markedly reduce the rate of wound complications, thus improving the risk-to-benefit ratio of this procedure.

Dexmedetomidine controls agitation and facilitates reliable, serial neurological examinations in a non-intubated patient with traumatic brain injury.

INTRODUCTION: We report the effective use of dexmedetomidine in the treatment of a patient with a history of chronic alcohol abuse and an acute traumatic brain injury who developed agitation that was unresolved if from traumatic brain injury, or alcohol withdrawal or the combination of both. Treatment with benzodiazepines failed; lorazepam therapy obscured our ability to do reliable neurological testing to follow his brain injury and nearly resulted in intubation of the patient secondary to respiratory suppression. Upon admission to hospital, the patient was first treated with intermittent, prophylactic doses of lorazepam for potential alcohol withdrawal based upon our institution's standard of care. His neurological examinations including a motor score of 6 (obeying commands) on his Glasgow Coma Scale testing, laboratory studies, and repeat CT head imaging remained stable. For lack of published literature in diagnosing symptoms of patients with a history of both alcohol withdrawal and traumatic brain injury, a diagnosis of agitation secondary to presumed alcohol withdrawal was made when the patient developed acute onset of tachycardia, confusion, and extreme anxiety with tremor and attempts to climb out of bed requiring him to be restrained. Additional lorazepam doses were administered following a hospital-approved protocol for titration of benzodiazepine therapy for alcohol withdrawal. The patient's mental status and respiratory function deteriorated with the frequent lorazepam dosing needed to control his agitation. Dexmedetomidine IV infusion at a rate of 0.5 mcg/kg/h was then administered and was titrated ultimately to 1.5 mcg/kg/h. After 8 days of therapy with dexmedetomidine, the patient was transferred from the ICU to a step-down unit with an intact neurological examination and no evidence of alcohol withdrawal. Airway intubation was avoided during the patient's entire hospitalization. This case report highlights the intricate balance between the side effects of benzodiazepine sedation for treatment of agitation and the difficulties of monitoring the neurological status of non-intubated patients with traumatic brain injury. CONCLUSION: Given the large numbers of alcohol-dependent patients who suffer a traumatic brain injury and subsequently develop agitation and alcohol withdrawal in hospital, dexmedetomidine offers a novel strategy to facilitate sedation without neurological or respiratory depression. As this case report demonstrates, dexmedetomidine is an emerging treatment option for agitation in patients who require reliable, serial neurological testing to monitor the course of their traumatic brain injury.

Benign anterior temporal epidural hematoma: indolent lesion with a characteristic CT imaging appearance after blunt head trauma.

PURPOSE: To study the incidence, pathogenesis, imaging characteristics, and clinical importance of a unique subtype of epidural hematoma (EDH) associated with blunt head trauma. MATERIALS AND METHODS: This study was reviewed and approved by the hospital's Institutional Review Board and was compliant with HIPAA. Informed consent was waived. The investigation was a retrospective study of 200 patients with acute supratentorial EDH, defined as a biconvex, high-attenuating, extraaxial hematoma. A subgroup of 21 patients in whom the EDH was located at the anterior aspect of the middle cranial fossa was defined. Computed tomographic images and inpatient medical records of these 21 patients were evaluated for imaging characteristics of the EDH, presence or absence of associated fracture, presence or absence of midline shift and/or mass effect, additional intracranial injury, and hospital clinical course. RESULTS: Twenty-one (10.5%) of 200 traumatic EDHs localized to the anterior middle cranial fossa. All of these 21 anterior temporal EDHs were juxtaposed to the sphenoparietal sinus, and all but one were limited laterally by the sphenotemporal suture and medially by the orbital fissure; none extended above the lesser sphenoid wing. Maximum thickness was less than 1 cm in 13 (62%) of 21 and less than 2 cm in 20 (95%) of 21 patients. Isolated fractures of the greater sphenoid wing and ipsilateral zygomaticomaxillary fractures were present in 12 (57%) of 21 and nine (43%) of 21 patients, respectively. Concomitant intracranial injury was identified in 15 (71%) of 21 patients. Twenty (95%) of 21 lesions were present at the admission study, and all 21 were stable or smaller at follow-up imaging. No patient required neurosurgical intervention of their anterior temporal EDH. CONCLUSION: Acute EDHs isolated to the anterior aspect of the middle cranial fossa constitute a subgroup of traumatic EDHs with a benign natural history. It is postulated that they arise from venous bleeding due to disruption of the sphenoparietal sinus.

Interobserver variability in the assessment of CT imaging features of traumatic brain injury.

The goal of our study was to determine the interobserver variability between observers with different backgrounds and experience when interpreting computed tomography (CT) imaging features of traumatic brain injury (TBI). We retrospectively identified a consecutive series of 50 adult patients admitted at our institution with a suspicion of TBI, and displaying a Glasgow Coma Scale score < or =12. Noncontrast CT (NCT) studies were anonymized and sent to five reviewers with different backgrounds and levels of experience, who independently reviewed each NCT scan. Each reviewer assessed multiple CT imaging features of TBI and assigned every NCT scan a Marshall and a Rotterdam grading score. The interobserver agreement and coefficient of variation were calculated for individual CT imaging features of TBI as well as for the two scores. Our results indicated that the imaging review by both neuroradiologists and neurosurgeons were consistent with each other. The kappa coefficient of agreement for all CT characteristics showed no significant difference in interpretation between the neurosurgeons and neuroradiologists. The average Bland and Altman coefficients of variation for the Marshall and Rotterdam classification systems were 12.7% and 21.9%, respectively, which indicates acceptable agreement among all five reviewers. In conclusion, there is good interobserver reproducibility between neuroradiologists and neurosurgeons in the interpretation of CT imaging features of TBI and calculation of Marshall and Rotterdam scores.

Hemicraniectomy: a new model for human electrophysiology with high spatio-temporal resolution.

Human electrophysiological research is generally restricted to scalp EEG, magneto-encephalography, and intracranial electrophysiology. Here we examine a unique patient cohort that has undergone decompressive hemicraniectomy, a surgical procedure wherein a portion of the calvaria is removed for several months during which time the scalp overlies the brain without intervening bone. We quantify the differences in signals between electrodes over areas with no underlying skull and scalp EEG electrodes over the intact skull in the same subjects. Signals over the hemicraniectomy have enhanced amplitude and greater task-related power at higher frequencies (60-115 Hz) compared with signals over skull. We also provide evidence of a metric for trial-by-trial EMG/EEG coupling that is effective over the hemicraniectomy but not intact skull at frequencies >60 Hz. Taken together, these results provide evidence that the hemicraniectomy model provides a means for studying neural dynamics in humans with enhanced spatial and temporal resolution.

Complications of decompressive craniectomy for traumatic brain injury.

Decompressive craniectomy is widely used to treat intracranial hypertension following traumatic brain injury (TBI). Two randomized trials are currently underway to further evaluate the effectiveness of decompressive craniectomy for TBI. Complications of this procedure have major ramifications on the risk-benefit balance in decision-making during evaluation of potential surgical candidates. To further evaluate the complications of decompressive craniectomy, a review of the literature was performed following a detailed search of PubMed between 1980 and 2009. The author restricted her study to literature pertaining to decompressive craniectomy for patients with TBI. An understanding of the pathophysiological events that accompany removal of a large piece of skull bone provides a foundation for understanding many of the complications associated with decompressive craniectomy. The author determined that decompressive craniectomy is not a simple, straightforward operation without adverse effects. Rather, numerous complications may arise, and they do so in a sequential fashion at specific time points following surgical decompression. Expansion of contusions, new subdural and epidural hematomas contralateral to the decompressed hemisphere, and external cerebral herniation typify the early perioperative complications of decompressive craniectomy for TBI. Within the 1st week following decompression, CSF circulation derangements manifest commonly as subdural hygromas. Paradoxical herniation following lumbar puncture in the setting of a large skull defect is a rare, potentially fatal complication that can be prevented and treated if recognized early. During the later phases of recovery, patients may develop a new cognitive, neurological, or psychological deficit termed syndrome of the trephined. In the longer term, a persistent vegetative state is the most devastating of outcomes of decompressive craniectomy. The risk of complications following decompressive craniectomy is weighed against the life-threatening circumstances under which this surgery is performed. Ongoing trials will define whether this balance supports surgical decompression as a first-line treatment for TBI.

Role of aquaporin-4 in cerebral edema and stroke.

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.

Survival with good outcome after cerebral herniation and Duret hemorrhage caused by traumatic brain injury.

Brainstem hemorrhage can occur as a primary or secondary event in traumatic brain injury (TBI). Secondary brainstem hemorrhage that evolves from raised intracranial pressure and transtentorial herniation is referred to as Duret hemorrhage. Duret hemorrhage following TBI has been considered an irreversible and terminal event. The authors report on the case of a young adult patient with TBI who presented with a low Glasgow Coma Scale score and advanced signs of cerebral herniation. She underwent an urgent decompressive hemicraniectomy for evacuation of an acute epidural hematoma and developed a Duret hemorrhage postoperatively. In accordance with the family's wishes, aggressive TBI monitoring and treatment in the intensive care unit was continued even though the anticipated outcome was poor. After a lengthy hospital course, the patient improved dramatically and was discharged ambulatory, with good cognitive functioning and a Glasgow Outcome Scale score of 4. Duret hemorrhage secondary to raised intracranial pressure is not always a terminal event, and by itself should not trigger a decision to withdraw care. Aggressive intracranial monitoring and treatment of a Duret hemorrhage arising secondary to cerebral herniation may enable a good recovery in selected patients after severe TBI.

Prehospital management of traumatic brain injury.

The aim of this study was to review the current protocols of prehospital practice and their impact on outcome in the management of traumatic brain injury. A literature review of the National Library of Medicine encompassing the years 1980 to May 2008 was performed. The primary impact of a head injury sets in motion a cascade of secondary events that can worsen neurological injury and outcome. The goals of care during prehospital triage, stabilization, and transport are to recognize life-threatening raised intracranial pressure and to circumvent cerebral herniation. In that process, prevention of secondary injury and secondary insults is a major determinant of both short- and longterm outcome. Management of brain oxygenation, blood pressure, cerebral perfusion pressure, and raised intracranial pressure in the prehospital setting are discussed. Patient outcomes are dependent upon an organized trauma response system. Dispatch and transport timing, field stabilization, modes of transport, and destination levels of care are addressed. In addition, special considerations for mass casualty and disaster planning are outlined and recommendations are made regarding early response efforts and the ethical impact of aggressive prehospital resuscitation. The most sophisticated of emergency, operative, or intensive care units cannot reverse damage that has been set in motion by suboptimal protocols of triage and resuscitation, either at the injury scene or en route to the hospital. The quality of prehospital care is a major determinant of long-term outcome for patients with traumatic brain injury.

Reversible monoparesis following decompressive hemicraniectomy for traumatic brain injury.

OBJECT: The "syndrome of the trephined" is an uncommon and poorly understood disorder of delayed neurological deficit following craniectomy. From the authors' extensive experience with decompressive hemicraniectomy for traumatic brain injury (TBI), they have encountered a number of patients who developed delayed motor deficits, also called "motor trephine syndrome," and reversal of the weakness following cranioplasty repair. The authors set out to study motor function systematically in this patient population to define the incidence, contributing factors, and outcome of patients with motor trephine syndrome. METHODS: The authors evaluated patient demographics, injury characteristics, detailed motor examinations, and CT scans in 38 patients with long-term follow-up after decompressive hemicraniectomy for TBI. RESULTS: Ten patients (26%) experienced delayed contralateral upper-extremity weakness, beginning 4.9 +/- 0.4 months (mean +/- standard error) after decompressive hemicraniectomy. Motor deficits improved markedly within 72 hours of cranioplasty repair, and all patients recovered full motor function. The CT perfusion scans, performed in 2 patients, demonstrated improvements in cerebral blood flow commensurate with resolution of cerebrospinal fluid flow disturbances on CT scanning and return of motor strength. Comparisons between 10 patients with and 20 patients (53%) without delayed motor deficits identified 3 factors--ipsilateral contusions, abnormal cerebrospinal fluid circulation, and longer intervals to cranioplasty repair--to be strongly associated with delayed, reversible monoparesis following decompressive hemicraniectomy. CONCLUSIONS: Delayed, reversible monoparesis, also called motor trephine syndrome, is common following decompressive hemicraniectomy for TBI. The results of this study suggest that close follow-up of motor strength with early cranioplasty repair may prevent delayed motor complications of decompressive hemicraniectomy.

Motor trephine syndrome: a mechanistic hypothesis.

BACKGROUND: In our neurotrauma practice, "motor trephine syndrome" was defined as a contralateral monoparesis that developed as a delayed and reversible complication in patients treated with decompressive hemicraniectomy for traumatic brain injury (TBI). The goal of this study was to define causal factors associated with this syndrome. METHODS: We retrospectively reviewed clinical records and imaging studies of all patients undergoing decompressive hemicraniectomy followed by cranioplasty repair in our comprehensive database of TBI patients. Detailed analysis of motor function from the time of injury to 6 months following cranioplasty repair identified three patterns of motor recovery. RESULTS: Blossoming of contusions, CSF circulation dysfunction, and longer times to cranioplasty repair were strongly associated with "motor trephine syndrome". We hypothesize that "motor trephine syndrome" arises from decompensated CSF flow with transgression of CSF fluid and edema into brain parenchyma, together with associated decrements in cerebral blood flow. CONCLUSION: Prior contusion injury, decreased skull resistance with large hemispheric decompressions, and longer intervals to cranioplasty repair facilitate transparenchymal flow of CSF and edema. "Motor trephine syndrome" is rapidly reversible following cranioplasty repair. CSF and edema fluid changes within the parenchyma and CBF normalize, coincident with improvements in the patient's motor function, upon replacement of the bone.

Angiogenesis and its role in the behavior of astrocytic brain tumors.

Angiogenesis, the development of new vessels from a pre-existing vasculature, accompanies the growth and malignant transformation of astrocytic brain tumors. Neovascularization is essential for sustained tumor growth, and with increasing grade, astrocytic tumors undergo an, angiogenic switch, manifested by marked increases in vessel density and changes in vascular morphology. In the quiescent state, endogenous anti-angiogenic factors including endostatin, thrombospondin, and soluble vascular endothelial growth factor receptor-1 (sVEGFR-1) balance the actions of pro-angiogenic stimuli and restrain the angiogenic switch. Once activated, pro-angiogenic factors including most notably basic fibroblast growth factor (FGF), vascular endothelial growth factor (VEGF-A), and platelet-derived growth factor (PDGF) incite robust astrocytoma neovascularization. Recent studies have also explored the expression patterns and functional importance of the angiopoietins, Tie2 and neuropilin receptors, and hepatocyte growth factor/scatter factor (HGF). Together these angiogenic factors have diverse actions on endothelium and perivascular supporting cells that engender tumor neovessels with a unique phenotype, distinct from normal vessels. Properties of the astrocytoma neovasculature contribute to tumor growth, malignant progression, invasion, hemorrhage, and edema formation. Thus, the mechanistic actions of angiogenic factors on cerebral microvessels and the nature of the resultant tumor neovasculature establish a framework for understanding many of the characteristic behaviors of astrocytoma tumors.