Deborah L. Benzil

Optic nerve sheath meningiomas: visual improvement after stereotactic radiotherapy.

OBJECTIVE The management of primary optic nerve sheath meningioma (ONSM) is controversial. Surgery often results in postoperative blindness in the affected eye and thus has been abandoned as a treatment option for most patients. When these tumors are left untreated, however, progressive visual impairment ensues, which also leads to blindness. Recently, radiation therapy has gained wider acceptance in the treatment of these lesions. Experience with stereotactic radiotherapy (SRT) in the treatment of ONSMs is limited because of the rare incidence of this tumor. We present a series of patients with ONSM who were treated with SRT. METHODS Five patients (three women, two men), ranging in age from 40 to 73 years, presented with progressive visual loss with decreased visual field, visual acuity, and color vision affecting six eyes (one patient had tumor involving both optic nerves). One patient also presented with proptosis and diplopia. Five eyes had functional residual vision (range, 20/20 to 20/40), and one eye was completely blind. All five patients were diagnosed clinically and radiographically to have an ONSM. Three were intraorbital, one was intracanalicular as well as intraorbital, and one was a left ONSM extending through the optic foramen into the intracranial space and involving the right optic nerve. The five functional eyes were treated with SRT by use of 1.8-Gy fractions to a cumulative dose of 45 to 54 Gy. RESULTS Follow-up ranged from 1 to 7 years, and serial magnetic resonance imaging revealed no changes in the size of the tumor in all five patients. Four patients experienced dramatic improvement in visual acuity, visual field, and color vision within 3 months after SRT. One patient remained stable without evidence of visual deterioration or disease progression. None had radiation-induced optic neuropathy. CONCLUSION SRT may be a viable option for treatment of primary ONSM in patients with documented progressive visual deterioration, and it may be effective in improving or stabilizing remaining functional vision.

The future of neurosurgery: a white paper on the recruitment and retention of women in neurosurgery

PREFACE The leadership of Women in Neurosurgery (WINS) has been asked by the Board of Directors of the American Association of Neurological Surgeons (AANS) to compose a white paper on the recruitment and retention of female neurosurgical residents and practitioners. INTRODUCTION Neurosurgery must attract the best and the brightest. Women now constitute a larger percentage of medical school classes than men, representing approximately 60% of each graduating medical school class. Neurosurgery is facing a potential crisis in the US workforce pipeline, with the number of neurosurgeons in the US (per capita) decreasing. WOMEN IN THE NEUROSURGERY WORKFORCE The number of women entering neurosurgery training programs and the number of board-certified female neurosurgeons is not increasing. Personal anecdotes demonstrating gender inequity abound among female neurosurgeons at every level of training and career development. Gender inequity exists in neurosurgery training programs, in the neurosurgery workplace, and within organized neurosurgery. OBSTACLES The consistently low numbers of women in neurosurgery training programs and in the workplace results in a dearth of female role models for the mentoring of residents and junior faculty/practitioners. This lack of guidance contributes to perpetuation of barriers to women considering careers in neurosurgery, and to the lack of professional advancement experienced by women already in the field. There is ample evidence that mentors and role models play a critical role in the training and retention of women faculty within academic medicine. The absence of a critical mass of female neurosurgeons in academic medicine may serve as a deterrent to female medical students deciding whether or not to pursue careers in neurosurgery. There is limited exposure to neurosurgery during medical school. Medical students have concerns regarding gender inequities (acceptance into residency, salaries, promotion, and achieving leadership positions). Gender inequity in academic medicine is not unique to neurosurgery; nonetheless, promotion to full professor, to neurosurgery department chair, or to a national leadership position is exceedingly rare within neurosurgery. Bright, competent, committed female neurosurgeons exist in the workforce, yet they are not being promoted in numbers comparable to their male counterparts. No female neurosurgeon has ever been president of the AANS, Congress of Neurological Surgeons, or Society of Neurological Surgeons (SNS), or chair of the American Board of Neurological Surgery (ABNS). No female neurosurgeon has even been on the ABNS or the Neurological Surgery Residency Review Committee and, until this year, no more than 2 women have simultaneously been members of the SNS. Gender inequity serves as a barrier to the advancement of women within both academic and community-based neurosurgery. STRATEGIC APPROACH TO ADDRESS ISSUES IDENTIFIED To overcome the issues identified above, the authors recommend that the AANS join WINS in implementing a strategic plan, as follows: 1) Characterize the barriers. 2) Identify and eliminate discriminatory practices in the recruitment of medical students, in the training of residents, and in the hiring and advancement of neurosurgeons. 3) Promote women into leadership positions within organized neurosurgery. 4) Foster the development of female neurosurgeon role models by the training and promotion of competent, enthusiastic, female trainees and surgeons.

Mortality risk after head injury increases at 30 years

BACKGROUND Age has long been recognized as a critical factor in predicting outcomes after head injury, with individuals older than 60 years predicted to have a worse outcome than those younger than 60. The object of this study was to determine the effect of age by decade of life beginning at birth in patients with head injuries of all levels of severity. STUDY DESIGN The New York State Trauma Registry was searched for head injuries from January 1, 1994 to December 31, 1995; the 13,908 cases found were placed into age groups by decade. Data were sought for each patient on demographics, Glasgow Coma Score, ICD-9 injury code, New Injury Severity Score (NISS), and mechanism of injury. These data were analyzed with chi-square and one-way ANOVA tests, with significance set at p < 0.05. RESULTS The risk of dying was significantly increased in patients beginning at 30 years of age compared with those in the younger age groups, with the greatest increases occurring after age 60 (p < 0.001). For the population with available Glasgow Coma Score data (n = 12,844), the mortality rate for patients ages 0 to 30 was 10.9%, and for patients ages 31 to 50 was 12.4%. The mean Glasgow Coma Score for nonsurvivors ages 0 to 20 (3.9) and for nonsurvivors ages 31 to 50 (5.1) were significantly different, with a risk ratio of 1.3 (p < 0.001). CONCLUSIONS The risk of dying for patients suffering head injuries increases as early as 30 years of age, making it necessary for health-care providers to consider increased monitoring and treatment for patients in this younger age group.

Hypophysopexy technique for radiosurgical treatment of cavernous sinus pituitary adenoma.

Stereotactic radiosurgery is being used with increased frequency in the treatment of residual or recurrent pituitary adenomas. The major risk associated with radiosurgical treatment of residual or recurrent pituitary tumor adjacent to normal functional pituitary gland is radiation of the pituitary, which frequently leads to the development of hypopituitarism. The authors describe a technique of pituitary transposition to reduce the radiation dose to the normal pituitary gland in cases of planned radiosurgical treatment of residual pituitary adenoma within the cavernous sinus. A sellar exploration for tumor resection is performed, the pituitary gland is transposed from the region of the cavernous sinus, and a fat and fascia graft is interposed between the normal pituitary gland and the residual tumor in the cavernous sinus. The residual tumor may then be treated with stereotactic radiosurgery. The increased distance between the normal pituitary gland and the residual tumor facilitates treatment of the tumor with radiosurgery and reduces the radiation to the normal pituitary gland. An illustrative case of a young female with recurrent acromegaly and a pituitary adenoma invading the cavernous sinus is described.

Safety of multiple stereotactic radiosurgery treatments for multiple brain lesions

AbstractBackground: Stereotactic radiosurgery (SRS) is a widely used therapy for multiple brain lesions, and studies have clearly established the safety and efficacy of single-dose SRS. However, as patient survival has increased, the recurrence of tumors and the development of metastases to new sites within the brain have made it desirable to repeat treatments over time. The cumulative toxicity of multi-isocenter, multiple treatments has not been well defined. We have retrospectively studied 10 patients who received multiple SRS treatments for multiple brain lesions to assess the cumulative toxicity of these treatments. Methods: In a retrospective review of all patients treated with SRS using the X-knife (Radionics, Burlington, MA) at Westchester Medical Center/New York Medical College between December 1995 and December 2000, 10 patients were identified who received at least two treatments to at least 3 isocenters and had a minimum follow-up period of 6 months. Image fusion technique was used to determine cumulative doses to targeted lesions, whole brain and critical brain structures. Toxicities and complications were identified by chart and radiological review. Results: The average of the maximum doses (cGy) to a point within the whole brain was 2402 (range 1617–3953); to the brainstem, 1059 (range 48–4126); to the right optic nerve, 223 (range 14–1012); to the left optic nerve, 159 (range 17–475); and to the optic chiasm, 219 (range 15–909). There were no focal neurological toxicities, including visual disturbances, cranial nerve palsies, or ataxia in any of the 10 patients. There were also no global toxicities, including cognitive decline or secondary tumors. Only one patient developed seizures that were difficult to control in association with radiation necrosis. Conclusions: Multiple SRS treatments at the cumulative doses used in our study are a safe therapy for patients with multiple brain lesions.

Mutant human tumor suppressor p53 modulates the activation of mitogen‐activated protein kinase and nuclear factor‐κB, but not c‐Jun N‐terminal kinase and activated protein‐1

The roles of the mitogen‐activated kinase protein (MAPK) pathway, nuclear factor‐kappa B (NF‐κB), and activator protein‐1 (AP‐1) in cellular responses to growth factors and mitogen are well established. However, the manner by which these proliferative pathways are affected by the tumor suppressor protein p53 is not fully understood. We report here the results of an investigation of the status of p53 on two human melanoma cell lines with wild‐type p53 (SK‐Mel‐186) or mutant p53 (SK‐Mel‐110). The basal levels of the activated extracellular‐signal regulated kinases 1 and 2 (ERK1/2) were high in cells with wild‐type p53, but low in cells with mutant p53. The 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA)‐induced activation of ERK1/2 through the phosphorylation of threonine and tyrosine at 202 and 204, respectively, was demonstrated in both cell lines, however, in a discrete manner. TPA‐induced activation of ERK1/2 was sustained in wild‐type p53 cells, while only a transient activation was seen in mutant p53 cells. Inhibition of MAPK kinase (MEK), an upstream kinase, by U0126, blocked TPA‐induced activation of ERK1/2 in wild‐type p53 cells and in mutant p53 cells. Treatment of wild‐type p53 (SK‐Mel 186) cells with small interfering RNA (siRNA) of p53 displayed a transient induction of activation of ERK1/2 following TPA treatment, indicating that p53 has a role in the regulation of the activation of ERK1/2. NF‐κB activity decreased significantly in cells with wild‐type p53, while enhanced NF‐κB activity was evident in cells with mutant p53. The expression of either wild‐type or mutant p53 had a similar effect on TPA‐induced Jun N‐terminal kinase (JNK) activation, indicating specificity for the ERK pathway. Similarly, AP‐1 binding activity showed a transient variation in both cell lines after TPA treatment but with different kinetics. These observations suggest that both wild‐type and mutant p53 can modulate the activation pathways for ERK1/2, and NF‐κB distinctively, while modulating the pathways of JNK and AP‐1 similarly. These differences may influence cellular processes such as proliferation, differentiation, and apoptosis.

Knife wound to the posterior fossa in a child

BackgroundKnife wounds to the posterior fossa are a rare occurrence, especially in children. We report an 8-year-old girl who sustained a penetrating knife injury through the occipital bone into the posterior fossa. On presentation, the large knife blade was firmly embedded in her head.MethodsRadiographic evaluation was limited to plain X-rays because of the large size and sharpness of the embedded blade. Innovative positioning was used during intubation and then the patient was positioned semi-prone on the operating room table. The blade was surgically removed and the dura was closed.ConclusionsAtypical penetrating cranial injuries in children may require the treatment team to take a creative approach to the evaluation and repair of the lesion in order to maximize patient safety and minimize the risk of neurological injury.

Sympathectomy for Chronic Pain Management

Learning Objectives: After reading this article, the participant should be able to:1. Explain the role of the sympathetic nervous system in chronic pain.2. Identify the pain syndromes that are mediated by the sympathetic nervous system.3. List the indications for, outcomes of, and possible complications associated with sympathectomy.4. Describe the surgical procedures available for sympathetic ablation.