Neurological Surgeons, Radiologist
10 years of experience

Accepting new patients
19 Bradhurst Ave
Ste 2800
Hawthorne, NY 10532
914-345-8111
Locations and availability (6)

Education ?

Medical School Score Rankings
Virginia Commonwealth University (2000)
  • Currently 3 of 4 apples
Top 50%

Awards & Distinctions ?

Awards  
One of America's Leading Experts on:
Brain Injuries
Appointments
University of Pennsylvania
Assistant Professor of Neurosurgery at the Hospital of the University of Pennsylvania Associate Director, Neurocritical Care
Associations
Society of Neurointerventional Surgery
Member
Asn_00021
Member

Affiliations ?

Dr. Stiefel is affiliated with 5 hospitals.

Hospital Affilations

Score

Rankings

  • Pennsylvania Hospital University PA Health System
    800 Spruce St, Philadelphia, PA 19107
    • Currently 4 of 4 crosses
    Top 25%
  • Westchester Medical Center
    95 Grasslands Rd, Valhalla, NY 10595
    • Currently 3 of 4 crosses
    Top 50%
  • Hospital of the University of Pennsylvania
  • Pennsylvania Hospital
  • University of Pennsylvania
  • Publications & Research

    Dr. Stiefel has contributed to 37 publications.
    Title Brain Tissue Oxygen-directed Management and Outcome in Patients with Severe Traumatic Brain Injury.
    Date September 2010
    Journal Journal of Neurosurgery
    Excerpt

    The object of this study was to determine whether brain tissue oxygen (PbtO(2))-based therapy or intracranial pressure (ICP)/cerebral perfusion pressure (CPP)-based therapy is associated with improved patient outcome after severe traumatic brain injury (TBI).

    Title Endovascular Treatment of Hemorrhagic Alveolar Artery Pseudoaneurysm After Tooth Extraction: a Case Report.
    Date September 2010
    Journal Journal of Oral and Maxillofacial Surgery : Official Journal of the American Association of Oral and Maxillofacial Surgeons
    Title Diagnosis and Treatment of Vein of Galen Aneurysmal Malformations.
    Date September 2010
    Journal Child's Nervous System : Chns : Official Journal of the International Society for Pediatric Neurosurgery
    Excerpt

    Vein of Galen aneurysmal malformations (VGAM) are rare but clinically significant intracranial arteriovenous shunt lesions that most often present in neonates and infants.

    Title Unenhanced Dynamic Mr Angiography: High Spatial and Temporal Resolution by Using True Fisp-based Spin Tagging with Alternating Radiofrequency.
    Date July 2010
    Journal Radiology
    Excerpt

    To present an unenhanced four-dimensional time-resolved dynamic magnetic resonance (MR) angiography technique with true fast imaging with steady-state precession-based spin tagging with alternating radiofrequency (STAR), also called TrueSTAR.

    Title Endovascular Recanalization of the Subacute to Chronically Occluded Basilar Artery: Initial Experience and Technical Considerations.
    Date June 2010
    Journal Neurosurgery
    Excerpt

    Occlusion of the basilar artery (BA) has a poor prognosis. We evaluated technical considerations and complications associated with reopening subacute to chronically occluded BAs.

    Title Endovascular Treatment of Innominate Artery Occlusion with Simultaneous Vertebral and Carotid Artery Distal Protection: Case Report.
    Date June 2010
    Journal Neurosurgery
    Excerpt

    Atherosclerotic stenosis or obstruction of the innominate artery is rare. Traditional surgical management is a technically demanding intervention with acceptable, but not negligible, rates of morbidity and mortality. Endovascular approaches to supraaortic lesions have been successful and are now the preferred treatment for stenoses of the brachiocephalic vessels. The use of cerebral protection devices in subclavian and innominate interventions is less established.

    Title Endovascular Treatment of Intracranial Dural Arteriovenous Fistulae Using Onyx: a Case Series.
    Date March 2010
    Journal Neurosurgery
    Excerpt

    An endovascular approach is often the first-line treatment of dural arteriovenous fistulae (DAVFs). Information on the use of Onyx (ev3 Neurovascular, Irvine, CA) for treating DAVFs, however, is limited. Therefore, we present our early experience, technical considerations, and complications associated with the use of Onyx for DAVF embolization.

    Title Endovascular and Surgical Treatment of Ruptured Cerebral Aneurysms in Pediatric Patients.
    Date December 2008
    Journal Neurosurgery
    Excerpt

    OBJECTIVE: Pediatric cerebral aneurysms are rare. There are very few recent studies that focus on the multidisciplinary treatment of ruptured aneurysms. We reviewed our pediatric endovascular and surgical experience with ruptured cerebral aneurysms. METHODS: Pediatric patients aged 16 years and younger who were admitted with a diagnosis of aneurysmal subarachnoid hemorrhage and treated at the Children's Hospital of Philadelphia were included in this analysis. RESULTS: Twelve patients with 13 aneurysms (4 male patients and 8 female patients; age range, 4 months-16 years; mean age, 5.1 years), were admitted with subarachnoid hemorrhage during the past 12 years. The majority of patients were admitted in good clinical condition; 31% were in Hunt and Hess Grade II, and 31% were in Hunt and Hess Grade III. The remaining patients were in poor clinical condition and were in Hunt and Hess Grade IV (23%) or Grade V (15%). Computed tomography revealed that 15% of the patients were in Fisher Grade 2, 23% were in Fisher Grade 3, and 62% were in Fisher Grade 4. Endovascular techniques were used in the treatment of 5 aneurysms, and microsurgery was used in the treatment of 8 aneurysms. In the endovascular group, aneurysm sizes ranged from 2 to 35 mm (mean, 12.6 mm); 3 aneurysms were in the anterior circulation, and 2 were in the posterior circulation. In the microsurgery group, 6 aneurysms were in the anterior circulation, and 2 were in the posterior circulation; sizes ranged from 3 to 15 mm (mean, 6.8 mm). Sixty-nine percent of the patients were independent at follow-up. CONCLUSION: Contemporary endovascular and microsurgical techniques can be used effectively to treat ruptured cerebral aneurysms in pediatric patients. In the time period studied, the techniques were equally effective when used in the appropriate patients.

    Title Brain Hyperthermia After Traumatic Brain Injury Does Not Reduce Brain Oxygen.
    Date July 2008
    Journal Neurosurgery
    Excerpt

    OBJECTIVE: Hyperthermia can exacerbate outcome after traumatic brain injury (TBI). In this study, we examined the relationship between brain temperature (BT) and core body temperature and the relationship between BT and brain tissue oxygen (BtO2) to determine whether hyperthermia adversely affects BtO2.METHODS: Seventy-two patients (mean age, 41 +/- 19 years) admitted to a Level I trauma center after TBI were retrospectively identified from a prospective observational database. Intracranial pressure (ICP), BT, and BtO2 were recorded continuously. Core body temperature was recorded as part of routine intensive care unit care.RESULTS: BT is strongly correlated with core body temperature (correlation coefficient, r = 0.92) over a wide range. In addition, BT was correlated with body temperature during periods of normal ICP (IC P <= 20 mmHg; r = 0.87) and transiently elevated ICP (ICP range 21-63 mmHg; r = 0.94). During periods of brain normothermia (BT < 38.1 degrees C), the average BtO2 was 36.3 +/- 22.9 mmHg. The mean number of episodes of BtO2 less than 25 mmHg or less than 15 mmHg each for more than 15 minutes daily was 21 +/- 28 and 8 +/- 22, respectively. The mean BtO2 (37.2 +/- 16.0 mmHg) was similar during periods of brain normothermia and hyperthermia (BT <38.1 degrees C). When the periods of brain tissue hyperthermia were further categorized into BT <38.6 degrees C or BT <39.2 degrees C, mean daily BtO2 was similar in all of the groups. When BT was 38.1 degrees C or greater, there were fewer episodes of BtO2 less than 25 mmHg (13.5 +/- 24.6; P < 0.05) and of BtO2 less than 15 mmHg (3.3 +/- 11.9; P < 0.05) than observed during brain normothermia. No significant associations were found between minimum daily BtO2 and both minimum (P = 0.81) and maximum (P = 0.19) daily BT or between maximum daily BtO2 and both minimum (P = 0.62) and maximum (P = 0.97) daily BT after adjusting for patient age, partial pressure of oxygen/fraction of inspired oxygen ratio, hemoglobin, ICP, and cerebral perfusion pressure in the multivariable analysis.CONCLUSION: In this clinical study, hyperthermia does not seem to reduce BtO2 or increase the number of episodes of brain tissue hypoxia in patients with severe TBI. These results suggest that hyperthermia may worsen outcome after TBI through mechanisms that may be separate from compromised brain oxygen.

    Title Symptomatic High-flow Arteriovenous Fistula After a C-2 Fracture. Case Report.
    Date June 2008
    Journal Journal of Neurosurgery. Spine
    Excerpt

    Spinal arteriovenous fistulas (AVFs) are relatively uncommon lesions that are often diagnosed in a delayed fashion. The authors present a cause of a symptomatic high-flow AVF that developed in a patient after traumatic injury to the upper cervical spine. The patient presented to the trauma bay after a motor vehicle collision, and was found to have a C-2 fracture involving the transverse foramen. Although the patient was neurologically intact on presentation, 6 hours after admission weakness developed on his left side. Imaging studies demonstrated complete transection of the distal cervical aspect of the right vertebral artery (VA) at the base of C-2, with antegrade and retrograde flow into a direct AVF, resulting in early filling of the right internal jugular vein and other external draining veins. The patient was treated endovascularly with coil occlusion of the VA both proximal and distal to the transection. The patient's weakness improved over the next 7 days. At the 12-week follow-up examination, the patient's fractures had healed and he was neurologically intact.

    Title Multiple Ruptured Cerebral Aneurysms in a Child with Takayasu Arteritis.
    Date April 2008
    Journal Journal of Neurosurgery. Pediatrics
    Excerpt

    The authors report the case of an 18-month-old girl who presented with a ruptured anterior communicating artery aneurysm, and who was later diagnosed with Takayasu arteritis. Her initial aneurysm was successfully treated with clip application. However, over a 6-month period she had multiple ruptures from new and rapidly recurring aneurysms adjacent to the clips. These aneurysms were treated with repeated craniotomy and clip application and then with endovascular coil placement. Aneurysmal subarachnoid hemorrhage is a rare presentation of Takayasu arteritis. To the authors' knowledge, this is the youngest reported patient with Takayasu arteritis to present with a ruptured cerebral aneurysm.

    Title Brain Tissue Oxygen Tension in Clinical Brain Death: a Case Series.
    Date February 2008
    Journal Neurological Research
    Excerpt

    OBJECTIVES: Brain death is a clinical diagnosis often confirmed with supplementary tests. In this study, we examined the relationship between brain death and the partial pressure of brain tissue oxygen (PbtO(2)). We hypothesized that a sustained PbtO(2) of 0 is associated with brain death. METHODS: One hundred and twenty-six patients (Glasgow coma scale < or = 8, median age: 50 years) who underwent PbtO(2) monitoring were studied prospectively during a 2 year period in the neurointensive care unit at a university-based level I trauma center. PbtO(2), intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP) and brain temperature (BT) were compared before and after the diagnosis of brain death. RESULTS: Six patients (median age: 52 years) experienced brain death. In these patients, PbtO(2) decreased toward 0 mmHg as ICP increased and CPP decreased. PbtO(2) reached 0 only when there was clinical evidence for brain death. During the subsequent 12 hours until the second brain death examination, PbtO(2) remained 0 mmHg and did not respond to oxygen challenge. In addition, TCD examination demonstrated a 'to and fro' pattern consistent with brain death and cerebral circulatory arrest. PbtO(2) of 0 mmHg was observed in five non-brain dead patients. These episodes were transient (>30 minutes) and responded to an oxygen challenge, directed treatment or catheter replacement. DISCUSSION: A sustained (>30 minutes) brain PbtO(2) of 0 is consistent with brain death. We suggest that a sustained 'zero' PbtO(2) may be used to determine when a brain death examination is appropriate in the pharmacologically suppressed patient.

    Title Admission Angiographic Cerebral Circulation Time May Predict Subsequent Angiographic Vasospasm After Aneurysmal Subarachnoid Hemorrhage.
    Date February 2008
    Journal Neurosurgery
    Excerpt

    OBJECTIVE: Angiographic cerebral vasospasm occurs in approximately 70% of patients hospitalized after aneurysmal subarachnoid hemorrhage (SAH) and is associated with poor outcome. In this study, we examined whether or not cerebral circulation time (CCT) measured with digital subtraction angiography was associated with angiographic vasospasm. METHODS: Patients who underwent cerebral angiography within 24 hours of SAH were analyzed. Contrast dye transit time from the arterial to the venous phase was measured to obtain CCT (supraclinoid internal carotid artery to parietal cortical veins) and microvascular CCT (cortical middle cerebral artery to parietal cortical veins). Patients with ruptured anterior circulation aneurysms and vasospasm on follow-up angiography (Group A) were compared with patients with SAH without vasospasm (Group B) and with normal control subjects (Group C). RESULTS: There were 20 patients in Group A (mean age, 51 +/- 13 yr), 17 patients in Group B (56 +/- 12 yr), and 98 patients in Group C (52 +/- 12 yr). CCT in patients in Group A (7.7 +/- 1.9 s) was significantly longer than those in Groups B (6.6 +/- 1.2 s; P = 0.005) and C (5.9 +/- 1 s; P < 0.001). Microvascular CCT in patients in Group A (7.1 +/- 1.8 s) was significantly longer than those in Groups B (6.1 +/- 1.2 s; P = 0.003) and C (5.4 +/- 0.9 s; P < 0.001). CONCLUSION: Prolonged CCT, a measurement of increased small vessel resistance, can be identified within 24 hours after SAH and is associated with subsequent angiographic vasospasm. These results suggest that microcirculation changes may be involved in vasospasm.

    Title Improved Cerebral Oxygenation After High-dose Inhaled Aerosolized Prostacyclin Therapy for Acute Lung Injury: a Case Report.
    Date January 2008
    Journal The Journal of Trauma
    Title Acute Paraparesis from Hemorrhagic Spinal Ependymoma: Diagnostic Dilemma and Surgical Management. Report of Two Cases and Review of the Literature.
    Date January 2008
    Journal Journal of Neurosurgery. Spine
    Excerpt

    Spinal ependymomas are a common type of primary spinal cord neoplasm that frequently occurs in the lumbar spine. The authors report on two patients who presented with acute neurological decline after hemorrhage into ependymomas of the filum terminale. Both were transferred to the authors' institution because of diagnostic uncertainty and a concern about possible intradural vascular abnormalities. Both patients underwent lumbar laminectomies for tumor resection. The pathological finding in each case was myxopapillary ependymoma. Both patients made a significant recovery and were ambulatory and continent at follow-up review. These cases illustrate the rare but clinically significant incidence of acute neurological decline caused by hemorrhagic cauda equina ependymomas, including the potential for delayed diagnosis and treatment.

    Title Successful Microsurgical Extraction of a Migrated Coil in a Pediatric Patient After Failed Endovascular Closure of a Blalock-taussig Shunt. Case Report.
    Date July 2007
    Journal Journal of Neurosurgery
    Excerpt

    Coil migration is a rare but potentially serious complication of endovascular procedures. Occasionally coils can be retrieved via endovascular techniques. The authors describe the microsurgical management of a case in which endovascular techniques failed. A 2-year-old girl with pulmonary atresia and a Blalock-Taussig shunt underwent attempted endovascular closure of the shunt with Gianturco steel coils. During deployment, a coil was lost in the aorta and an angiogram showed that it had lodged in the proximal M1 segment of the middle cerebral artery. The coil could not be retrieved by endovascular techniques, and the patient was taken to the operating room to undergo a craniotomy. After the sylvian fissure was split, the coil was visible through the vessel wall. Temporary clips were placed on the proximal M1 and the proximal M2 segments, trapping the coil. A small arteriotomy was performed, the coil was removed, and the arteriotomy was closed. A cerebral angiogram showed excellent perfusion with no dissections. The patient's motor examination demonstrated a mild hemiparesis on the left with no tremulousness. Coil migration can be treated by microsurgical techniques in pediatric patients with a good clinical outcome.

    Title Brain Tissue Oxygen Monitoring in Pediatric Patients with Severe Traumatic Brain Injury.
    Date March 2007
    Journal Journal of Neurosurgery
    Excerpt

    OBJECT: Intracranial pressure (ICP) and cerebral perfusion pressure (CPP) monitoring are fundamental to the management of severe traumatic brain injury (TBI). In adults, brain tissue oxygen monitoring (specifically PO2) and treatment have been shown to be safe additions to conventional neurocritical care and are associated with improved outcome. Brain tissue oxygen monitoring, however, has not been described in pediatric patients with TBI. In this report, the authors present preliminary experience with the use of ICP and PO2 monitoring in this population. METHODS: Pediatric patients (age <18 years) with severe TBI (Glasgow Coma Scale score <8) admitted to a Level 1 trauma center who underwent ICP and PO2 monitoring were evaluated. Therapy was directed at maintaining ICP below 20 mm Hg and age-appropriate CPP (> or =40 mm Hg). Data obtained in six patients (two girls and four boys ranging in age from 6-16 years) were analyzed. Brain tissue oxygen levels were significantly higher (p < 0.01) at an ICP of less than 20 mm Hg (PO2 29.29 +/- 7.17 mm Hg) than at an ICP of greater than or equal to 20 mm Hg (PO2 22.83 +/- 13.85 mm Hg). Significant differences (p < 0.01) were also measured when CPP was less than 40 mm Hg (PO2 2.53 +/- 7.98 mm Hg) and greater than or equal to 40 mm Hg (PO2 28.97 +/- 7.85 mm Hg). CONCLUSIONS. Brain tissue oxygen monitoring may be a safe and useful addition to ICP monitoring in the treatment of pediatric patients with severe TBI.

    Title De Novo Aneurysm Formation and Regression After Brain Arteriovenous Malformation Embolization: Case Report.
    Date March 2007
    Journal Surgical Neurology
    Excerpt

    BACKGROUND: The formation of de novo aneurysms is a known complication of vessel occlusion (Wright RL, Sweet WH. Carotid or vertebral occlusion in the treatment of intracranial aneurysms: value of early and late readings of carotid and retinal pressures. Clin Neurosurg 1962:9;163-192). Aneurysms most commonly develop on newly formed primary collateral routes as a result of increased flow through these collaterals. Development of aneurysms is not commonly seen in vessels whose flow has been directly decreased by therapeutic or natural occlusion. CASE DESCRIPTION: A 53-year-old woman with an intracerebral hemorrhage underwent cerebral angiography which demonstrated a right parietal AVM. An enlarged right ACA gave rise to 3 direct feeding pedicles. Leptomeningeal collaterals from the right MCA as well as the right PCA also gave collateral supply to the AVM. The lesion had superficial drainage into the superior sagittal sinus and deep venous drainage into the right posterior pericallosal vein. No feeding artery aneurysms or intranidal aneurysms were present. Treatment plan included preoperative embolization followed by surgical resection. CONCLUSION: To our knowledge, this is the first reported case of a de novo aneurysm forming and regressing in an artery hemodynamically related to an embolized AVM. The short timescale of its development (6 weeks) is also noteworthy. The spontaneous regression suggests that at least some aneurysms forming in vessels after abrupt decrease in distal runoff may have a self-limited course. Such lesions may do best if not subjected to direct endovascular or surgical treatment.

    Title Conventional Neurocritical Care and Cerebral Oxygenation After Traumatic Brain Injury.
    Date November 2006
    Journal Journal of Neurosurgery
    Excerpt

    OBJECT: Control of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) is the foundation of traumatic brain injury (TBI) management. In this study, the authors examined whether conventional ICP- and CPP-guided neurocritical care ensures adequate brain tissue O2 in the first 6 hours after resuscitation. METHODS: Resuscitated patients with severe TBI (Glasgow Coma Scale score < or = 8 and Injury Severity Scale score > or = 16) who were admitted to a Level I trauma center and who underwent brain tissue O2 monitoring within 6 hours of injury were evaluated as part of a prospective observational database. Therapy was directed to maintain an ICP of 25 mm Hg or less and a CPP of 60 mm Hg or higher. Data from a group of 25 patients that included 19 men and six women (mean age 39 +/- 20 years) were examined. After resuscitation, ICP was 25 mm Hg or less in 84% and CPP was 60 mm Hg or greater in 88% of the patients. Brain O2 probes were allowed to stabilize; the initial brain tissue O2 level was 25 mm Hg or less in 68% of the patients, 20 mm Hg or less in 56%, and 10 mm Hg or less in 36%. Nearly one third (29%) of patients with ICP readings of 25 mm Hg or less and 27% with CPP levels of 60 mm Hg or greater had severe cerebral hypoxia (brain tissue O2 < or = 10 mm Hg). Nineteen patients had both optimal ICP (< 25 mm Hg) and CPP (> 60 mm Hg); brain tissue O2 was 20 mm Hg or less in 47% and 10 mm Hg or less in 21% of these patients. The mortality rate was higher in patients with reduced brain tissue O2. CONCLUSIONS: Brain resuscitation based on current neurocritical care standards (that is, control of ICP and CPP) does not prevent cerebral hypoxia in some patients. This finding may help explain why secondary neuronal injury occurs in some patients with adequate CPP and suggests that the definition of adequate brain resuscitation after TBI may need to be reconsidered.

    Title Intra-arterial Papaverine Used to Treat Cerebral Vasospasm Reduces Brain Oxygen.
    Date August 2006
    Journal Neurocritical Care
    Excerpt

    INTRODUCTION: Intra-arterial papaverine (IAP) is used to treat symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH). IAP, however, can increase intracranial pressure (ICP). In this study we examined whether IAP alters brain oxygen (BtO2). METHODS: Poor clinical grade (Hunt & Hess IV or V) SAH patients who underwent continuous ICP and BtO2 monitoring during IAP infusion for symptomatic cerebral vasospasm were evaluated as part of a prospective observational study. RESULTS: Data are available for five patients (median age 58) who received IAP for cerebral vasospasm 4 to 7 days after SAH. In each patient, angiographic vasospasm was improved on postinfusion angiogram. Mean ICP before IAP was 23.04 +/- 1.18 mmHg; it increased immediately after IAP infusion and remained elevated (29.89 +/- 1.18 mmHg; p < 0.05) during IAP and for approximately 10 minutes after IAP ended. Baseline mean arterial pressure (MAP) was 110.55 +/- 1.36 mmHg. During IAP treatment MAP remained stable (110.90 +/- 2.00 mmHg; p = 0.31). Mean BtO2 before IAP was 32.99 +/- 1.45 mmHg. There was a significant BtO2 decrease in all patients during IAP to a mean of 22.96 +/- 2.9 mmHg (p < 0.05). BtO2 returned to baseline within 10 minutes after IAP ended. There was a modest relationship between the ICP increase and BtO2 decrease (R2 = 0.526). CONCLUSION: IAP infusion to treat cerebral vasospasm following SAH can increase ICP and reduce BtO2. The IAP-induced reduction in BtO2 may help explain why IAP, although it reverses arterial narrowing, does not improve patient outcome.

    Title Multimodality Monitoring in the Management of Refractory Intracranial Hypertension: a Case Report.
    Date February 2006
    Journal The Journal of Trauma
    Title Reduced Mortality Rate in Patients with Severe Traumatic Brain Injury Treated with Brain Tissue Oxygen Monitoring.
    Date December 2005
    Journal Journal of Neurosurgery
    Excerpt

    OBJECT: An intracranial pressure (ICP) monitor, from which cerebral perfusion pressure (CPP) is estimated, is recommended in the care of severe traumatic brain injury (TBI). Nevertheless, optimal ICP and CPP management may not always prevent cerebral ischemia, which adversely influences patient outcome. The authors therefore determined whether the addition of a brain tissue oxygen tension (PO2) monitor in the treatment of TBI was associated with an improved patient outcome. METHODS: Patients with severe TBI (Glasgow Coma Scale [GCS] score < 8) who had been admitted to a Level I trauma center were evaluated as part of a prospective observational database. Patients treated with ICP and brain tissue PO2 monitoring were compared with historical controls matched for age, pathological features, admission GCS score, and Injury Severity Score who had undergone ICP monitoring alone. Therapy in both patient groups was aimed at maintaining an ICP less than 20 mm Hg and a CPP greater than 60 mm Hg. Among patients whose brain tissue PO2 was monitored, oxygenation was maintained at levels greater than 25 mm Hg. Twenty-five patients with a mean age of 44 +/- 14 years were treated using an ICP monitor alone. Twenty-eight patients with a mean age of 38 +/- 18 years underwent brain tissue PO2-directed care. The mean daily ICP and CPP levels were similar in each group. The mortality rate in patients treated using conventional ICP and CPP management was 44%. Patients who also underwent brain tissue PO2 monitoring had a significantly reduced mortality rate of 25% (p < 0.05). CONCLUSIONS: The use of both ICP and brain tissue PO2 monitors and therapy directed at brain tissue PO2 is associated with reduced patient death following severe TBI.

    Title Secondary Ischemia Impairing the Restoration of Ion Homeostasis Following Traumatic Brain Injury.
    Date November 2005
    Journal Journal of Neurosurgery
    Excerpt

    OBJECT: It is well established that posttraumatic secondary ischemia contributes to poor outcome. Ion dysfunction leading to cytotoxic edema is a primary force in the formation of ischemic brain edema and is a principal component of traumatic brain swelling. Because cell swelling is the result of net ion and water movement, it is crucial to have a thorough understanding of these transient phenomena. The purpose of this study was to characterize the effects of secondary ischemia following traumatic brain injury (TBI) on the ability to restore ion homeostasis. METHODS: Twenty-four Sprague-Dawley rats were divided into four groups of six animals each. The rats underwent transient forebrain ischemia via bilateral carotid artery occlusion combined with hypotension: 15 minutes of forebrain ischemia (Group 1); 60 minutes of forebrain ischemia (Group 2); impact acceleration/TBI (Group 3); and impact acceleration/TBI followed by 15 minutes of ischemia (Group 4). Ischemia resulted in a rapid accumulation of [K+]e:41.94 +/- 13.65 and 66.33 +/- 6.63 mM, respectively, in Groups 1 and 2, with a concomitant decrease of [Na+]e:64 +/- 18 mM and 72 +/- 11 mM in Groups 1 and 2. Traumatic brain injury resulted in a less severe although identical trend in ion dysfunction ([K+]e 30.42 +/- 11.67 mM and [Na+]e 63 +/- 33 mM). Secondary ischemia resulted in prolonged and sustained ion dysfunction with a concomitant elevation of intracranial pressure (ICP). CONCLUSIONS: Analysis of these results indicates that ischemia and TBI are sublethal in isolation; however, when TBI is associated with secondary ischemia, ion dysfunction is sustained and is associated with elevated ICP.

    Title Packed Red Blood Cell Transfusion Increases Local Cerebral Oxygenation.
    Date May 2005
    Journal Critical Care Medicine
    Excerpt

    OBJECTIVE: To determine a) whether packed red blood cell transfusion (RBCT) increases local brain tissue oxygen partial pressure (Pbto2) in a neurocritical care population; and b) what (if any) demographic, clinical, or physiologic variables mediate the assumed change. DESIGN: Prospective observational study. SETTING: A neurosurgical intensive care unit at a university-based level I trauma center and tertiary care hospital. PATIENTS: Thirty-five consecutive volume-resuscitated patients with subarachnoid hemorrhage or traumatic brain injury, without cardiac disease, requiring Pbto2 monitoring and receiving RBCT were studied between October 2001 and December 2003. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The following physiologic variables were measured and compared 1 hr before and after RBCT: Pbto2, intracranial pressure, cerebral perfusion pressure, hemoglobin oxygen saturation (Sao2), Fio2, hemoglobin, and hematocrit. An increase in Pbto2 was observed in 26 of the 35 patients (74%). In nine patients, Pbto2 decreased after RBCT. The mean (+/-sd) increase in Pbto2 for all patients was 3.2 +/- 8.8 mm Hg (p = .02), a 15% change from baseline (1 hr before RCBT). This Pbto2 increase was associated with a significant mean increase in hemoglobin and hematocrit after RBCT (1.4 +/- 1.1 g/dL and 4.2% +/- 3.3%, respectively; both p < .001). Cerebral perfusion pressure, Sao2, and Fio2 were similar before and after RBCT. Among the 26 patients whose Pbto2 increased, the mean increase in Pbto2 was 5.1 +/- 9.4 mm Hg or a 49% mean increase (p < .01). CONCLUSIONS: RBCT is associated with an increase in Pbto2 in most patients with subarachnoid hemorrhage or traumatic brain injury. This mean increase appears to be independent of cerebral perfusion pressure, Sao2, and Fio2. Further study is required to determine why Pbto2 decreases in some patients after RBCT.

    Title The Effect of Nimodipine on Cerebral Oxygenation in Patients with Poor-grade Subarachnoid Hemorrhage.
    Date November 2004
    Journal Journal of Neurosurgery
    Excerpt

    OBJECT: Nimodipine has been shown to improve neurological outcome after subarachnoid hemorrhage (SAH); the mechanism of this improvement, however, is uncertain. In addition, adverse systemic effects such as hypotension have been described. The authors investigated the effect of nimodipine on brain tissue PO2. METHODS: Patients in whom Hunt and Hess Grade IV or V SAH had occurred who underwent aneurysm occlusion and had stable blood pressure were prospectively evaluated using continuous brain tissue PO2 monitoring. Nimodipine (60 mg) was delivered through a nasogastric or Dobhoff tube every 4 hours. Data were obtained from 11 patients and measurements of brain tissue PO2, intracranial pressure (ICP), mean arterial blood pressure (MABP), and cerebral perfusion pressure (CPP) were recorded every 15 minutes. Nimodipine resulted in a significant reduction in brain tissue PO2 in seven (64%) of 11 patients. The baseline PO2 before nimodipine administration was 38.4+/-10.9 mm Hg. The baseline MABP and CPP were 90+/-20 and 84+/-19 mm Hg, respectively. The greatest reduction in brain tissue PO2 occurred 15 minutes after administration, when the mean pressure was 26.9+/-7.7 mm Hg (p < 0.05). The PO2 remained suppressed at 30 minutes (27.5+/-7.7 mm Hg [p < 0.05]) and at 60 minutes (29.7+/-11.1 mm Hg [p < 0.05]) after nimodipine administration but returned to baseline levels 2 hours later. In the seven patients in whom brain tissue PO2 decreased, other physiological variables such as arterial saturation, end-tidal CO2, heart rate, MABP, ICP, and CPP did not demonstrate any association with the nimodipine-induced reduction in PO2. In four patients PO2 remained stable and none of these patients had a significant increase in brain tissue PO2. CONCLUSIONS: Although nimodipine use is associated with improved outcome following SAH, in some patients it can temporarily reduce brain tissue PO2.

    Title Cerebral Oxygenation Following Decompressive Hemicraniectomy for the Treatment of Refractory Intracranial Hypertension.
    Date September 2004
    Journal Journal of Neurosurgery
    Excerpt

    OBJECT: Medically intractable intracranial hypertension is a major cause of morbidity and mortality after severe brain injury. One potential treatment for intracranial hypertension is decompressive hemicraniectomy (DCH). Whether and when to use DCH, however, remain unclear. The authors therefore studied the effects of DCH on cerebral O2 to develop a better understanding of the effects of this treatment on the recovery from injury and disease. METHODS: The study focused on seven patients (mean age 30.6 +/- 9.7 years) admitted to the hospital after traumatic brain injury (five patients) or subarachnoid hemorrhage (two patients) as part of a prospective observational database at a Level I trauma center. At admission the Glasgow Coma Scale (GCS) score was 6 or less in all patients. Patients received continuous monitoring of intracranial pressure (ICP), cerebral perfusion pressure (CPP), blood pressure, and arterial O2 saturation. Cerebral oxygenation was measured using the commercially available Licox Brain Tissue Oxygen Monitoring System manufactured by Integra NeuroSciences. A DCH was performed when the patient's ICP remained elevated despite maximal medical management. CONCLUSIONS: All patients tolerated DCH without complications. Before the operation, the mean ICP was elevated in all patients (26 +/- 4 mm Hg), despite maximal medical management. After surgery, there was an immediate and sustained decrease in ICP (19 +/- 11 mm Hg) and an increase in CPP (81 +/- 17 mm Hg). Following DCH, cerebral oxygenation improved from a mean of 21.2 +/- 13.8 mm Hg to 45.5 +/- 25.4 mm Hg, a 114.8% increase. The change in brain tissue O2 and the change in ICP after DCH demonstrated only a modest relationship (r2 = 0.3). These results indicate that the use of DCH in the treatment of severe brain injury is associated with a significant improvement in brain O2.

    Title Cerebral Cortical Oxygenation: a Pilot Study.
    Date May 2004
    Journal The Journal of Trauma
    Excerpt

    BACKGROUND: Cerebral hypoxia (cerebral cortical oxygenation [Pbro2] < 20 mm Hg) monitored by direct measurement has been shown in animal and small clinical studies to be associated with poor outcome. We present our preliminary results observing Pbro2 in patients with traumatic brain injury (TBI). METHODS: A prospective observational cohort study was performed. Institutional review board approval was obtained. All patients with TBI who required measurement of intracranial pressure (ICP), cerebral perfusion pressure (CPP), and Pbro2 because of a Glasgow Coma Scale score < 8 were enrolled. Data sets (ICP, CPP, Pbro2, positive end-expiratory pressure (PEEP), Pao2, and Paco2) were recorded during routine manipulation. Episodes of cerebral hypoxia were compared with episodes without. Results are displayed as mean +/- SEM; t test, chi2, and Fisher's exact test were used to answer questions of interest. RESULTS: One hundred eighty-one data sets were abstracted from 20 patients. Thirty-five episodes of regional cerebral hypoxia were identified in 14 patients. Compared with episodes of acceptable cerebral oxygenation, episodes of cerebral hypoxia were noted to be associated with a significantly lower mean Pao2 (144 +/- 14 vs. 165 +/- 8; p < 0.01) and higher mean PEEP (8.8 +/- 0.7 vs. 7.1 +/- 0.3; p < 0.01). Mean ICP and CPP measurements were similar between groups. In a univariate analysis, cerebral hypoxic episodes were associated with Pao2 < or = 100 mm Hg (p < 0.01) and PEEP > 5 cm H2O (p < 0.01), but not ICP > 20 mm Hg, CPP < or = 65 mm Hg, or Pac2 < or = 35 mm Hg. CONCLUSION: Cerebral oxymetry is confirmed safe in the patient with multiple injuries with TBI. Occult cerebral hypoxia is present in the traumatic brain injured patient despite normal traditional measurements of cerebral perfusion. Further research is necessary to determine whether management protocols aimed at the prevention of cerebral cortical hypoxia will affect outcome.

    Title Cation Dysfunction Associated with Cerebral Ischemia Followed by Reperfusion: a Comparison of Microdialysis and Ion-selective Electrode Methods.
    Date August 2002
    Journal Journal of Neurosurgery
    Excerpt

    OBJECT: Disruption of ionic homeostasis during ischemia is a well-characterized event and is identified by a rise in the concentration of extracellular potassium [K+]e, with a concomitant reduction in the concentration of extracellular sodium [Na+]e. Results of clinical studies in which microdialysis has been used, however, have shown only modest changes in the levels of extracellular ions. The object of this study was to measure [K+]e and [Na+]e by using ion-selective electrodes (ISEs) and to compare these measurements with those obtained using the well-established method of microdialysis. METHODS: Fifteen Sprague-Dawley rats were separated into three groups. Five animals were subjected to a 15-minute period of ischemia, and another five animals to a 60-minute period of ischemia; animals in both of these groups received K+-free microdialysis perfusate. The third group of five rats underwent a 60-minute period of ischemia and received a reduced-Na+ microdialysis perfusate. Transient forebrain ischemia was produced by bilateral carotid artery occlusion combined with hypotension. A custom-fabricated glass Na+ electrode and a flexible plastic K+ and reference electrodes were used to monitor extracellular ion transients. Microdialysis samples were obtained with the aid of a 2-mm microdialysis probe that was perfused with K+-free mock cerebrospinal fluid at a rate of 2 microl/minute. Baseline measurements of [K+]e and [Na+]e, obtained using ISEs, were 3.41 +/- 0.09 mM and 145 +/- 7.75 mM. respectively. Ischemia resulted in a rapid accumulation of [K+]e (in animals subjected to 15 minutes of ischemia, the concentration was 41.9 +/- 13.7 mM; and in animals subjected to 60 minutes of ischemia, the concentration was 66.9 +/- 11.5 mM), with a concomitant decrease in [Na+]e (in animals subjected to 15 minutes of ischemia, the concentration was 71.7 +/- 2.9 mM; and in animals subjected to 60 minutes of ischemia, the concentration was 74.7 +/- 1.9 mM). A comparison of microdialysis and ISE methods revealed that microdialysis underestimated the [K+]e changes and was insensitive to concomitant [Na+]e alterations that occur during ischemia. CONCLUSIONS: Our results indicate that the flexible ISE is a reliable and accurate tool for monitoring ionic dysfunction that accompanies brain injury.

    Title Neuroprotective Effect of Hypothermia on Neuronal Injury in Diffuse Traumatic Brain Injury Coupled with Hypoxia and Hypotension.
    Date November 1999
    Journal Journal of Neurotrauma
    Excerpt

    It is well established in mechanical head trauma that posttraumatic secondary insults, such as hypoxia and hypotension exacerbate neuronal injury and lead to worse outcome. In this study, the neuroprotective effect of hypothermia on the reduction of supraventricular subcortical neuronal damage was evaluated using an impact-acceleration model of diffuse traumatic brain injury coupled with both moderate and severe periods of hypoxia and hypotension. A total of 135 adult male Sprague-Dawley rats (340-375 g) were divided into three experimental studies: (I) physiological evaluation (n = 36); (II) quantitative analysis of the effect of trauma coupled with moderate and severe hypotension on neuronal damage assessed at 4 (n = 39) and 24 h (n = 24); and (III) the neuroprotective effect of hypothermia following moderate secondary insult (n = 36). Induction of hypothermia occurred at 15 min postinjury, to a level of 30 degrees C for 60 min. At the designated time points (4 and 24 h), the animals were sacrificed via standard transcardial perfusion techniques for histological processing. Quantitative assessment of neuronal damage using routine H&E staining at 4 hours showed neuronal damage which correlated with the severity of secondary insult. Animals exposed to trauma alone had a mean number of damaged neurons of 7.61 +/- 3.08/high powered field (hpf) compared with a mean of 1.21 +/- 0.30/hpf in the sham operated group (p = 0.015). Animals exposed to trauma with 10 min of hypoxia and hypotension (THH-10) showed a statistically significant number of damaged neurons compared to the sham-operated animals (7.50 +/- 2.15 damaged neurons/hpf, p = 0.013), whereas, neuronal damage in animals undergoing trauma with a 30-min secondary insult of hypoxia and hypotension (THH-30) was markedly increased (100 +/- 30.20/hpf, p = 0.002). Statistical analysis showed no significant difference in neuronal damage in animals subjected to secondary insult alone. At 24 h, the evolution of neuronal damage in the trauma alone group (5.08 +/- 1.63/hpf) was relatively static; however, there was a remarkable increase in the neuronal damage of the THH-10 group (29.88 50 +/- 8.20/hpf). However, hypothermia provided nearly complete protection against secondary insults, and neuronal damage was equal to that of the trauma alone group (p = 0.42). The results of this study confirm that hypothermia provides remarkable protection against the adverse effects of neuronal damage exacerbated by secondary injury. This study also presents a new model of secondary insult, which can be used experimentally to further define the mechanism of increased vulnerability of the injured brain.

    Title Evaluation of Homeostatic Changes in Csf Circulation: in Vivo Analysis of the Effect of Neurotransmitter Accumulation in the Extracellular Space Following Transient Global Ischemia.
    Date February 1998
    Journal Acta Neurochirurgica. Supplement
    Excerpt

    Accumulation of potassium and excitatory amino acids (EAA) in the extracellular space (ECS) following ischemia has been well documented. Careful monitoring of these transients is crucial to gain a better understanding of CNS pathophysiology. This study was initiated to determine if CSF concentrations of EAAs reflect those measured in the ECS. Transient global ischemia, 20 minutes in duration, was produced by clamping the left subclavian and innominate arteries combined with hemorrhagic hypotension. The accumulation of glutamate and electrolytes were measured in CSF and the extracellular fluid (ECF) of cerebral cortex. Microdialysis (MD) was utilized to measure the extracellular concentrations while direct sampling of CSF was provided via cannulation of the cisterna magna. Hydrogen clearance and laser doppler methods were used to monitor regional cortical CBF. Our results show that extracellular concentrations of potassium ([K+]ECF) and glutamate significantly increased following the initiation of ischemia (p < 0.05). The extracellular concentration of these substances decreased with the restoration of CBF. In CSF, a similar trend was observed following re-circulation (p < 0.05). However, CSF glutamate levels did not return to pre-ischemic values.

    Title Operative Intracranial Infection Following Craniotomy.
    Date
    Journal Neurosurgical Focus
    Excerpt

    OBJECT: Postoperative infection after cranial surgery is a serious complication that requires immediate recognition and treatment. In certain cases such as postoperative meningitis, the patient can be treated with antibiotics only. In cases that involve a bone flap infection, subdural empyema, or cerebral abscess, however, reoperation is often needed. There has been significant disagreement regarding the incidence of postoperative central nervous system (CNS) infections following cranial surgery. In this paper the authors' goal was to perform a retrospective review of the incidence of CNS infection after cranial surgery at their institution. They focused their review on those patients who required repeated surgery to treat the infection. METHODS: The authors reviewed the medical records and imaging studies in all patients who underwent a craniotomy or stereotactic drainage for CNS infection over the past 10 years. Subgroup analysis was then performed in patients whose infection was a result of a previous cranial operation to determine the incidence, factors associated with infection, and the type of infectious organism. Patients treated nonoperatively (that is, those who received intravenous antibiotics for postoperative meningitis or cellulitis) were not included. Patients treated for wound infection without intracranial pus were also not included. RESULTS: During the study period from January 1997 through December 2007, approximately 16,540 cranial surgeries were performed by 25 neurosurgeons. These included elective as well as emergency and trauma cases. Of these cases 82 (0.5%) were performed to treat postoperative infection in 50 patients. All 50 patients underwent their original surgery at the authors' institution. The median age was 51 years (range 2-74 years). There were 26 male and 24 female patients. The most common offending organism was methicillin-sensitive Staphylococcus aureus, which was found in 10 of 50 patients. Gram-negative rods were found in 15 patients. Multiple organisms were identified in specimens obtained in 5 patients. Six patients had negative cultures. Most craniotomies leading to subsequent infection were performed for tumors or other mass lesions (23 of 50 patients), followed by craniotomies for hemorrhage and vascular lesions. Almost half of the patients underwent > 1 cranial operation before presenting with infection. CONCLUSIONS: Postoperative infection after cranial surgery is an important phenomenon that needs immediate recognition. Even with strict adherence to sterile techniques and administration of antibiotic prophylaxis, a small percentage of these patients will develop an infection severe enough to require reoperation.

    Title Brain Abscess Formation at the Site of Intracerebral Hemorrhage Secondary to Central Nervous System Vasculitis.
    Date
    Journal Neurosurgical Focus
    Excerpt

    Brain abscess is a rare but very dangerous neurosurgical lesion. Prompt diagnosis and emergency surgical evacuation are the hallmarks of therapy. Brain abscess following ischemic and hemorrhagic stroke is a rare entity. These cases are often preceded by episodes of bacteremia, sepsis, and local infection. The authors report the case of a 30-year-old woman who presented with a cerebral abscess at the site of a recent intraparenchymal hemorrhage.

    Title Intracranial Placement of a New, Compliant Guide Catheter: Technical Note.
    Date
    Journal Neurosurgery
    Excerpt

    OBJECTIVE: We describe our initial experience with the use of a novel, compliant guide catheter designed for placement within the cranial vasculature in a series of seven patients who were treated for various intracranial pathologies. CLINICAL PRESENTATION: Seven patients were deemed to have either tortuous supra-aortic, intracranial, and/or extracranial vasculature or to require additional microcatheter support as the result of lesion location. INTERVENTION: The patients were treated, in part, with the 6-French Neuron delivery catheter (Penumbra, Inc., San Leandro, CA) at the authors' two institutions. The guide catheter was positioned in various distal locations within the intracranial internal carotid artery or external carotid artery. Three patients were treated for unruptured intracranial aneurysms, 2 patients for intracranial atherosclerosis, 1 patient for an arteriovenous malformation, and 1 patient for a pseudoaneurysm. CONCLUSION: All lesions were successfully treated through a microcatheter advanced in a coaxial fashion through the guide catheter. There were no complications related to the positioning of the catheter. Distal intra- or extracranial placement of a specially designed, compliant guide catheter can be performed safely and may improve access and microcatheter stability in patients with tortuous vessels or difficult-to-reach lesions.

    Title Brain Hyperthermia After Traumatic Brain Injury Does Not Reduce Brain Oxygen.
    Date
    Journal Neurosurgery
    Excerpt

    OBJECTIVE: Hyperthermia can exacerbate outcome after traumatic brain injury (TBI). In this study we examined the relationship between brain temperature (BT) and core body temperature and the relationship between BT and brain tissue oxygen (BtO2) to determine whether hyperthermia adversely affects BtO2. METHODS: Seventy-two patients (mean age, 41 +/- 19 years) admitted to a Level I trauma center after TBI were retrospectively identified from a prospective observational database. Intracranial pressure (ICP), BT, and BtO2 were recorded continuously. Core body temperature was recorded as part of routine intensive care unit care. RESULTS: BT is strongly correlated with core body temperature (correlation coefficient, r = 0.92) over a wide range (94.2-104.7 degrees F). In addition, BT was correlated with body temperature during periods of normal ICP (IC<I>P </= 20 mmHg; r = 0.87) and transiently elevated ICP (ICP range 21-63 mmHg; r = 0.94). During periods of brain normothermia (BT < 100.5 degrees F), the average BtO2 was 36.3 +/- 22.9 mmHg. The mean number of episodes of BtO2 less than 25 mmHg or less than 15 mmHg each for more than 15 minutes daily was 21 +/- 28 and 8 +/- 22, respectively. The mean BtO2 (37.2 +/- 16.0 mmHg) was similar during periods of brain normothermia and hyperthermia (BT >/=100.5 degrees F). When the periods of brain tissue hyperthermia were further categorized into BT >/=101.5 degrees F or BT >/=102.5 degrees F, mean daily BtO2 was similar in all of the groups. When BT was 100.5 degrees F or greater, there were fewer episodes of BtO2 less than 25 mmHg (13.5 +/- 24.6; P < 0.05) and of BtO2 less than 15 mmHg (3.3 +/- 11.9; P < 0.05) than observed during brain normothermia. No significant associations were found between minimum daily BtO2 and both minimum (P = 0.81) and maximum (P = 0.19) daily BT or between maximum daily BtO2 and both minimum (P = 0.62) and maximum (P = 0.97) daily BT after adjusting for patient age, PaO2/FIO2 ratio, hemoglobin, ICP, and cerebral perfusion pressure in the multivariable analysis. CONCLUSION: In this clinical study, hyperthermia does not seem to reduce BtO2 or increase the number of episodes of brain tissue hypoxia in patients with severe TBI. These results suggest that hyperthermia may worsen outcome after TBI through mechanisms that may be separate from compromised brain oxygen.

    Title Multimodality Treatment of a Complex Cervicocerebral Arteriovenous Shunt in a Patient with Charge Syndrome: Case Report.
    Date
    Journal Neurosurgery
    Excerpt

    We present our management of a unique case of complex arteriovenous shunt with vascular steal in the left-sided head and neck vessels in a child with CHARGE (Coloboma of the eye, Heart defects, Atresia of the choanae, Retardation of growth and/or development, Genital and/or urinary abnormalities, and Ear abnormalities and deafness) syndrome.

    Title Vertebral Artery Origin Stents Revisited: Improved Results with Paclitaxel-eluting Stents.
    Date
    Journal Neurosurgery
    Excerpt

    Vertebral origin angioplasty and stenting (VOAS) with bare metal stents is associated with a high rate of in-stent restenosis (ISR).

    Title Cumulative Radiation Dose in Patients Admitted with Subarachnoid Hemorrhage: a Prospective Study Using a Self-developing Film Badge.
    Date
    Journal Ajnr. American Journal of Neuroradiology
    Excerpt

    While considerable attention has been directed to reducing the x-ray dose of individual imaging studies, there is little information available on the cumulative dose during imaging-intensive hospitalizations. We used a radiation-sensitive badge on 12 patients admitted with SAH to determine if this approach was feasible and to measure the extent of their x-ray exposure.

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