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Biomedical subjects

Bernard R Bendok

Publications and source records attributed to Bernard R Bendok.

At least 19 recordsLinked to original sources

Endovascular treatment strategies for cerebral vasospasm.

Cerebral vasospasm is a significant cause of morbidity and mortality in patients who have sustained a subarachnoid hemorrhage from aneurysm rupture. Symptomatic cerebral vasospasm is also a strong predictor of poor clinical outcome and has thus drawn a great deal of interest from cerebrovascular surgeons. Although medical management is the cornerstone of treatment for this condition, endovascular intervention may be warranted for those in whom this treatment fails and in whom symptomatic vasospasm subsequently develops. The rapid advancements in endovascular techniques and pharmacological agents used to combat this pathological state continue to offer promise in broadening the available treatment armamentarium. In this article the authors discuss the rationale and basis for using the various endovascular options for the treatment of cerebral vasospasm, and they also discuss the limitations, complications, and efficacy of these treatment strategies in regard to neurological condition and outcome.

Aneurysm, Ruptured↗

Current updates in perioperative management of intracerebral hemorrhage.

Spontaneous ICH remains a formidable disease that continues to disable and kill the majority of its victims. Treatment of the disease continues to be controversial and without any proved success, such as improvement in the disease mortality or the resulting disability in survivors. Primary prevention is the most effective medical intervention. Nevertheless, as the population continues to age and patients remain undertreated for hypertension, the incidence of ICH likely will increase, resulting in significant socioeconomic impact on society in the coming years. It is imperative that more research be conducted to improve treatment and outcomes of patients who have ICH. Unlike ischemic stokes or other causes of hemorrhagic stroke, such as SAH, where major advancement of treatment has led to improved outcomes, the increased incidence of ICH has not been matched with any considerable improvement in treatment. This burden to improve therapeutic interventions for patients who have ICH should be shared by all neurosurgeons, stroke neurologists, and critical care physicians who care for these patients on a regular basis. It is hoped that early diagnosis and resuscitation, prevention of hematoma growth, selective surgery or minimally invasive clot evacuation, and judicious critical care and rehabilitation will combine to lessen the burden of this disease.

Brain↗

Return of vision after transarterial coiling of a carotid cavernous sinus fistula: case report.

BACKGROUND: Carotid cavernous sinus fistulae are abnormal communications between the carotid circulation and cavernous sinus that may arise spontaneously or develop after craniocerebral trauma. They may present with a constellation of signs and symptoms characteristic of raised cavernous sinus pressure, including orbital or retro-orbital pain, pulsatile proptosis, chemosis, ocular or cranial bruit, deterioration of visual acuity, or ophthalmoplegia. Visual loss is likely the result of multiple insults to the visual system, including reversal of venous drainage from the fistula, arterial flow into the superior ophthalmic vein, increased intraocular venous pressure, venous stasis retinopathy, and eventually ischemic optic neuropathy [Brodsky MC, Hoyt WF, Halbach VV, et al. Recovery from total monocular blindness after balloon embolization of carotid-cavernous fistula. Am J Ophthalmol 1987;104:86-87; Sanders MD, Hoyt WF. Hypoxic ocular sequelae of carotid-cavernous fistulae: study of the causes of visual failure before and after neurosurgical treatment in a series of 25 cases. Br J Ophthalmol 1969;53:82-97]. CASE DESCRIPTION: With few exceptions, the literature is replete with evidence of persistent blindness despite successful treatment of the CCF [Albuquerque FC, Heinz GW, McDougall CG. Reversal of blindness after transvenous embolization of a carotid-cavernous fistula: case report. Neurosurgery 2003;52:233-237; Brodsky MC, Hoyt WF, Halbach VV, et al. Recovery from total monocular blindness after balloon embolization of carotid-cavernous fistula. Am J Ophthalmol 1987;104:86-87; Weinstein JM, Rufenacht DA, Partington CR, et al. Delayed visual loss due to trauma of the internal carotid artery. Arch Neurol. 1991;48:490-497]. Here, we report a patient who experienced recovery of vision after endovascular obliteration of the offending CCF. DISCUSSION: To our knowledge, this is the second reported case of recovery of visual function in a patient presenting with loss of light perception after treatment of a direct CCF.

Blindness↗

Use of heparin-coated stents in neurovascular interventional procedures: preliminary experience with 10 patients.

OBJECTIVE: Currently, there is minimal published data on the use of heparin-coated stents in the neurovasculature; however, these stents have a proven clinical record in the treatment of coronary disease. This article details our experience with the safety and technical aspects of stent deployment in the first 10 patients who had heparin-coated stents placed in the intracranial and cervical vasculature and the preliminary follow-up in most cases. METHODS: We retrospectively reviewed the clinical history, intra- and periprocedural data, and imaging for the patients who received heparin-coated stents in the cervical and intracranial vasculature for cerebrovascular disease between October 2002 and October 2003. RESULTS: Thirteen heparin-coated stents were placed in 10 patients. Seven out of the 10 patients had heparin-coated stents placed in the posterior circulation; the remaining three patients had stents placed in the anterior circulation. Four patients had stents placed intracranially. There was no acute or subacute in-stent thrombosis and no procedure-related complications. Follow-up was performed on most patients, with no clinical symptoms attributable to restenosis in any patient. CONCLUSION: This small series suggests that heparin-coated stents are safe for use in the treatment of cervical and intracranial atherosclerotic disease. Longer-term follow-up is needed to study the heparin coating effect on in-stent restenosis rates and to assess the long-term durability and clinical efficacy of this stent. The use of drug-coated stents in the cerebrovascular circulation is an area that warrants further investigation.

Adult↗

Giant intracranial aneurysms: endovascular challenges.

The treatment of giant aneurysms remains a formidable challenge for endovascular and surgical strategies. The use of endovascular techniques in a deconstructive (e.g., parent vessel occlusion) and reconstructive (e.g., stent coiling) methodology is reviewed. The results of endovascular coiling as a primary therapy for giant aneurysm occlusion have been disappointing. Hunterian strategies have had more success in published series, but recent developments in coil, glue, and stent technology show great promise in allowing parent vessel reconstruction as a primary endovascular target, with acceptable morbidity, mortality, and durability. A literature review of giant aneurysm endovascular treatment strategies was undertaken after 1994, when Guglielmi detachable coils were approved by the Food and Drug Administration. Where possible, follow-up, durability, and occlusion rates are also reviewed.

Blood Vessel Prosthesis↗

Retrograde suction decompression of giant paraclinoid aneurysms using a No. 7 French balloon-containing guide catheter. Technical note.

The treatment of large and giant paraclinoid carotid artery (CA) aneurysms often requires the use of suction decompression for safe and effective occlusion. Both open and endovascular suction decompression techniques have been described previously. In this article the authors describe a revised endovascular suction decompression technique that provides several advantages in the treatment of large and giant paraclinoid and CA aneurysms. A 51-year-old woman presented with a relatively brief history of progressive visual loss in the right eye, nonspecific headache, and an afferent pupillary defect. After angiography studies had been obtained, it was determined that she had a giant right paraclinoid internal CA aneurysm with a dome size of approximately 26 mm on the right and a neck diameter of 10 mm. A modified technique was performed in which suction decompression was used. With the aid of a No. 7 French Concentric balloon guide catheter (Concentric Medical, Inc., Mountain View, CA) and application of a temporary clip distal to the aneurysm, the aneurysm was trapped and decompressed using retrograde suction through the guide catheter when the balloon was inflated. After satisfactory placement of three permanent clips, an intraoperative angiogram obtained through the same guide catheter confirmed CA patency. The aneurysm was then punctured and aspirated, ensuring complete occlusion of the aneurysm sac and reconstruction of the parent vessel. The patient made an excellent recovery and did not suffer any complications. She did not experience worsening in her vision. This technical modification to endovascular suction decompression allows several potential advantages, including higher volume decompression and the ability to deliver endovascular devices to distal arterial locations.

Carotid Artery Diseases↗

Acquired Chiari malformation Type I associated with a supratentorial arteriovenous malformation. Case report and review of the literature.

Chiari malformation Type I (CM-I), a condition defined by caudal descent of the cerebellar tonsils through the foramen magnum, is generally considered a congenital lesion. Several authors, however, have described an acquired form that appears identical to the congenital lesion on neuroimages. The most commonly reported cause of an acquired CM-I is cerebrospinal fluid diversion through a lumboperitoneal shunt. In this paper, the authors report the case of a patient in whom an acquired CM-I developed in association with a supratentorial arteriovenous malformation (AVM) of the brain. Development of the acquired CM was documented on serial magnetic resonance images. Moreover, the CM was seen to originate and worsen in concert with the clinicoradiological progression of the AVM. The underlying mechanism responsible for the acquired CM in this case is thought to be a high-flow venopathy of the transverse and sigmoid sinuses causing occlusion on the right and redirection of venous outflow into posterior fossa veins, with consequent venous congestion and swelling of the posterior fossa structures.

Adult↗

Deficiencies in estrogen-mediated regulation of cerebrovascular homeostasis may contribute to an increased risk of cerebral aneurysm pathogenesis and rupture in menopausal and postmenopausal women.

Despite the catastrophic consequence of ruptured intracranial aneurysms, very little is understood regarding their pathogenesis, and there are no reliable predictive markers for identifying at-risk individuals. Few studies have addressed the molecular pathological basis and mechanisms of intracranial aneurysm formation, growth, and rupture. The pathogenesis and rupture of cerebral aneurysms have been associated with inflammatory processes, and these have been implicated in the digestion and breakdown of vascular wall matrix. Epidemiological data indicate that the risk of cerebral aneurysm pathogenesis and rupture in women rises during and after menopause as compared to premenopausal women, and has been attributed to hormonal factors. Moreover, experimental evidence supports a role for estrogen in the modulation of each phase of the inflammatory response implicated in cerebral aneurysm pathogenesis and rupture. While the risk of aneurysm rupture in men also increases with age, this increased risk has been attributed to other recognized risk factors including cigarette smoking, use of alcohol, and history of hypertension, all of which are more common in men than women. We hypothesize, therefore, that decreases in both circulating estrogen levels and cerebrovascular estrogen receptor density may contribute to an increased risk of cerebral aneurysm pathogenesis and rupture in women during and after menopause. To test our hypothesis, experiments are needed to identify genes regulated by estrogen and to evaluate gene expression and intracellular mechanisms in cells/tissues exposed to varying concentrations and duration of treatment with estrogen, metabolites of estrogen, and selective estrogen receptor modulators (SERMs). Furthermore, it is not likely that the regulation of cerebrovascular homeostasis is due to the actions of estrogen alone, but rather the interplay of estrogen and other hormones and their associated receptor expression. The potential interactions of these hormones in the maintenance of normal cerebrovascular tone need to be elucidated. Additional studies are needed to define the role that estrogen and other sex hormones may play in the cerebrovascular circulation and the pathogenesis and rupture of cerebral aneurysms. Efforts directed at understanding the basic pathophysiological mechanisms of aneurysm pathogenesis and rupture promise to yield dividends that may have important therapeutic and clinical implications. The development of non-invasive tools such as molecular MRI for the detection of specific cells, molecular markers, and tissues may facilitate early diagnosis of initial pathophysiological changes that are undetectable by clinical examination or other diagnostic tools, and can also be used to evaluate the state of activity of cerebral aneurysm pathogenesis before, during, and after treatment.

Brain↗

Microsurgical resection of infratentorial arteriovenous malformations.

Successful microsurgical resection of an infratentorial arteriovenous malformation (AVM) requires both surgical skill and intraoperative judgment. Extensive practical experience in treating these complex lesions, which is acquired over many years, is of substantial value during each new operation. The authors present the surgical approaches and techniques used for the treatment of posterior fossa AVMs based largely on the strategies acquired and developed by the senior author (H.H.B.). Emphasis is placed on conceptual principles of AVM excision, as well as principles incorporated for the treatment of each specific type of infratentorial malformation.

Brain Stem↗

Update on current registries and trials of carotid artery angioplasty and stent placement.

Stroke remains the leading cause of disability in adults and the third leading cause of death in the US. Carotid artery (CA) occlusive disease is the primary pathophysiological source of 10 to 20% of all strokes. Carotid endarterectomy (CEA) has been shown to reduce the risk of stroke in patients with both symptomatic and asymptomatic extracranial CA stenosis. Carotid artery angioplasty and stent placement has recently emerged as an alternative to CEA for primary and secondary prevention of stroke related to CA stenosis. With the advent of the embolic protection device, the safety of CA angioplasty and stent placement has approached, if not surpassed, that of CEA. In particular, the former has come to be considered as a first-line therapy in the management of CA stenotic disease in individuals at high risk for complications related to surgical intervention. Preliminary data from multiple registries have demonstrated that CA angioplasty and stent placement is an effective means of treating CA stenosis. The results of the Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy trial have demonstrated that this modality has a significant role in the management of CA disease in symptomatic and asymptomatic patients with risk factors for high rates of surgery-related morbidity or mortality. With the completion of the Carotid Revascularization Endarterectomy versus Stent Trial, the role of CA angioplasty and stent placement in the prevention of stroke in all individuals with significant CA stenosis should be better demarcated. This treatment modality promises to assume a central role in stroke prophylaxis in patients with CA disease who are at high risk for complications related to surgery.

Angioplasty↗

Interactions between melatonin and estrogen may regulate cerebrovascular function in women: clinical implications for the effective use of HRT during menopause and aging.

A number of clinical trials associated with the Women's Health Initiative (WHI) have assessed the potential benefits of hormone replacement therapy (HRT) for protection against the development of cardiovascular disease and memory loss in menopausal women. The results of the WHI Memory Study suggest that HRT increases the risk of stroke and dementia in menopausal women. This finding has called into question the results of hundreds of basic science studies that have suggested that estrogen could protect brain cells from damage and improve cognition. A number of researchers have argued that inappropriate formulation, improper dosing, a limited study population, and poor timing of administration likely contributed to the reported findings from the clinical trial. Regarding appropriate formulation, it has been suggested that interactions between estrogen and other hormones should be considered for further investigation. A review of the literature has led us to conclude that a thorough investigation into such hormonal interactions is warranted. We hypothesize that the increased risk of cerebrovascular disease observed in menopausal women may, in part, be due to changes in the circulating levels of melatonin and estrogen and their modulatory affects on many relevant endothelial cell biological activities, such as regulation of vascular tone, adhesion to leukocytes, and angiogenesis, among others. Our hypothesis is supported by numerous studies demonstrating the reciprocal inhibitory effects of melatonin and estrogen on vascular tone, neuroprotection, and receptor expression. We believe that a thorough analysis of the distribution, localization, expression, quantification, and characterization of hormonal receptor subtypes, as well as changes in structural morphology in diseased and normal, healthy cerebrovascular tissue, will substantially aid in our understanding of the effects of HRT on the cerebrovascular circulation. The application of new molecular biological techniques such as tissue microarray analysis, gene and protein arrays, and multi-photon confocal microscopy may be of tremendous benefit in this regard.

Cerebrovascular Circulation↗

Combination treatment of vertebral metastases using image-guided percutaneous radiofrequency ablation and vertebroplasty: a case report.

BACKGROUND: We describe a case of vertebral metastases treated with a combination of percutaneous radiofrequency ablation (RFA) and vertebroplasty in a single session. CASE DESCRIPTION: A 45-year-old female with recently diagnosed metastatic non-small cell lung cancer was referred for consideration of vertebroplasty after having several weeks of back pain. Computed tomography and magnetic resonance imaging scans of the thoracic spine revealed metastatic lesions at the T9 and T12 bodies. Radiofrequency ablation was performed using a starburst array electrode (Rita Medical Systems, Mountain View, Calif). The metastatic lesion in the T9 vertebral body measured 1.5 x 1.5 cm and was heated to 100 degrees C for 5 minutes. Vertebroplasty was then performed on this lesion as well as a lesion at T12 with no complications. The patient was discharged home the same day without complaints. CONCLUSION: Radiofrequency ablation and vertebroplasty are minimally invasive procedures that can be used in combination to treat spinal metastases. The pain relief from these treatments is often immediate. RFA can also be used to minimize procedure-related complications during the vertebroplasty. In properly selected patients, RFA may also increase the duration of local spinal stabilization afforded by the vertebroplasty alone. Long-term studies are warranted to assess the efficacy and durability of this unique approach.

Back Pain↗

Late morphological progression of a dissecting basilar artery aneurysm after staged bilateral vertebral artery occlusion: case report.

BACKGROUND: The authors present a patient who experienced late (5-year follow-up) morphological progression of a dissecting aneurysm of the distal basilar artery after treatment with a combined microsurgical and neuroendovascular Hunterian strategy. In addition to postulating about the possible reasons underlying the evolution of this lesion, the role of stenting is discussed. CASE DESCRIPTION: The patient was 37 years old when she suffered a subarachnoid hemorrhage from spontaneous basilar artery dissection. At the time of the hemorrhage, minimal aneurysmal enlargement was noted angiographically, and she was therefore treated nonoperatively. On reimaging 5 months later, massive enlargement of the aneurysm was noted. The patient was treated with staged bilateral vertebral artery sacrifice using a combination of microsurgical and neuroendovascular techniques. The dominant vertebral artery was clip-ligated distal to the posteroinferior cerebellar artery, whereas the contralateral vertebral artery was coil-occluded cervically 1 week later. CONCLUSIONS: Despite the patient remaining asymptomatic, follow-up angiography 5 years after the initial hemorrhage revealed further enlargement of the aneurysm as well as a newly discovered inferiorly projecting daughter sac measuring 5 mm in diameter. Clearly, certain aneurysms exist for which indirect approaches involving hemodynamic attenuation fail to prevent progression. With greater refinements in stent technology, such lesions may be more effectively treated.

Adult↗

Transarterial coil embolization of a high-flow vertebrojugular fistula due to penetrating craniocervical trauma: case report.

BACKGROUND: Vertebrojugular fistulas after penetrating cervical trauma (gunshot or stab wounds) are rarely reported. Successful endovascular coil embolization of an acute fistulizing vertebral artery pseudoaneurysm involving an obstructed internal jugular vein is presented and the various treatment strategies for such a lesion are described. CASE DESCRIPTION: A 23-year-old man presented from an outside institution after sustaining 2 gunshot wounds in a civilian conflict. Neuroimaging revealed a right vertebral artery pseudoaneurysm, which formed a fistulous connection with the internal jugular vein. Because venous outflow obstruction was present just below the fistula, a high-flow shunt was directed intracranially. Both the pseudoaneurysm and arteriovenous fistula were accessed percutaneously via a transfemoral route and coil embolization was performed. Perfusion of the basilar artery circulation was assumed by the contralateral vertebral artery. The ipsilateral posteroinferior cerebellar artery filled through retrograde flow down the vertebral confluence. CONCLUSIONS: Coil embolization is a safe and reliable strategy by which to obliterate an acute traumatic vertebrojugular fistula as well as pseudoaneurysm. Serial angiographic follow-up is mandatory to document a persistent cure.

Adult↗

Mathematical model of the rupture mechanism of intracranial saccular aneurysms through daughter aneurysm formation and growth.

OBJECTIVES: Daughter aneurysms have been strongly associated with saccular aneurysm rupture. We constructed a mathematical model to help explain this association as a possible hemodynamic mechanism for intracranial saccular aneurysm rupture. METHODS: Our model is based on the assumption that when an aneurysm reaches a state of imminent rupture, the weakest area of the aneurysm wall responds passively to a surge of intra-aneurysmal pressure by forming a daughter aneurysm that will be the site of the eventual rupture. The daughter and parent aneurysms were assumed to be spherical. Using mathematical modeling, the growth of the daughter aneurysm was observed. To obtain the change in tensile stress in the daughter aneurysm wall under constant pressure and changing geometry, the Law of Laplace was applied to the parent and the daughter aneurysms. RESULTS: The model reveals that the stress factor, i.e. tensile stress in the daughter aneurysm wall relative to the wall strength (rupture point), is dependent on two geometric parameters: the orifice factor (mu), which represents the relative size of the daughter aneurysm orifice radius to the parent aneurysm radius; and the aspect ratio (lambda), which represents the height-to-orifice ratio of the daughter aneurysm. As the daughter aneurysm develops, the stress factor first decreases to protect against rupture. Minimal stress is attained at an aspect ratio (lambda) of 0.577 regardless of the orifice factor. This is a relatively stable state. Further growth of the daughter aneurysm results in an increase of stress above the minimum, eventually leading to rupture at a stress factor of 1. A smaller orifice factor mu allows this aneurysm to grow to a higher aspect ratio lambda before rupture. DISCUSSION: Daughter aneurysm formation is a likely path to aneurysm rupture. The formation of a daughter aneurysm temporarily decreases the tensile stress within a parent aneurysm in which rupture is imminent, indicating a temporary protective role of daughter aneurysm development. Aneurysms harboring daughter aneurysms are at a more advanced stage of development, hence at a greater risk for rupture. The severity of the rupture risk can be estimated on the basis of daughter aneurysm geometry; aspect ratio lambda > 0.577 indicates a greater risk of rupture. Furthermore, daughter aneurysms with larger orifices are associated with a greater risk of rupture.

Aneurysm, Ruptured↗

Prediction of cerebral vasospasm in patients presenting with aneurysmal subarachnoid hemorrhage: a review.

OBJECTIVE: Cerebral vasospasm is a devastating medical complication of aneurysmal subarachnoid hemorrhage (SAH). It is associated with high morbidity and mortality rates, even after the aneurysm has been treated. A substantial amount of experimental and clinical research has been conducted in an effort to predict and prevent its occurrence. This research has contributed to significant advances in the understanding of the mechanisms leading to cerebral vasospasm. The ability to accurately and consistently predict the onset of cerebral vasospasm, however, has been challenging. This topic review describes the various methodologies and approaches that have been studied in an effort to predict the occurrence of cerebral vasospasm in patients presenting with SAH. METHODS: The English-language literature on the prediction of cerebral vasospasm after aneurysmal SAH was reviewed using the MEDLINE PubMed (1966-present) database. RESULTS: The risk factors, diagnostic imaging, bedside monitoring approaches, and pathological markers that have been evaluated to predict the occurrence of cerebral vasospasm after SAH are presented. CONCLUSION: To date, a large blood burden is the only consistently demonstrated risk factor for the prediction of cerebral vasospasm after SAH. Because vasospasm is such a multifactorial problem, attempts to predict its occurrence will probably require several different approaches and methodologies, as is done at present. Future improvements in the prevention of cerebral vasospasm from aneurysmal SAH will most likely require advances in our understanding of its pathophysiology and our ability to predict its onset.

Humans↗