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Dive into the research topics where Todd A. Kuether is active.

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Featured researches published by Todd A. Kuether.


Neurosurgery | 1998

Clinical and angiographic outcomes, with treatment data, for patients with cerebral aneurysms treated with Guglielmi detachable coils: a single-center experience.

Todd A. Kuether; Gary M. Nesbit; Stanley L. Barnwell

OBJECTIVE The purpose of this report is to provide the most detailed treatment and outcome data currently available in the literature, to allow for the further evaluation of Guglielmi detachable coils (GDC) as an appropriate treatment option for patients with cerebral aneurysms. METHODS During a period of 4.5 years, 74 patients with intracerebral aneurysms were treated with GDC in the Department of Neurosurgery at Oregon Health Sciences University. A comprehensive retrospective and prospective analysis of these patients was performed, to assess the overall angiographic and clinical outcomes for these patients. RESULTS Seventy-seven aneurysms were treated, with an average angiographic follow-up period of 1.4 years. Initially, 40% of aneurysms exhibited complete (100%) occlusion, 52% near complete (90-99%) occlusion, and 8% incomplete (<90%) occlusion. The average clinical follow-up period was 2.2 years. For unruptured aneurysms, 85% of patients returned to independent status. Of patients of Hunt and Hess Grade I/II status, 81% were independent; of patients of Grade III status, 100% were independent; and, of patients of Grade IV/V status, 50% were independent. The procedure-related morbidity rate was 9.1%, with a 7.8% risk of death from aneurysm perforation, stroke, or delayed hemorrhage. No completely occluded aneurysm hemorrhaged after GDC treatment (follow-up period, 1.9 yr). Of near complete occlusions, 2.6% hemorrhaged after embolization, at a rate of 1.4%/yr (follow-up period, 1.9 yr). CONCLUSION This study details long-term clinical outcomes after GDC treatment and describes factors affecting the need for retreatment. Although complete anatomic cure was not obtained in all cases and the long-term protection from subarachnoid hemorrhage remains to be determined, these data indicate that GDC are a safe and efficacious treatment for cerebral aneurysms.


Neurosurgery | 1997

Rotational Vertebral Artery Occlusion: A Mechanism of Vertebrobasilar Insufficiency

Todd A. Kuether; Gary M. Nesbit; Wayne M. Clark; Stanley L. Barnwell

OBJECTIVE Symptomatic dynamic changes in blood flow secondary to vertebral artery compression with rotational head motion are evaluated in a series of patients as a cause for posterior circulation transient ischemic attacks. These cases are classic examples of rotational vertebral artery occlusion and allow for the discussion of the anatomic basis, angiographic features, and treatment options. ILLUSTRATIVE CASES In our series, symptoms of vertebrobasilar insufficiency were reproducible with rotational head movement. Compression of the vertebral artery was demonstrated angiographically. The correct site of occlusion of the vertebral artery was apparent only by dynamic angiography with progressive head rotation. All of the patients presented in the illustrative cases had occlusion at the C2 level; however, one patient had been previously misdiagnosed and another had an additional site of occlusion. The anatomic course of the vertebral artery is described in addition to the sites of rotational occlusion. CONCLUSION Rotational vertebral occlusion is an important cause of vertebrobasilar symptoms, which may lead to permanent neurological deficit if left undiagnosed. Dynamic angiography is the established method of diagnosis. Great care must be taken to avoid misdiagnosing the site of occlusion or missing a second occlusive site. For this reason, it is crucial to have a thorough understanding of the anatomic course of the vertebral artery and the muscular and tendinous insertions, which may cause rotational occlusion. The decision for treatment must be based on the site of occlusion as well as the assessment of the patient as a surgical candidate. A review of the literature reveals that surgical treatment is effective and must be considered to avoid further morbidity.


Neurosurgery | 1998

Endovascular Treatment of Traumatic Dural Sinus Thrombosis: Case Report

Todd A. Kuether; Oisin R. O'Neill; Gary M. Nesbit; Stanley L. Barnwell

OBJECTIVE Dural sinus thrombosis has rarely been associated with closed head injury. We present a unique case involving the use of endovascular thrombolysis in the treatment of traumatic dural sinus thrombosis, which has not been reported. CLINICAL PRESENTATION A 20-year-old male patient suffered a severe closed head injury while skiing. He developed refractory elevated intracranial pressure requiring barbiturate coma. Angiography demonstrated thrombosis of the dominant right transverse and sigmoid sinuses, with partial thrombosis of the superior sagittal sinus. Urokinase was administered via a microcatheter within the thrombus as a bolus of 250,000 units and then as a continuous infusion of 60,000 to 100,000 units per hour for 48 hours. The patient was maintained in a barbiturate coma and heparinized. Serial angiography was performed to assess the sinus patency and efficacy of thrombolysis. RESULTS After 48 hours of thrombolysis, angiography demonstrated normal patency of the superior sagittal, right transverse, and right sigmoid sinuses. The intracranial pressure decreased after thrombolysis and was manageable with conventional techniques. Within 48 hours of the completed thrombolysis, the barbiturates were withdrawn and the patients neurological status rapidly improved until the time of discharge 2 weeks later. DISCUSSION AND CONCLUSION This case documents a rare instance of traumatic dural sinus thrombosis resulting from a closed head injury. In addition, endovascular thrombolysis resulted in subsequent opening of the dural sinuses and effective intracranial pressure management, despite the presence of a hemorrhagic contusion. Heparin was effective in maintaining sinus patency and was used safely in conjunction with urokinase in this setting of head injury.


Neurosurgery | 1996

Direct carotid cavernous fistula after trigeminal balloon microcompression gangliolysis: Case report

Todd A. Kuether; Oisin R. O'Neill; Gary M. Nesbit; Stanley L. Barnwell

OBJECTIVE AND IMPORTANCE Percutaneous gangliolysis procedures may rarely be associated with vascular complications. There are three reported cases of carotid cavernous fistulas occurring after percutaneous microcompressive trigeminal gangliolysis. This is the only reported case of this complication associated with microcompression gangliolysis. CLINICAL PRESENTATION A 78-year-old woman was referred to our institution with a history of abrupt onset of left-sided bruit, proptosis, chemosis, and diplopia after a percutaneous retrogasserian microcompression. INTERVENTION Cerebral angiography revealed a large left direct carotid cavernous fistula. Attempts at balloon embolization were unsuccessful, and the lesion was ultimately cured by transarterial and transvenous coil embolization. CONCLUSION Follow-up examination revealed no evidence of bruit or neurological deficit. This report highlights a unique complication of balloon gangliolysis and describes coil embolization of the fistula as the mode of treatment.


Neurosurgery | 1998

Chiari malformation associated with vitamin D-resistant rickets: case report.

Todd A. Kuether; Joseph H. Piatt

INTRODUCTION Craniocervical junction abnormalities have a wide range of origins, from rare congenital conditions to common arthritic processes. We present a rare case of foramen magnum stenosis with Chiari I malformation and associated syringomyelia, which resulted from vitamin D-resistant hypophosphatemic rickets. METHODS This 12-year-old male patient had a history of vitamin D-resistant rickets, and he presented with a 1-year history of increasing upper extremity weakness and sharp pain in the left shoulder and arm. Magnetic resonance imaging of his spine showed a large syrinx from C2 to T7, with significant foramen magnum stenosis and a Chiari Type I malformation. RESULTS The patient underwent craniocervical decompression, consisting of a suboccipital craniectomy and C1 laminectomy with duraplasty. A pathological evaluation of bone yielded no diagnostic abnormality. Postoperative magnetic resonance imaging showed significant reduction in the diameter of the cervical thoracic spinal cord syrinx 3 months after surgery. The patients pain and sensation in his left arm had not improved by that time, and he still had some diffuse weakness in his arms. Two years later, he had persistent left shoulder girdle pain and his syrinx had collapsed, except for a small residual from T2 to T6. DISCUSSION AND CONCLUSION The bone disease of vitamin D-resistant rickets can involve the base of the cranium, precipitating the development of the Chiari malformation and associated syringomyelia. We review the association between rickets and Chiari malformation and discuss the management of these patients.


Neurosurgery | 1996

Embolization as Treatment for Spinal Cord Compression from Renal Cell Carcinoma: Case Report

Todd A. Kuether; Gary M. Nesbit; Stanley L. Barnwell

OBJECTIVE AND IMPORTANCE Metastatic renal cell carcinoma may involve the vertebrae, resulting in acute spinal cord compression. Embolization has been used to reduce operative blood loss during surgical decompression, but it has not been considered as an alternative that may eliminate the need for open debulking. CLINICAL PRESENTATION A case is presented of a 30-year-old woman with renal cell carcinoma who developed increasing severe back pain, lower extremity weakness, and sensory loss. Magnetic resonance evaluation revealed a T5 metastasis, resulting in significant spinal cord compression. INTERVENTION Transarterial embolization was performed with polyvinyl alcohol particles and platinum microcoils. One month after embolization, the patients lower extremity strength and sensation had improved, and magnetic resonance imaging demonstrated a dramatic response with a significant reduction of cord compression. She deteriorated again 4 months later, and a new sacral mass was embolized. She again improved after treatment. CONCLUSION This report illustrates that embolization may be used as palliative treatment for spinal cord compression and obviate the need for open surgical decompression.


Critical Care Clinics | 1999

DURAL SINUS THROMBOSIS ENDOVASCULAR THERAPY

Frank P. K. Hsu; Todd A. Kuether; Gary M. Nesbit; Stanley L. Barnwell

Dural sinus thrombosis is a relatively rare, but potentially devastating disease. The problem occurs when there is extensive thrombosis of the intracranial dural sinuses, the outflow channels of venous blood from the brain. If recanalization does not occur, venous hypertension can lead to cerebral edema, infarction, and hemorrhage. Treatment of this disease usually involves anticoagulants, but with mixed results. Endovascular approaches using direct infusion of thrombolytic drugs into the occluded sinuses may result in excellent recanalization and improved patient outcomes.


Surgical Neurology | 2000

Spontaneous brachial plexus hemorrhage—case report

A.Chris Heller; Todd A. Kuether; Stanley L. Barnwell; Gary M. Nesbit; Kim A Wayson

BACKGROUND Shoulder hemorrhage resulting in brachial plexus neuropathy is a rare occurrence most often seen in cases of traumatic injury or anticoagulation therapy. We report a unique case of spontaneous brachial plexus hemorrhage. CASE DESCRIPTION This is the first report of a spontaneous shoulder hemorrhage in which a 48-year-old jackhammer operator presented to the emergency department with a sudden onset of right shoulder pain and upper extremity pain and numbness. Imaging studies revealed a hematoma in the right axilla and chest wall. Without evidence of active bleeding or worsening neurologic deficit, this patient was treated conservatively with pain control and observation and eventually experienced a full recovery. Had there been persistent neurologic deficit, however, surgical evacuation would have been indicated. CONCLUSIONS Cases of nerve compression caused by a hematoma should be analyzed on the basis of the severity of the neurologic deficit and not on the underlying cause of bleeding. Conservative treatment may be indicated in cases of mild or improving neurologic deficit, but regardless of its etiology, a hematoma that results in severe or worsening neurologic symptoms must be surgically evacuated to prevent permanent nerve damage.


Journal of Clinical Neuroscience | 1998

Endoscopic treatment of spinal epidural hematoma

Timothy Steel; Jordi X. Kellogg; Todd A. Kuether; Jacques Favre; Edmund Frank

We report the use of a spinal endoscope via a limited cervical laminotomy to evacuate a spinal epidural hematoma. The patient was a 75-year-old male with a 32-year history of ankylosing spondylitis. Following a low speed motor vehicle accident he developed a cervicothoracic epidural hematoma without an associated fracture. Despite a rapidly improving neurological state, his rapidly deteriorating cardiorespiratory state required systemic anticoagulation necessitating decompression of the hematoma. The hematoma was successfully removed via a limited C6 and C7 laminotomy using the endoscope and a malleable disposable aspirator. We conclude that epidural hematomas can be readily evacuated via endoscopic techniques without extensive laminectomy. This technique may be used for approaching intraspinal pathology in high risk patients where extensive exposure may be contraindicated.


CNS Drugs | 2000

Cerebral venous thrombosis: A guide to diagnosis and drug treatment

Frank P. K. Hsu; Gary M. Nesbit; Todd A. Kuether; Stanley L. Barnwell

Cerebral venous thrombosis (CVT) is a relatively rare pathological condition. The clinical presentations can be nonspecific and quite variable, frequently resulting in delayed or missed diagnosis. The symptoms include headache, nausea, vomiting, visual disturbance, altered consciousness and seizures. These symptoms are believed to be caused by increased intracranial pressure secondary to impeded venous drainage.The diagnosis can be made with computed tomography (CT), magnetic resonant imaging (MRI) and cerebral angiography. CT is usually the initial diagnostic test that may show dense clot in the cerebral veins along with hemorrhagic venous infarctions. Empty delta sign can be seen on contrast-enhanced CT. MRI has become the preferred modality for detecting CVT; magnetic resonance angiography (MRA) and venography (MRV) are the best methods for detecting the condition. Angiography, once the standard, is now only indicated when MRI has resulted in an uncertain diagnosis or when endovascular intervention is desired.Therapy should be directed at treating the underlying causative process and symptoms secondary to elevated intracranial pressure. Although there is no consensus regarding antithrombotic treatment, the current trend is to use intravenous heparin initially, followed by warfarin. A newer approach has been developed using interventional endovascular modalities. Local infusion of thrombolytics can be achieved by transvenous catheterisation and catheter navigation. This may offer potential advantages over the established systemic antithrombotic therapy.

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