Cases reported "Subarachnoid Hemorrhage"

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11/48. brain stem and cerebellar dysfunction after lumbar spinal fluid drainage: case report.

    Lumbar spinal fluid drainage is a common procedure to reduce the risks of cerebrospinal fluid (CSF) fistula after skull base fractures or various transdural neurosurgical procedures. Nevertheless, this simple and effective technique can lead to overdrainage and CSF hypovolaemia. This report describes the case of a young patient who had a lumbar drain inserted, to avoid CSF fistula after a pterional craniotomy with opening of the frontal sinus for the clipping of a ruptured aneurysm. The drain was removed after 48 hours because of underdrainage (<1 ml/h). Three days after drain removal, she developed rapid deterioration of her level of consciousness and signs of cranial nerves involvement, brain stem and cerebellar dysfunction. intracranial pressure was low (<5 cm H(2)O) and MRI showed brain sagging and cerebellar foramen magnum herniation. The patient was successfully treated with epidural blood patch, ventricular drainage, and Trendelenburg position. The authors report this case because CSF hypovolaemia attributable to lumbar overdrainage is an insidious and threatening condition not easy to diagnose in the absence of detectable CSF leak. MRI and intracranial pressure monitoring confirm the diagnosis and permit better understanding of the physiopathology of brain sagging.
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12/48. Treatment of wide-necked intracranial aneurysms with a self-expanding stent system: initial clinical experience.

    BACKGROUND AND PURPOSE: Currently available stents for intracranial use usually are balloon-expandable coronary stents that carry the risk of damaging a dysplastic segment of the artery, with potential vessel rupture. We assessed the technical feasibility and efficacy of the combined application of a flexible, self-expanding neurovascular stent and detachable coils in the management of wide-necked intracranial aneurysms in humans. methods: Four consecutive patients with a wide-necked intracranial aneurysm were treated with a combined approach that consisted of delivery of a flexible self-expanding neurovascular stent through a microcather to cover the neck of the aneurysm and subsequent filling of the aneurysm with coils through the stent interstices. The aneurysms were located at the internal carotid artery (n=2) and the basilar tip encroaching the P1 segment (n=2). Previous attempts with conventional endosaccular coil packing alone failed in all cases. RESULTS: Stent placement in the desired position with complete or nearly complete occlusion of the aneurysms was feasible in all patients. In one patient, aneurysm perforation with the microcatheter occurred and necessitated ventricular drainage, which led to a large parenchymal and intraventricular hemorrhage because of the strong anticoagulation regimen. Six-month follow-up demonstrated no focal neurologic sequelae in any of the patients, except slight memory dysfunction in the patient with bleeding. CONCLUSION: Preliminary data demonstrate that this extremely flexible stent is technically easy to deploy and can be easily and safely maneuvered through severely tortuous vessels, enabling the treatment of intracranial wide-necked aneurysms. The combination of endovascular reconstruction of the parent vessel with use of a self-expanding stent followed by coil embolization offers a promising therapeutic alternative for wide-necked aneurysms not amenable to coil embolization alone. Although immediate angiographic results are promising, long-term angiographic and clinical follow-up is essential to determine permanent vessel patency and aneurysm occlusion rate.
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13/48. diagnosis of subarachnoid hemorrhage indicated by transthoracic echocardiography.

    We report the case of a 63-year-old woman who presented to her local emergency department unresponsive and in a state of cardiogenic shock 4 hours after the sudden onset of a severe headache. Her electrocardiogram revealed nonprogressive 1-mm S-T elevation in leads V(5) to V(6) and a prolonged QTc. A transthoracic echocardiogram performed at the time of her resuscitation revealed regional wall-motion abnormalities not consistent with any known coronary artery territory but consistent with a diagnosis of acute subarachnoid hemorrhage. This diagnosis was subsequently confirmed on computed tomography brain imaging. Although subarachnoid hemorrhage is known to be associated with cardiopulmonary dysfunction, and electrocardiogram and echocardiogram abnormalities, the diagnosis of subarachnoid hemorrhage suspected by echocardiography before brain imaging has not previously been described.
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14/48. Management of patients with stunned myocardium associated with subarachnoid hemorrhage.

    Cardiac complications are well known after aneurysmal subarachnoid hemorrhage. Electrocardiographic changes occur in 50% to 100% of such cases. Arrhythmias, left ventricular dysfunction, and frank myocardial infarction are infrequently observed. myocardial infarction must be differentiated from neurogenic stunned myocardium, which is a reversible condition. From 1996 to 2001, 105 patients with aneurysmal subarachnoid hemorrhage underwent endovascular treatment at the University of michigan. Of these, four patients with no history of cardiac disease experienced cardiac failure related to neurogenic stunned myocardium. All had signs of left ventricular dysfunction, electrocardiographic changes, and elevated cardiac enzymes. Three had pulmonary edema at presentation. All were diagnosed with myocardial infarction. One underwent coronary angiography, which was normal. All were considered poor surgical candidates and underwent endovascular treatment of the aneurysms. Three of four patients developed symptomatic vasospasm, and two required balloon angioplasty. Three patients achieved good outcomes. The eldest died from severe vasospasm that was unresponsive to angioplasty. Reversible cardiac failure associated with subarachnoid hemorrhage may be due the neurogenic stunned myocardium. Frequent symptomatic vasospasm occurs, possibly related to poor cardiac output and the inability to optimize hyperdynamic hypervolemic therapy, particularly with compromised volume status. These patients can be treated with endovascular therapy of the aneurysms and balloon angioplasty as needed. With aggressive management, patients can recover from these reversible cardiac complications.
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15/48. Global cerebral edema and subarachnoid hemorrhage in a patient with systemic lupus erythematosus.

    Systemic lupus erythematosus is a multifactorial autoimmune disease of complex etiology, which may be associated with cognitive dysfunction, seizures, and headache. The authors present an unusual presentation of systemic lupus erythematosus complicated by global cerebral edema and subarachnoid hemorrhage secondary to rupture of a cerebral aneurysm. The complicated patient management issues are discussed.
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16/48. Pseudoaneurysm of the thoracic radiculomedullary artery with subarachnoid hemorrhage. Case report.

    The authors report a rare case of a patient with a left-sided T-5 radiculomedullary artery pseudoaneurysm who presented with spinal subarachnoid hemorrhage (SAH). The patient, a 71-year-old woman, was hospitalized for progressive paraplegia and sensory loss with bladder and rectal dysfunction. Computerized tomography scanning revealed an SAH at the posterior fossa. Spinal T2-weighted magnetic resonance imaging demonstrated SAH and an inhomogeneous and slightly low signal intensity mass at T4-5. Spinal angiography revealed a tiny masslike staining without arteriovenous shunting. The resected specimen, which caused the spinal SAH, was diagnosed as a pseudoaneurysm based on operative and pathological findings.
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17/48. pupil-sparing, painless compression of the oculomotor nerve by expanding basilar artery aneurysm: a case of ocular pseudomyasthenia.

    BACKGROUND: oculomotor nerve paresis may have relatively benign but also life-threatening causes. Distinguishing between these is of great clinical importance. OBJECTIVE: To reveal a potential pitfall of the clinical evaluation of oculomotor nerve paresis. PATIENT: Single case observation. RESULTS: A 56-year-old man had fluctuating diplopia and fatigable ptosis, promptly relieved by intravenous edrophonium, leading to the diagnosis of ocular myasthenia gravis. His pupillary function was intact. A few days after the initial diagnosis, he suffered a subarachnoid hemorrhage secondary to the rupture of a basilar artery aneurysm. His ocular symptoms were related to aneurysmal oculomotor nerve compression. CONCLUSION: patients with oculomotor nerve dysfunction need more detailed evaluation because the underlying cause cannot be safely determined on a clinical basis.
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18/48. Early myocardial dysfunction following subarachnoid haemorrhage.

    Like systolic dysfunction (SD), diastolic dysfunction (DD) has recently been proposed as a contributing factor in haemodynamic instability and in the genesis of pulmonary oedema, but its occurrence in subarachnoid haemorrhage (SAH) patients has not been described. Following aneurysmal SAH, three patients arrived at our institution with haemodynamic instability requiring vasoactive drugs and with pulmonary oedema. Transoesophageal echocardiographic study during aneurysm surgery documented mild to severe left ventricular SD and DD. Right ventricular SD and DD were also present. Documented biventricular systolic and diastolic myocardial dysfunctions may contribute to haemodynamic instability and pulmonary oedema following SAH due to intracranial aneurysmal rupture.
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19/48. Posterior reversible encephalopathy syndrome on computed tomography perfusion in a patient on "Triple H" therapy.

    INTRODUCTION: This article reports a case of posterior reversible encephalopathy syndrome on compyted tomography (CT) perfusion in a patient on "Triple H" (hypertension, hypervolemia, and hemodilution) therapy following aneurysmal rupture repair. CASE REPORT: "Triple H" therapy is used in the postoperative course for treatment of vasospasm to prevent stroke and hemorrhage by maintaining cerebral perfusion pressure. DISCUSSION: A potential complication includes vasogenic edema from dysfunction of cerebral blood vessel autoregulation. CT perfusion can detect alterations in cerebral blood flow and volume caused by these hemodynamic changes.
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20/48. Neurogenic pulmonary edema during intracranial endovascular therapy.

    Neurogenic pulmonary edema (NPE) is a well-known complication of acute brain injury. Neurogenic stunned myocardium (NSM) occurs clinically in a significant subset of patients with NPE. A 49-year-old woman developed refractory cerebral vasospasm requiring angioplasty following a subarachnoid hemorrhage. During angioplasty, NPE with NSM manifested as acute pulmonary edema associated with elevated pulmonary artery occlusion pressure and reduced cardiac output. Evaluations disclosed a right insular infarction, cardiac wall motion abnormalities, and electrocardiographic characteristics of NSM. The NSM completely resolved, and the neurological outcome was good. A 56-year-old woman developed NPE during complicated coil embolization of an internal carotid artery aneurysm. Cardiac function was normal, and the NPE resolved with a brief period of mechanical ventilation and diuresis. The delayed appearance of NSM and NPE during endovascular therapy in these patients implies a degree of risk for sympathetically mediated cardiopulmonary dysfunction during complex intracranial endovascular procedures.
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