Cases reported "Subarachnoid Hemorrhage"

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1/101. Early rebleeding from intracranial dural arteriovenous fistulas: report of 20 cases and review of the literature.

    OBJECT: In this study the authors sought to estimate the frequency, seriousness, and delay of rebleeding in a homogeneous series of 20 patients whom they treated between May 1987 and May 1997 for arteriovenous fistulas (AVFs) that were revealed by intracranial hemorrhage (ICH). The natural history of intracranial dural AVFs remains obscure. In many studies attempts have been made to evaluate the risk of spontaneous hemorrhage, especially as a function of the pattern of venous drainage: a higher occurrence of bleeding was reported in AVFs with retrograde cortical venous drainage, with an overall estimated rate of 1.8% per year in the largest series in the literature. However, very few studies have been designed to establish the risk of rebleeding, an omission that the authors seek to remedy. methods: Presenting symptoms in the 20 patients (17 men and three women, mean age 54 years) were acute headache in 12 patients (60%), acute neurological deficit in eight (40%), loss of consciousness in five (25%), and generalized seizures in one (5%). Results of the clinical examination were normal in five patients and demonstrated a neurological deficit in 12 and coma in three. Computerized tomography scanning revealed intracranial bleeding in all cases (15 intraparenchymal hematomas, three subarachnoid hemorrhages, and two subdural hematomas). A diagnosis of AVF was made with the aid of angiographic studies in 19 patients, whereas it was a perioperative discovery in the remaining patient. There were 12 Type III and eight Type IV AVFs according to the revised classification of Djindjian and Merland, which meant that all AVFs in this study had retrograde cortical venous drainage. The mean duration between the first hemorrhage and treatment was 20 days. Seven patients (35%) presented with acute worsening during this delay due to radiologically proven early rebleeding. Treatment consisted of surgery alone in 10 patients, combined embolization and surgery in eight, embolization only in one, and stereotactic radiosurgery in one. Three patients died, one worsened, and in 16 (80%) neurological status improved, with 15 of 16 AVFs totally occluded on repeated angiographic studies (median follow up 10 months). CONCLUSIONS: The authors found that AVFs with retrograde cortical venous drainage present a high risk of early rebleeding (35% within 2 weeks after the first hemorrhage), with graver consequences than the first hemorrhage. They therefore advocate complete and early treatment in all cases of AVF with cortical venous drainage revealed by an ICH.
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2/101. Nontraumatic acute spinal subdural hematoma: report of five cases and review of the literature.

    Acute subdural spinal hematoma occurs rarely; however, when it does occur, it may have disastrous consequences. The authors assessed the outcome of surgery for this lesion in relation to causative factors and diagnostic imaging (computerized tomography [CT], CT myelography), as well as eventual preservation of the subarachnoid space. The authors reviewed 106 cases of nontraumatic acute subdural spinal hematoma (101 published cases and five of their own) in terms of cause, diagnosis, treatment, and long-term outcome. Fifty-one patients (49%) were men and 55 (51%) were women. In 70% of patients the spinal segment involved was in the lumbar or thoracolumbar spine. In 57 cases (54%) there was a defect in the hemostatic mechanism. spinal puncture was performed in 50 patients (47%). Late surgical treatment was performed in 59 cases (56%): outcome was good in 25 cases (42%) (in 20 of these patients preoperative neurological evaluation had shown mild deficits or paraparesis, and three patients had presented with subarachnoid hemorrhage [SAH]). The outcome was poor in 34 cases (58%; 23 patients with paraplegia and 11 with SAH). The formation of nontraumatic acute spinal subdural hematomas may result from coagulation abnormalities and iatrogenic causes such as spinal puncture. Their effect on the spinal cord and/or nerve roots may be limited to a mere compressive mechanism when the subarachnoid space is preserved and the hematoma is confined between the dura and the arachnoid. It seems likely that the theory regarding the opening of the dural compartment, verified at the cerebral level, is applicable to the spinal level too. Early surgical treatment is always indicated when the patient's neurological status progressively deteriorates. The best results can be obtained in patients who do not experience SAH. In a few selected patients in whom neurological impairment is minimal, conservative treatment is possible.
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3/101. Weber's syndrome secondary to subarachnoid hemorrhage.

    BACKGROUND: Since a large intracranial hemorrhage is a space-occupying mass, it may cause the brain to shift, resulting in neurologic deficits both at the location of the bleeding and at a site distal to the hemorrhage. A parietal lobe hemorrhage may push the brain downward, causing the uncus of the temporal lobe to herniate through the tentorial notch, compressing the midbrain. The signs of parietal lobe damage, uncal herniation, and several midbrain syndromes that effect ocular motility are discussed. CASE REPORT: A 66-year-old Hispanic man came to us with a history of a subarachnoid hemorrhage that involved the right parietal lobe. Several signs of damage to both the right parietal lobe and midbrain were evident, including an ipsilateral third nerve paresis with contralateral hemiplegia, Weber's syndrome. CONCLUSION: A patient who survives a subarachnoid hemorrhage may demonstrate permanent residual neurologic deficits subsequent to the acute event. The presentation is particularly complex when the hemorrhage is large and damage occurs at multiple locations. Damage at the level of the midbrain is evident when the findings include Weber's syndrome, which is one of several syndromes that involves the oculomotor nerve.
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4/101. Using transcranial Doppler sonography to augment the neurological examination after aneurysmal subarachnoid hemorrhage.

    Vasospasm is the leading cause of death in patients who survive initial subarachnoid hemorrhage (SAH). Evidence of blood in the subarachnoid space on computed tomography (CT) scan can often predict the occurrence of vasospasm. Clinically, the onset of new or worsening neurological symptoms is the most reliable indicator of vasospasm. Transcranial Doppler (TCD) sonography studies can further aid the neuroscience nurse's assessment for vasospasm by measuring cerebral blood flow velocities. Physiological changes that occur during vasospasm cause the lumen of the blood vessel to decrease, increasing blood flow velocity through the affected area. Although vasospasm can only be definitively diagnosed by cerebral angiogram, TCD sonography provides a noninvasive, low-risk assessment tool that can be done at the beside. By coupling a patient's vital neurological data with blood flow velocity trends, the neuroscience nurse can anticipate the onset or worsening of vasospasm. This advanced nursing assessment allows for collaboration with the medical team to initiate and adjust appropriate therapies to improve patient outcomes.
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5/101. False positive appearance of subarachnoid hemorrhage on CT with bilateral subdural hematomas.

    We describe a patient with bilateral traumatic subdural hematomas in whom CT findings of hyperattenuation in the basal cisterns and subarachnoid spaces falsely suggested superimposed acute subarachnoid hemorrhage.
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6/101. Spontaneous occlusion of ruptured vertebral artery dissection at the extradural fenestration associated with extradural origin of the posterior inferior cerebellar artery--case report.

    A 69-year-old female suffered from sudden onset of severe headache. Computed tomography showed subarachnoid hemorrhage primarily located in the posterior fossa. Initial angiography demonstrated a fenestration of the vertebral artery and an extracranial origin of the posterior inferior cerebellar artery. However, no bleeding points could be clearly detected. The operative findings revealed a massive clot in subarachnoid space, but no bleeding point. Serial angiography demonstrated dissection in one of the limbs of the fenestrated vertebral artery on the 25th day after the onset. On the 100th day, the lesion was spontaneously occluded. The patient is presently doing well at 8 years after surgery.
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7/101. meningioma presented as subarachnoid haemorrhage: case report.

    A case of parasagittal meningioma causing subarachnoidal haemorrhage (SAH) is reported. Computed tomography (CT) was found negative in the patient with acute severe headache and haemorrhage was observed on cerebrospinal fluid (CSF) examination. Digital subtraction angiography (DSA) showed an avascular space over the convexity and magnetic resonance imaging (MRI) revealed the tumour. The importance of MRI for the detection of underlying pathology in SAH with unknown aetiology is emphasised.
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8/101. Tentorium cerebelli subdural haematoma complicating subarachnoid haemorrhage.

    Acute subdural haematoma (SDH) as a result of aneurysmal rupture is a rare event. We report a tentorium cerebelli SDH, secondary to a ruptured aneurysm which we believe is unique in the literature. This report also gives further support to the theory that a sentinel bleed causes inflammation and adhesion between the aneurysm and arachnoid as the underlying pathology in these unusual subdural haematomas. Since the first report of acute SDH from a ruptured aneurysm by Hasse in 1855, only about 150 further cases have been reported in the literature. We describe a further case, but at an as yet unreported site with radiological evidence of a sentinel bleed.
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9/101. subarachnoid hemorrhage associated with cyclosporine A neurotoxicity in a bone-marrow transplant recipient.

    We report subarachnoid hemorrhage associated with cyclosporine A (CSA) neurotoxicity after bone-marrow transplantation for chronic myelogenous leukemia. CT showed occipital subarachnoid hemorrhage. MRI confirmed this, and demonstrated cortical and subcortical edema in the posterior temporal, occipital, and posterior frontal lobes bilaterally, which was typical of CSA neurotoxicity. Recognition of CSA neurotoxicity as the cause of the subarachnoid hemorrhage obviated angiographic investigation. After cessation of cyclosporine therapy, the cortical and subcortical edema resolved on follow-up MRI with some residual blood products in the subarachnoid space.
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10/101. Aneurysms of the lateral spinal artery: report of two cases.

    OBJECTIVE AND IMPORTANCE: The goal of this report was to describe aneurysms arising from the lateral spinal artery. The locations of aneurysms contributing to subarachnoid hemorrhage (SAH) have been well characterized and are primarily in the circle of willis or at the bifurcation points of the internal carotid artery or the vertebrobasilar system. Although the spinal arteries are also in direct communication with the subarachnoid space, aneurysms of these arteries that lead to SAH are rare. To date, only aneurysms of the anterior and posterior spinal arteries have been described. In this communication, we report two patients with aneurysms of the lateral spinal artery who presented with SAH. CLINICAL PRESENTATION: review of our neurointerventional database from 1997 to the present revealed two patients with lateral spinal artery aneurysms. The medical records, as well as the operative and radiological findings, were reviewed for both patients. In both cases, the lateral spinal arteries were involved as collateral pathways for occlusive vertebral lesions, suggesting hemodynamic stress as a cause. INTERVENTION: Endovascular treatment was attempted in both cases and was successful in one; open surgery, with aneurysm resection, was performed in the other case. We review the vascular anatomic features of the spinal cord as they relate to the lateral spinal artery, as well as treatment options for lateral spinal artery aneurysms. CONCLUSION: Lateral spinal artery aneurysms are a rare cause of SAH. Both endovascular and surgical treatment options are available.
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