PubMed Health⌕ Search

Biomedical subjects

W I Schievink

Publications and source records attributed to W I Schievink.

At least 37 records · Page 2Linked to original sources

The dilemma of discontinuation of anticoagulation therapy for patients with intracranial hemorrhage and mechanical heart valves.

BACKGROUND: Anticoagulant-related hemorrhage occurs with an incidence of approximately 1%/patient-year in mechanical heart valve recipients. Intracranial hemorrhage poses a difficult clinical choice; continuing anticoagulation therapy may enlarge the volume of the hemorrhage, early reinstitution of anticoagulation therapy may predispose patients to recurrence, and reversal of anticoagulation therapy may place patients at risk for systemic embolization involving the brain. The risk of embolization may also be greater for patients with atrial fibrillation, cage-ball valves in the mitral position, and reduced ventricular function. This dilemma exists because of a lack of data for a large series of patients. METHODS: We reviewed the medical records and neuroimaging studies for a consecutive group of patients admitted with intracranial hemorrhage and mechanical heart valves. We reviewed neurological presenting data, cardiac risk factors for systemic embolization (atrial fibrillation, enlarged atrial chambers, reduced ventricular function, and the type and location of the metallic valve), and hospital management. RESULTS: We studied 39 patients with intracranial hemorrhage and mechanical heart valves (median age, 69 yr). Four patients had experienced previous transient ischemic attacks or minor strokes. The time from valve replacement to intracranial hemorrhage ranged from 2 months to 19 years (median, 6 yr). The type of intracranial hemorrhage was acute subdural hematoma (n = 20), lobar hematoma (n = 10), subarachnoid hemorrhage (n = 4), cerebellar hematoma (n = 3), or basal ganglionic hematoma (n = 2). Thirteen patients died within 2 days of admission. All 26 surviving patients received fresh frozen plasma and vitamin K. Fifteen patients underwent evacuation of acute subdural hematoma, and in one patient an anterior communicating aneurysm was clipped. The duration of discontinuation of anticoagulation therapy varied from 2 days to 3 months (median, 8 d). None of the patients developed transient ischemic attacks, ischemic strokes, valve thrombosis, or systemic embolization. No recurrence of intracranial hemorrhaging was observed during hospitalization and reinstitution of anticoagulation or antiplatelet agent administration. CONCLUSION: Temporary interruption of anticoagulation therapy seems safe for patients with intracranial hemorrhage and mechanical heart valves but without previous evidence of systemic embolization. For most patients, discontinuation for 1 to 2 weeks should be sufficient to observe the evolution of a parenchymal hematoma, to clip or coil a ruptured aneurysm, or to evacuate an acute subdural hematoma.

Adult↗

Fibromuscular dysplasia of the internal carotid artery associated with alpha1-antitrypsin deficiency.

OBJECTIVE: A deficiency of alpha1-antitrypsin has been implicated in the development of various disorders affecting medium-sized arteries, including intracranial aneurysms, cervicocephalic arterial dissections, and fibromuscular dysplasia (FMD). We performed alpha1-antitrypsin phenotyping in three consecutive patients who underwent bypass surgery for FMD of the extracranial internal carotid artery to test the hypothesis that alpha1-antitrypsin deficiency is a genetic risk factor for the development of FMD. METHODS: The study population consisted of three women (aged 37, 49, and 53 years, respectively) who had bilateral internal carotid artery stenosis caused by FMD. The indications for surgery included ocular or cerebral ischemic symptoms in two patients and progressive stenosis in one patient. The diagnosis of FMD was confirmed by histological examination of the resected segment of artery. The alpha1-antitrypsin phenotype was determined by isoelectric focusing in polyacrylamide gels. RESULTS: Two of the three patients had a heterozygous alpha1-antitrypsin deficiency (PiMZ phenotype). Pathological examination of the resected arterial segment showed typical medial FMD with focal intimal fibroplasia in both patients with the PiMZ phenotype. CONCLUSION: These findings suggest that a heterozygous alpha1-antitrypsin deficiency may be a genetic risk factor for the development of FMD of the internal carotid artery.

Adult↗

Long-term graft patency rates and clinical outcomes after revascularization for symptomatic traumatic internal carotid artery dissection.

INTRODUCTION: Surgical management of traumatic internal carotid artery (ICA) dissection remains controversial. Therefore, the delayed outcomes and graft patency rates of patients who underwent bypass procedures for symptomatic traumatic ICA dissection were studied. METHODS: Between September 1989 and August 1996, 13 patients (9 male and 4 female patients; mean age, 30.6 yr) underwent 16 revascularization procedures for symptomatic traumatic ICA dissection. The duration of clinical follow-up averaged 47.3 months (range, 12-94 mo) from the date of diagnosis. The duration of radiographic follow-up (catheter or magnetic resonance angiography, duplex Doppler ultrasonography) averaged 24 months (range, 12-60 mo). RESULTS: ICA dissection was caused by blunt (n = 11) or penetrating trauma (n = 2). Associated angiographic abnormalities included seven ipsilateral ICA occlusions, six dissecting aneurysms, two carotid-cavernous fistulae, and six contralateral traumatic ICA dissections. Patients requiring early revascularization (n = 6) underwent bypass procedures an average of 19.2 days after their injuries. Medically managed patients who developed ischemia later were revascularized a mean of 7.8 months after injury. The mean Glasgow Coma Scale score at the time of presentation was 10 (range, scores of 6-15), and the mean Glasgow Coma Scale score before revascularization was 14 (range, scores of 9-15). There were 14 saphenous vein ICA bypasses (8 cervical-to-petrous, 3 cervical-to-middle cerebral artery, 3 petrous-to-supraclinoid) and 2 superficial temporal artery-to-middle cerebral artery bypasses. There was one early postoperative graft occlusion, which responded to surgical thrombectomy. One patient with multiple other traumatic injuries died as a result of a pulmonary embolus 12 months after revascularization. All remaining patients had Glasgow Outcome Scale scores of 5, with patent bypass grafts confirmed during follow-up. CONCLUSION: Revascularization for persistently symptomatic traumatic ICA dissection eliminated ischemia and was associated with excellent long-term outcomes and graft patency rates.

Adolescent↗

MR imaging in pretruncal nonaneurysmal subarachnoid hemorrhage: is it worthwhile?

BACKGROUND AND PURPOSE: The cause of pretruncal (perimesencephalic) nonaneurysmal subarachnoid hemorrhage is not known. MRI of the brain or spine is often performed to exclude any other vascular abnormalities. Its diagnostic value is not known. METHODS: We used MR imaging of the brain with routine sequences, gadolinium enhancement, and additional thin T1-weighted axial sections following a triple dose of contrast. RESULTS: We performed MR imaging of the brain in 18 patients with a pretruncal nonaneurysmal subarachnoid hemorrhage. The focal nature of the subarachnoid hemorrhage exclusively in front of the brain stem was confirmed in 14 patients studied within 7 days of the ictus. No vascular abnormalities were found in 17 cases, including 14 patients with gadolinium enhancement. An incidental capillary telangiectasia was found in 1 patient. Fluid-attenuated inverse recovery MR additionally documented blood in the sulci due to cerebrospinal fluid recirculation of blood. Five patients underwent MR imaging of the spine, and no arteriovenous malformations were found. CONCLUSIONS: MR imaging did not reveal a source of pretruncal subarachnoid hemorrhage. The cost of MR imaging probably outweighs the benefit in the evaluation of this variant of subarachnoid hemorrhage.

Brain↗

Heritable connective tissue disorders in cervical artery dissections: a prospective study.

We prospectively evaluated 15 consecutive patients with spontaneous cervical artery dissections. Three patients (20%) had a heritable connective tissue disorder, each with a unique phenotype. None of these patients met the criteria of any of the named syndromes, and collagen and fibrillin analyses were normal. Heritable connective tissue disorders are common among patients with spontaneous cervical artery dissections, but, despite intensive investigations, the type of disorder usually cannot be identified. The underlying arteriopathy in cervical artery dissections is likely to be heterogeneous.

Adult↗

Surgical treatment of spontaneous spinal cerebrospinal fluid leaks.

OBJECT: Spontaneous spinal cerebrospinal fluid (CSF) leaks are an increasingly recognized cause of intracranial hypotension and may require neurosurgical intervention. In the present report the authors review their experience with the surgical management of spontaneous spinal CSF leaks. METHODS: Between 1992 and 1997, 10 patients with spontaneous spinal CSF leaks and intracranial hypotension were treated surgically. The mean age of the seven women and three men was 42.3 years (range 22-61 years). Preoperative imaging showed a single meningeal diverticulum in two patients, a complex of diverticula in one patient, and a focal CSF leak alone in seven patients. Surgical exploration in these seven patients demonstrated meningeal diverticula in one patient; no clear source of CSF leakage could be identified in the remaining six patients. Treatment consisted of ligation of the diverticula or packing of the epidural space with muscle or Gelfoam. Multiple simultaneous spinal CSF leaks were identified in three patients. CONCLUSIONS: All patients experienced complete relief of their headaches postoperatively. There has been no recurrence of symptoms in any of the patients during a mean follow-up period of 19 months (range 3-58 months; 16 person-years of cumulative follow up). Complications consisted of transient intracranial hypertension in one patient and leg numbness in another patient. Although the disease is often self-limiting, surgical treatment has an important role in the management of spontaneous spinal CSF leaks. Surgery is effective in eliminating the headaches and the morbidity is generally low. Surgical exploration for a focal CSF leak, as demonstrated on radiographic studies, usually does not reveal a clear source of the leak. Some patients may have multiple simultaneous CSF leaks.

Adult↗

Seasonal pattern of spontaneous cervical artery dissection.

OBJECT: The etiology of spontaneous cervical artery dissection is poorly understood; however, it may involve genetic and environmental factors. The purpose of this study was to determine whether seasonality of spontaneous cervical artery dissection exists. METHODS: The seasonal pattern of spontaneous cervical artery dissection was analyzed in a group of 200 consecutive patients (104 females and 96 males with a mean age of 44.9 years) who were evaluated using the Rayleigh test during the period from 1970 to 1990. The majority of patients resided in the midwestern section of the United States, where large seasonal fluctuations in climate occur. A circannual periodicity was found in the frequency of spontaneous cervical artery dissections with a peak occurring in October (p < 0.02). The seasonal variation was substantial, with approximately 58% more patients suffering a cervical artery dissection during autumn than during other seasons. CONCLUSIONS: A seasonal pattern of spontaneous cervical artery dissection exists with a peak occurring in October. The cause of the seasonality remains to be explained; however, weather- or infectious disease-related factors may provide etiological leads.

Adolescent↗

Rupture of a previously documented small asymptomatic intracranial aneurysm in a patient with autosomal dominant polycystic kidney disease. Case report.

Intracranial aneurysms are common extrarenal manifestations of autosomal dominant polycystic kidney disease (ADPKD). Although their natural history is not completely understood, small asymptomatic intracranial aneurysms in patients with ADPKD often are not treated but are followed with serial magnetic resonance (MR) angiography. The authors report the unique case of a patient with ADPKD who bled from a previously documented asymptomatic 3-mm intracranial aneurysm. This 42-year-old man with ADPKD suffered a subarachnoid hemorrhage (SAH) from a 7-mm left pericallosal artery aneurysm. This aneurysm was clipped and the patient made an excellent recovery. An irregular asymptomatic 3-mm right middle cerebral artery (MCA) aneurysm had also been demonstrated on angiography. While the patient was considering elective surgery for the MCA aneurysm, he suffered a hemorrhage from this lesion 10 weeks after the initial SAH. The aneurysm was clipped and the patient made a satisfactory recovery (he was moderately disabled). In this report the authors indicate that small asymptomatic intracranial aneurysms are not always innocuous in patients with ADPKD, and they suggest that treatment should be strongly considered for these lesions in this group of patients when there is a history of SAH or the aneurysm is irregular in appearance. Because MR angiography studies may not adequately define the configuration of small aneurysms and irregularity may easily be missed, conventional angiography is recommended for patients with ADPKD who are found to have an intracranial aneurysm on screening with MR angiography.

Adult↗

Cervical bone spur presenting with spontaneous intracranial hypotension. Case report.

Spontaneous intracranial hypotension due to a spinal cerebrospinal fluid (CSF) leak is a rare but increasingly recognized cause of postural headaches. The exact cause of these CSF leaks often remains unknown. The authors treated a 32-year-old man with a unique cause of spontaneous intracranial hypotension. He suffered an excruciating headache that was exacerbated by his being in an upright position. The results of four-vessel cerebral angiography were negative; however, magnetic resonance (MR) imaging of the brain revealed pachymeningeal enhancement and hindbrain herniation. A presumptive diagnosis of spontaneous intracranial hypotension was made. Myelography revealed extrathecal contrast material ventral to the cervical spinal cord as well as an unusual midline bone spur at C5-6. The patient's symptoms did not resolve with the application of epidural blood patches, and he subsequently underwent an anterior approach to the C5-6 spur. After discectomy, a slender bone spur that had pierced the thecal sac was found. After its removal, the dural rent was closed using two interrupted prolene sutures. The patient was discharged home 2 days later. On follow up his symptoms had resolved, and on MR imaging the pachymeningeal enhancement had resolved and the cerebellar herniation had improved slightly.

Adult↗

Screening for intracranial aneurysms in patients with isolated polycystic liver disease.

OBJECT: Isolated polycystic liver disease, that is, polycystic liver disease without kidney cysts, is an entity distinct from polycystic kidney disease. It is not known whether patients with isolated polycystic liver disease are at an increased risk for developing intracranial aneurysms, similar to patients with polycystic kidney disease. The authors screened individuals for intracranial aneurysms in a family in which isolated polycystic liver disease occurred to study the relationship between these two disorders. METHODS: Six siblings requested screening for intracranial aneurysms. Their father had died of a middle cerebral artery aneurysm. Isolated polycystic liver disease was found at autopsy. Their paternal aunt had died of a basilar artery aneurysm, but no autopsy had been performed in that case. Screening with magnetic resonance (MR) angiography and subsequent conventional angiography showed a 5-mm posterior communicating artery aneurysm in one sibling in whom abdominal ultrasound examination yielded normal findings and a posterior communicating artery infundibulum in another sibling in whom an ultrasound examination detected isolated polycystic liver disease. Screening did not detect aneurysms or polycystic liver disease in the other siblings. Thus, of the two patients with isolated polycystic liver disease in this family, one had a ruptured aneurysm and the other had an infundibulum. CONCLUSIONS: Findings in this family suggest an association between isolated polycystic liver disease and intracranial aneurysms. However, because of the delay in onset of the appearance of liver cysts in individuals who carry the disease gene, abdominal ultrasonography is not a useful method to exclude those family members at risk for aneurysm development.

Adult↗

Surgical treatment of superficial siderosis associated with a spinal arteriovenous malformation. Case report.

In many patients with superficial siderosis of the central nervous system (CNS) no source of bleeding can be established, despite extensive examinations. The authors report a patient with superficial siderosis and a spinal arteriovenous malformation (AVM) that was not visible on magnetic resonance (MR) imaging or myelography but was identified on angiographic studies. This 71-year-old man presented with a 2-year history of progressive gait difficulties and hearing loss. Examination showed ataxia, hearing loss, and quadriparesis. On MR imaging superficial siderosis of the brain and spinal cord as seen; however, MR imaging of the CNS, as well as cerebral angiography and myelography studies, did not reveal the source of hemorrhage. Spinal angiography revealed a small slow-flow pial AVM at the C-5 level originating from the anterior spinal artery. A C-5 corpectomy was performed and the AVM was obliterated. The patient did well and reported no further progression of his symptoms during 3 months of follow up. Spinal angiography is indicated to complete the evaluation of patients with superficial siderosis, even if results of spinal MR imaging and myelography studies are normal. Obliteration of spinal AVMs may successfully prevent the progression of superficial siderosis.

Aged↗

Pretruncal nonaneurysmal subarachnoid hemorrhage.

OBJECTIVE: To review the diagnostic evaluation and the clinical course of patients with pretruncal nonaneurysmal subarachnoid hemorrhage. MATERIAL AND METHODS: The study population consisted of a consecutive series of patients with a pretruncal nonaneurysmal subarachnoid hemorrhage encountered at Mayo Clinic Rochester during a 6-year interval. We reviewed the clinical manifestations, the neuroimaging characteristics, and the appropriate management. RESULTS: The 15 male and 9 female patients with a pretruncal nonaneurysmal subarachnoid hemorrhage ranged from 3 to 72 years of age (median, 45). Of the 24 patients, 18 had a sudden explosive headache at the time of initial assessment. Ventricular shunting for acute hydrocephalus was indicated in one patient. Neuroimaging studies demonstrated that the center of the hemorrhage was prepontine, and it extended into the interpeduncular or premedullary cisterns. In two patients, a small focal hemorrhage was not noted on an admission computed tomographic scan but was identified on repeated study. A second four-vessel cerebral angiogram, obtained in most patients, showed normal findings in four patients who had had cerebral vasospasm on the first study. In one patient, moderate cerebral vasospasm was found on the second angiogram. No patient had rebleeding. One patient had transient dysphasia associated with cerebral vasospasm after cerebral angiography. Two patients had a family history of aneurysmal subarachnoid hemorrhage. CONCLUSION: The excellent outcome in patients with pretruncal nonaneurysmal subarachnoid hemorrhage is in distinct contrast to the overall somber outcome associated with aneurysmal subarachnoid hemorrhage. A ruptured aneurysm of the posterior circulation may mimic a pretruncal nonaneurysmal subarachnoid hemorrhage and should be excluded on the basis of a technically satisfactory cerebral angiogram.

Adolescent↗

Genetics and aneurysm formation.

This article reviews the current understanding of genetic factors involved in the development of intracranial aneurysms. Of the large number of heritable connective tissue disorders that have been associated with intracranial aneurysms, three are discussed in detail: autosomal dominant polycystic kidney disease, Ehlers-Danlos syndrome type IV, and alpha 1-antitrypsin deficiency. The author reviews the familial occurrence of intracranial aneurysms, which is found in about one-fifth of patients with aneurysm subarachnoid hemorrhage. Guidelines are provided for the evaluation of patients with familial intracranial aneurysms and screening of their relatives.

Connective Tissue Diseases↗

Brain protection for cerebral aneurysm surgery.

The modern management of patients undergoing surgery for intracranial aneurysm often includes temporary periods of cerebral ischemia to minimize the risks final dissection and clipping or to allow vascular reconstruction. This article reviews the concepts of ischemic thresholds and examines the effects of the physiologic variables that may affect outcome from an ischemic episode. The protective agents presently available and the agents in development that may limit the extent of ischemic injury are reviewed extensively as well.

Brain Ischemia↗