Intracerebral hemorrhage (ICH) and lacunar infarction (LI) are the major acute clinical manifestations of cerebral small vessel diseases (cSVDs). Hypertensive small vessel disease, cerebral amyloid angiopathy, and hereditary causes, such as Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL), constitute the three common cSVD categories. Diagnosing the underlying vascular pathology in these patients is important because the risk and types of recurrent strokes show significant differences. Recent advances in our understanding of the cSVD-related radiological markers have improved our ability to stratify ICH risk in individual patients, which helps guide antithrombotic decisions. There are general good-practice measures for stroke prevention in patients with cSVD, such as optimal blood pressure and glycemic control, while individualized measures tailored for particular patients are often needed. Antithrombotic combinations and anticoagulants should be avoided in cSVD treatment, as they increase the risk of potentially fatal ICH without necessarily lowering LI risk in these patients. Even when indicated for a concurrent pathology, such as nonvalvular atrial fibrillation, nonpharmacological approaches should be considered in the presence of cSVD. More data are emerging regarding the presentation, clinical course, and diagnostic markers of hereditary cSVD, allowing accurate diagnosis, and therefore, guiding management of symptomatic patients. When suspicion for asymptomatic hereditary cSVD exists, the pros and cons of prescribing genetic testing should be discussed in detail in the absence of any curative treatment. Recent data regarding diagnosis, risk stratification, and specific preventive approaches for both sporadic and hereditary cSVDs are discussed in this review article.
Anticoagulants ; Atrial Fibrillation ; Blood Pressure ; CADASIL ; Cerebral Amyloid Angiopathy ; Cerebral Hemorrhage ; Cerebral Small Vessel Diseases ; Diagnosis ; Genetic Testing ; Humans ; Pathology ; Stroke ; Stroke, Lacunar*

OBJECTIVES: The spontaneous spinal epidural hematoma (SSEH) is a rare clinical entity. Patients typically present with sudden onset back pain followed by neurological deficits. METHODS: Diagnosis of SSEH is usually made with MRI and standard treatment is surgical evacuation. In 1996, Groen published the most comprehensive review on the SSEH in which he analyzed 333 cases. We review 104 cases of SSEH presented in the English literature since the last major review and add three of our own cases, for a total of 107 cases. RESULTS: Our patients presented with back pain and neurologic deficits. Two made excellent functional recovery with prompt surgical decompression while one continued to have significant deficits despite evacuation. Better postoperative outcome was associated with less initial neurological dysfunction, shorter time to operation from symptom onset and male patients. CONCLUSION: We discuss the etiology of SSEH and report current trends in diagnosis, treatment, and outcome.
Back Pain ; Decompression, Surgical ; Hematoma, Epidural, Spinal ; Humans ; Male ; Neurologic Manifestations ; Retrospective Studies

The purpose of this study was to visualize the spatial patterns and connection of channels created after percutaneous transmyocardial revascularization (PTMR) in normal porcine hearts, and to estimate the relative contributions of transmyocardial and coronary perfusion. Six pigs underwent PTMR creating channels using radiofrequency ablative energy. Three-dimensional computed tomography imaging of channels 1 hr after PTMR showed the direct connection of PTMR channels to the myocardial capillary network and to epicardial coronary vessels. In the heart, examined 28 day after PTMR, there was a fine, extensive, network of microvessels originating from the site of the original PTMR channel, also connecting the left ventricular cavity to myocardial capillaries. Histopathologic examination of the 1-hr specimens showed numerous regions of myocardial hemorrhage and associated inflammatory cell infiltration. In the 28-day specimens, newly developed new vascular network suggested neovascularization within the core of these channel remnants. The immunoreactivity for basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) were intense within myocardium and neovascular structure surrounding PTMR channel remnants. The vascular connections occur by direct communication with existing myocardial vasculature acutely, and angiogenesis in these channel remnant chronically.
Animal ; Coronary Angiography ; Coronary Circulation ; Coronary Vessels/pathology ; Heart/radiography* ; Heart Ventricle/radiography ; Image Enhancement/methods ; Immunohistochemistry ; Myocardial Revascularization/methods* ; Myocardium/pathology* ; Neovascularization, Pathologic/radiography ; Neovascularization, Pathologic/pathology* ; Perfusion ; Swine ; Tomography, X-Ray Computed