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Perivascular Inflammation (perivascular + inflammation)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Autopsy case of neuro-Behçet's disease with multifocal neutrophilic perivascular inflammation

NEUROPATHOLOGY, Issue 6 2006
Yoshifumi Arai
We report here an autopsy case of neuro-Behçet's disease. The patient was a 28-year-old man, who developed a slight fever, right uveitis, and right sensory neural hearing loss at the age of 25. These symptoms relapsed repeatedly despite treatment. Eventually he was admitted to hospital because of progressing neurological deficits such as pyramidal symptoms, somatic sensorial and autonomic disorders, and bulbar palsy. The patient's condition deteriorated and he died of heart failure. Total clinical course was about three years. In postmortem examination, various-sized necrotic foci, often accompanied by gliosis and foamy macrophage infiltration, were scattered in the diencephalic region and brain stem. Meningitis was observed on the ventral side of the brain stem as well as inferior cerebral surface. Non-bacterial or non-fungal acute perivascular inflammatory foci were also present in the brain stem and cerebellar parenchyma. These histopathological findings suggest that a destructive multifocal neutrophilic inflammation might have caused the neurological deficits. Perivascular inflammation might be important to understanding the pathogenesis of neuro-Behçet's disease. [source]

Vascular pathology in dermatomyositis and anatomic relations to myopathology

MUSCLE AND NERVE, Issue 1 2010
Alan Pestronk MD
Abstract The causes of perifascicular myofiber atrophy and capillary pathology in dermatomyositis are incompletely understood. We studied 11 dermatomyositis muscles by histochemistry, immunohistochemistry, and ultrastructure. We found that endomysial capillaries within regions of perifascicular atrophy are not entirely lost, but they have reduced size, endothelial loss, C5b9 complement deposits, and relatively preserved connective tissue molecules and pericytes. In all muscles, the perimysium varies regionally. Some areas contain intermediate-sized vessels. Others are avascular. In dermatomyositis, vascular perimysium contains abnormal vessel fragments, perivascular inflammation, and increased PECAM-1. Perifascicular myofiber atrophy and capillary pathology are concentrated near the avascular perimysium. We conclude that both perimysial intermediate-sized vessels and endomysial capillaries within regions of perifascicular myofiber atrophy are abnormal in dermatomyositis. Capillary damage and myofiber atrophy are concentrated in regions distant from intermediate-sized perimysial vessels. Chronic immune vascular damage and insufficiency in dermatomyositis may cause ischemia, myofiber atrophy, and capillary damage in "watershed" regions of muscle near the avascular perimysium. Muscle Nerve, 2010 [source]

Diabetic and nondiabetic lumbosacral radiculoplexus neuropathies: New insights into pathophysiology and treatment

MUSCLE AND NERVE, Issue 4 2002
P. James B. Dyck MD
Abstract Diabetic lumbosacral radiculoplexus neuropathy (DLRPN) (also called diabetic amyotrophy) is a well-recognized subacute, painful, asymmetric lower-limb neuropathy that is associated with weight loss and type II diabetes mellitus. Nondiabetic lumbosacral radiculoplexus neuropathy (LRPN) has received less attention. Comparison of large cohorts with DLRPN and LRPN demonstrated that age at onset, course, type and distribution of symptoms and impairments, laboratory findings, and outcomes are similar. Both conditions are lumbosacral radiculoplexus neuropathies that are associated with weight loss and begin focally with pain but that evolve into widespread, bilateral paralytic disorders. Although both are monophasic illnesses, patients have prolonged morbidity from pain and weakness, and many patients become wheelchair-dependent. Although motor-predominant, there is unequivocal evidence that autonomic and sensory nerves are also involved. Cutaneous nerves from patients with DLRPN and LRPN show pathological evidence of ischemic injury (multifocal fiber loss, perineurial thickening and degeneration, neovascularization, microfasciculation, and swollen axons with accumulated organelles) and microvasculitis (mural and perivascular inflammation, separation and fragmentation of mural smooth muscle layers of microvessels and hemosiderin-laden macrophages). Controlled trials with immune-modulating therapies in DLRPN are in progress, and preliminary data suggest that such therapy may be beneficial in LRPN. It is likely that DLRPN and LRPN are immune-mediated neuropathies that should be separated from chronic inflammatory demyelinating polyneuropathy and from systemic necrotizing vasculitis. © 2002 Wiley Periodicals, Inc. Muscle Nerve 25: 000,000, 2002 [source]