Book contents
- Frontmatter
- Contents
- List of contributors
- 1 Blood–brain barrier methodology and biology
- Part I Methodology
- Part II Transport biology
- Part III General aspects of CNS transport
- Part IV Signal transduction/biochemical aspects
- Part V Pathophysiology in disease states
- 41 Cerebral amyloid angiopathy
- 42 Brain microvasculature in multiple sclerosis
- 43 Hemostasis and the blood–brain barrier
- 44 Microvascular pathology in cerebrovascular ischemia
- 45 HIV infection and the blood–brain barrier
- 46 Hypertension
- 47 The blood-brain barrier in brain tumours
- 48 The pathophysiology of blood–brain barrier dysfunction due to traumatic brain injury
- 49 Cerebral malaria and the brain microvasculature
- 50 Molecular basis of tissue tropism of bacterial meningitis
- Index
42 - Brain microvasculature in multiple sclerosis
from Part V - Pathophysiology in disease states
Published online by Cambridge University Press: 10 December 2009
- Frontmatter
- Contents
- List of contributors
- 1 Blood–brain barrier methodology and biology
- Part I Methodology
- Part II Transport biology
- Part III General aspects of CNS transport
- Part IV Signal transduction/biochemical aspects
- Part V Pathophysiology in disease states
- 41 Cerebral amyloid angiopathy
- 42 Brain microvasculature in multiple sclerosis
- 43 Hemostasis and the blood–brain barrier
- 44 Microvascular pathology in cerebrovascular ischemia
- 45 HIV infection and the blood–brain barrier
- 46 Hypertension
- 47 The blood-brain barrier in brain tumours
- 48 The pathophysiology of blood–brain barrier dysfunction due to traumatic brain injury
- 49 Cerebral malaria and the brain microvasculature
- 50 Molecular basis of tissue tropism of bacterial meningitis
- Index
Summary
Introduction
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disorder of the central nervous system (CNS) that is the most common cause of acquired neurological dysfunction in young adults. The clinical manifestations and progression of MS vary widely amongst patients but are characterized by focal involvement of the optic nerves, spinal cord and brain that remit to a varying extent and recur over a period of years. Although the etiology remains unknown, there is strong circumstantial evidence to support the conclusion that it is mediated by an autoimmune attack directed against CNS myelin (Hafler and Weiner, 1995). A substantial genetic component to the disease process has been implicated by the observations that the risk for first degree relatives is increased over the general population, but environmental factors have also been shown to play a role (Ebers, et al., 1995). Active lesions are characterized by perivascular cuffs of lymphocytes and macrophages centered on post-capillary venules, particularly in the periventricular white matter, the optic nerve and tract, the corpus callosum and brainstem. Older lesions are immunologically silent in terms of inflammation and comprise large astroglial scars and demyelinated axons (Raine, 1990). Lesions are rarely noted beyond the root entry zones of the cranial and spinal nerves.
- Type
- Chapter
- Information
- Introduction to the Blood-Brain BarrierMethodology, Biology and Pathology, pp. 386 - 400Publisher: Cambridge University PressPrint publication year: 1998
- 7
- Cited by