title: Morphogenesis of the demyelinating lesions in Baló's concentric sclerosis.
abstract: In tissues with elastic properties, an edema causes a raised tissue pressure and therefore a diminished blood flow. The authors assume that an increased tissue pressure due to local and/or relapsing edema may be the cause for incomplete necrosis (e.g. demyelinated lesions) or seldom complete necrosis in the brain. Newly forming demyelinating lesions seldom show small tissue bands with normal appearing myelin sheaths in the immediate vicinity of precursor lesions (Baló type of MS). The small myelinated bands are the result of a "protected zone" on the edge of previous demyelinated lesions. The authors explain this protected zone with two arguments. Firstly, the resorptive granulation tissue of more or less older lesions is relatively rich in capillaries. These capillaries may act as an energy reservoir that can nourish not only the plaque, but also a narrow adjacent myelinated tissue band by diffusion, even if the capillary blood flow in this tissue band is limited due to the greater tissue pressure of a new developing lesion in the neighborhood. Secondly, another protective mechanism may act simultaneously: older or more sclerosed lesions and small adherent bands of myelinated tissue with them may swell less in cases of an edema than in normal tissue. The hardening of the older lesions is caused by proliferated fiber-forming astrocytes in the sense of scarring. In an area with an increased tissue pressure, the capillaries are less compressed in a sclerosed lesion than in regions of normal grey and white matter. In addition, the adherent myelinated tissue band closest to the edge of a hardened plaque is better protected against swelling and compression than the further away tissue. Theoretically, this protection zone is comparable with protected blood vessels in the Haversian canals or the medullary spaces of bones. Both theses of protecting mechanisms at the edges of demyelinated lesions support the assumption of a hypoxic causation principle of demyelinating lesions in Baló's concentric sclerosis and multiple sclerosis.
authors.affiliation: Holunderweg 17, D-18209 Bad Doberan, Germany; Neuropathology Department, Dietrich-Bonhoeffer Hospital, D-17022 Neubrandenburg, PF 400135 Mecklenburg-West Pomerania, Germany.
authors.forename: Helmut
authors.initials: H
authors.lastname: Barz
authors.affiliation: Hospital Martha-Maria Halle-Dölau, Röntgenstraße 1, D-06120 Halle-Saale, Saxony-Anhalt, Germany.
authors.forename: Ulrich
authors.initials: U
authors.lastname: Barz
authors.affiliation: Fit for Work, Bautzner Landstraße 91, D-01324 Dresden, Saxony, Germany.
authors.forename: Almut
authors.initials: A
authors.lastname: Schreiber
mesh_terms: D001253:Astrocytes / Q000166:cytology; D001783:Blood Flow Velocity; D001921:Brain / Q000473:pathology; D002196:Capillaries / Q000378:metabolism; D049109:Cell Proliferation; D002560:Cerebrovascular Circulation; D003711:Demyelinating Diseases; D002549:Diffuse Cerebral Sclerosis of Schilder / Q000503:physiopathology*; D004058:Diffusion; D004487:Edema / Q000473:pathology; D004548:Elasticity; D066128:Gray Matter / Q000473:pathology; D006801:Humans; D000860:Hypoxia; D008833:Microcirculation; D020768:Middle Cerebral Artery / Q000473:pathology; D009024:Morphogenesis; D009103:Multiple Sclerosis / Q000503:physiopathology; D009186:Myelin Sheath / Q000737:chemistry; D009336:Necrosis; D012008:Recurrence; D066127:White Matter / Q000473:pathology