Effects of enzymatic blood defibrination in subcortical arteriosclerotic encephalopathy.

Abstract

SUMMARY Plasma hyperviscosity is a striking abnormality in patients suffering from subcortical arteriosclerotic encephalopathy (SAE) and is thought to perpetuate the chronic ischaemic demyelinating process of the periventricular white matter. Ancrod, a defibrinating enzyme, was given to 10 patients with SAE in an attempt to reduce plasma fibrinogen, which would thus normalise hyperviscosity. This was paralleled by a significant improvement of the initially abnormal retinal arteriovenous passage time, as well as a significant augmentation of the C02-induced cerebral vasomotor response. This did not lead, however, to any clinical improvement with respect to performance of neuropsychological tests, recurrence of strokes during a 6 month observation period or improvement of various audiological parameters. The findings indicate that hyperviscosity in patients with SAE is merely an epiphenomenon. A potentially reversible, chronic penumbral state of the brain tissue apparently does not exist in SAE.

Effects of an Antithrombin Drug in Patients with Subacute Exacerbations of Binswanger Disease.

“…Elevated plasma levels of fibrinogen, one of the major determinants of plasma viscosity, may worsen the microcirculation in BD (2,3). However, a clinical trial to decrease the fibrinogen levels using defibrinating agents was not effective in improving the neurological deficits (4). The release of p-thromboglobulin, a platelet activation marker, was observed to be increased in the cerebral circulation of BD patients (5).…”

Immunohematologic characteristics of infection-associated cerebral infarction.

“…We interpret this finding in the following way: when studied early, acute-phase responses in stroke patients may be primarily related to events other than the stroke, (e.g., prior infection); beyond 48 hours, acute-phase responses from the stroke itself predominate, resulting in comparable fibrinogen levels for patients with and without infection. Increased fibrinogen levels may contribute to the pathogenesis of cerebral infarction by multiple mechanisms; there is an inverse relation between fibrinogen levels and cerebral blood flow, 32 middle cerebral artery blood velocity in the elderly, 33 cerebral vascular reactivity, 34 and, perhaps, fibrinolytic activity. 35 In addition, fibrinogen serves as the major intercellular link for platelet aggregation via the glycoprotein Ilb-IIIa complex.…”

Fibrinogen and the Amount of Leukoaraiosis in Patients with Symptomatic Small-Vessel Disease

“…A therapeutic trial with ancrod did not produce any benefit for BD patients [40], although this was an open and small (n = 12) trial with only a 1-month treatment, and a 6-month follow-up.…”