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Effects of enzymatic blood defibrination in subcortical arteriosclerotic encephalopathy
E B Ringelstein1, A Mauckner, R Schneider
1Department of Neurology, University Hospital of the RWTH Aachen, Federal Republic of Germany.
Insights
Plasma hyperviscosity in subcortical arteriosclerotic encephalopathy (SAE) did not improve clinically after treatment with ancrod. This suggests hyperviscosity is an epiphenomenon, not a cause of the disease.
Area of Science:
- Neurology
- Vascular Biology
Background:
- Subcortical arteriosclerotic encephalopathy (SAE) is associated with plasma hyperviscosity.
- This hyperviscosity is hypothesized to worsen chronic white matter ischemia.
Purpose of the Study:
- To investigate if reducing plasma hyperviscosity with ancrod improves clinical outcomes in SAE patients.
- To assess the role of hyperviscosity in the pathophysiology of SAE.
Main Methods:
- Administered ancrod, a defibrinating enzyme, to 10 SAE patients.
- Monitored plasma fibrinogen, retinal arteriovenous passage time, and CO2-induced cerebral vasomotor response.
- Evaluated clinical outcomes including neuropsychological tests, stroke recurrence, and audiological parameters over 6 months.
Main Results:
- Ancrod significantly reduced plasma fibrinogen, normalizing hyperviscosity.
- Retinal arteriovenous passage time and cerebral vasomotor response improved significantly.
- No clinical improvement was observed in neuropsychological tests, stroke recurrence, or audiological parameters.
Conclusions:
- Plasma hyperviscosity in SAE appears to be an epiphenomenon, not a primary driver of the disease.
- The findings suggest that a reversible chronic penumbral state does not exist in SAE.
Abstract:
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 CO2-induced cerebral vasomotor response. This did not lead, however, to any clinical improvement with respect to performance of neuropsychological tests, recurrences 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.