Coagulation Disturbances in Cerebrovascular Disorders

Antithrombin III deficiency in ischaemic stroke

“…Hypercoagulability of the blood and disseminated intravascular coagulation have been demonstrated during the initial stages of cerebral ischaemia and stroke in several clinical studies and animal experiments (Pilgeram 1974;Fletcher et al 1976;Hossmann 1977;Hossmann and Hossmann 1977). The most likely explanation for the activation of the coagulation system is an enhanced liberation of thromboplastin from the damaged brain tissue (Donati and d'Angelo 1979).…”

Cerebrovascular Agents in Gerontopsychopharmacotherapy

“…As a consequence the possibility exists that hemorrhages are provoked and/or that emboli will result from the dissolution of an extracranial thrombus. Thus the administration of the fibrinolytic enzymes such as plasmin, streptokinase, and urokinase is limited to a few cases (HOSSMANN, 1977), because the benefit risk/ratio is considered sufficiently high and clinical emergency care must be at hand when this therapy is in use.…”

The impact of aging on spreading depolarization in the intact and ischemic rat brain

“…Furthermore, waves of SD were shown to evolve minutes after the onset of focal ischemia in the rat brain 11,12 . The observation that SD appearance for days after the acute infarction was associated with delayed neurological deficits has led to promote SDs as causal biomarkers for the estimation of tissue metabolic failure in neurocritical care 13 .…”

“…Taken that SDs occur in a recurrent fashion in ischemic zones 11,12 , and that tissue pH remains acidic for at least 10 min after an SD event propagating under penumbra-like conditions (Fig. 19), SDs are suggested to prolong tissue acidosis, thereby also increasing the risk of neuronal injury.…”