Immunological Abnormalities

Circulating antibodies, like lupus anticoagulant (LA) and anticardiolipin antibodies, may be related to stroke. The LA is a phospholipid antibody that interferes with the formation of the prothrombin activator. In the laboratory, there is a prolonged activated partial thromboplastin time (PTT). Some patients with LA have SLE, but most do not. When antiphospholipids of the IgG, IgM, or IgA classes are found in the absence of a known systemic illness, and patients present with an increased incidence of spontaneous abortions, thrombophlebitis, pulmonary embolism, and large- and small-artery occlusions, the disorder is now referred to as primary antiphospholipid lupus anticoagulant (APLA) syndrome. The APLA-associated stroke syndrome is characterized by its younger age at onset, predominance in women, and high risk of recurrent thrombo-occlusive events. Some patients have mitral and aortic valve vegetations and ocular ischemia. In addition to the presence of LA or anticardiolipins, or both, laboratory abnormalities include false-positive Venereal Disease Research Laboratory (VDRL), thrombocytopenia, antinuclear antibodies, and prolonged activated PTT. The risk of recurrent thrombosis in patients with the antiphospholipid-antibody syndrome is high. More than one-half of the patients have at least one recurrent thrombo-occlusive stroke, most occurring within the first year. y Long-term anticoagulation therapy is recommended, maintaining the international normalized ratio at or above 3. y

Disseminated intravascular coagulation occurs when a primary disorder leads to local or diffuse clotting and the coagulation cascade is activated, with generation of excess intravascular thrombin. The coagulation system then is activated further, fibrin is deposited into the microcirculation, hemostatic elements have a shortened survival, and the fibrinolytic system is activated. The most common disorders inciting disseminated intravascular coagulation


1. Deficiencies of natural coagulation inhibitors Antithrombin III

Protein C Protein S

2. Resistance to activated protein C

3. Increased levels of serine protein coagulation factors (can occur in patients with inflammatory diseases), factors V, VII, and VIII

4. Cancer, especially mucinous adenocarcinomas

5. Abnormalities of the normal fibrinolytic system Tissue plasminogen activator (t-PA) Plasminogen activator inhibitor (PAI)

6. Dysfibrinogenemias including increased levels of fibrinogen

are infections, obstetric and vascular emergencies, cancer, nonbacterial thrombotic endocarditis, head trauma, SAH, brain tumors, and vascular malformations. The laboratory findings usually include thrombocytopenia, reduced fibrinogen levels, prolongation of prothrombin time (PT) and PTT, and increased levels of fibrin split products. Neurological findings are frequent and include an encephalopathy with multifocal signs and frank thrombotic and embolic infarcts. Bleeding can also occur.y , [63]

Whole blood viscosity is one of the major determinants of cerebral blood flow, especially in the microcirculation. Whole blood viscosity is very dependent on the hematocrit and fibrinogen levels, and these are often elevated in patients with stroke. y Hyperviscosity also is probably pathogenetically related to Binswanger's disease (subcortical arteriosclerotic encephalopathy). y Less often, viscosity is increased by high levels of globulins as in Waldenstrom's macroglobulinemia or in other disorders with abnormal proteins or cryoglobulins, such as multiple myeloma, or by very high levels of serum lipids, especially chylomicron.

Thrombotic thrombocytopenic purpura is characterized clinically by fever, renal failure, thrombocytopenia, and microangiopathic hemolytic anemia. Transient focal neurological signs and a more diffuse encephalopathy are common, but occasionally, persistent neurological deficits due to occlusion of medium-sized arteries or brain hemorrhages occur.y Plasma exchange can be an effective treatment.


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