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Fifty-one patients of cerebral hemorrhage were observed on controlled study which were treated with the Zhu-Yu Hua-Tan Decoction (ZYHTD) and Western medicine. The results revealed that ZYHTD could reduce the serum IgG (P < 0.05), and lymphocyte transformation rate (P < 0.05). Meanwhile, the patient's health condition of treated group was better than the control group in the fields of eliminating brain hematoma, evaluating patients condition score in TCM and compromised neurologic function (P < 0.05). It is assumed that there is positive significance in anti-inflammatory effect and promoting the absorption of brain hematoma in the acute phase of cerebral hemorrhage.

Unlabelled: Premature children (n = 25) with respiratory distress (RD) were studied regarding complement activation and formation of the anaphylatoxins C3a and C5a. Blood samples were drawn on admission to the paediatric intensive care unit. In 18 of the patients RD was accompanied by other perinatal complications like pneumothorax or intracerebral haemorrhages. Seven of the premature children had RD without such complications. Preterm children with RD and with peri- and postnatal complications such as pneumothorax or intracerebral haemorrhage had increased concentrations in plasma of the anaphylatoxins C3a and C5a compared with preterm children with RD without these complications. There was a positive correlation between the plasma C3a and C5a concentrations in the preterm children., Conclusion: The present study indicates that isolated RD will appear without signs of complement activation and that complications like pneumothorax or intracerebral haemorrhages are associated with release of the anaphylatoxins C3a and C5a.

Neonatal alloimmune thrombocytopenia (NAIT) is caused by maternal immunisation against a paternal antigen on fetal platelets. The antigen involved in the majority of cases is HPA-1 a (PIA1). Usually circulating platelet alloantibodies are detectable in the mother. In this report, we present a thrombocytopenic newborn with severe hemorrhagic diathesis due to materno-fetal HPA-1 a (PIA1) incompatibility. Platelet antibodies could initially not be demonstrated in the mother's serum but became detectable after four weeks. Because of the severe and protracted course of the disease, repeated platelet substitution was necessary throughout the first two months of life.

Neonatal alloimmune thrombocytopenic purpura (NAITP) is one of the causes of thrombocytopenia in the newborn period. The thrombocytopenia is caused by maternal transplacental antiplatelet alloantibodies. We report a case of NAITP in a newborn infant having subarachnoid hemorrhage. Examination of platelet antibodies revealed anti-Yukb, that is, human platelet antigen (HPA)-4a incompatibility. Cranial ultrasound and brain magnetic resonance imaging revealed subarachnoid hemorrhage in the temporal region inferior to the cephalohematoma. The lesion seemed to have been sustained during delivery. The patient was treated with high-dose gamma-globulin and several transfusions of random donor platelets and showed a good clinical course. This is the second reported case of NAITP associated with the Yuk antigen system having intracranial hemorrhage.

Background and Purpose: The aims of this prospective and multicenter study were to determine the frequency of anticardiolipin and antinuclear antibodies in an unselected ischemic and hemorrhagic stroke population and to evaluate the clinical significance of these autoantibodies., Methods: Over a 1-year period, we collected plasma from 481 consecutive patients with ischemic or hemorrhagic stroke attending four different hospitals. Blood (10 mL) was drawn from each subject into a citrated glass tube. Plasma was obtained immediately by centrifugation and was stored at -70 degrees C until use. Concentrations of IgM and IgG anticardiolipin antibodies were measured at room temperature in normal (not heat-treated) plasma by standardized enzyme-linked immunosorbent assay. All sera were treated by indirect immunofluorescence on mouse liver and kidney sections for antinuclear antibodies., Results: A total of 481 patients (325 men, 156 women) 16 to 90 years in age (mean age, 61 years) were studied. Anticardiolipin antibodies were present in 5 of 481 (1.04%) patients. One patient was IgG positive and four patients were IgM positive. Of 481 patients, 35 (7.2%) were positive for antinuclear antibodies. Anti-DNA antibodies were not demonstrable in any patient., Conclusions: The frequency of anticardiolipin antibodies in a heterogeneous stroke population is possibly lower than reported. The routine screening of anticardiolipin and antinuclear antibodies in a stroke population is of questionable value.

Objective: Our goal was to describe the neuroradiologic findings in hemorrhagic venous infarction related to a hypercoagulable state caused by antiphospholipid antibodies (aPA)., Materials and Methods: Magnetic resonance imaging was performed on two patients with superior sagittal thrombosis related to the presence of aPA., Results: A parenchymal region of hyperintense signal due to hemorrhagic venous infarction was demonstrated in both patients, along with abnormal signal within the thrombosed superior sagittal sinus., Conclusion: Hemorrhagic venous infarction may result from the hypercoagulable state related to aPA. The presence of these antibodies should be considered in the setting of otherwise unexplained dural sinus thrombosis and/or venous infarction.

We report a family with a neonate who was severely damaged by intracranial haemorrhages. These probably occurred before the 20th week of gestation. The neonate had a moderate thrombocytopenia. In the maternal serum anti-HPA-1b and anti-HPA-2a alloantibodies were detected. Third-generation assays were applied to identify the alloantibodies. No other cause for the bleeding was found. Probably the combination of anti-HPA-1b and anti-HPA-2a alloantibodies, directed against the platelet fibrinogen receptor and the von Willebrand receptor, respectively, induced a thrombocytopenia and a thrombocytopathy.

The changes occurring in the immunity of 118 patients with focal brain injuries verified at surgery and during computed tomography were studied in relation to hemispheric lateralization. Patients with left-sided brain injuries showed more severe abnormalities of immunity and had a considerable lot of pyoinflammatory complications, including extracerebral ones. In patients with right-sided brain injuries, compensation of the changed immune responses occurred more rapidly, but intracranial pyoinflammatory complications took place more frequently. The magnitude and changes in immunity were found to depend upon the hemispheric lateralization of focal brain injuries, which characterizes that the brain regions play unequal role in the formation of an immune response. Differences become significant at week 3 at the peak of secondary immunodeficiency.

The oedema which forms around an intracerebral haemorrhage has a complex aetiology. The immune response may have a role in its formation. There is clinical and experimental evidence that circulating leucocytes and platelets may mediate oedema formation. Global depletion of circulating leucocytes and platelets by whole body irradiation in a rodent model of intracerebral haemorrhage was found to confer protection against both ischaemia and oedema formation. This was not a direct effect of irradiation of the brain. The possible mechanisms for this protection are discussed.

We report a case of neonatal alloimmune thrombocytopenia and intracranial hemorrhage in an infant whose mother received immunizations of paternal mononuclear cells. This therapy is designed to prevent unexplained first trimester miscarriages. No previous cases of platelet autoimmunization associated with maternal immunization with paternal mononuclear cells has been reported. Treatment with antenatal maternal infusions of intravenous gamma globulin (IVGG) did not prevent fetal thrombocytopenia, but IVGG may become the treatment of choice for postnatal, antibody-mediated thrombocytopenia of the newborn.

Cerebral vasculitis may occur in isolation or in conjunction with a systemic illness. Although a relatively infrequent cause of intracerebral or subarachnoid hemorrhage, it should be considered in a setting of relevant systemic symptoms, an unexplained progressive neurologic disorder, or in a patient lacking risk factors for hemorrhagic stroke. Diagnosis may be difficult because the results of most studies may be normal or nonspecific. Because treatment is effective in many of the cerebral vasculitides, vigorous pursuit of the diagnosis is warranted.

The associated antigen of factor VIII in plasma of 124 cases of cerebrovascular disease and 40 normal cases were detected using immune rocket electrophoresis. There were significant differences between the 3 illness groups and the normal group. The results suggest that the associated antigen of factor VIII may be one of the useful markers for forecasting the danger of cerebrovascular disease.

Lymphocyte capping with concanavalin A was studied in 11 patients with hereditary cerebral haemorrhage with amyloidosis (Dutch type) and 10 controls. No difference in capping was found between patients and controls. Abnormal lymphocyte concanavalin A capping has been reported in patients with the Icelandic type of cerebral amyloidosis and in patients with Alzheimer's disease, a disease in which cerebral amyloid angiopathy can also be found. The results suggest a difference in pathogenesis between the Dutch type of cerebral amyloidosis and the other amyloid diseases.

The usefulness of in vivo skin test reaction to phytohemagglutinin to assess cell-mediated immunity was investigated in 109 subjects, including 37 normal controls, 35 patients without brain tumor and 37 patients with brain tumor. Intradermal injection at forearm of 10 microgram of Bacto-phytohemagglutinin-P (PHA-P) produced an erythema within 24 hours. Upon PHA skin reaction the mean diameter of erythema was 25.3 mm with the normal in the control and 18.6 mm with other diseases than brain tumor, while it was 13.0 mm with brain tumor. Furthermore when mean diameter of those with longer than 15.0 mm are classified as positive in the PHA skin test, the normal in the control revealed 89.2% positive and the patients with brain tumor indicated only 37.8% positive. A positive reaction was observed in 10 (77.0%) of 13 benign brain tumor and 5 (26.3%) of 19 malignant brain tumor. A correlation was found between in vivo and in vitro responses to PHA, and between PHA and PPD skin reaction. In repeated PHA skin test at intervals of about one month, the skin reaction to PHA of patients with brain tumor varied depending on the clinical states. Other advantages of this test are no presensitization and it can be used repeatedly. The PHA skin test is a useful and simple screening test for cellular immune function of patients with brain tumor and as a simple method applicable clinically indicating accurate immuno-reactivity the PHA skin tests have been carried out during the course of treatment with an interval of about one month repeatedly.

Changes in immunological responsiveness, including humoral and cellular immunity, spontaneous rosette formation of neutrophils and their phagocytic activity were investigated in 100 patients with acute disorder of the cerebral circulation, in 25 clinically healthy individuals and in 20 patients with essential hypertension. The findings made it possible to confirm the presence of immunological changes following cerebral strokes as well as their influence on the course and outcome of acute impairments of the cerebral circulation.

Circulating immune complexes (CIC) and complement activation (plasma C3d levels) were monitored during a 2-week period in patients with ruptured cerebral aneurysms and also in patients with cerebral hematoma unrelated to saccular aneurysms. Thirteen of 18 aneurysm patients were found to have CIC on admission as compared to three of 21 healthy blood donors (p less than 0.001). The presence of CIC in aneurysm patients was associated with a poor prognosis. Eight of nine patients who developed angiographic vasospasm had CIC on admission compared with one of four without vasospasm. Patients with vasospasm showed a twofold increase in plasma C3d levels at the time when the spasm occurred, whereas no significant changes in the C3d concentration could be demonstrated in aneurysm patients without spasm or in patients with hematoma unrelated to aneurysm rupture. These findings suggest that immunological processes involving complement-activating immune complexes are involved in the pathogenesis of cerebral vasospasm following rupture of saccular aneurysms.

Cell-mediated and humoral immunity was studied in 74 patients with acute cerebral vascular disease. During the first two days after the onset of disease marked changes of cell-mediated immunity were observed, manifested as a decrease in total lymphocyte count in the peripheral blood, decrease in number of T lymphocytes, depression in lymphocyte blastogenesis and production of the migration inhibition factor, and a delayed-type skin reactivity. The changes were most evident in patients with severe lesions of brain tissue resulting from primary cerebral haemorrhage and cerebral infarction with fatal outcome. In the group of patients with cerebral infarction with improvement of neurological symptoms the immunological changes were not so pronounced as in the two above-mentioned groups, the smallest changes being found in patients with subarachnoid haemorrhage. We suppose that the depression in the immunne function was caused by severe stress during the course of disease. Impairment of the immune function may increase susceptibility to infection. The humoral immune response was not so evidently changed, and the observed increase of IgA in the sera was probably present before the stroke. In cases with good clinical course some improvement in the immunological parameters was observed, but full recovery did not occur until 3 weeks after the onset of disease.

Parameters of blood-brain barrier (BBB) function and of humoral and cellular immune response were determined in lumbar CSF and blood serum samples from 717 patients and statistically compared to "healthy" controls (n = 190). Leucocyte counts (mainly mononuclear cells), total protein and IgG levels in CSF were significantly higher, and prealbumin fraction mostly lower in patients, besides other alterations of protein electrophoresis. Serum fractions (median) of protein electrophoresis were within the reference range. When parameters were correlated with age, a significant increase of total protein of 1.62 mg/dl and of IgG of 0.13 mg/dl per 10 years of age was found in lumbar CSF of controls. Elevated leucocyte counts did not correlate with age of patients, but they increased significantly with age, with respect to controls, to a higher extent in patients with polyneuritis, ischemia and injury; they decreased in patients with brain tumors and polyneuropathy. When compared to controls, elevated total protein levels significantly increased with age only with tumors and injury patients. In multiple sclerosis, IgG increased and beta-globulin fraction decreased significantly in CSF with age. The findings point to age-dependent alterations of BBB and immune response only in some patients groups which were different from those of controls.

The lymphocyte transformation test was performed in 32 risk newborns and 32 comparative persons (17 adults, 15 children). In the void controls without antigen addition the newborns had a significantly higher spontaneous blastic reaction than the control group. The phenomenon may be explained by lymphatic stem cells in the blood or an ontogenetically higher content of "embryonic tissue" respectively being present as unspecific stimulant or an immunological defence reaction against maternal immunoglobulins transmitted diaplacentally (formation of antigammaglobulin factors) or against maternal lymphocytes to prevent a "runt disease".

A clinical-immunologic study of 133 patients was carried out to elucidate the status of the T- and B-immune systems in atherosclerotic dyscirculatory encephalopathy (ADE) in the acute period of cerebral infarction and hemorrhagic stroke. A similar pattern of elevation in humoral and tissue immunity, with quantitative fluctuations in the intensity of individual parameters in various dyscirculatory disorders, was found. The changes indicate that cerebral stroke develops in the body already sensitized in the prestroke period and its development involves the central and peripheric links of the immune system.

Examinations of the clinical and immunological state of 68 patients with the acute stage of cerebral stroke were carried out, and so were immunomorphological examinations of the spleen and the subclavicular lymph nodes in 36 of them whose disease ended in death. An analysis of the results obtained has shown that the immunological reactivity increases from the very first day of the disease. The authors believe that the early immunological response, especially in cases of brain infarction, is due to development of the cerebral stroke in a sensitized body. A rise of selective antibody titres depending on the character of the cerebrovascular disorder was noted: there were: anti-encephalic antibodies targeted at the malacia focus in cases of brain infarction, and antivascular, and to a lesser extent anti-encephalic antibodies in cases of a hemorrhagic stroke. The informative value of the complement fixation test was found to be greater than that of the hemagglutination inhibition test. High degrees of plasmatization of the splenic tissue and the presence of the anti-encephalic immune complexes in it, mainly in cases of brain infarction, also point to the activity of the immunogenesis in the acute stage of the cerebral stroke.

The immunoelectrophoresis in cerebral tumours, craniocerebral injuries and cerebral haemorrhages showed antibodies against the pathologically changed cerebral tissue, especially in the case of severe traumata and malignant cerebral tumours. Serum and cerebrospinal fluid of 85 patients were examined. Eight of them showed positive results with antibodies (4 gliomas, 1 craniopharyngioma, 3 severe cerebral contusions with disturbance of consciousness).

We demonstrate the sonographic and computer-tomographic findings in a newborn with neonatal alloimmune thrombocytopenia (NAITP). Initial examination on the third day of life showed an extensive old and already partially resolved haematoma as well as a new perinatal haematoma in the left cerebral white matter. Follow-up investigations revealed enlargement of the cystic defect, midline-shift to the right and progressive dilatation of the right lateral ventricle caused by compression of the Foramina Monroi. Peritoneal drainage of the cyst resulted in prompt diminution of the enlarged right lateral ventricle. The case report emphasises that in patients with NAITP intracranial haemorrhage may occur in utero and during the perinatal period as well. In pregnant women suspected to produce antibodies against PLA 1 positive thrombocytes, we recommend regular ultrasonic cranial examinations of the fetus. Delivery should be as careful as possible.

This is a report of a 62-year-old male patient who had a bleeding disorder due to the presence of a factor VII (proconvertin) inhibitor. After treatment with a high-dose intravenous (IV) immunoglobulin failed and a life-threatening intracranial hemorrhage occurred, plasma exchanges were performed and immunosuppressive therapy was given. The factor VII inhibitor promptly disappeared, and the patient's parameters of hemostasis became normal. Even though a relapse occurred some months later, the patient responded to immunosuppressive therapy. No underlying disorder was evidenced after 17 months of follow-up.