Cerebral Artery Thrombosis Research Articles

Ischemic Brain Injury After Intracerebral Hemorrhage

Intracerebral hemorrhage (ICH) is the second most common cause of stroke and accounts for 8% to 15% of strokes in Western societies with an estimated incidence of 10 to 25 per 100 000 persons.1–3 Despite advances in the field of stroke and neurocritical care,4 the 30-day mortality has not changed significantly over the past 20 years.3 Indeed, ICH has the highest rates of dependence or death among stroke types and proven treatments are lacking. Clinical trials aimed at limiting hemorrhage growth, procoagulant agents for hemostasis,5 and surgical evacuation6 have not translated into improved clinical outcomes. Antihypertensive therapy for the purpose of reducing hematoma growth has been a mainstay of acute management. Guidelines recommend maintaining mean arterial pressure <130 mm Hg during the acute phase7; however, controversies exist given the lack of randomized clinical trial data and uncertainties about the rapidity and target level of blood pressure (BP)-lowering. Recent Phase 2 clinical trials evaluating acute BP control have shown promise in reducing hematoma expansion with an adequate safety profile and Phase 3 trials are underway.8,9 Besides hematoma growth, other pathophysiological processes occur in the setting of ICH and may serve as potential therapeutic targets. In the acute period after ICH, a rapid rise in intracranial pressure (ICP) from an expanding hematoma may reduce cerebral perfusion pressure. In this setting, interventions aimed at BP-lowering and hemostasis may theoretically induce thrombosis or exacerbate brain ischemia, particularly in patients with pre-existing cerebrovascular disease. A recent publication suggests that aggressive BP-lowering may actually cause acute brain ischemia and worsen outcomes after ICH.10 In this review, we outline the data on secondary acute ischemic injury after ICH, review the prevalence of remote ischemic lesions and risk factors associated with their occurrence, explore potential …

The kunitz protease inhibitor domain of protease nexin-2 inhibits factor XIa and murine carotid artery and middle cerebral artery thrombosis

AbstractCoagulation factor XI (FXI) plays an important part in both venous and arterial thrombosis, rendering FXIa a potential target for the development of antithrombotic therapy. The kunitz protease inhibitor (KPI) domain of protease nexin-2 (PN2) is a potent, highly specific inhibitor of FXIa, suggesting its possible role in the inhibition of FXI-dependent thrombosis in vivo. Therefore, we examined the effect of PN2KPI on thrombosis in the murine carotid artery and the middle cerebral artery. Intravenous administration of PN2KPI prolonged the clotting time of both human and murine plasma, and PN2KPI inhibited FXIa activity in both human and murine plasma in vitro. The intravenous administration of PN2KPI into WT mice dramatically decreased the progress of FeCl3-induced thrombus formation in the carotid artery. After a similar initial rate of thrombus formation with and without PN2KPI treatment, the propagation of thrombus formation after 10 minutes and the amount of thrombus formed were significantly decreased in mice treated with PN2KPI injection compared with untreated mice. In the middle cerebral artery occlusion model, the volume and fraction of ischemic brain tissue were significantly decreased in PN2KPI-treated compared with untreated mice. Thus, inhibition of FXIa by PN2KPI is a promising approach to antithrombotic therapy.

Cerebral Venous Sinus Thrombosis: Association with Primary Varicella Zoster Virus Infection

Varicella zoster virus (VZV) has been known to cause cerebral arterial vasculopathy and an acquired antibody-mediated coagulopathy associated with purpura fulminans and generalized thromboembolism. There are no published reports of cerebral venous sinus thrombosis (CVST) associated with primary VZV infection. We report 2 cases that highlight an unusual presentation of VZV infection: CVST with primary varicella infection. One patient had extensive CVST with coexistent middle cerebral artery involvement. Primary VZV infection can be associated with thrombosis of cerebral arteries and venous sinuses.

Recurrent thrombosis in an HIV-1 infected child

Though thromboembolic complications in HIV infected patients have been described in literature, recurrent thrombosis is very rare. We present a six-year-old HIV infected boy who presented with recurrent thrombosis. He initially had renal artery thrombosis, then middle cerebral artery thrombosis and finally hepatic vein thrombosis that was fatal.

Visual Anosognosia (Anton-Babinski Syndrome): Report of Two Cases Associated with Ischemic Cerebrovascular Disease

Visual anosognosia or Anton-Babinski syndrome is a rare neurological condition related to cortical blindness. The patients deny their blindness and affirm adamantly that they are capable of seeing. The clinical presentation includes confabulations and sometimes confusional states. In this article we report two patients with anosognosia related to ischemic stroke in two different sets of etiology and pathogenesis. We describe the major clinical manifestations of this syndrome and review the current medical literature. Two patients were identified, a 96-year-old male with visual anosognosia secondary to a right posterior cerebral artery thrombosis, and a 56-year-old female with the same syndrome but related to central nervous system angiitis in relation with multiple sclerosis and Hashimoto’s thyroiditis. Visual anosognosia or Anton-Babinski syndrome is a rare neurological condition, however the ischemic vascular cerebral disease is a frequent etiology. We believe that this is the first report of this syndrome in relation to angiitis with a clear autoimmune pathogenesis.

Study on epidemiological characteristics and risk factors of stroke among adult residents in the urban areas of Tianjin

ObjectiveTo investigate the epidemiological characteristics and risk factors of stroke among adult residents in the urban areas of Tianjin, and provide references for directive population intervention.MethodsA total of 28 515...

Clinical application of different cerebral protection devices in Carotid angioplasty and stenting in 1148 patients with carotid stenosis

ObjectiveTo investigate the efficacy and safety of Carotid angioplasty and stenting (CAS) by different cerebral protection devices in 1148 patients with carotid stenosis.MethodsCarotid angioplasty and stenting by different cerebral protection...

Middle cerebral artery thrombosis after IVF and ovarian hyperstimulation: a case report

To report a rare case of left middle cerebral artery thrombosis in a patient after controlled ovarian hyperstimulation and IVF. Case report. University-affiliated teaching hospital. A 30-year-old woman who had undergone invitro fertilization and subsequently developed left middle cerebral artery thrombosis. Ovulation induction with gonadotropins, IVF-ET, sodium ozagrel injection, and mannitol and albumin administration. Outcome of treatment. The patient survived with some neurologic sequelae. Prevention of ovarian hyperstimulation syndrome is key to reducing incidence of thrombosis. Be aware of any neurologic symptoms after IVF-ET. Immediate and correct therapy should be given after thrombosis is suspected.

Traumatic Cerebral Infarction - Basketball

HISTORY: A 19 year old white male was struck by an elbow in his left neck during a basketball game. He was knocked to the ground but did not lose consciousness or sustain head trauma. He did, however, immediately develop right-sided hemiparesis and dysarthria. His symptoms improved after a short period of time and he went home. The next day the patient still had difficulty speaking and noticed right-sided visual loss. He was taken to the hospital where MRI/MRA of his brain was negative for carotid dissection but did show a left occipital lobe infarct. Subsequent CT angiogram revealed a sub-acute occlusive thrombus in the left posterior communicating artery. The patient was started on intravenous heparin and transferred to a tertiary care center where he was medically stabilized and underwent additional diagnostic testing that confirmed the thrombus and cerebral infarction. PHYSICAL EXAMINATION: His PHYSICAL EXAMINATION was significant for left hemiparesis and ataxia and right homonymous hemianopsia with moderate expressive aphasia, dysarthria and parasphasic errors. He also displayed significant cognitive deficits. DIFFERENTIAL DIAGNOSIS: 1. Vertebral Artery Dissection 2. Cerebral Vascular Accident 3. Epidural Hematoma 4. Traumatic Brain Injury TEST AND RESULTS: VIR arteriography: Slight dilation of the left internal carotid artery without clearly demonstrated dissection. Complete occlusion of the left posterior cerebral artery without partial filling around a clot. Occlusion is complete and posterior cerebral artery was likely fetal, filling from the internal carotid artery. MR angiography neck: Subtle contour abnormality of the left internal carotid artery but no findings to suggest acute dissection. CT head/brain without contrast: Small infarction in the left occipital lobe. FINAL WORKING DIAGNOSIS: Traumatic left posterior cerebral artery thrombosis with occipital lobe infarction. TREATMENT AND OUTCOMES: The patient was treated with intravenous heparin therapy and gradually showed improvement with functional restoration measures including multi-disciplinary therapy and rehabilitation. More rapid recognition of the possibility of this condition in the field of play could lead to potentially improved neurologic outcomes with thrombolytic therapy.

Phospholipid inhibitors

The antiphospholipid syndrome (APS) is defined by the association of arterial and/or venous thrombosis and/or pregnancy complications with the presence of at least one among the main antiphospholipid antibodies (aPL) (i. e., Lupus anticoagulants, LA, IgG and/or IgM anticardiolipin antibodies, aCL, IgG and/or IgM antiβ2-glycoprotein I antibodies, aβ2-GPI). Several clinical studies have consistently reported that LA is a stronger risk factor for both arterial and venous thrombosis compared to aCL and aβ2-GPI. In particular, LA activity dependent on the first domain of β2-GPI and triple aPL positivity are associated with the risk of thrombosis and obstetrical complications. Asymptomatic aPL-positive subjects do not require primary thromboprophylaxis. Venous thromboembolism is the most common initial clinical manifestation of APS. To prevent its recurrence indefinite anticoagulation is recommended. Long duration treatment with warfarin or aspirin is used after a first cerebral arterial thrombosis. Low molecular weight heparin (LMWH) with or without aspirin is recommended to reduce the rate of obstetrical complications of APS pregnant women.

Cerebrovascular Complications in Patients with Cancer

Stroke in the cancer patient is often caused by disorders of coagulation that are induced by the cancer, by cancer metastatic to the central nervous system, or by coagulation disorders or vascular injury due to cancer therapy. Nonbacterial thrombotic endocarditis in association with diffuse thrombosis of cerebral vessels is often the cause of cerebral infarction. Venous occlusion is most common in leukemic patients, but can also result from growth of solid tumor in the adjacent skull or dura. Chemotherapy administration is associated with a small risk of cerebral arterial or venous thrombosis. Radiation that is administered to the neck can result in delayed carotid atherosclerosis. Tumor embolization to the brain is a rare cause of stroke. Fungal septic cerebral emboli occur most commonly in leukemic patients who have undergone bone marrow transplantation. Hemorrhages occur in the brain parenchyma or the subdural and subarachnoid spaces and are most commonly caused by acute disseminated intravascular coagulation or metastatic tumor. Hemolysis from chemotherapy administration is a rare cause of brain hemorrhage. Careful clinical assessment, neuroimaging studies, measurement of coagulation function, and echocardiography are the most useful modalities to identify the cause of stroke.

Changes in serum ghrelin and small intestinal motility in rats with cerebral arterial thrombosis

Changes in serum ghrelin and small intestinal motility in rats with cerebral arterial thrombosis

Infarctus cérébral et myocardique après consommation de cannabis chez une femme jeune

Cannabis is the most consumed drug in the world particularly in young adults. Few reports have suggested a causal role of cannabis in the development of cerebral or cardiovascular events. We describe the first association of myocardial infarction and stroke after heavy cannabis consumption in a 45-year-old woman. Stroke occurred in relation with a right carotid and middle cerebral artery thrombosis after cannabis abuse. The patient was successfully treated with intravenous rt-PA. Two days after her admission, she presented a myocardial infarction due to a coronary thrombosis. Cerebral and coronary arteries were angiographically normal. Etiological tests were negative and a toxic cause in relation with cannabis consumption was concluded. Cannabis can be associated with vascular events by different mechanisms. Thrombosis may occur in cerebral and/or coronary arteries. We suggest that it might be useful to search for cannabis consumption systematically in young subjects victims of stroke and myocardial infarction.

Effect and nursing main points of Fluvastatin on patients with cerebral arterial thrombosis

Objective To explore the effect and nursing main points of fluvastatin on the patients with cerebral arterial thrombosis. Methods Eighty-five patients with cerebral arterial thrombosis were randomly divided into three groups. Group Ⅰ was the negative control group. Group Ⅱ was the conventional-dose therapy group and group Ⅲ was the high-dose therapy group. Each group was treated with related therapy and care. The blood lipids in all groups were tested before the treatment, 4 weeks, 12 weeks and 24 weeks after the treatment; the carotid intima-media thickness (IMT) were measured by the Germany SEQUOIAS-512-B ultra machine before the treatment and 24 weeks after the treatment; At the same time, the side effects of fluvastatin were recorded. Results The results of blood lipid tests showed that the LDL, TC and TG in two treated groups were significantly decreased compared to negative control group (P 0.05). Conclusion The effects of different doses of fluvastatin on cerebral arterial thrombosis were significantly different. With the dose of fluvastatin increased, the serum LDL-L and TC reduced more obvious and the inhibition on carotid atherosclerosis shows more obvious, and the side effects did not increased. Key words: Fluvastatin; Cerebral arterial thrombosis; Effect; Nursing

Stroke due to septic embolism resulting from Aspergillus aortitis in an immunocompetent patient

IntroductionCerebral infarction secondary to Aspergillus arteritis or septic embolism is an exceptional finding. We present a case of multiple systemic embolism and cerebral infarction resulting from Aspergillus aortitis in an immunocompetent patient. PatientA 65-year-old male with hypertension, hyperglycaemia and myocardial infarction with aorto-coronary by-pass surgery three years before admission, that suffered cerebral infarction in middle right cerebral artery territory and right cubital artery embolism. One month later he presented abrupt increase of his left hemiparesia and left central facial palsy associated with fever of unknown origin. Laboratory test, cranial CT and echocardiogram were performed. He died ten days later. ResultsHemogram: leucocytes 34.700/μL (85% N, 4.8%L). Cranial CT: cerebral infarction in middle right cerebral artery territory. Transthoracic and transesophageal echocardiogram: moderate left ventricular hypertrophy and slight inferior hypokinesis. Arteriography: complete thrombosis of the left internal carotid. Necropsy: parietal aortic aspergillosis with generalized septic embolisms (brain, kidney, liver, fingers), cerebral infarction in middle right cerebral artery territory and thrombosis of the left carotid siphon with Aspergillus arteritis. ConclusionsAspergillosis is an exceptional cause of cerebral infarction, especially in immunocompetent patients, and their diagnosis is complicated, being usually found at necropsy.

Effects of prasugrel, a novel P2Y 12 inhibitor, in rat models of cerebral and peripheral artery occlusive diseases

Prasugrel is an orally available thienopyridyl prodrug with more potent in vivo antiplatelet effects compared to clopidogrel. In the present study, we examined the effects of prasugrel in rat models of cerebral and peripheral arterial occlusive diseases. Cerebral arterial thrombosis was induced by photochemical irradiation of the middle cerebral artery. Prasugrel (3 and 10 mg/kg) dose-relatedly and significantly reduced thrombus-mediated cerebral infarction 24 h after the irradiation. The effect of prasugrel was further examined in an embolic infarction model. Four h after an oral administration of prasugrel, non-occlusive thrombus formation in the right common carotid artery was initiated. In this model, prasugrel (0.3—3 mg/kg) reduced incidence, total area, and total number of cerebral infarcts in a dose-related manner 24 h after the vascular injury. Clopidogrel (10 or 30 mg/kg) was less potent than prasugrel at the doses tested on these thrombotic and embolic infarctions. Finally, the effect of prasugrel on lauric acid-induced peripheral arterial occlusive diseases was evaluated. After injection of lauric acid into the femoral artery, the lesions were scored for the following 10 days as they gradually progressed from the toe throughout the leg. Prasugrel (0.03–3 mg/kg/day) administered from the day before the lauric acid injection for 11 successive days inhibited the progression of the disease in a dose-related manner. Clopidogrel (3–30 mg/kg/day) showed similar effect but its effect was less potent than prasugrel. These results suggest that prasugrel could be a useful drug for preventing thromboembolic diseases including cerebral infarction and peripheral arterial occlusive diseases.

Liposome‐Encapsulated Hemoglobin Reduces the Size of Cerebral Infarction in Rats: Effect of Oxygen Affinity

Liposome-encapsulated hemoglobin (LEH) with a low oxygen affinity (l-LEH, P(50) = 45 mm Hg) was found to be protective in the rodent and primate models of ischemic stroke. This study investigated the role of LEH with a high O(2) affinity (h-LEH, P(50) = 10 mm Hg) in its protective effect on brain ischemia. The extent of cerebral infarction was determined 24 h after photochemically induced thrombosis of the middle cerebral artery from the integrated area of infarction detected by triphenyltetrazolium chloride staining in rats receiving various doses of h-LEH as well as l-LEH. Both h-LEH and l-LEH significantly reduced the extent of cortical infarction. h-LEH remained protective at a lower concentration (minimal effective dose [MED]: 0.08 mL/kg) than l-LEH (MED: 2 mL/kg) in the cortex. h-LEH reduced the infarction extent in basal ganglia as well (MED: 0.4 mL/kg), whereas l-LEH provided no significant protection. h-LEH provided better protection than l-LEH. The protective effect of both high- and low-affinity LEH may suggest the importance of its small particle size (230 nm) as compared to red blood cells. The superiority of h-LEH over l-LEH supports an optimal O(2) delivery to the ischemic penumbra as the mechanism of action in protecting against brain ischemia and reperfusion.

S‐Nitrosylated Pegylated Hemoglobin Reduces the Size of Cerebral Infarction in Rats

Cell-free hemoglobin-based oxygen carriers have well-documented safety and efficacy problems such as nitric oxide (NO) scavenging and extravasation that preclude clinical use. To counteract these effects, we developed S-nitrosylated pegylated hemoglobin (SNO-PEG-Hb, P(50) = 12 mm Hg) and tested it in a brain ischemia and reperfusion model. Neurological function and extent of cerebral infarction was determined 24 h after photochemically induced thrombosis of the middle cerebral artery in the rat. Infarction extent was determined from the integrated area in the cortex and basal ganglia detected by triphenyltetrazolium chloride staining in rats receiving various doses of SNO-PEG-Hb (2, 0.4, and 0.08 mL/kg) and compared with rats receiving pegylated hemoglobin without S-nitrosylation (PEG-Hb) or saline of the same dosage. Results indicated that successive dilution revealed SNO-PEG-Hb but not PEG-Hb to be effective in reducing the size of cortical infarction but not neurological function at a dose of 0.4 mL/kg. In conclusion, SNO-PEG-Hb in a dose of 0.4 mL/kg (Hb 24 mg/kg) showed to be most effective in reducing the size of cortical infarction, however, without functional improvement.

Extensive cerebral arteries thrombosis.

Cerebral artery thrombosis is one of the major causes of death. It is usually not clear what kind of pathologic processes participate in this pathological entity. We report a case of a 47-year old female patient with recurrent episodes of cerebral arterial thrombosis, without permanent neurological deficits and history of heavy smoking, hypertension, hypothyroidism, hypercholesterolemia, metabolic syndrome and insulin resistant postprandial hyperglycemia. Brain magnetic resonance angiography (MRA) revealed total thrombosis of the left internal carotid artery (ICA) and partial thrombosis of the right ICA. Although, the extent of the cerebral arteries thrombosis due to the coexistence of many risk factors, the clinical symptoms are mild, because of the sufficient blood supply from the vertebrobasilar system and the efficient collateral circulation.

Vaskulitis als Ursache von Kopfschmerzen

A 13-year-old girl presented to our emergency with a one week history of fever and skin rash and new onset of chorea for the last three days. There was a long standing history of right predominant headache; followed by personality change, fatigue, arthralgia and weight loss over the last few months. Previous investigations by head CT and ophthalmological examination did not explain the symptoms. Further investigations revealed peri- and pancarditis with aortic insufficiency, a renal involvement with elevated creatinin, protein- and hematuria and a hemolytic anemia. Diagnosis of lupus eythematodes was confirmed by high ANA, anti-dsDNS and Anticardiolipin antibodies. Within the first 48 hours after admission there was significant deterioration with reduced vigilance and dysarthria. MRI of the brain and dopplersonography of cerebral vessels showed a complete thrombosis of the right medial cerebral artery with a small net of collaterals, irregularities of the left cerebral artery due to vasculitis and several subacute leftsided ischemias. Immunosuppressive therapy with high-dose corticosteroids and cyclophosphamid together with antithrombotic therapy induced an improvement of neurologic, renal and cardiac function.