Brain Hemorrhages最新文献

Cerebral amyloid angiopathy (CAA) is a cerebrovascular disease with vascular amyloid-β deposits and is commonly observed among the elderly. Often associated with Alzheimer’s disease, CAA is among the leading causes of intracerebral hemorrhage (ICH) and age-related cognitive decline. Several research studies have tried to understand the mechanisms underlying CAA, but further use of in vivo models is needed to fully understand its pathophysiology. In this review, we provide information gathered from key findings dealing with the mechanisms of beta deposition in cerebral arteries, the diagnosis of different CAA types, and advances in treatment for CAA. Since CAA is a risk factor for ICH, we also review previously used in vivo and in vitro models of CAA and their features with respect to CAA-related ICH. Currently available transgenic mouse models of CAA show a limited occurrence of hemorrhage at variable locations, which often do not produce any obvious neurological deficits. Thus, the development of novel models to more closely mimic the clinical condition of CAA-related ICH is warranted.

Delayed cerebral ischemia (DCI) is a life-threatening complication of aneurysmal subarachnoid hemorrhage (aSAH). The vasoactive P450 eicosanoids 20-hydroxyeicosatretraenoate (20-HETE) and 14,15-epoxyeicosatrenoate (14,15-EET) are associated with the development of DCI and may play opposing roles in DCI risk. We hypothesized that the ratio of these opposing eicosanoids in cerebrospinal fluid (CSF) is associated with hemorrhage severity and the risk of developing DCI after aSAH. In a preclinical model, rats received intracisternal blood injections to approximate aSAH. Hemorrhage severity, cerebral blood flow (CBF), cortical spreading depolarizations were recorded, and CSF eicosanoid levels were quantified using mass spectrometry. In a parallel clinical study, CSF samples were collected and analyzed prospectively from subjects with aSAH and outcomes were tracked. Preclinically, rats with greater hemorrhage severity had impaired CBF and lower median 14,15-EET/20-HETE ratios compared to those with lesser or no hemorrhage. In aSAH patients, the CSF 14,15-EET/20-HETE ratio was negatively correlated with hemorrhage grade on imaging. Patients who developed DCI had lower median 14,15-EET/20-HETE ratios compared to those without DCI. The CSF 14,15-EET/20-HETE ratio correlates with hemorrhage severity and may reflect a mechanistic underpinning of microvascular dysfunction that contributes to DCI. These results suggest that vasoactive eicosanoids may be a therapeutic target in aSAH.

Purpose

A prospective, observational study was done at the country leading tertiary care hospital to evaluate etiologies, clinical features, diagnosis, and prognosis of cerebral venous sinus thrombosis (CVST) in the Pakistani population.

Methods

34 patients with clinical and MRI features suggestive of CVST were evaluated. Modified Rankin Score (mRS) was assessed of all patients at presentation.

Results

The mean age of presentation was 30.69 years with female predominance (n = 28). Headache was most common presenting symptoms (97%, n = 33) followed by seizure (59%, n = 20), hemiparesis (56%; n = 19), altered sensorium (47%; n = 16), vomiting (21%; n-7) and cranial nerve involvement (18%; n = 6). 72% of patients (n = 23) had thrombosis of superior sagittal sinus, 53% of patients (n = 17) had thrombosis of the transverse sinus, 25% patients (n = 8) of patients had sigmoid sinus thrombosis, 16 % patients (n = 8) had straight sinus thrombosis. The most common cause for provoked CVST was found to be pregnancy/puerperium in 53% (n = 18 patients), followed by previous CVST/DVT in 12% (n = 4), and then OCP and parainfectious causes which were 3% (n = 1) for each and elevated factor VIII and protein deficiency were found in 7 patients. MRS between 3 and 5 was assessed in most patients on presentation (n = 23).

Conclusion

CVST is an under-recognized cause of stroke in the young population, especially in the puerperium period. Clinical presentation is highly variable, and correction with magnetic resonance imaging with venography is the current diagnostic modality of choice. Aggressive management with anticoagulants is safe with excellent clinical outcomes.

Parkinson's disease (PD) presents clinical heterogeneity in late-stage patients who show a varied responsivity to subthalamic nucleus deep brain stimulation (STN-DBS) on motor symptoms. To explore the heterogeneity of STN-DBS effect on motor symptoms in late-stage PD patients and to categorize the patients, basic characteristics, preoperative motor symptoms, and motor symptoms one month and one year after the operation of 28 late-stage PD patients were collected and analyzed with agglomerative hierarchical clustering. Preoperative motor complications, non-motor symptoms, and late-stage related manifestations were also collected and compared among the clusters. The analysis revealed three patient clusters with different motor features: 1) high response; 2) low response, and 3) moderate response with fast progression. Clinical characteristics showed significant differences in disease duration, postoperative UPDRS-III, decrease in UPDRS-III, and index of progression. Patterns of the six major motor symptoms can clearly differentiate the three clusters. Preoperative dyskinesia, memory decline, and visual hallucination were also found to differ in the three clusters. The current study identified three clusters of late-stage PD patients showing distinct responses to STN-DBS on motor symptoms. These clustering patterns may relate with diverse dopaminergic/non-dopaminergic impairments and hopefully help to categorize late-stage PD patients and to select adequate STN-DBS candidates.

Ras-related C3 botulinum toxin substrate (Rac1) is a small GTPase that monitors external signals and activates downstream cascades by transmitting information from membrane-bound receptors to exert its physiological and pathological effects. It is essential for regulating actin cytoskeleton polymerization, organization, function, and dynamics. Rac1 is a widely studied molecule, and its role in various brain disorders and diseases has been studied in rodent and vitro models. This review discusses the involvement of Rac1 in the pathophysiology of neurological diseases, its molecular pathway in different neurological diseases, and its beneficial and detrimental pathophysiological role in different cell-type and neurological disease phases.

Objective

We report a rare case of subarachnoid hemorrhage (SAH) caused by a ruptured vertebral artery (VA) dissecting aneurysm (DA) under severe COVID-19 treatment, and discuss the potential relationships.

Case presentation

A 58-year-old woman with COVID-19 fell into severe pneumonia needing mechanical ventilation at 10 days post-onset (day 10). The patient had no risk factors for DA or stroke other than COVID-19 infection. At day 17 when weaning ventilatory management, her systolic blood pressure was transiently elevated, and her consciousness did not recover thereafter. Computed tomography (CT) at day 21 revealed SAH with modified Fisher grade 4, and CT angiography revealed a DA in the right VA just distal to the right posterior inferior cerebellar artery (PICA). The DA was treated emergently with internal trapping by endovascular coiling, while the right PICA was preserved. Postoperative course was uneventful, and 2-time negative SARS-CoV-2 PCR results were obtained at day 45. The patient recovered to 4-month modified Rankin Scale 2.

Conclusions

Although it is not clear from the present case alone whether SARS-CoV-2 infection causes SAH by a ruptured VA DA, the accumulation of more cases and further studies are warranted to clarify the relationships between SARS-CoV-2 infection and ruptured intracranial DAs.

Hemorrhagic transformation is a common complication of acute cerebral infarction, and rtPA thrombolytic therapy will increase the risk of hemorrhagic transformation. Cerebral microbleeds (CMBs) have become an important and independent predictor of cerebral hemorrhage. However, it is still controversial whether CMBs increase the risk of intracranial hemorrhage (ICH) and poor prognosis (PFO) after intravenous thrombolysis (IVT) in patients with acute ischemic stroke (AIS).This review summarizes a number of studies on microbleeds in clinical patients, and discusses whether the presence, number, and distribution of CMBs are related to ICH and PFO after IVT in AIS patients, as well as the significance of CMBs in IVT decision-making in AIS.