“…Besides, other pathologies have been described as independently associated with CMB, some of them of special relevance in the older population as traumatic brain injury 25 and obstructive sleep apnea, 26 which prevalence increases with aging. Finally, other studies also reported CMB associated with cocaine abuse, brain radiotherapy, infectious endocarditis, thrombotic thrombocytopenic purpura and posterior reversible encephalopathy syndrome 27 …”
Objectives
To determine the prevalence, localization and associations of cerebral microbleeds (CMB) in dementia with Lewy bodies (DLB) with its core clinical symptoms and cerebrospinal fluid (CSF) biomarkers of Alzheimer's disease (AD). We hypothesize DLB patients with CMB have increased amyloid burden compared to those without CMB, which could also translate into clinical differences.
Methods
Retrospective cross‐sectional analysis from the AlphaLewyMA study (https://clinicaltrials.gov/ct2/show/NCT01876459). Patients underwent a standardized protocol of brain MRI including 3D T1, 3D FLAIR and T2* sequences, and CSF analysis of AD biomarkers. CMB and white matter hyperintensities (WMHs) were visually assessed in prodromal and mild demented (DLB, N = 91) and AD (AD, N = 67) patients.
Results
CMB prevalence did not differ among DLB and AD (24.2% vs. 37.3%; p = 0.081). CMB were mainly distributed in lobar topographies in both DLB (74%) and AD (89%). CMB in DLB was not associated with global cognitive performance, executive functioning, speed of information processing, or AD CSF biomarkers. Similarly, there was no difference regarding specific clinical symptoms: fluctuations, psychotic phenomena, sleep behavior disorder and Parkinsonism between DLB patients with and without CMB. AD patients with CMB had increased burden of WMH compared to those without (2.1 ± 0.86 vs. 1.4 ± 0.89; p = 0.005), according to Fazekas scale, whereas no significant difference was observed in DLB patients (1.68 ± 0.95 vs. 1.42 ± 0.91; p = 0.25).
Conclusion
CMB were equally prevalent with similar topographic distribution in both DLB and AD patients. CMB was not associated with CSF AD biomarkers or core clinical symptoms in DLB.
“…Besides, other pathologies have been described as independently associated with CMB, some of them of special relevance in the older population as traumatic brain injury 25 and obstructive sleep apnea, 26 which prevalence increases with aging. Finally, other studies also reported CMB associated with cocaine abuse, brain radiotherapy, infectious endocarditis, thrombotic thrombocytopenic purpura and posterior reversible encephalopathy syndrome 27 …”
Objectives
To determine the prevalence, localization and associations of cerebral microbleeds (CMB) in dementia with Lewy bodies (DLB) with its core clinical symptoms and cerebrospinal fluid (CSF) biomarkers of Alzheimer's disease (AD). We hypothesize DLB patients with CMB have increased amyloid burden compared to those without CMB, which could also translate into clinical differences.
Methods
Retrospective cross‐sectional analysis from the AlphaLewyMA study (https://clinicaltrials.gov/ct2/show/NCT01876459). Patients underwent a standardized protocol of brain MRI including 3D T1, 3D FLAIR and T2* sequences, and CSF analysis of AD biomarkers. CMB and white matter hyperintensities (WMHs) were visually assessed in prodromal and mild demented (DLB, N = 91) and AD (AD, N = 67) patients.
Results
CMB prevalence did not differ among DLB and AD (24.2% vs. 37.3%; p = 0.081). CMB were mainly distributed in lobar topographies in both DLB (74%) and AD (89%). CMB in DLB was not associated with global cognitive performance, executive functioning, speed of information processing, or AD CSF biomarkers. Similarly, there was no difference regarding specific clinical symptoms: fluctuations, psychotic phenomena, sleep behavior disorder and Parkinsonism between DLB patients with and without CMB. AD patients with CMB had increased burden of WMH compared to those without (2.1 ± 0.86 vs. 1.4 ± 0.89; p = 0.005), according to Fazekas scale, whereas no significant difference was observed in DLB patients (1.68 ± 0.95 vs. 1.42 ± 0.91; p = 0.25).
Conclusion
CMB were equally prevalent with similar topographic distribution in both DLB and AD patients. CMB was not associated with CSF AD biomarkers or core clinical symptoms in DLB.
“…This suggests that individuals that are more susceptible to vasculature impairments, such as patients affected by genetic blood disorders like sickle cell or thalassemia, could present higher risk of cerebral microbleeds. Those microhemorrhages could contribute to neurological conditions that these subjects might suffer from [69]. In fact, this is supported by a study with children affected by hemoglobinopathies [70], and developing a reversible neurological complication, known as leukoencephalopathy syndrome, upon blood transfusion [71].…”
Section: The Cytotoxicity Of Iron In the Brainmentioning
Iron is a critical element for most organisms, which plays a fundamental role in the great majority of physiological processes. So much so, that disruption of iron homeostasis has severe multi-organ impacts with the brain being particularly sensitive to such modifications. More specifically, disruption of iron homeostasis in the brain can affect neurophysiological mechanisms, cognition, and social behavior, which eventually contributes to the development of a diverse set of neuro-pathologies. This article starts by exploring the mechanisms of iron action in the brain and follows with a discussion on cognitive and behavioral implications of iron deficiency and overload and how these are framed by the social context. Subsequently, we scrutinize the implications of the disruption of iron homeostasis for the onset and progression of psychosocial disorders. Lastly, we discuss the links between biological, psychological, and social dimensions and outline potential avenues of research. The study of these interactions could ultimately contribute to a broader understanding of how individuals think and act under physiological and pathophysiological conditions.
Patients with hematological diseases often experience cerebrovascular complications including ischemic stroke, intracerebral and subarachnoid hemorrhage, microbleeds, posterior reversible encephalopathy syndrome, and dural sinus and cerebral vein thrombosis (CVT). In this update, we will review recent advances in the management of cerebrovascular diseases in the context of myeloproliferative neoplasms, leukemias, lymphomas, multiple myeloma, POEMS, paroxysmal nocturnal hemoglobinuria (PNH), thrombotic thrombocytopenic purpura (TTP), and sickle-cell disease. In acute ischemic stroke associated with hematological diseases, thrombectomy can in general be applied if there is a large vessel occlusion. Intravenous thrombolysis can be used in myeloproliferative neoplasms and sickle-cell anemia, but in other diseases, a case-by-case evaluation of the bleeding risks is mandatory. Patients with sickle-cell disease and acute stroke need very often to be transfused. In PNH, acute ischemic stroke patients must be anticoagulated. Most patients with CVT can be treated with low-molecular weight heparin (LMWH) acutely, even those with leukemias. Prevention of recurrence of cerebral thrombotic events depends on the control of the underlying disease, combined in some conditions with antithrombotic drugs. The recent introduction of specific monoclonal antibodies in the treatment of PHN and TTP has dramatically reduced the risk of arterial and venous thrombosis.
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