Multiple Microhemorrhages Research Articles

SWAN MRI revealing multiple microhemorrhages secondary to septic emboli from mucormycosis

A 77-year-old man with myelodysplastic syndrome presented with fever and acute renal failure, followed by right-sided hemiparesis, neglect, and aphasia. Neuroimaging revealed a left parietal-occipital ICH with extensive edema. T2-star susceptibility weighted angiography (SWAN) revealed multiple

Microhemorrhages in the Brains of Mountaineers who Survived High Altitude Cerebral Edema (HACE)

Ziele: Brain MRI during high altitude illness is not easy. Usually no scanner is around during the illness. Post-mortem exams showed multiple micro-hemorrhages (MH) in brains of HACE victims. We hypothesized MH may also occur in non-lethal HACE and deposits of hemosiderin indicative of previous MH can be found in HACE survivors. Methode: We performed brain MRI in 36 mountaineers: HACE survivors (n=10), subjects who had suffered from severe acute mountain sickness (AMS, n=11), subjects who had had high altitude pulmonary edema (HAPE, n=8) and mountaineers with repeated high altitude exposure (>7000m without additional oxygen), but without HACE (n=7). MR protocol included susceptibility-weighted imaging, which is very sensitive in detection of previous MH. Ergebnis: MH were almost exclusively found in the group of HACE survivors. Distribution: most MH were found in the corpus callosum, especially the splenium. In severe HACE MH were also found in cerebral hemispheres. MH were detectable years after HACE. Schlussfolgerung: Cerebral Microhemorrhages were found almost exclusively and consistently in the brains of HACE surviors. They are found predominantly in the Corpus callosum and are detectable years after HACE. This diagnostic sign has not been previously described and may become an important conerstone in the diagnosis of high altitude cerebral edema (HACE).

Longitudinal brain imaging of five malignant glioma patients treated with bevacizumab using susceptibility-weighted magnetic resonance imaging at 7 T

Malignant glioma is a rare tumor type characterized by prominent vascular proliferation. Antiangiogenic therapy with the monoclonal antibody bevacizumab is considered as a promising therapeutic strategy, although the effect on tumor vascularization is unclear. High-field susceptibility-weighted imaging (SWI) visualizes the microvasculature and may contribute to the investigation of antiangiogenic therapy responses in gliomas. We prospectively studied five adult malignant glioma patients treated with bevacizumab-containing regimens. In each patient, we performed three 7-T SWI and T1-weighted imaging investigations (baseline and 2 and 4 weeks after the start of bevacizumab treatment). In addition, we imaged a postmortem brain of a patient with glioblastoma using 7-T SWI and performed detailed histopathological analysis. We observed almost total resolution of brain edema in three of five patients after initiation of bevacizumab therapy. In one case with rapid increase of the lesion size despite bevacizumab therapy, SWI showed progressive increase of irregular hypointense structures, most likely corresponding to increasing amounts of pathological microvasculature. In one case with progressive neurological decline, 7-T images showed multiple intratumoral microhemorrhages after the first bevacizumab application. Correlation of postmortem neuroimaging with histopathology confirmed that SWI-positive structures correspond to tumor vasculature. The experience from our case series indicates that longitudinal 7-T SWI seems to be an appropriate method for investigation of changes in brain tumor vascularization over time under antiangiogenic therapy.

T cell mediated cerebral hemorrhages and microhemorrhages during passive Aβ immunization in APPPS1 transgenic mice

BackgroundImmunization against amyloid-β (Aβ), the peptide that accumulates in the form of senile plaques and in the cerebrovasculature in Alzheimer's disease (AD), causes a dramatic immune response that prevents plaque formation and clears accumulated Aβ in transgenic mice. In a clinical trial of Aβ immunization, some patients developed meningoencephalitis and hemorrhages. Neuropathological investigations of patients who died after the trial showed clearance of amyloid pathology, but also a powerful immune response involving activated T cells probably underlying the negative effects of the immunization.ResultsTo define the impact of T cells on this inflammatory response we used passive immunization and adoptive transfer to separate the effect of IgG and T cell mediated effects on microhemorrhage in APPPS1 transgenic mice. Neither anti Aβ IgG nor adoptively transferred T cells, alone, led to increased cerebrovascular damage. However, the combination of adoptively transferred T cells and passive immunization led to massive cerebrovascular bleeding that ranged from multiple microhemorrhages in the parenchyma to large hematomas.ConclusionsOur results indicate that vaccination can lead to Aβ and T cell induced cerebral micro-hemorrhages and acute hematomas, which are greatly exacerbated by T cell mediated activity.

Cortical petechial hemorrhage, subarachnoid hemorrhage and corticosteroid-responsive leukoencephalopathy in a patient with cerebral amyloid angiopathy

We describe a 69-year-old woman who developed subacute onset cognitive decline after hitting the left side of her head. Cerebral spinal fluid showed yellowish discoloration with highly elevated protein content. FLAIR MRI revealed diffuse high signal intensity in all cortical sulci, and leptomeningeal enhancement in the left cerebral hemisphere was seen in the T1 image after contrast administration. She was treated with a corticosteroid. Consciousness disturbance was temporarily relieved but again worsened, resulting in an apathetic state due to communicating hydrocephalus. A shunt tube was placed in her right lateral ventricle. A brain biopsy disclosed multiple cortical microbleeds and heavy deposition of Aβ-immuoreactive amyloid on vascular walls. Inflammatory mononuclear cells surrounded a few leptomeningeal vessels. After the operation her condition further deteriorated and she fell into a coma. MRI showed diffuse swelling of the right cerebral white matter. She again received high-dose corticosteroid and gradually recovered during the following 2 months. On MRI the vast majority of abnormal signals in the right cerebral white matter disappeared. An initial manifestation of this patient was possibly caused by multiple microhemorrhages from fragile cortical and subarachnoid vessels with Aβ-amyloid deposition, which was triggered by head trauma. CAA-related inflammation possibly worsened this condition. Additionally, surgical intervention for communicating hydrocephalus might have induced cerebral amyloid angiopathy (CAA)-related leukoencephalopathy in her right cerebral hemisphere. These CAA-derived manifestations are unusual and high-dose corticosteroids seems to be useful for vascular events in CAA patients.

Report of an angiosarcoma mimic: cutaneous aneurysmal fibrous histiocytoma

Aneurysmal fibrous histiocytoma is an unusual variant of the spectrum of fibrous histiocytomas with the peculiar morphologic appearance of a benign aneurysmal vasoformative process that ultimately culminates in multiple microhemorrhages within the tumor. It looks strikingly different from the usual cutaneous lesions encountered in clinical dermatology practice. A single report of a cutaneous aneurysmal fibrous histiocytoma in the skin of the back of a 60-year-old male is described with emphasis on the immunostaining pattern and review of the literature. There is a significant potential for confusion of this lesion with other cutaneous lesions, clinically as well as pathologically. In our case, the patient presented with a lesion that clinically resembled a hemangioma, was pathologically interpreted initially to be an angiosarcoma, and finally, the revised pathology was interpreted as an aneurysmal variant of a fibrous histiocytoma. Caution is warranted to avoid misinterpretation of cutaneous fibrohistiocytic tumors.

The Prevalence of Microhemorrhage on Gradient-echo Magnetic Resonance Imaging in Acute Lacunar Infarction

Microhemorrhages seen on gradient-echo magnetic resonance imaging are thought to be a manifestation of small-vessel disease. It was the aim of our study to evaluate the prevalence of microhemorrhage for patients presenting with acute lacunar infarction. We obtained gradient-echo and diffusion-weighted magnetic resonance imaging as part of the acute stroke workup in 46 patients presenting with lacunar infarction. Gradient-echo magnetic resonance imaging was abnormal in 24 of 46 (52%) patients. Microhemorrhage was seen in 21 patients (46%), 2 patients had multiple microhemorrhages and a frank hemorrhage, and 3 patients had frank hemorrhage in the absence of microhemorrhage. Prior symptomatic stroke was the only significant risk factor for the presence of microhemorrhages. Microhemorrhages are present in approximately half of patients with lacunar infarcts and appear to be a marker of severity of small-vessel disease.

Alzheimer disease and cerebrovascular pathology: an update.

Recent epidemiological and clinico-pathologic data suggest overlaps between Alzheimer disease (AD) and cerebrovascular lesions that may magnify the effect of mild AD pathology and promote progression of cognitive decline or even may precede neuronal damage and dementia. Vascular pathology in the aging brain and in AD includes: 1. cerebral amyloid angiopathy (CAA) with an incidence of 82-98% often associated with ApoE epsilon 2 and causing a) cerebral mass hemorrhages (around 70%, mainly in the frontal and parietal lobes), b) multiple or recurrent microhemorrhages (15%), and c) ischemic (micro-)infarcts or lacunes (around 20%). The frequency of these lesions increases with the severity of CAA and shows no correlation with that of senile amyloid plaques. CAA, significantly more frequent in patients with cerebral hemorrhages or infarcts than in aged controls, is an important risk factor for cerebrovascular lesions in AD. 2. Microvascular changes with decreased density and structural abnormalities causing regional metabolic and blood-brain barrier dysfunctions with ensuing neuronal damage. In large autopsy series of demented aged subjects, around 80% show Alzheimer type pathology, 20-40% with additional, often minor vascular lesions, 7-10% "pure" vascular dementia, and 3-5% "mixed" dementia (combination of AD and vascular encephalopathy). AD cases with additional minor cerebrovascular lesions have significantly more frequent histories of hypertension or infarcts than "pure" AD patients. Vascular lesions in AD include cortical microinfarcts, subcortical lacunes, white matter lesions / leukoencephalopathy, small hemorrhages and corticosubcortical infarcts, while in mixed type dementia multiple larger or hemispheral infarcts are more frequent. Small infarcts in AD patients have no essential impact on global cognitive decline which mainly depends on the severity of Alzheimer pathology, but in early stage of AD they may influence and promote the development of dementia. Recent studies showed lower density of plaques and tangles in brains with cerebrovascular lesions, and similar severity of dementia was related to fewer AD lesions in brains with than in those without small vascular lesions. Further studies will help to elucidate the risk factors and impact of cerebrovascular lesions on the development and progression of dementia in AD.