Hemorragia encefálica por angiopatía amiloidea / Amyloid angiopathy brain hemorrhage

Amyloid angiopathy (AA) is a selective deposition of amyloid in the walls of the brain vessels. It is a form of sporadic and localized amyloidosis, constituted by the Aβ4 protein, the same of Alzheimer's disease senile plaques. The most consistent clinical effect of AA is spontaneous brain hemorrhage (BH). It is the second most common cause of BH after arterial hypertension (HT). Other clinical manifestations are cognitive impairment and transient focal neurological episodes. AA BH is characteristically localized in the cerebral cortex and subcortical white matter (lobar hemorrhage), consistent with the preferential deposit of amyloid in the walls of leptomeningeal and intracortical small cerebral vessels. Other types of AA hemorrhagic complications are microbleeds (MB), cerebral convexity subarachnoid hemorrhage (cSAH) and superficial hemosiderosis (cSS). The diagnosis of AA BH is based on the Boston criteria. Using these criteria, several non-hemorrhagic biomarkers of AA have been identified that can be useful in its diagnosis. The principal AA BH risk factor is age, followed by cSS, MB, Apolipoprotein E gen ε2 and ε4 alleles, HT and the use of antithrombotics. This condition has a high recurrence rate that shares the same risk factors. There is no specific treatment for AA BH. It has a better prognosis than HT BH during the acute period, but worse on the long term, due to its high recurrence rate and cognitive impairment.

Hemorragia subaracnoídea no traumática con angiografía por tomografía computada inicial "negativa / Non-traumatic subarachnoid hemorrhage with "negative" initial computed tomography angiography

La hemorragia subaracnoidea (HSA) no traumática es un subtipo de ictus hemorrágico que representa aproximadamente el 5% de todos los accidentes vasculares encefálicos (AVE). El 85% de los casos de HSA espontánea (no traumática) son secundarios a un aneurisma intracraneano roto, el 10% a hemorragia perimesencefálica no aneurismática y el otro 5% a otras causas. Entre estas se incluyen malformaciones arterio-venosas, fístulas durales, vasculits, trombosis de vena cortical, síndrome de vasoconstricción reversible, angiopatía amiloidea y síndrome de encefalopatía posterior reversible. La aproximación inicial a una HSA no traumática requiere un estudio angiográfico no invasivo con tomografía computada para la toma de decisiones terapéuticas. Si no se detecta un aneurisma sacular intradural que explique el sangrado, las conductas a seguir dependerán del patrón de distribución de la sangre. En esta revisión sugerimos una aproximación basada en 1) revisar el estudio inicial tomando en cuenta los puntos ciegos para la detección de aneurismas, 2) analizar el patrón de distribución de la sangre y 3) analizar los hallazgos en imágenes de acuerdo a las posibles causas según patrón.

Non-traumatic subarachnoid hemorrhage represents approximately 5% of strokes. From these, 85% of nontraumatic subarachnoid hemorrhage are secondary to a ruptured aneurysm, 10% to nonaneurysmal perimesencephalic hemorrhage and the other 5% to other causes. These include but are not limited to arteriovenous malformations, dural fistulae, vasculitis, cortical vein thrombosis, reversible cerebral vasoconstriction syndrome, amyloid angiopathy and posterior reversible encephalopathy syndrome. Initial workup of nontraumatic subarachnoid hemorrhage requires a non-enhanced CT and CT angiography for decision making and management. If there is no aneurysm as a source of hemorrhage, subsequent imaging studies will depend on blood distribution pattern. In this review we suggest an approach: 1) review blind spots for aneurysm detection in the initial CT angiography, 2) analyze blood distribution pattern and 3) evaluate imaging findings and possible causes according to each pattern.

Interrelationship between implant and orthognathic surgery for the rehabilitation of edentulous cleft palate patients: a case report

A 43-year-old woman with a unilateral cleft lip and palate, presenting a totally edentulous maxilla and mandible with marked maxillomandibular discrepancy, attended the Prosthodontics section of the Hospital for Rehabilitation of Craniofacial Anomalies, University of São Paulo for treatment. She could not close her mouth and was dissatisfied with her complete dentures. Treatment planning comprised placement of six implants in the maxilla, four in the mandible followed by prostheses installation and orthognathic surgery. The mandibular full arch prosthesis guided the occlusion for orthognathic positioning of the maxilla. The maxillary complete prosthesis was designed to assist the orthognathic surgery with a provisional prosthesis (no metal framework), allowing reverse treatment planning. Maxillary and mandibular realignment was performed. Three months later, a relapse in the position of the maxilla was observed, which was offset with a new maxillary prosthesis. This isa complex interdisciplinary treatment and two-year follow-up is presented and discussed. It should be considered that this type of treatment could also be applied in non-cleft patients.

Non-hypertensive intracerebral haemorrhage: some interesting observations.

Hypertension is the commonest cause of intracerebral hemorrhage (ICH) but non-hypertensive intracerebral hemorrhages (NHICH) are not rare. We report three interesting cases of NHICH subsequent to amyloid angiopathy, alcoholic hepatitis and amphetamine abuse. They suggest the importance of recognizing these conditions and need for urgent specific therapy which may play a vital role in therapeutic planning and prevention of ICH.

Pericardite constritiva em paciente com passado de múltiplas trocas de valva mitral, complicada com insuficiência tricúspide grave e hemorragia cerebral por angiopatia amilóide / Constrictive pericarditis in the patient with a history of numerous mitral valve replacements, complicated by serious tricuspid regurgitation and cerebral hemorrhage for amyloid angiopathy

Paciente do sexo feminino, portadora de cardiopatia reumática, com passado de cirurgias de troca valvar mitral que desenvolveu insuficiência tricúspide grave e pericardite constritive, fez hemorragia cerebral grave por angiopatia amilóide, tendo evoluído para óbito

Hemorragias cerebrales y angiopatía amiloidea / Cerebral amyloid angiopathy in brains of patients dying of non traumatic cerebral hemorrhages

Background: Cerebral amyloid angiopathy is considered pathogenic in non traumatic cerebral lobar hemorrhages. Aim: To study the frequency of cerebral amyloid angiopathy in brains of patients dying of non traumatic cerebral hemorrhages. Material and methods: Thirty seven brains from patients, 25 men and aged 65ñ10 years old, with cerebral hemorrhages (14 lobar, 18 in basal ganglia and 5 in cerebellum or brainstem) were studied. As controls, the brains of 30 subjects, 14 men and aged 64ñ16 years old, dying of non neurological causes were studied. Deep and cortical vessels were stained with hematoxylin eosin, Gomori, Thioflavin T and Bodian. Definitive cerebral amyloid angiopathy was diagnosed when amyloid deposition was observed in the media of vessels. Results: Twenty six out of 32 patients dying of cerebral hemorrhage and 3 of 21 controls had chronic hypertension. Cerebral amyloid angiopathy was present in 19 of 37 brains of patients with cerebral hemorrhage and 13 of 30 control brains. In patients with hypertension, vascular changes independent of the location and volume of amyloid deposition, were observed. Such changes were dilatation, tortuousness, thickening of walls specially in muscular and adventitia and hyaline degeneration. Thirteen brains with hemorrhage had fibrinoid necrosis and 10 had microaneurysms. Conclusions: In this series of patients, cerebral amyloid deposition was unspecific and its role in the pathogenesis of cerebral hemorrhages was not confirmed. Hypertension was associated with vascular degenerative changes that can lead to cerebral hemorrhages