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Marcos Devanir Silva da Costa, Bruno Fernandes de O. Santos, Felipe Bouchabki de Almeida Guardini and Feres Chaddad-Neto

The management of arteriovenous malformations (AVMs) of the corpus callosum and choroidal fissure is challenging because they commonly receive arterial feeders from the anterior and posterior circulation, and drain to deep veins. In this video the authors present the case of a 20-year-old man who presented with acute onset of headache, loss of consciousness, and nuchal rigidity. Computed tomography, MRI, and cerebral angiography performed in tandem revealed a ruptured, large, Grade IV AVM of the corpus callosum and choroidal fissure with two groups of arterial feeders: one from the pericallosal artery and the other from the medial and lateral posterior choroidal arteries. The treatment strategy included two stages. The first stage involved preoperative embolization of the arterial feeders from the posterior circulation, which promoted reduction of the nidus flow of the AVM. The second involved a microsurgical resection, using the interhemispheric approach, with the patient in the prone position, which allowed accessing the anterior circulation feeders and the complete resection of the AVM, without associated morbidity.

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Bernardo Oliveira Ratilal, Mariana Moreira Coutinho Arroja, Joao Pedro Fidalgo Rocha, Adelaide Maria Afonso Fernandes, Andreia Pereira Barateiro, Dora Maria Tuna Oliveira Brites, Rui Manuel Amaro Pinto, Bruno Miguel Nogueira Sepodes and Helder Dias Mota-Filipe


There is an unmet clinical need to develop neuroprotective agents for neurosurgical and endovascular procedures that require transient cerebral artery occlusion. The aim in this study was to explore the effects of a single dose of recombinant human erythropoietin (rhEPO) before middle cerebral artery (MCA) occlusion in a focal cerebral ischemia/reperfusion model.


Twenty-eight adult male Wistar rats were subjected to right MCA occlusion via the intraluminal thread technique for 60 minutes under continuous cortical perfusion monitoring by laser Doppler flowmetry. Rats were divided into 2 groups: control and treatment. In the treated group, rhEPO (1000 IU/kg intravenously) was administered 10 minutes before the onset of the MCA ischemia. At 24-hour reperfusion, animals were examined for neurological deficits, blood samples were collected, and animals were killed. The following parameters were evaluated: brain infarct volume, ipsilateral hemispheric edema, neuron-specific enolase plasma levels, parenchyma histological features (H & E staining), Fluoro-Jade–positive neurons, p-Akt and total Akt expression by Western blot analysis, and p-Akt–positive nuclei by immunohistochemical investigation.


Infarct volume and Fluoro-Jade staining of degenerating neurons in the infarct area did not vary between groups. The severity of neurological deficit (p < 0.001), amount of brain edema (78% reduction in treatment group, p < 0.001), and neuron-specific enolase plasma levels (p < 0.001) were reduced in the treatment group. Perivascular edema was histologically less marked in the treatment group. No variations in the expression or localization of p-Akt were seen.


Administration of rhEPO before the onset of 60-minute transient MCA ischemia protected the brain from this insult. It is unlikely that rhEPO pretreatment leads to direct neuronal antiapoptotic effects, as supported by the lack of Akt activation, and its benefits are most probably related to an indirect effect on brain edema as a consequence of blood-brain barrier preservation. Although research on EPO derivatives is increasing, rhEPO acts through distinct neuroprotective pathways and its clinical safety profile is well known. Clinically available rhEPO is a potential therapy for prevention of neuronal injury induced by transitory artery occlusion during neurovascular procedures.

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Daniela de Souza Coelho, Bruno Fernandes de Oliveira Santos, Marcos Devanir Silva da Costa, Gisele Sampaio Silva, Sergio Cavalheiro, Flávia H. Santos and Feres Chaddad-Neto


A cerebral arteriovenous malformation (cAVM) can change over time and cause symptoms, but clinical studies tend to define only the patients with ruptured cAVMs as symptomatic and do not consider neurocognitive aspects prior to neurosurgical intervention. The objective of this study was to describe the neurocognitive function of patients with ruptured and unruptured cAVMs according to the Spetzler-Martin (SM) grade, flow status, and anatomical topography.


In this blinded cross-sectional study, 70 patients of both sexes and ages 18–60 years were evaluated using the Brazilian Brief Neuropsychological Assessment Battery Neupsilin.


Of the 70 patients with cAVMs, 50 (71.4%) demonstrated deficits in at least one of the eight neurocognitive domains surveyed, although they did not exhibit neurological deficits. cAVMs in the temporal lobe were associated with memory deficits compared with the general population. The SM grade was not significantly associated with the results of patients with unruptured cAVMs. However, among patients with ruptured cAVMs, there were deficits in working memory in those with high-grade (SM grade) cAVMs and deficits in executive function (verbal fluency) in those with low-grade cAVMs (p < 0.001).


This study indicates that patients with untreated cAVMs, either ruptured or unruptured, already exhibit neurocognitive deficits, even the patients without other neurological symptoms. However, the scales used to evaluate disability in the main clinical studies, such as A Randomized Trial of Unruptured Brain Arteriovenous Malformations (ARUBA), do not assess neurocognitive alterations and therefore disregard any deficits that may affect quality of life. The authors’ finding raises an important question about the effects of interventional treatment because it reinforces the hypothesis that cognitive alterations may be preexisting and not determined by interventions.