Cerebral arteriovenous malformation (AVM)
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Epidemiology
Classification
Grading
Rupture risk
Pathogenesis
Significant progress in the understanding of their pathogenesis has been made during the last decade, particularly using whole genome sequencing and biomolecular analysis 1)
Pathophysiology
Clinical Features
Differential diagnosis
Primary lobar hemorrhages (usually due to cerebral amyloid angiopathy) are typically seen in elderly. Younger patients may also develop lobar haemorrhages, but in such cases they usually have an underlying lesion (e.g. cerebral arteriovenous malformation).
Treatment
Outcome
Complications
Case series
Case reports
Bhanot et al. presented a patient with intraparenchymal hemorrhage due to cerebral arteriovenous malformation (AVM) who exhibited acute ST segment myocardial infarction (STEMI) after neurosurgery. Serial cardiac biomarkers and echocardiograms were performed which did not reveal any evidence of acute myocardial infarction. The patient was managed conservatively from cardiac stand point with no employment of anticoagulants, antiplatelet therapy, fibrinolytic agents, or angioplasty and recovered well with minimal neurological deficit. This case highlights that diffuse cardiac ischemic signs on the ECG can occur in the setting of an ICH after neurosurgery, potentially posing a difficult diagnostic and management conundrum 2).
Cerebral Arteriovenous Malformation General University Hospital of Alicante Cases
A 31-year-old man with a cerebral arteriovenous malformation in the deep and medial aspect of the right cerebral hemisphere, whose arterial contributions are established through the branches of the anterior choroidal artery and posterior choroidal arteryes, lenticulostriate arteries and perforating thalamus, whose venous drainage is through the right internal cerebral vein that reaches the vein of Galen and other medial venous branches that reach the superior sagittal sinus. The malformation nest has diameters of approximately 30 x 50mm.
After developing hydrocephalus he was operated on with ventriculoperitoneal shunt + endoscopic septostomy. Ventriculoperitoneal shunt infection removal of the infected hardware and ventriculoatrial shunt placement
7 years later he presents with a headache of two days of evolution in the frontal area that does not subside with paracetamol, associated with nausea with dizziness, and appreciating a BP of 140/90 mmHg, for which reason he has taken 50 mg captopril on his own and comments that it has made him sick with nausea.
Post-surgical changes after insertion of a ventriculoatrial shunt catheter through the right frontal trephine, with the distal end of the catheter not appearing to reach the anterior horn of the right lateral ventricle. Already known large right frontotemporal arteriovenous malformation, with an imprint of the drainage vein on the interventricular septum deviated to the left, and with dilatation of the vein of Galen that has not changed with respect to the previous control. Its drainage vein is ectatic and empties into the vein of Galen, without significant changes. There are no signs of intracranial hemorrhage or signs of established acute ischemia. Diffuse increase in ventricular size with respect to MRI, this increase being very evident in relation to the parietal and temporal horns, probably related to progressive hydrocephalus from Cerebrospinal fluid shunt malfunction.
Pedicled horseshoe incision at basal left occipital. A trephine is made and inserted with a DVE navigator in the left occipital horn about 6cm with a high-pressure CSF outlet. A short distance from the same incision, obstruction of the previous proximal EVD is checked and a new connection is made at the level of the previous valve. The old catheter was left tied (because it did not pull the previous EVD very close to the AVM).