Journal of Clinical Images and Case Reports

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Case Report, J Clin Image Case Rep Vol: 7 Issue: 1

Evidence of Old Hemorrhage in a Patient with a Brain Arteriovenous Malformation

Michael T Lawton*, Visish M Srinivasan and Lea Scherschinski

Department of Neurosurgery, Barrow Neurological Institute, Phoenix, Arizona

*Corresponding Author: Michael T Lawton
Department of Neurosurgery, Barrow Neurological Institute, Phoenix, Arizona
Tel: 6024063593

Received date: 29 August, 2022, Manuscript No. CICR-22-73230;
Editor assigned date: 31 August, 2022, PreQC No. CICR-22-73230 (PQ);
Reviewed date: 14 September, 2022, QC No. CICR-22-73230;
Revised date: 17 January, 2023, Manuscript No. CICR-22-73230 (R);
Published date: 24 January, 2023, DOI: 10.4172/CICR.1000230
Citation: Lawton MT, Srinivasan VM, Scherschinski L (2023) Evidence of Old Hemorrhage in a Patient with a Brain Arteriovenous Malformation. J Clin Image Case Rep 12:1.


A brain arteriovenous malformation (AVM) is a tangle of blood vessels that connects arteries and veins in the brain. The arteries take oxygen-rich blood from the heart to the brain. Veins carry the oxygen depleted blood back to the lungs and heart. A brain AVM disrupts this vital process. Arteriovenous malformations, or AVMs, are irregular connections between arteries and veins. They can occur anywhere in the body but are most common in the brain and spinal cord. The greatest risk of an AVM is that it will rupture and cause a stroke. Your arteries carry blood from your heart to the rest of your body.

Keywords: Arteriovenous malformatio, Oxygen rich, Brain and spinal cord, Stroke, Oxygen depleted blood


Arteriovenous malformation; Oxygen rich; Brain and spinal cord; Stroke; Oxygen depleted blood


A right temporal sylvian Arteriovenous Malformation (AVM) was incidentally discovered as part of a diagnostic workup for cognitive deficits in a patient in his middle 60’s. The patient’s medical history was unremarkable, without clinical evidence of prior brain AVM (bAVM) rupture. An axial T1 weighted Magnetic Resonance Imaging (MRI) showed a temporal sylvian AVM that was classified as a Spetzler Martin grade II lesion (S1V0E0) and Lawton Young grade IV lesion (A3B1C1). The bAVM had adjacent hypointense signaling suggestive of previous hemorrhage (Panel A, arrow). An axial T2 weighted MRI showed the AVM nidus in the absence of acute hemorrhage (Panel B, arrow). Intraoperatively, the radiographic findings of old hemorrhage correlated with hemosiderin stained parenchyma, indicating silent microhemorrhages (Panel C). This finding was confirmed by the presence of hemosiderin on hematoxylin and eosin staining and abundant hemosiderin laden macrophages (Panel D).

Case Presentation

This patient presented with silent hemorrhage from a bAVM, without a bleeding history but with radiographic and intraoperative evidence of old hemorrhage.

Figure 1: Right temporal sylvian Arteriovenous Malformation (AVM).

This case demonstrates radiographic and intraoperative Evidence of Old Hemorrhage (EOOH) in a patient with a medical history insignificant for bAVM rupture. Hemosiderin staining is a definitive marker of silent hemorrhage and is present in one-third of patients with unruptured BAVMs. Silent intralesional microhemorrhages are associated with an aggressive natural history and the identification of these high risk lesions offers opportunities for risk stratification among patients with unruptured bAVMs.

Lesions with EOOH can be diagnosed with iron sensitive MRI studies and visible intracellular hemosiderin positivity on pathology.


The intraoperative finding of hemosiderin stained parenchyma supports the diagnosis of EOOH. Primary surgical resection of unruptured BAVMs with EOOH is associated with improved final modified Rankin Scale scores and outcomes, suggesting primary surgical resection as the preferred treatment approach for these lesions.

Typically, the heart sends oxygen rich blood to the brain through arteries. The arteries slow blood flow by passing it through a series of progressively smaller networks of blood vessels, ending with the smallest blood vessels (capillaries). The capillaries slowly deliver oxygen through their thin, porous walls to the surrounding brain tissue.


Bleeding in the brain: An AVM puts extreme pressure on the walls of the affected arteries and veins, causing them to become thin or weak. This may result in the AVM rupturing and bleeding into the brain. This risk of a brain AVM bleeding ranges from around 2% to 3% each year. The risk of bleeding may be higher for certain types of AVMs or if there's been a previous AVM rupture. Some hemorrhages associated with AVMs go undetected because they cause no major brain damage or signs or symptoms. However, potentially life threatening bleeding episodes may occur. Brain AVMs account for about 2% of all hemorrhagic strokes each year. They're often the cause of hemorrhage in children and young adults who experience brain hemorrhage.


The authors have no personal, financial, or institutional interest in any of the drugs, materials, or devices described in this manuscript.

Financial Support



We thank the staff of Neuroscience Publications at Barrow Neurological Institute for assistance with manuscript preparation.


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