Cerebral Arterio-Venous Malformation - Erler Zimmer
Clinical History
This patient succumbed at the age of 58 due to post-operative complications following transurethral resection of the prostate. Notably, at 28 and 35, he experienced two episodes of transient neurological deficit. However, at the age of 50, he developed permanent hemiparesis of the left leg, primarily affecting his ankle.
Pathology
The specimen, a coronal slice passing through the parietal lobes, reveals the replacement of cortex and white matter on the medial aspect of the right cerebral hemisphere by a 4 cm diameter mass of abnormal tissue. This lesion extends from the superior surface down to the roof of the lateral ventricle. A closer inspection identifies the tissue as a network of tortuous vascular channels and intervening tissue. Histological examination of this arteriovenous malformation (AVM) reveals glial tissue surrounding dilated vessels. All vessels exhibit a typical endothelial lining, with some displaying thick muscular walls (arteries) and others thin walls (veins).
Further Information
Cerebral AVMs often manifest as headaches, seizures, cranial nerve deficits, back pain, and nausea, especially when coagulated blood escapes into the cerebrospinal fluid in the vertebral column. Some AVM patients may remain asymptomatic. Progressive weakness, numbness, vision changes, and debilitating pain may occur based on AVM location. In severe cases, AVM vessels may rupture, leading to intracranial hemorrhage. Symptoms of bleeding-induced AVM include loss of consciousness, sudden and severe headache, nausea, vomiting, incontinence, and blurred vision, among others. Local damage at the bleeding site can cause seizures, hemiparesis (as seen in this patient), loss of touch sensation on one side of the body, and language processing deficits (aphasia). Ruptured AVMs contribute significantly to mortality and morbidity.