Left Thalamus Arteriovenous Malformation Secondary to Radiation Therapy of Original Vermian Arteriovenous Malformation: Case Report.

A 70-year-old gentleman with history of hypothyroidism, hyperlipidemia, hypertension, and right superior cerebellar aneurysm presented to the neurosurgery service in 2008 with vertigo. Diagnostic cerebral angiography performed that year demonstrated a vermian arteriovenous malformations (AVM). The patient underwent stereotactic proton beam radiosurgery, which resulted in a decrease in flow and size of the lesion, and the patient was lost to follow-up. Now at the age of 80, the patient presented with acute gait instability. Cerebral angiogram demonstrated his stable vermian AVM and a new 1.1 cm AVM nidus in the region of the left posterior thalamus. Although AVMs are often described as congenital lesions, there is a growing body of literature suggesting that AVMs can grow, spontaneously regress, and even arise de novo in response to some insult. Understanding what leads to the growth, remodeling, regression, and hemorrhage of AVMs is crucial in order to better direct therapeutic endeavors. We would argue that this patient's AVM is secondary to endothelial cell damage from radiation therapy. Radiation can cause endothelial cell injury and upregulation of factors, such as vascular endothelial growth factor and transforming growth factor beta expression, which are implicated in AVM development pathways. We believe that this patient's new AVM is secondary to entrance radiation dosing affecting the thalamus during radiation therapy for the original vermian AVM.

The unilateral spatial neglect phenomenon in patients with arteriovenous malformations of deep brain structures.

Clinical-neuropsychological investigations were performed in 187 patients with arteriovenous malformations (AVM) of deep brain structures; 28 had AVM of the caudate nucleus, 35 of the thalamus, 45 of the cingulate gyrus, 43 of the hippocampus, and 36 of the corpus callosum. A total of 47 patients displayed neglect phenomena of different modalities, while unfixed neglect was demonstrated in 40 cases using special tests. The vast majority of patients showed neglect of left-sided space and the left side of the body, while only three patients showed right-sided neglect. These three patients had signs of left-handedness. In the development of neglect in all patients was associated with post-hemorrhagic or post-operative damage to the white matter (the projections of sensory bundles of the parietal and occipital lobes, the periventricular white matter) or the thalamus and corpus callosum. In hemispheric lesions, neglect developed on the background of the corresponding derangements (hemihypesthesia hemianopsia) and were of the same modality. In cases of damage to the corpus callosum, neglect could develop without accompanying sensory disturbances or the phenomenon could occur on different sides (in cases of simultaneous left hemisphere damage). This supports the independent nature of the neglect phenomenon.