Palliative embolisation of brain arteriovenous malformations presenting with progressive neurological deficit

Abstract

Large arteriovenous malformations (AVMs) located in eloquent areas of the brain are generally considered incurable because of the high morbidity and mortality associated with their treatment. When these patients develop a progressive neurological deficit they in time often become severely disabled. This report presents the results of palliative embolisation in this subgroup of patients. Analysis of our data-base of 714 patients with known brain AVMs revealed 17 patients who presented with progressive neurological deficit and who underwent palliative embolisation as the therapeutic modality of choice for management of their AVM. One patient was excluded due to lack of follow-up and two were excluded because they later received radiation therapy. Following embolisation 43% had improvement of their neurological deficit, 50% stabilized and 7% continued to deteriorate and these clinical results persisted for an average of more than 2 years follow-up. Transient neurological morbidity associated with embolisation treatment was 7% and there was no permanent morbidity and no mortality. Palliative embolisation of brain AVMs presenting with progressive neurological deficits arrested deterioration in more than 90% of patients and was associated with low morbidity and no mortality.

Figure 1

67-year-male presenting with progressive neurological deficit. A) Left internal carotid artery angiogram (lateral view) demonstrates left temporal-pareital AVM prior to embolisation. B) Left internal carotid angiogram (lateral view) immediately following the embolisation procedure shows residual AVM. C) Left internal carotid angiogram (lateral view) one year after the first angiogram demonstrates complete obliteration of the AVM. D) MRI examination (T2 weighted, axial view) prior to embolisation demonstrates white matter edema (arrows) surrounding the ectatic draining veins at the left parietal cortex level. E) MRI examination (T2 weighted, axial view) 4 months after embolisation demonstrates reduction of the white matter edema (arrow) coinciding with the clinical improvement in the neurological deficit in this patient following partial embolisation. F) MRI examination (T2 weighted, axial view) one year after embolisation demonstrates near complete regression of the white matter edema.

Figure 1

67-year-male presenting with progressive neurological deficit. A) Left internal carotid artery angiogram (lateral view) demonstrates left temporal-pareital AVM prior to embolisation. B) Left internal carotid angiogram (lateral view) immediately following the embolisation procedure shows residual AVM. C) Left internal carotid angiogram (lateral view) one year after the first angiogram demonstrates complete obliteration of the AVM. D) MRI examination (T2 weighted, axial view) prior to embolisation demonstrates white matter edema (arrows) surrounding the ectatic draining veins at the left parietal cortex level. E) MRI examination (T2 weighted, axial view) 4 months after embolisation demonstrates reduction of the white matter edema (arrow) coinciding with the clinical improvement in the neurological deficit in this patient following partial embolisation. F) MRI examination (T2 weighted, axial view) one year after embolisation demonstrates near complete regression of the white matter edema.

Figure 2

22-year-old female presenting with progressive neurological deficit. A) MRI examination (T2 weighted, axial view) demonstrates a large AVM involving the right basal ganglia and thalamic regions with ectatic draining internal cerebral vein. B) Left vertebral angiogram (lateral view) demonstrates a large deep-seated AVM prior to embolisation. C) Left vertebral angiogram (lateral view) following partial embolisation demonstrates moderate changes in the appearance of the AVM resulting in marked clinical improvement.