Neuropathological studies have shown that brain tissue around an AVM is frequently gliotic and exhibits cystic changes. Besides these subcortical changes which may extend very deep into the white matter there may occasionally be seen cases of severe encephalomalacia with atrophy of gyri or lobules in the neighbourhood of the AVM and also changes of the arachnoid-pialayer. In some cases this change is combined with hemorrhage, but in others there is no sign of bleeding. The superficial and deep changes are not clearly related to the site or size of the AVM. Neurosurgical observations do not confirm that gliotic change around the convolutions is, as often stated, a “pseudocapsule or matrix” in every case.
The gliotic area surrounding an AVM may represent the brain reaction to pulsation of the AVM, to ischemia, to microhemorrhage or to a primary developmental phenomenon (lack of an astrocytic layer around vessels, therefore diffusion of metabolites).
It is assumed that because of the dysplasia of a capillary bed, there is no functioning brain tissue within the AVM itself, at least in compact lesions. However, we do not know at what distance from the lesion normal cerebral architecture is preserved and this must vary in each case. A better understanding of the pathophysiology of the lesion thus awaits a more comprehensive embryological and histological analysis.
Localization
Besides the ‘pure’ AVM occupying a single intracranial compartment we have seen examples of AVMs involving multiple anatomical layers including skin, muscle, bone, dura, arachnoid, brain, and ventricle.
The following combinations have been described:
Localization of the AVM Within the Brain
AVMs do not always involve all layers of the brain from surface arachnoid down to the ventricle (Figs 3.7A–B, 3.8). From the surgical perspective they may be divided into the following groups and subgroups:
I. Surface Lesions (visible on exploration on the surface of the brain)
II. Deep Lesions (invisible at exploration on the surface)
Fig 3.7A–B A Typical relationship of cortical-subcortical AVMs to the ventricular system. 1 = frontal, 2 = temporal dorsal, 3 = temporal (amygdala + hippocampus), 4 = parietooccipital dorsal, 5 = parietal paramedian, 6 = callosal.
Fig 3.7B Infratentorial AVMs with extension to the IVth ventricle, with (1) and without (2) ventricular obstruction.
I 1–2–3 Surface Lesions
Surface lesions may involve only the cortex or the white matter and the subependymal layer to extend into the white matter or extend through reach the ventricular system (Figs 3.8, 3.9A–D).
Fig 3.8 Artistic drawing of the possible locations and extensions of hemispheric AVMs:
A with connection to ventricular system
B without connection to ventricular system.
Fig 3.9A–D Cortical-subcortical AVM (A–B) on the visible surface, with (D) and without (C) subependymal extension.
II 1 Within the Sulci
An AVM may appear to be superficial on angiography but at operation only a red draining vein is present, or there may be no evidence of the AVM at all as it is deep within the sulci. The lesion is still a cortical + subcortical one but hidden deep within a sulcus which may be two or three centimeters or more below the actual surface of the brain. Dissection through the arachnoid of the sulcus will expose the lesion (Fig 3.10A–D).
Fig 3.10A–D Cortical-subcortical AVM located in the depth of sulci (with [D] and without [C] subependymal extension) (B) and therefore not visible on the surface (A).
II 2 Within the Deep Fissures
Similarly, an AVM may lie deep within the interhemispheric (median surface of frontal, parietal, occipital lobe), Sylvian (insula and adjacent operculum) or transverse fissures respectively or in the sulci of these fissures. These AVMs are deeply located but actually are still superficial in relation to the corpus callosum, cingulate gyrus, insula, parahippocampus, and pulvinar thalami (see Fig 3.13B).
Exposure of these lesions can be gained with minimal retraction of the adjacent lobuli and by opening the subarachnoid cisterns.
II 3 Within the Deep White Matter
(see Fig 3.8B)
These often small lesions may be found in every part of the brain, but more frequently around the paraventricular area and within the internal capsule. An approach can be made through the fissures or sulci, or sometimes transcallosally. In some cases it is necessary to employ a transcortical incision or stereotactic or ultrasound techniques or to use stereotactic irradiation.
II 4 Within the Deep Gray Matter (see Fig 3.8)
These AVMs are localized within the amygdala, putamen, pallidum, nucleus caudatus, thalamus, hypothalamus, nucleus ruber and substantia nigra, nucleus dentatus and other nuclei. They are supplied primarily by perforating arteries of the ACA, MCA, PCA, PcoA, anterior and posterior choroidal arteries, AICA, PICA, SCA, vertebral and basilar arteries.
II 5 Cisternal (Subarachnoidal)
(see Fig 3.13B)
Although angiography of an AVM of the vein of Galen shows the lesion in the very center of the brain, surgical experience has shown that they lie entirely within the cisternal system. Surgical explorations have further demonstrated that there exist pure cisternal (subarachnoidal) AVMs which may be paramesencephalic (ventral or dorsal), parapontine (ventral or ventrolateral within the cerebellopontine angle) and parabulbar (around the medulla oblongata).
These paramedullary superficial AVMs of the brain stem seem to be an intracranial equivalent to some paramedullary spinal AVMs.
II 6 Intraventricular (see Fig 3.11)
A few totally intraventricular AVMs of the choroid plexus within the trigonum are known. These lesions may be approached through the corpus callosum. We have seen 2 cases with an AVM of the tela chorioidea of IIIrd ventricle, three cases of lateral ventricle, and two cases of an AVM of the plexus chorioideus of the IVth ventricle.
Fig 3.11A–C Surgically observed locations of para- and intraventricular AVMs with obstruction of ventricular system. A Anterior callosal and septal (1), posterior callosal (2), choroid plexus of Illrd ventricle (3),