(1) A series of 32 cases form the basis of a radiological investigation of the intracranial arteriovenous malformations. (2) The incidence of the intracranial arterio- venous malformations has been estimated at one% of the neurological admissions to hospital (Mackenzie 1953). They comprise two to five% of the reported cases examined by cerebral angiography (4.8% in the present series). (3) The pathology of the lesion is described and its relationship to the other vascular anomalies is defined. Arteriovenous malformation is considered to be the most suitable terminology. (4) Abnormal appearances in the preliminary skull radiographs, attributable to the presence of an arteriovenous malformation, may be seen in approximately 30% of the cases. They are as follows: (a) Enlargement of foramina and grooves for the meningeal vessels and occasionally anomalous vascular channels. Perforations in the skull due to communications between branches of the external carotid artery in the scalp and the meningeal vessels. Thickening of the skull, when the vascularity of the hone is greatly increased, which may simulate the hyperostosis of a meningioma. (b) Enlarged and pulsating drainage veins or the malformation itself may lead to localised areas of erosion of the inner table of the skull. Enlargement of the sagittal sinus groove may be demonstrable when there is a large shunt situated so that its effluents drain into the sinus. This observation may be of some value, since it may be the only visible radiographic change occurring with a lesion confined to the intracerebral circulation. Pour of the present cases showed marked widening and deepening of the sinus groove and in three others enlargement was probable. (c) Calcification may be found in the walls of the vessels of the malformation or in adjacent haematomata. It is present in approximately 15% of cases. (5) Ventriculography and encephalography have been superseded by cerebral angiography in the investigation of intracranial vascular lesions. In approximately 70% of cases of arteriovenous malformation plain radiography and ventriculography combined show some abnormality. An undulating, serrated or ripple contour of the walls of the lateral ventricle, without shift of the ventricular system has been considered typical of the conditions. Other changes result from cerebral atrophy, organisation of blood clot in the ventricle leading to coarctation, or to filling of a porencephalic cyst with air. Hydrocephalus commonly occurs with mid-brain lesions. (6) The technique of cerebral angiography as it applies to the demonstration of the arteriovenous malformations is described. Possible pitfalls in diagnosis are considered. (7) The angiographic appearances of the arteriovenous malformations, their feeding arteries and drainage veins are described. There were 17 large lesions, 10 small and 5 of intermediate size. The middle cerebral artery was the feeding vessel in 75% of cases. (8) A case is presented to support the hypothesis that a true increase in size of the arteriovenous malformations occurs. (9) Epilepsy was the presenting symptom in 25% and present eventually in 44 cent. of the present cases. The attacks were mainly focal in type and in those presenting with epilepsy the common situation of the lesion was fronto-parietal. If haemorrhage proceeded the onset of the attacks the lesion was elsewhere in the brain. (10) Headache was a presenting feature in 44% of the cases. It was commoner with the large (11 of 17 cases) than with the small (3 of 10 cases). Six lesions in relation to the occipital lobe were associated with headache of a migrainous type. (11) Haemorrhage occurred from 41% of the large, 70% of the small and all 5 lesions of medium size. It is suggested that the difference in incidence in bleeding from the small and large malformations, is due to the fact that the large ones are found during the course of investigation for symptoms such as headache and epilepsy, whereas small lesions are frequently asymptomatic until bleeding occurs. The relative liability of the small and large lesions to bleed cannot however be assessed until the number of small lesions at risk is known. The possibility that the small lesions are in fact more liable to haemorrhage than the large is not excluded. There are no characteristic angiographic features whereby the liability of a particular lesion to haemorrhage can be forecast. (12) The frequency with which an intracranial bruit can be heard on auscultation of the skull has varied widely in different reports. It was present in 8 cases (25% ), all large lesions, of the author's series. In 5 of the cases there was clinical or radiographic evidence of hypertrophy of branches of the external carotid artery. (13) The differentiating features between highly vascular tumours such as glioblastoma multiforme and meningioma and the arteriovenous malformations are described. There were no difficulties of this type in the present series of cases. (14) The value of cerebral angiography in the assessment of the operability of a lesion and in showing the results of excision are exemplified