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We reviewed 11 cases of intramedullary cavernous haemangiomas (IMCH) studied by MRI, to assess its diagnostic value in these lesions. Follow-up MRI was obtained in five patients 7 days-2 years following the initial study. In one case a postoperative examination was obtained. The diagnosis was pathologically proven in ten cases, and supported in the last by a family and personal history of cavernous haemangiomas. A reticulate appearance with areas of mixed signal intensity in both T1- and T2-weighted images was the most common finding. Homogeneous high, low or intermediate signal intensity was each found in one case. Two small lesions gave low signal. A rim of low signal was less common than in cerebral cavernous haemangiomas. In one case, the brain showed more than 20 lesions with the MRI appearances of cavernous haemangiomas. In two of five patients, serial preoperative MRI showed progressive disappearance of high-signal areas on both T1- and T2-weighted images. To find a haemorrhagic intramedullary lesion on MRI is not rare. Although the appearances are not pathognomonic, an IMCH can be suggested. We suggest that the following characteristics may help: (1) a personal and/or family history of cavernous haemangiomas; (2) typical MRI appearances of mixed acute, subacute and chronic haemorrhage; (3) a tendency for signal intensity to decrease on follow-up; (4) normal spinal angiography; and (5) associated brain lesions.

We present three cases of suprasellar cavernous haemangioma with characteristic high-field MRI features. Clinical, CT and MRI data were retrospectively analysed. The patients had progressive neurological, endocrinological and visual complaints. In the three cases CT revealed a high-density suprasellar mass. In all cases the combination of a reticulated core of mized signal intensity with a surrounding rim of decreased signal on T1- and T2-weighted MRI scans suggested the presence of a cavernous haemangioma. Two patients underwent surgical biopsy after their first MRI examination. Cavernous haemangiomas located in the suprasellar area may show typical MRI features.

A total of 162 patients with suspected acoustic neuromas underwent MR imaging at 1.5 T. All patients were injected with Gd DTPA or DOTA. In 72 patients, uni- or bilateral acoustic neuromas were detected. 18 cases were equivocal: In 9 cases, contrast enhancement was due to other tumors (5 meningiomas, 2 metastases, 1 hemangioma). In 1 case, misinterpretation resulted from partial volume effects with the petrous bone marrow. In one patient, previously operated on, increased signal was due to postoperative fat graft. Four hypersignals were due to intracanalicular venous or meningeal enhancement. Three cases are still equivocal. Most of the diagnostic problems may be obviated by precontrast MR imaging, multidimensional 3-mm sections, and fast imaging.

The successful treatment of a congenital vertebral fistula with the balloon catheter occlusion technique is reported. A new approach is presented (the occipital approach), based upon the pathological enlargement of the second intervertebral space anastomosis between occipital and vertebral arteries.

The normal development of the hyoidostapedial system and its branches and anastomosis are outlined. The intrapetrous facial nerve receives its arterial suplly from the network. The arterial arch of the facial nerve is seen more frequently in angiograms of infants than in those of adults. The fact that the same vessel supplies the VIIth and the Vth nerves suggests that an ischemic mechanism may frequently be involved in Bell's palsy. The facial nerve from the point of view of its arterial supply must be considered as a nerve of the middle fossa and represent the major risk of embolization in the propinal middle meningeal artery.

Many arguments lead us to think that a possible etiologic factor in idiopathic Bell's palsy is the ischemia of the facial nerve and that angiography could help in diagnosis: (1) the rapid progress of the paralysis; (2) the correlation between Bell's palsy occurring after embolization of the internal maxillary artery, the middle meningeal artery, the occipital or posterior auricular artery, and their participation in the blood supply of the facial nerve; (3) the already known ischemic third nerve paralysis reported in diabetes and extending further to the facial nerve. Even if it is technically impossible to study Bell's palsy by angiography, it is interesting to understand and consider some complications of embolization and perhaps to envisage a new kind of treatment.

The middle meningeal artery can sometimes supply the complete vascularisation of the posterior fossa, i.e., the dura mater of the cerebellar fossa and the tentorium cerebelli. The authors present an anatomic and radiologic correlative study based upon an unusual case where the middle meningeal artery arose from the ascending pharyngeal artery and vascularised the entire posterior cerebellar fossa.

Since Parkinson's original description, the C5 collaterals are always presented as originating from a common trunk (meningo-hypophyseal). This is the least frequent anatomical variation. In fact, the posterior (C5) group of collaterals corresponds to the remnant of two transient embryonic vessels (primitive maxillary and trigeminal arteries), branches of which will give rise to the two main groups of collaterals originating from this area: medially, the inferior hypophyseal and the medial clival arteries; laterally, the basal tentorial and lateral clival arteries, which are constantly anastomosed with the ascending pharyngeal artery. Only in some cases (10%) do these two groups arise in common from the C5 carotid siphon. Apart from these branches the so-called Bernasconi's artery may originate from eight different pedicles, the C5 siphon representing only one of them.