We studied 20 patients with intraspinal tuberculosis (TB), to characterise the MRI features of tuberculous meningitis and myelitis. MRI leptomeningitis and intramedullary involvement in 11 patients, intramedullary lesions alone in 5, leptomeningitis alone in 2, and isolated extradural disease in 2. TB leptomeningitis was characterised by loculation of the cerebrospinal fluid (CSF), nerve root thickening and clumping (seen only in the lumbar region) or complete obliteration of the subarachnoid space on unenhanced images. Gd-DTPA-enhanced images proved useful in 6 cases, revealing linear enhancement of the surface of the spinal cord and nerve roots or plaque-like enhancement of the dura-arachnoid mater complex. Intramedullary lesions included tuberculomas (8), cord oedema (5) and cavitation (3). In seven cases of intramedullary tuberculoma multiple lesions with skip areas were seen, without significant cord swelling. One patient had an isolated lesion in the conus medullaris. The lesions were iso- or hypointense on T1-weighted images, iso-, hypo- or hyperintense on T2-weighted images and showed rim or nodular enhancement with contrast medium.

MRI was performed on 26 patients with tuberculous meningitis, with particular reference to document the cranial nerve abnormalities. MR angiography (MRA) was performed in 20 of the patients. Meningeal enhancement in the basal cisterns or over the convexity of brain was seen in all patients; two show ependymal enhancement. Tuberculomas, single (3), multiple (12) or miliary (2) were detected in 17 patients. Of the 9 patients with cranial nerve palsies, 7 showed contrast enhancement with or without thickening of the involved nerve. Abnormality signal intensity of the involved nerve was seen on proton density and T2-weighted images in one of these patients. MRA revealed focal arterial narrowing in 10 patients, the vessels commonly affected being the terminal segment of the internal carotid artery and the proximal segments of the middle and anterior cerebral arteries. One patient also had a small aneurysm of the proximal middle cerebral artery. Infarcts, haemorrhagic (8) or bland (6), were detected in 14 patients; most were the basal ganglia and internal capsules, large middle or anterior cerebral arterial territory infarcts being seen in only two cases.

We document the MRI features in seven patients with Japanese encephalitis. MRI was carried out on a 1.5 T system within 10-60 days of onset. In all the patients MRI revealed bilateral thalamic lesions, haemorrhagic in five. Signal changes were present in the cerebrum in four patients, the midbrain and cerebellum in three each, the pons in two and the basal ganglia in one. The lesions were haemorrhagic in three of the four patients with lesions in the cortex, two of the three with lesions in the midbrain and cerebellum, but the pontine lesions were haemorrhagic in both patients. Spinal cord involvement was seen in one of the three patients who underwent MRI. In two patients MRI was repeated 3 years after the onset, showing marked reduction in abnormal signal; and all the lesions gave low signal on both T1- and T2-weighted images. Bilateral thalamic involvement, especially haemorrhagic, may be considered characteristic of Japanese encephalitis, especially in endemic areas.

The purpose of this paper was to describe our experience with the endovascular management of splenic artery pseudoaneurysms (SAPA). Seven patients with documented SAPA on CT and/or angiography were considered for endovascular treatment. The pseudoaneurysms were located in the main splenic artery (n = 4) or its branches (n = 3). In one patient in whom the pseudoaneurysm was located in a hilar branch, selective catheterization of splenic artery failed. Metallic coils (n = 1), gelfoam and hydrogel particles (n = 1), metallic coils and gelfoam (n = 2), metallic coil, gelfoam and acrylic glue (n = 2) were used as embolization material in the remaining six patients. These patients were followed for a mean period of 11.3 months. Transcatheter embolization was successful in five patients with no procedure-related complications. In one patient, embolization was incomplete and the patient underwent surgery, but died on the 10th postoperative day because of irreversible shock. Another patient, after successful embolization, underwent surgery for management of an associated pseudocyst. Endovascular treatment is a safe and effective method of management of SAPA.