Although cure of cerebral arteriovenous malformations (AVMs) is the ideal goal it is often only possible with smaller sized lesions. This is certainly true if surgery or radiotherapy is used as the treatment strategy. Endovascular treatment, however, allows the possibility of partial treatment directed at specific areas of AVM architecture. With this in mind we retrospectively reviewed our cohort of AVMs to establish which morphological areas we had identified as targets and how the treatment of the AVM influenced the clinical picture. Over a 36-month period 42 AVMs were treated. In 22 of the patients who presented with a hemorrhage an intranidal aneurysm was identified as a target and treated in nine patients. Other patients presented with headaches (2), neurological deficit (4) and seizures (16) with two patients having their AVM picked up coincidentally. Targets identified included high flow fistulas (12), decreasing venous flow (17) and cure of the AVM (8). Results of targeted treatment showed a lower rehemorrhage rate than anticipated by the natural history. Patients cured did best and targeted embolization improved seizures in nine patients, neurological deficit in four patients and headache in 20 patients. Until safer methods exist to cure large AVMs the use of targeted embolization is acceptable as it protects patients against rehemorrhage and translates into an improvement in their clinical picture.

Arteriovenous malformation (AVM) patients who initially present with intracerebral haemorrhage may have an identifiable source of bleeding on angiogram, which can be a treatment target. Previous work suggests that the re-bleed rate may be lowered if a weak area is eliminated. A retrospective cohort study was conducted on patients who presented over a six-year period with a bled AVM. Cases were reviewed looking for the source of the hemorrhage by correlating haematoma location on CT or MRI and any angio-architectural weakness seen on digital subtraction angiography (DSA). Neuroendovascular notes were reviewed to identify the treatment targets. One hundred patients presented with a brain AVM with a 1.7:1 male: female ratio, 41 patients had an initial presentation of hemorrhage. The source of hemorrhage was identified in 18 subjects with 11 intranidal false aneurysms, five flow-related aneurysms, two associated aneurysms and one venous pouch. The location of haemorrhage on the presenting scan significantly correlated with the identified bleeding source using Chi-square analysis (P-value 0.039). Partial targeted embolization was used successfully in 90% with a 9% related technical complication rate not resulting in long-term morbidity or mortality. The mean follow-up period was 34 months with an annual hemorrhage rate of 0.7%. In just under half the patients with AVM bleeding a source of haemorrhage can be identified on DSA and in most cases this will be an intranidal false aneurysm. Flow-related and associated aneurysms in patients with brain AVM can cause haemorrhage and these patients are more likely to have SAH than intracerebral haemorrhage. These weak points are a good target for partial endovascular treatment, are usually accessible and may reduce the higher haemorrhage rate expected over the next two years.

A retrospective review of all angiograms done for craniocervical trauma, over an eight-year period at Groote Schuur Hospital identified 61 patients out of 823 angiographically studied who had extradural vascular injury and required endovascular treatment. Multiple lesions were identified in nine (14,8%) patients and associated injuries were found in 23 patients (37%). The mechanism of injury was blunt in nine (14.8%) patients and penetrating in 52 (85.2%). There was a statistically significant correlation between the presenting clinical feature and the underlying angiographic lesion. Patients with active bleeding were more likely to have a vessel laceration, an expanding hematoma was associated with false aneurysm and a pulsatile mass with arteriovenous fistula. Endovascular treatment with emphasis on vessel occlusion rather than preservation was successful in all cases except one which required surgical vessel ligation.

Post-transplant lymphoproliferative disorder (PTLD) occurs in 1 -10% of patients undergoing solid-organ transplantation and presents predominantly in the first year. It is a heterogeneous entity and encompasses indolent B-or T-cell lymphoproliferation to aggressive monomorphic lymphoma. Sirolimus is an inhibitor of the response to interleukin-2 and blocks T-and B-cell activation. The drug has been used to treat renal transplant-related PTLD, but cases of PTLD related to stopping sirolimus have not been reported. We present a case of rapidly progressive central nervous system (CNS) PTLD 11 years after transplantation, in which sirolimus had been stopped 1 month prior to symptom onset. Case reportThe patient was a 31-year-old man who had undergone cadaveric renal transplantation 9 years previously for end-stage renal failure of undetermined cause. He presented with ataxia and acute confusion. In the 3 months preceding presentation he had experienced unexplained, asymptomatic weight loss.Clinical examination was unremarkable. Sirolimus had been stopped 1 month before the onset of symptoms, owing to an apparent functional iron deficiency in the absence of evident gastro-intestinal blood loss. The patient remained on mycophenolate mofetil and prednisone.On the morning of presentation, the patient's wife witnessed his confusion and unsteadiness. He was afebrile and normotensive,

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