Etiology of cortical and white matter lesions in cyclosporin-A and FK-506 neurotoxicity.

BACKGROUND AND PURPOSE: The etiology of the neurotoxicity associated with cyclosporin-A (CsA) and FK-506 treatment is not fully understood. At our institution, we noticed a distinct, abrupt change in the imaging characteristics of CsA and FK-506 neurotoxicity, which consisted of a shift in lesion morphology from a white matter abnormality to a mixed cortical and white matter pattern. The purpose of this study was to assess clinical parameters that might explain this change. METHODS: Twenty-two patients had a neurotoxic reaction and brain imaging changes while receiving CsA or FK-506. Nineteen patients received allogeneic bone marrow transplants, and three had aplastic marrow disorders. Fifty-one imaging studies (CT or MR imaging) were obtained, and lesion characteristics, locations, and time courses were evaluated along with relevant clinical data. RESULTS: Nine patients who had been conditioned for transplantation with cyclophosphamide and chemotherapy (busulfan or thiotepa) had a mixed pattern of cortical and white matter involvement (57 lesions). Isolated white matter involvement (62 lesions) developed in three nontransplant patients and 10 transplant patients conditioned with cyclophosphamide and total-body irradiation. All lesions occurred at typical brain watershed zones. Lesion enhancement was noted in two patients conditioned with chemotherapy. Initial images demonstrated characteristic lesions in 15 patients (68%). Initial images were normal in four patients (18%) and nonspecific in three patients (14%). CONCLUSION: Lesion location in CsA and FK-506 neurotoxicity may depend on the presence or type of conditioning used before bone marrow transplantation. Nontransplant patients or those conditioned with total-body irradiation develop white matter lesions, whereas those conditioned with chemotherapy develop mixed cortical and white matter lesions.

The adult radiographic shuntogram.

We describe the adult radiographic shuntogram, a simple method to evaluate the function and patency of a ventriculoperitoneal or ventriculoatrial shunt. The procedure involves placing contrast material into the valve of a shunt system and following the flow for appropriate clearing of contrast agent from the shunt tubing. Twenty-three studies were obtained in 15 patients in whom shunt malfunction was suspected. The method can be used to establish valve malfunction, ventricular or distal catheter obstruction, and peritoneal encystment.

Isolated deep cerebral venous thrombosis treated by direct endovascular thrombolysis.

BACKGROUND: Isolated thrombosis of the deep cerebral venous system is very rare and is associated with a poor prognosis. Antithrombin III (AT III) deficiency is a disorder of hypercoagulability associated with deep venous thrombosis and recurrent pulmonary emboli. We report a case of an 18-year-old man who presented with spontaneous thrombosis of the deep cerebral veins and straight dural sinus as the initial presentation of a previously undiagnosed AT III deficiency. METHODS: The patient was managed using direct endovascular infusion of the fibrinolytic agent urokinase followed by intravenous heparin. RESULTS: The technique was successful in establishing patency of the deep cerebral venous system. The patient experienced a good clinical outcome. CONCLUSIONS: Direct endovascular thrombolysis is a potentially effective management strategy for isolated thrombosis of the deep cerebral venous system.

Endovascular thrombolysis in deep cerebral venous thrombosis.

We present two cases of acute thrombosis of the internal cerebral veins, vein of Galen, and straight sinus without sagittal sinus involvement. Both patients had hydrocephalus and severe edema of the basal ganglia and thalami, one with hemorrhagic infarction of the thalamus. Because both patients rapidly deteriorated to a comatose state, endovascular thrombolysis was performed with urokinase infusion of the deep venous structures. Thrombolysis was continued until a patent channel with brisk flow in the venous structures was achieved. Both patients survived with minimal neurologic deficits.

Paradoxical aggravation of vasospasm with papaverine infusion following aneurysmal subarachnoid hemorrhage. Case report.

Reports of intraarterial papaverine infusion as treatment for cerebral vasospasm are few and documented complications are uncommon. The authors report the case of a patient with paradoxical aggravation of cerebral arterial narrowing during selective intraarterial papaverine infusion intended to treat vasospasm following aneurysmal subarachnoid hemorrhage (SAH). A 48-year-old man presented to the authors' service with symptomatic vasospasm 10 days after experiencing an SAH. The ruptured anterior communicating artery aneurysm was surgically obliterated the following day, and thereafter maximum hypervolemic and hypertensive therapies were used. However, the patient remained lethargic, and a stable xenon-computerized tomography (CT) cerebral blood flow (CBF) study revealed CBF to be 15 cc/100 g/minute in the left anterior cerebral artery (ACA) and 25 cc/100 g/minute in the right ACA territories. Cerebral arteriography demonstrated diffuse severe left ACA and mild left middle cerebral artery (MCA) vasospasm. In response intraarterial papaverine was infused into the internal carotid artery just proximal to the ophthalmic artery. During the infusion the patient became aphasic and exhibited right hemiplegia. Arteriography performed immediately after the intraarterial papaverine infusion revealed diffuse exacerbation of vasospasm in the distal ACA and MCA territories. A repeat xenon-CT CBF study showed that CBF in the left ACA and the MCA had drastically decreased (2 cc/100 g/minute and 10 cc/100 g/minute, respectively). Despite aggressive management, infarction ultimately developed. This is the first clinical case to illustrate a paradoxical effect of intraarterial papaverine treatment for vasospasm following aneurysmal SAH. The possible mechanisms of this paradoxical response and potential therapeutic reactions are reviewed.

Angioplasty of the occluded internal carotid artery.

PURPOSE: To review patients who have presented with acute strokes from a middle cerebral artery occlusion in whom in addition to the middle cerebral artery thromboembolus, an internal carotid artery occlusion has been present, and in whom angioplasty of these totally occluded internal carotid arteries has bee n successful. METHODS: We reviewed retrospectively our experience in treating a cute stroke patients with intracranial, intraarterial urokinase. Six of 27 patients had internal carotid artery occlusions in addition to middle cerebral artery occlusions. Two patients presented with spontaneous carotid dissections for wh ich no further intervention from the ipsilateral internal carotid artery was attempted. In the remaining four internal carotid artery occlusions secondary to atherosclerotic disease, standard guide wires and catheters were negotiated across the level of the internal carotid artery occlusion, which expedited intracranial catheterization for thrombolysis. Subsequently, angioplasty of the internal carotid artery was performed. RESULTS: All four occluded internal carotid arteries could be traversed. No new neurologic deficits occurred. No vascular injuries occurred. No deaths occurred. Four- to 6-month follow-up showed all four internal carotid arteries remained patent. CONCLUSION: In acute occlusions of the internal carotid artery from atherosclerosis, the occluded vessel can sometimes be recanalized with low morbidity. In addition, endovascular access to the intracranial circulation can be expedited by using the recanalized internal carotid artery.

Is bilateral lower extremity compression sonography useful and cost-effective in the evaluation of suspected pulmonary embolism?

OBJECTIVE: Because deep venous thrombosis is clinically linked with pulmonary embolism and often treated similarly, we sought to assess the usefulness of obtaining bilateral lower extremity compression sonograms when findings on ventilation-perfusion lung scans indicate a low or indeterminate probability of pulmonary embolism. Demonstration of deep venous thrombosis would provide a rationale for treating both pulmonary embolism and deep venous thrombosis. MATERIALS AND METHODS: Two hundred twenty-three consecutive patients with suspected pulmonary embolism had ventilation-perfusion lung scans and concurrent bilateral lower extremity compression sonograms; 34 also had pulmonary arteriography. RESULTS: In 75 cases, the results of ventilation-perfusion lung scanning indicated an indeterminate probability of pulmonary embolism. Evidence of thrombosis was seen on sonograms in 11 of these 75. In the remaining 64, 17 underwent pulmonary arteriography and four (24%) had pulmonary embolism. Findings on lung scans indicated a low probability of pulmonary embolism in 70 of 223 patients. Evidence of thrombosis was seen on sonograms in 11 of these 70. Five of the remaining 59 underwent pulmonary arteriography and one (20%) had pulmonary embolism. According to the 1993 Medicare Fee Schedule, if all 145 patients whose lung scans were nondiagnostic had sonography and only those with normal sonograms had pulmonary arteriography, the professional and hospital charges would be $359,552. If all 145 had pulmonary arteriography without sonography, the charges would be $395,031. CONCLUSION: If ventilation-perfusion lung scans indicate a low or an indeterminate probability of pulmonary embolism and bilateral lower extremity compression sonography is performed, only those patients with normal sonographic findings would need further study. Thus, 15% (22/145) of patients could be spared pulmonary arteriography, and the estimated savings in cost would be 9%.