Background and PurposeComputed tomography is insufficient in evaluation of medullary lesions. Although lateral medullary infarction is a relatively common type of cerebrovascular disease, detailed correlation between clinical findings and magnetic resonance imaging (MRI) has not yet been reported.Methods We studied 33 consecutive patients with lateral medullary infarction who showed appropriate MRI lesions and correlated their clinical findings with the MRI results.Results Gait ataxia (88%), vertigo/dizziness (91%), nausea/ vomiting (73%), dysphagia (61%), hoarseness (55%), Horner sign (73%), and facial (85%) and hemibody (94%) sensory changes were frequent clinical findings. MRI results showed that the lesions located in the rostral part of the medulla were usually diagonal band-shaped and were associated with more

Summary:Factors that enhance hypercoagulability following BMT may have a pathogenetic role in VOD. To investigate the relevance of hemostatic parameters for the development of VOD, we prospectively measured protein C, protein S, antithrombin III (AT III), von Willebrand factor, and factor VIII in 50 consecutive patients undergoing allogeneic BMT. Each parameter was determined before conditioning, on day 0 of BMT and weekly for 3 weeks, and patients were monitored prospectively for the occurrence of VOD. VOD occurred in 26 patients at median post-BMT day 8.5 (range, day ؊2 to 17). Thirteen patients had mild, 10 had moderate and three had severe VOD. No coagulation parameters were significantly different at the baseline or on day 0 of BMT between patients with no/mild VOD and moderate to severe VOD. On day 7 and thereafter, levels of protein C and AT III were significantly lower in patients with moderate to severe VOD when compared to patients with no/mild VOD. Levels of protein C and AT III decreased before the clinical onset of VOD in patients with moderate to severe VOD. Early post-BMT reduction of these parameters may indicate the development of moderate to severe VOD.

Summary:We performed a randomized trial to determine whether there are differential effects of G-CSF when it is either started on the day (day 0 group) or on the 6th day of marrow infusion (day 5 group) in the allogeneic BMT setting. G-CSF 450 g was given intravenously daily until the peripheral blood ANC was over 3000/ l. Between May 1995 and April 1998, 60 patients were enrolled (30 in each group). Median number of days of G-CSF administration was significantly longer for the day 0 group (18.5 vs 14.0 days, P Ͻ 0.001). Median days to an ANC over 500/ l were the same in both groups (16 days). Median days to an unsupported platelet count of 20 000/ l did not show significant differences (29.5 vs 28 days, P = 0.202). The frequency of hepatic VOD was higher for the day 0 group (66.7 vs 40.0%, P = 0.038). Mean plasma antithrombin III level was significantly lower in the day 0 group on post-transplant day 7 (83.6 vs 93.9%, P = 0.009). Patients in the day 0 group showed significantly worse 100-day survival (25/30 vs 30/30 surviving respectively, P = 0.019). In conclusion, early initiation of G-CSF after allogeneic BMT did not facilitate marrow engraftment. In addition, early administration of G-CSF was associated with a higher frequency of VOD and a significant fall in plasma antithrombin III level.