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Both Gliadel wafers [1,3-bis(2-chloroethyl)-1-nitrosourea] and temozolomide (TEMO) have been shown in independent studies to prolong survival of patients with recurrent malignant glioma following surgery and radiotherapy. On the basis of preclinical evidence of synergism between Gliadel wafers and TEMO, a phase I study was designed to evaluate the toxicity of combining these 2 agents in the treatment of patients with recurrent supratentorial malignant glioma. All patients had surgical resection of the tumor at relapse, and up to 8 Gliadel (3.85%) wafers were placed in the surgical cavity following resection. Two weeks after surgery, TEMO was given orally daily for 5 days. Cohorts of 3 patients received TEMO at daily doses of 100 mg/m2, 150 mg/m2, and 200 mg/m2, respectively. Patients were assessed for toxicity 4 weeks after start of the first course of TEMO. Contrast-enhanced MRI of the brain was used to assesstumor response after the first cycle of TEMO. Patients with stable disease or response after the first cycle of TEMO were allowed to continue treatment at the same dose every 4 weeks for 12 cycles or until disease progression or unacceptable toxicity. Ten patients with a median age of 47 years (range, 22-66 years) were enrolled in this study. There were 7 patients with glioblastoma multiforme and 3 patients with anaplastic astrocytoma. Three patients were treated with TEMO at the first dose level of 100 mg/m2, 4 at the second dose level of 150 mg/m2, and 3 at the third dose level of 200 mg/m2. The 10 patients received a median of 3 cycles (range, 1-12 cycles) of TEMO following placement of Gliadel wafers. The treatment was well tolerated, with only 1 patient suffering grade III thrombocytopenia at the highest dose level. Two patients at each dose level had no evidence of disease progression after treatment. Four patients suffered progressive disease on therapy. Our study demonstrates that TEMO can be given safely after placement of Gliadel (3.85%) wafers. The recommended dosage for TEMO for a phase II study of this combination is 200 mg/m2 per day for 5 days.

Abstract: The combination of high signal and reduced apparent diffusion coefficients (ADC) within abscesses on diffusion-weighted MRI (DWI) has been reported as characteristic of abscesses, and useful for distinguishing them from cystic or necrotic neoplasms. To assess whether these are consistent findings in abscesses, we used DWI-derived ADC to investigate changes in water diffusibility in cerebral abscesses. We reviewed the MRI studies and clinical records of five patients with brain abscesses, who underwent DWI. Regions of interest were drawn within the abscesses on ADC maps, to obtain the ADC. The center of all five abscesses gave signal higher than that of white matter on DWI. The three largest also appeared bright on ADC maps, i. e., showed ADC substantially lower than those of normal white matter, consistent with restricted diffusion. However, the two smaller abscesses were not visible on ADC maps because their ADC were essentially the same as that of white matter; they did not show restricted diffusion. The absence of restricted diffusion within small abscesses may be related to intrinsic differences in molecular microenvironment between small and large abscesses, or to greater influence of volume averaging with surrounding edema on the ADC in smaller abscesses.

Objective. Diffusion‐weighted magnetic resonance imaging (DWI) detects acute ischemic infarcts with high lesion conspicuity. Determination of infarct age is difficult on DWI alone because infarct signal intensity (SIinfarct) on DWI is influenced by T2properties (“T2shine‐through”). Maps of the apparent diffusion coefficient (ADC) reflect pure diffusion characteristics without T2effects but have low lesion conspicuity. Thus, in clinical practice, combined use of DWI and ADC maps is required. Exponential DWI (eDWI) is an innovative means of MRI‐diffusion data analysis that merges the advantages of DWI and ADC maps. The authors hypothesized that SIinfarcton eDWI would correlate with infarct age. The authors studied 114 consecutive patients who had 120 ischemic strokes with clearly determined onset times and who underwent echo‐planar DWI. The eDWI were generated by dividing the signal intensity on DWI by that on the corresponding T2image on a pixel‐by‐pixel basis. SIinfarcton eDWI was measured in the lesion core and expressed as a percentage of contralateral control tissue. On eDWI, relative SIinfarctchanged significantly with infarct age (P< .0001). When patients were sorted in infarct‐age groups, no significant differences were found within the first 120 hours. However, for patients studied within 5 days, the mean relative SIinfarctwas significantly higher compared with patients studied ≥8 days after stroke (P< .05). For all infarcts up to 5 days old, the eDWI signal intensity was higher than control tissue (hyperintense appearance). All infarcts >10 days old had an eDWI signal intensity lower than control tissue (hypointense appearance). The authors concluded that the use of eDWI, as a single set of images, reliably differentiates acute infarcts (≤5 days old) from infarcts >10 days old. This feature would be expected to be helpful when the distinction between acute and nonacute infarction cannot be determined on clinical grounds.

Abstract: Previously reported methods of dynamic, contrast-enhanced, CT perfusion imaging in acute stroke have been promising but substantially limited by their dependence on very rapid rates of injection (typically 10–20 ml/s in an arm vein). Newly available deconvolution software permits the use of lower rates of injection (e. g., 3–4 ml/s), and rapidly provides maps of cerebral blood flow, cerebral blood volume and mean transit time. We report the potential of CT perfusion imaging performed with an injection rate of 4 ml/s to provide information on the extent of hemodynamic abnormality, and to help distinguish viable from nonviable ischemic tissue. The slower injection rates permitted by deconvolution analysis substantially enhance the practicality of CT perfusion imaging for studying stroke.

Abstract: We qualitatively assessed the regional distribution of vasogenic edema in a case of postpartum eclampsia. Although diffusion-weighted imaging showed no abnormalities, bilateral high signal was seen on T2-weighted images and apparent diffusion coefficient (ADC) maps. ADC of 1.45 0.10 mm2/s 10–3 for the posterior cerebral artery (PCA) territory and 1.22 0.12 mm2/s 10–3 for the watershed areas were significantly higher than those in the territories of the anterior (0.85 0.07 mm2/s 10–3) and middle cerebral (0.79 0.06 mm2/s 10–3)arteries (P < 0.05). The predilection of ADC changes within the PCA territory and in a previously undescribed watershed distribution supports the hypothesis that vasogenic edema in eclampsia is due to hypertension-induced failure of vascular autoregulation.

A 60-year-old man developed hemiballismus due to an intracranial hemorrhage involving the subthalamic nucleus 8 weeks after orthotopic liver transplantation. The hemorrhage was thought to be due to alterations in cerebral blood flow following a period of hypotensive shock due to sepsis, in the presence of anticoagulant therapy and thrombocytopenia. This represents a rare neurologic complication of liver transplantation.

Abstract: The purpose of this report is to describe imaging findings in activated protein C resistance, a hereditary cause of recurrent thrombosis. The case described was unusual in that a neonate was affected, whereas the vast majority of cases occur in adulthood. This entity is important to diagnose because of the recurrent nature of thromboses and the fact that relatives are often affected.