Norio Tsuchiya

Quantitative evaluation of norcholesterol scintigraphy, CT attenuation value, and chemical-shift MR imaging for characterizing adrenal adenomas

ObjectiveThe objective of our study was to evaluate diagnostic ability and features of quantitative indices of three modalities: uptake rate on norcholesterol scintigraphy, computed tomography (CT) attenuation value, and fat suppression on chemical-shift magnetic resonance imaging (MRI) for characterizing adrenal adenomas.MethodsImage findings of norcholesterol scintigraphy, CT, and MRI were reviewed for 78 patients with functioning (n = 48) or nonfunctioning (n = 30) adrenal masses. The norcholesterol uptake rate, attenuation value on unenhanced CT, and suppression on in-phase to opposed-phase MRI were measured for adrenal masses.ResultsThe norcholesterol uptake rate, CT attenuation value, and MR suppression index showed the sensitivity of 60%, 82%, and 100%, respectively, for functioning adenomas of <2.0 cm, and 96%, 79%, and 67%, respectively, for those of ≥2.0 cm. A statistically significant correlation was observed between size and norcholesterol uptake, and between CT attenuation value and MR suppression index. Regarding norcholesterol uptake, the adenoma-to-contralateral gland ratio was significantly higher in cortisol releasing than in aldosterone-releasing adenomas.ConclusionsThe norcholesterol uptake rate was reliable for characterization of adenomas among adrenal masses of ≥2.0 cm. CT attenuation value and MR suppression index were well correlated with each other, and were useful regardless of mass size.

Impact of CT attenuation correction by SPECT/CT in brain perfusion images

PurposeThe aim of this study was to elucidate the regional differences between brain perfusion single photon emission computed tomography (SPECT) images reconstructed with a uniform attenuation correction using Chang’s method (AC-Chang) and a non-uniform attenuation correction with CT using SPECT/CT (AC-CT).MethodsSPECT images of a phantom with and without head holder were obtained, and reconstructed images of AC-Chang and AC-CT were compared. Twenty-eight consecutive patients with brain disease examined by SPECT/CT brain perfusion imaging were selected, and images were reconstructed with AC-Chang and AC-CT. The AC-Chang and AC-CT reconstructed images were then compared by voxel-based analysis using three-dimensional stereotactic surface projections.ResultsCounts in the frontal area of the AC-Chang phantom image with head holder were higher than those in the posterior area. Counts in the frontal area of the AC-Chang clinical images were significantly higher than those in the AC-CT images, while the counts in the margin of the frontal lobe and posterior margin of the parietal, occipital cortices and cerebellum of the AC-Chang images were significantly lower. Relative frontal perfusion was 5.0% higher and relative cerebellar perfusion was 4.6% lower in the AC-Chang images relative to the AC-CT images, on average.ConclusionWe demonstrated the frontal dominant hyper-perfusion and parieto-occipital and cerebellar hypo-perfusion in brain SPECT images reconstructed with AC-Chang compared to those reconstructed with AC-CT. We suggest that to obtain an accurate attenuation-corrected brain perfusion SPECT image, attenuation correction by Chang’s method is inadequate.

Fluorodeoxyglucose uptake in the bone marrow after granulocyte colony-stimulating factor administration in patients with non-Hodgkinʼs lymphoma

PurposeTo clarify the change in the fluorodeoxyglucose (FDG) uptake by the bone marrow over time after administration of granulocyte colony-stimulating factor (G-CSF), we evaluated the correlation between the interval from the last day of administration of G-CSF to positron emission tomography/computed tomography (PET/CT) study and spinal bone marrow accumulation in patients with non-Hodgkins lymphoma. MethodsA total of 127 patients with confirmed non-Hodgkins lymphoma who underwent FDG PET within 60 days from the last administration of G-CSF were retrospectively reviewed. Thirty age-matched and sex-matched healthy controls were also included to evaluate physiological FDG uptake. PET/CT examinations were retrospectively reviewed, and maximum standardized uptake value (SUVmax) was measured by placing volumetric regions of interest over each thoracic and lumbar vertebra on PET images referring to CT images. Bone marrow SUV was defined as the mean SUVmax of the vertebra. The correlation between the interval after G-CSF and the bone marrow SUV was plotted and analyzed with polynomial approximation. ResultsIn controls, physiological bone marrow SUV of the spine was determined. In patients with lymphoma, bone marrow SUV decreased over time and reached a plateau at about 14 days after G-CSF administration, and this was higher by 5% than the plateau at 10 days. SUV declined to the ‘physiological range’, that is, mean+1 standard deviation of patients, at about 7 days. ConclusionFor a PET/CT study, an interval of 10 days after G-CSF administration is recommended to minimize the influence of G-CSF on the bone marrow when evaluating treatment response in patients with non-Hodgkins lymphoma.

Decreased brain FDG uptake in patients with extensive non-Hodgkin’s lymphoma lesions

ObjectiveFaint brain [18F]fluoro-2-deoxyglucose (FDG) uptake has sporadically been reported in patients with FDG-avid large or diffusely extended tumors. The purpose of this study was to investigate whether there is a correlation between massive tumor uptake and decreased brain uptake on FDG positron emission tomography/computed tomography (PET/CT).MethodsSixty-five patients with histologically confirmed non-Hodgkin’s lymphoma who underwent FDG-PET/CT were enrolled. Thirty control subjects were also included to evaluate normal brain FDG uptake. PET/CT examinations were retrospectively reviewed. The volumetric regions of interest were placed over lesions by referring to CT and PET/CT fusion images to measure mean standardized uptake value (SUVavg). The products of SUVavg and tumor volume were calculated as total glycolytic volume (TGV). The maximum SUV (SUVmax) and SUVavg were measured in the cerebrum and cerebellum. The values of TGV and brain FDG uptake were plotted and analyzed with a linear regression method.ResultsIn the lymphoma patients, there were statistically significant negative correlations between TGV and brain SUVs.ConclusionDemonstrating a significant negative correlation between TGV and brain uptake validated the phenomenon of decreased brain FDG uptake. Diversion of FDG from the brain to the lymphoma tissue may occur during the FDG accumulation process. Recognition of this phenomenon prevents unnecessary further neurological examinations in such cases.

Naloxone and flumazenil fail to antagonize the isoflurane-induced suppression of dorsal horn neurons in cats.

Effects of naloxone and flumazenil on isoflurane activities were examined on dorsal horn neurons in cats. Isoflurane suppressed bradykinin-induced nociceptive responses in transected feline spinal cords. The bradykinin-induced neuronal firing rates were significantly suppressed by 60.0%, 35.3% and 32.2% at 10, 20 and 30 min after isoflurane administration, respectively. The 32.2% suppression on bradykinin-induced neuronal responses at 30 min after isoflurane administration was not reversed 5 min after administration of naloxone (36.4% suppression). The suppressive effects of isoflurane were not reversed by naloxone (0.2 mg·kg−1, i.v. Similarly, the benzodiazepine antagonist, flumazenil (0.2 mg·kg−1 i.v., did not affect the suppressive effects of isoflurane. Failure of naloxone and flumazenil to reverse the suppressive effects of isoflurane suggests that isoflurane interacts with neither opioid nor benzodiazepine receptors in producing its suppressive action on nociceptive responses in dorsal horn neurons of the feline spinal cord.

Yohimbine and flumazenil: effect on nitrous oxide-induced suppression of dorsal horn neurons in cats

PurposeThe purpose of this study was to determine the mechanisms of nitrous oxide (N2O) antinociception at the spinal level with yohimbine (an α2-adrenergic antagonist) and flumazenil (a specific benzodiazepine antagonist) using chemonociceptive stimuli in spinal dorsal horn neurons in the cat.MethodsA lumbar laminectomy extending from L4 to L6 was performed to allow insertion of a extracellular recording device via a microelectrode. Additional laminectomy was performed at the T12 level to transect the spinal cord. As a noxious stimulus, bradykinin (BK) was injected via the cannula inserted into the femoral artery. Animals were divided into four treatment groups for subsequent experiments: N2O+flumazenil, N2O+yohimbine, flumazenil (alone), and yohimbine (alone).ResultsN2O suppressed BK-induced nociceptive responses in transected feline spinal cords. The BK-induced neuronal firing rates were significantly suppressed: to 69.2%, 61.8%, and 52.2% of the baseline firing rate at 10, 20, and 30 min, respectively, after N2O administration. The 47.8% suppression on BK-induced neuronal responses at 30 min after N2O administration was reversed 5 min after administration of yohimbine (25.2% suppression). Similarly, N2O suppression (42.5%) on chemically induced neuronal responses was reversed by flumazenil (24.9% suppression) at identical postadministration intervals.ConclusionThese data imply that N2O suppresses the nociceptive responses in part probably through its agonistic binding activity to the α2-adrenergic, γ-aminobutyric acid (GABA)-benzodiazepine, or both receptor systems in dorsal born neurons of the feline spinal cord.

Suppressive action of enflurane on dorsal horn neurons in rabbits

The neurophysiologic mechanism of the suppressive action of enflurane on spinal nociceptive transmission was examined in rabbits with intact and with transected spinal cords. Enflurane suppressed nociceptive responses in both intact and transected spinal cord groups. The suppressive effects of enflurane were significantly greater in the intact group than in the transected group. The suppressive effects of enflurane were not reversed by the addition of 0.2 mg·kg−1 of naloxone. These results suggest that enflurane suppresses nociceptive responses by activating descending inhibitory systems and directly suppressing activity at the spinal level. This suppressive action of enflurane does not interact with the opioid receptor.