The solitary sellar plasmacytoma: a diagnostic challenge.

UNLABELLED: Solitary sellar plasmacytomas are exceedingly rare and difficult to distinguish from other pituitary tumors. We report a case of a 62-year-old woman presenting with blurred vision of the right eye and tenderness of the right temporal region, which was interpreted as temporal arteritis. MRI revealed a pituitary mass lesion (20mm×14mm×17mm) without compression of the optic chiasm and her pituitary function was normal. Pituitary surgery was undertaken due to growth of the lesion, and histopathological examination showed a highly cellular neoplasm composed of mature monoclonal plasma cells. Subsequent examinations revealed no evidence of extrasellar myeloma. The patient received pituitary irradiation and has remained well and free of symptoms apart from iatrogenic central diabetes insipidus. Until now, only eight cases of solitary sellar plasmacytoma have been reported. Most frequent symptoms stem from compression of the cranial nerves in the cavernous sinus (III, IV, V), whereas the anterior pituitary function is mostly intact. LEARNING POINTS: A solitary plasmacytoma is a rare cause of a sellar mass lesion.The radiological and clinical features are nonspecific, but cranial nerve affection and intact pituitary function are usually present.The diagnosis is made histologically and has important therapeutic implications.

Acute Vagal Nerve Stimulation Lowers α2 Adrenoceptor Availability: Possible Mechanism of Therapeutic Action.

BACKGROUND: Vagal nerve stimulation (VNS) emerged as an anti-epileptic therapy, and more recently as a potential antidepressant intervention. OBJECTIVE/HYPOTHESIS: We hypothesized that salutary effects of VNS are mediated, at least in part, by augmentation of the inhibitory effects of cortical monoaminergic neurotransmission at appropriate receptors, specifically adrenoceptors. Our objective was to measure the effect of acute VNS on α2 adrenoceptor binding. METHODS: Using positron emission tomography (PET), we measured changes in noradrenaline receptor binding associated with acute VNS stimulation in six anesthetized Göttingen minipigs. We used the selective α2 adrenoceptor antagonist [11C]yohimbine, previously shown to be sensitive to competition from the receptor's endogenous ligands, as a surrogate marker of monoamine release. PET records were acquired 4-6 weeks after the implant of a VNS electrode in minipigs before and within 30 min of the initiation of 1 mA stimulation. Kinetic analysis with the Logan graphical linearization generated tracer volumes of distribution for each condition. We used an averaged value of the distribution volume of non-displaceable ligand (VND), to calculate binding potentials for selected brain regions of each animal. RESULTS: VNS treatment markedly reduced the binding potential of yohimbine in limbic, thalamic and cortical brain regions, in inverse correlation with the baseline binding potential. CONCLUSION: The result is consistent with release of noradrenaline by antidepressant therapy, implying a possible explanation for the antidepressant effect of VNS.

Spatial distribution of malignant tissue in gliomas: correlations of 11C-L-methionine positron emission tomography and perfusion- and diffusion-weighted magnetic resonance imaging.

BACKGROUND: The prognosis of glioma patients is contingent on precise target selection for stereotactic biopsies and the extent of tumor resection. (11)C-L-methionine (MET) positron emission tomography (PET) demonstrates tumor heterogeneity and invasion with high diagnostic accuracy. PURPOSE: To compare the spatial tumor distribution delineated by MET PET with that by perfusion- and diffusion-weighted magnetic resonance imaging (MRI), in order to understand the diagnostic value of these MRI methods, when PET is not available. MATERIAL AND METHODS: Presurgical MET PET and MRI, including perfusion- and diffusion-weighted MRI, were acquired in 13 patients (7 high-grade gliomas, 6 low-grade gliomas). A quantitative volume of interest analysis was performed to compare the modalities objectively, supplemented by a qualitative evaluation that assessed the clinical applicability. RESULTS: The inaccuracy of conventional MRI was confirmed (area under the curve for predicting voxels with high MET uptake = 0.657), whereas cerebral blood volume (CBV) maps calculated from perfusion data improved accuracy (area under the curve = 0.760). We considered CBV maps diagnostically comparable to MET PET in 5/7 cases of high-grade gliomas, but insufficient in all cases of low-grade gliomas when evaluated subjectively. Cerebral blood flow and apparent diffusion coefficient maps did not contribute to further accuracy. CONCLUSION: Adding perfusion-weighted MRI to the presurgical protocol can increase the diagnostic accuracy of conventional MRI and is a simple and well-established method compared to MET PET. However, the definition of low-grade gliomas with subtle or no alterations on cerebral blood volume maps remains a diagnostic challenge for stand-alone MRI.

Inhibition of [11C]mirtazapine binding by alpha2-adrenoceptor antagonists studied by positron emission tomography in living porcine brain.

We have developed [(11)C]mirtazapine as a ligand for PET studies of antidepressant binding in living brain. However, previous studies have determined neither optimal methods for quantification of [(11)C]mirtazapine binding nor the pharmacological identity of this binding. To obtain that information, we have now mapped the distribution volume (V(d)) of [(11)C]mirtazapine relative to the arterial input in the brain of three pigs, in a baseline condition and after pretreatment with excess cold mirtazapine (3 mg/kg). Baseline V(d) ranged from 6 ml/ml in cerebellum to 18 ml/ml in frontal cortex, with some evidence for a small self-displaceable binding component in the cerebellum. Regional binding potentials (pBs) obtained by a constrained two-compartment model, using the V(d) observation in cerebellum, were consistently higher than pBs obtained by other arterial input or reference tissue methods. We found that adequate quantification of pB was obtained using the simplified reference tissue method. Concomitant PET studies with [(15)O]-water indicated that mirtazapine challenge increased CBF uniformly in cerebellum and other brain regions, supporting the use of this reference tissue for calculation of [(11)C]mirtazapine pB. Displacement by mirtazapine was complete in the cerebral cortex, but only 50% in diencephalon, suggesting the presence of multiple binding sites of differing affinities in that tissue. Competition studies with yohimbine and RX 821002 showed decreases in [(11)C]mirtazapine pB throughout the forebrain; use of the multireceptor version of the Michaelis-Menten equation indicated that 42% of [(11)C]mirtazapine binding in cortical regions is displaceable by yohimbine. Thus, PET studies confirm that [(11)C]mirtazapine affects alpha(2)-adrenoceptor binding sites in living brain.