Double Trouble: Association of Malignant Melanoma with Sporadic and Genetic Forms of Parkinson's Disease and Asymptomatic Carriers of Related Genes: A Brief Report.

Introduction: Previous epidemiological evidence has established the co-occurrence of malignant melanoma (MM) and Parkinson's disease (PD). Shared molecular mechanisms have been proposed to be implicated in this relationship. The aim of the present study was to assess the prevalence of MM in patients with sporadic and genetic types of PD, as well as in asymptomatic carriers of PD-related genes. Methods: Data regarding past medical history and concomitant disease of 1416 patients with PD (including 20 participants with prodromal disease who phenoconverted to PD), 275 healthy controls (HCs) and 670 asymptomatic carriers of PD-related genes were obtained from the database of the Parkinson's Progression Markers Initiative (PPMI). Focus was placed on information about a medical record of MM. We also retrieved data regarding the genetic status of selected PPMI participants with a positive MM history. Results: In total, 46 patients with PD reported a positive MM history. Concerning the genetic forms of PD, nine of these PD patients (2.47%) carried a Leucine Rich Repeat Kinase 2 (LRRK2) gene mutation (mainly the G2019S), while eight (4.49%) harbored a Glucocerebrosidase (GBA) gene mutation (mainly the N370S). No alpha-synuclein (SNCA) gene mutation was identified in patients with an MM history. The remaining 29 PD patients (3.5%) were genetically undetermined. In total, 18 asymptomatic carriers of PD-related genes had a positive medical history for MM: among them, 10 carried an LRRK2 gene mutation (2.69%) and 10 a GBA gene mutation (3.51%) (2 were dual carriers). MM history was identified for seven HCs (2.5%). Conclusions: We replicated the previously reported association between genetically undetermined PD (GU-PD) and MM. A correlation of LRRK2 mutations with the development of MM could not be verified in either symptomatic PD patients or asymptomatic carriers, implicating distinct pathogenetic mechanisms as compared to GU-PD. Importantly, despite the limited literature evidence on Gaucher disease, this study highlights for the first time the relatively high prevalence of MM among asymptomatic and symptomatic PD GBA mutation carriers, with potential clinical implications.

FLT PET/CT in a Case of Demyelinating Disease.

A 32-year-old woman, with spare previous medical history, presented with neurological symptoms of numbness and diplopia. The patient underwent brain MRI, which revealed a lesion of abnormal signal in the midbrain that could be attributed to subacute stroke; however, consecutive MRIs revealed multiple lesions of abnormal signal pointing to demyelinating disease. During symptoms investigation and MRI findings assessment, the patient underwent a FLT PET/CT examination, which revealed lesions of increased FLT uptake, probably indicating active disease and blood-brain barrier disruption.

Prospective PET image quality gain calculation method by optimizing detector parameters.

BACKGROUND: Lutetium-based scintillators with high-performance electronics introduced time-of-flight (TOF) reconstruction in the clinical setting. Let G' be the total signal to noise ratio gain in a reconstructed image using the TOF kernel compared with conventional reconstruction modes. G' is then the product of G1 gain arising from the reconstruction process itself and (n-1) other gain factors (G2, G3, … Gn) arising from the inherent properties of the detector. METHODS: We calculated G2 and G3 gains resulting from the optimization of the coincidence and energy window width for prompts and singles, respectively. Both quantitative and image-based validated Monte Carlo models of Lu2SiO5 (LSO) TOF-permitting and Bi4Ge3O12 (BGO) TOF-nonpermitting detectors were used for the calculations. RESULTS: G2 and G3 values were 1.05 and 1.08 for the BGO detector and G3 was 1.07 for the LSO. A value of almost unity for G2 of the LSO detector indicated a nonsignificant optimization by altering the energy window setting. G' was found to be ∼1.4 times higher for the TOF-permitting detector after reconstruction and optimization of the coincidence and energy windows. CONCLUSION: The method described could potentially predict image noise variations by altering detector acquisition parameters. It could also further contribute toward a long-lasting debate related to cost-efficiency issues of TOF scanners versus the non-TOF ones. Some vendors re-engage nowadays to non-TOF product line designs in an effort to reduce crystal costs. Therefore, exploring the limits of image quality gain by altering the parameters of these detectors remains a topical issue.

A review of PET normalization: striving for count rate uniformity.

The advent of PET instrumentation signaled the beginning of a new perspective in nuclear medicine diagnostic imaging. PET systems rely on several corrections that must be applied in order to establish accurate and reliable quantification. The inherent properties of PET detector architecture and the crystals themselves are sources of different types of systematic and random errors with subsequent count rate variability that should be accounted for. Normalization is the correction dealing with these errors. In this work, the reasons resulting in this variability are explored and the different normalization approaches are described. Special focus is paid to component-based normalization, with an attempt to describe the discrete factors and discuss the underlying mechanisms of their contribution to sensitivity variations of the lines of response.

Myocardial perfusion and adrenergic innervation in patients with RBBB and LAfB: the effect of altering the activation sequence with right ventricular apical pacing.

The aim of this study was to investigate myocardial perfusion and adrenergic innervation in patients with intraventricular conduction disturbances and to detect any changes caused by alteration of the ventricular activation sequence as a result of right ventricular apical pacing. We studied 15 patients with right bundle branch block (RBBB) and left anterior fascicular block (LAFB), while 15 healthy individuals served as controls. All patients underwent planar and single-photon emission computed tomography (SPECT) myocardial imaging after intravenous infusion of 5mCi 123I-metaiodobenzylguanidine (123I-MIBG) and a SPECT thallium201 myocardial perfusion study before and 3 months after pacemaker implantation. The heart to mediastinum ratio was calculated during the 123I-MIBG study in order to assess the global cardiac sympathetic activity and was significantly smaller in patients than in controls (P < 0.001). Patients with RBBB and LAFB revealed regional adrenergic innervation defects, mostly in the inferior and posterior walls. After a medium-term pacing period, a redistribution of 123I-MIBG uptake was detected, with aggravation of adrenergic innervation defects in the apical and posterior walls and amelioration in septal and anterior walls. Five patients showed perfusion defects that remained unchanged after pacing. Two others displayed mild myocardial perfusion defects that did not exist before pacing. In conclusion, patients with RBBB and LAFB reveal global and regional disturbances of myocardial adrenergic innervation, which shows redistribution as a result of the altered propagation of the ventricular electrical activation. To a smaller degree these patients reveal myocardial perfusion disturbances in which pacing has a limited medium-term effect.