ABSTRACT
Background Quantitative susceptibility mapping (QSM) is used to differentiate between calcification and iron deposits. Few studies have examined the relationship between CT attenuation values and magnetic susceptibility in such materials. Purpose To assess the relationship among metal concentration, CT attenuation values, and magnetic susceptibility in paramagnetic and diamagnetic phantoms, and the relationship between CT attenuation values and susceptibility in brain structures that have paramagnetic or diamagnetic properties. Materials and Methods In this retrospective study, CT and MRI with QSM were performed in gadolinium and calcium phantoms, patients, and healthy volunteers between June 2016 and September 2017. In the phantom study, we evaluated correlations among metal concentration, CT attenuation values, and susceptibility. In the human study, Pearson and Spearman correlations were performed to assess the relationship between CT attenuation values and susceptibility in regions of interest placed in the globus pallidus (GP), putamen, caudate nucleus, substantia nigra, red nucleus, dentate nucleus, choroid plexus, and hemorrhagic and calcified lesions. Results Eighty-four patients (mean age, 64.8 years ± 19.6; 49 women) and 20 healthy volunteers (mean age, 72.0 years ± 7.6; 11 men) were evaluated. In the phantoms, strong linear correlations were identified between gadolinium concentration and CT and MRI QSM values (Râ2 = 0.95 and 0.99, respectively; P < .001 for both) and between calcium concentration and CT and MRI QSM values (Râ2 = 0.89 [P = .005] and Râ2 = 0.98 [P < .001], respectively). In human studies, positive correlations between CT attenuation values and susceptibility were observed in the GP (Râ2 = 0.52, P < .001) and in hemorrhagic lesions (Râ2 = 0.38, P < .001), and negative correlations were found in the choroid plexus (Râ2 = 0.53, P < .001) and in calcified lesions (Râ2 = 0.38, P = .009). Conclusion CT attenuation values showed a positive correlation with susceptibility in the globus pallidus and hemorrhagic lesions and negative correlation in the choroid plexus and calcified lesions. © RSNA, 2020 Online supplemental material is available for this article.
Subject(s)
Brain Mapping/methods , Brain/diagnostic imaging , Magnetic Resonance Imaging/methods , Tomography, X-Ray Computed/methods , Adult , Aged , Aged, 80 and over , Brain Diseases/diagnostic imaging , Female , Humans , Image Interpretation, Computer-Assisted , Male , Middle Aged , Phantoms, Imaging , Retrospective StudiesABSTRACT
The authors present the case of a 6-year-old girl with typical absence epilepsy induced by hyperventilation associated with moyamoya disease (MMD). A diffuse 3-Hz spike-and-wave complex induced by hyperventilation was apparent on an electroencephalogram, and her seizures were intractable to medication. Significant ischemia in the bilateral frontal lobes was present. The epilepsy disappeared after superficial temporal artery-middle cerebral artery anastomosis with encephalomyosynangiosis on both sides. In the treatment of children with intractable absence epilepsy, the possibility of underlying MMD and indications that revascularization surgery may be needed should be taken into consideration.
Subject(s)
Electroencephalography , Epilepsy, Absence/diagnosis , Moyamoya Disease/diagnosis , Anticonvulsants/therapeutic use , Aspirin/therapeutic use , Carotid Artery, Internal/surgery , Carotid Stenosis/diagnosis , Carotid Stenosis/surgery , Cerebral Angiography , Cerebral Infarction/diagnosis , Cerebral Infarction/surgery , Cerebral Revascularization , Child , Child, Preschool , Combined Modality Therapy , Drug Resistance , Epilepsy, Absence/surgery , Female , Follow-Up Studies , Frontal Lobe/blood supply , Humans , Moyamoya Disease/surgery , Postoperative Complications/diagnosis , Tomography, Emission-Computed, Single-Photon , Valproic Acid/therapeutic useABSTRACT
During a screen for novel putative Ca(2+)/calmodulin-dependent protein kinase (CaMK)-like CREB kinases (CLICKs), we have cloned a full-length cDNA for CLICK-III/CaMKIgamma, an isoform of the CaMKI family with an extended C-terminal domain ending with CAAX motif (where AA is aliphatic acid). As expected from the similarity of its kinase domain with the other CaMKI isoforms, full activation of CLICK-III/CaMKIgamma required both Ca(2+)/CaM and phosphorylation by CaMKK. We also found that Ca(2+)/cAMP-response element-binding protein (CREB) was a good substrate for CLICK-III/CaMKIgamma, at least in vitro. Interestingly enough, CLICK-III/CaMKIgamma transcripts were most abundant in neurons, with the highest levels in limited nuclei such as the central nucleus of the amygdala (CeA) and the ventromedial hypothalamus. Consistent with the presence of the CAAX motif, CLICK-III/CaMKIgamma was found to be anchored to various membrane compartments, especially to Golgi and plasma membranes. Both point mutation in the CAAX motif and treatment with compactin, a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, disrupted such membrane localization, suggesting that membrane localization of CLICK-III/CaMKIgamma occurred in a prenylation-dependent way. These findings provide a novel mechanism by which neuronal CaMK activity could be targeted to specific membrane compartments.