DOCSLIB.ORG

Supplemental Data

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Supplemental Data Supplemental Figure 1. Individual model fits to parent fraction, plasma/blood and input function data 18 Supplemental Figure 2. Linear regression plots comparing (A)MA1 vs 2TC derived F-BCPP-EF VT, 11 11 (B)MA1 vs 2TC derived C-SA-4503 VT, (C)MA1 vs 1TC derived C-UCB-J VT. THE JOURNAL OF NUCLEAR MEDICINE • Vol. 61• No. 1 • xxx 2019 Mansur et al. 18 Supplemental Figure 3. Regional time stability plots for F-BCPP-EF VT. CS: Centrum semiovale, BST: Brainstem, SN: substantia nigra, THA: thalamus, VST: ventral striatum, CAU: caudate, PUT: putamen, HIP: hippocampus, INS: insular cortex, Tl; temporal lobe, PL: parietal lobe, FTCX: frontal cortex, CER: cerebellum THE JOURNAL OF NUCLEAR MEDICINE • Vol. 61• No. 1 • xxx 2019 Mansur et al. 11 Supplemental Figure 4. Regional time stability plots for C-SA-4503 VT. CS: Centrum semiovale, BST: Brainstem, SN: substantia nigra, THA: thalamus, VST: ventral striatum, CAU: caudate, PUT: putamen, HIP: hippocampus, INS: insular cortex, Tl; temporal lobe, PL: parietal lobe, FTCX: frontal cortex, CER: cerebellum THE JOURNAL OF NUCLEAR MEDICINE • Vol. 61• No. 1 • xxx 2019 Mansur et al. 11 Supplemental Figure 5. Regional time stability plots for C-UCB-J VT. CS: Centrum semiovale, BST: Brainstem, SN: substantia nigra, THA: thalamus, VST: ventral striatum, CAU: caudate, PUT: putamen, HIP: hippocampus, INS: insular cortex, Tl; temporal lobe, PL: parietal lobe, FTCX: frontal cortex, CER: cerebellum THE JOURNAL OF NUCLEAR MEDICINE • Vol. 61• No. 1 • xxx 2019 Mansur et al. 18 Supplemental Figure 6. Linear regression plots of age vs. (A)DVR and (B)VT/fp estimates for F-BCPP-EF for 11C-SA-4503 and for 11C-UCB-J. THE JOURNAL OF NUCLEAR MEDICINE • Vol. 61• No. 1 • xxx 2019 Mansur et al. Supplemental Figure 7. Linear regression plots for age vs fp THE JOURNAL OF NUCLEAR MEDICINE • Vol. 61• No. 1 • xxx 2019 Mansur et al. Supplemental Table 1. Demographic information and individual scan parameters Scan parameters Demographic Data 18F-BCPP-EF 11C-SA-4503 11C-UCB-J Inj. Inj. Inj. Inj. Inj. Inj. Age MMSE Sex Act Mass fp Act Mass fp Act Mass fp (y) score (MBq) (g) (MBq) (g) (MBq) (g) M 56 29 87 0.03 0.07 257 3.10 0.07 250 3.43 0.27 M 75 30 94 0.04 0.06 281 2.82 0.05 234 1.85 0.21 F 67 29 89 0.04 0.09 267 2.29 0.05 176 1.61 0.19 F 65 30 97 0.13 0.09 277 5.23 0.07 113 1.45 0.21 M 46 29 91 0.07 0.07 244 2.41 0.06 191 2.05 0.25 M 69 28 87 0.06 0.07 221 2.86 0.06 261 6.26 0.25 M 68 28 91 0.05 0.07 229 1.84 0.06 234 1.82 0.21 F 50 30 91 0.05 0.06 255 2.01 0.05 230 2.12 0.21 F 69 30 96 0.11 0.10 236 1.47 0.06 278 2.23 0.24 F 33 30 85 0.04 0.07 219 5.43 0.05 249 2.60 0.26 M 73 29 82 0.09 0.08 252 3.28 0.10 245 3.53 0.23 M 64 28 88 0.12 0.08 277 3.10 0.10 152 2.54 0.25 Mean 61 29 90 0.07 0.08 251 2.99 0.07 218 2.62 0.23 SD 13 1 4 0.03 0.01 22 1.23 0.02 49 1.32 0.03 COV 20% 3% 5% 50% 16% 9% 41% 27% 23% 50% 11% fp=plasma free fraction; MMSE=Mini-Mental state exam *Radiochemical purities were over 98% for all three tracers. THE JOURNAL OF NUCLEAR MEDICINE • Vol. 61• No. 1 • xxx 2019 Mansur et al. Supplemental Table 2. Mass effects on PET outcome measures 18F-BCPP-EF 11C-SA-4503 11C-UCB-J ROI r p r p r p Centrum semiovale 0.50 0.10 -0.26 0.42 -0.07 0.83 Brainstem 0.42 0.17 0.33 0.29 0.10 0.75 Substantia nigra 0.69 0.01 0.32 0.32 0.19 0.55 Thalamus 0.36 0.25 0.21 0.51 -0.10 0.76 Ventral striatum 0.45 0.14 0.32 0.31 -0.09 0.78 Caudate 0.08 0.80 0.16 0.62 -0.25 0.44 Putamen 0.56 0.06 0.22 0.49 -0.11 0.74 Hippocampus 0.49 0.10 0.14 0.67 0.05 0.88 Insular cortex 0.52 0.09 0.05 0.87 0.01 0.98 Temporal lobe 0.51 0.09 0.14 0.66 0.01 0.97 Parietal lobe 0.52 0.08 0.19 0.56 0.07 0.83 Frontal cortex 0.47 0.12 0.18 0.57 0.00 0.99 Cerebellum 0.50 0.10 0.37 0.24 0.16 0.61 r =correlation coefficient THE JOURNAL OF NUCLEAR MEDICINE • Vol. 61• No. 1 • xxx 2019 Mansur et al. THE JOURNAL OF NUCLEAR MEDICINE • Vol. 61• No. 1 • xxx 2019 Mansur et al. Supplemental Table 3. DVR estimates from 1TC, 2TC and MA1 Regions of interest Kinetic Radioligand FTC model BST SN THA VST CAU PUT HIP INS TL PL CER X 1.51 1.79 1.95 2.73 1.77 2.96 1.82 2.31 2.15 2.27 2.17 2.65 1TC 10% 9% 12% 10% 27% 9% 11% 9% 10% 10% 9% 8% 1.47 1.76 1.92 2.65 1.71 2.86 1.82 2.23 2.08 2.17 2.07 2.58 18F-BCPP-EF 2TC 12% 8% 13% 11% 28% 9% 11% 9% 10% 9% 8% 10% 1.58 1.78 1.93 2.67 1.71 2.87 1.83 2.25 2.10 2.19 2.09 2.59 MA1 12% 10% 14% 12% 29% 10% 11% 10% 10% 10% 9% 10% 1.43 1.39 1.26 1.50 0.96 1.66 1.45 1.76 1.60 1.47 1.53 1.88 1TC 18% 21% 14% 14% 24% 14% 17% 15% 16% 15% 14% 19% 1.59 1.44 1.27 1.49 1.04 1.81 1.58 1.87 1.71 1.51 1.52 2.04 11C-SA-5403 2TC 25% 38% 18% 16% 28% 18% 25% 17% 21% 19% 14% 24% 1.34 1.28 1.15 1.36 0.90 1.54 1.36 1.62 1.47 1.33 1.37 1.71 MA1 31% 35% 24% 23% 27% 26% 28% 22% 26% 25% 22% 31% 11C-UCB-J 1TC 1.26 1.50 1.96 3.66 2.17 3.67 2.50 3.63 3.34 3.11 3.07 2.80 7% 8% 13% 8% 24% 7% 10% 9% 8% 11% 10% 8% 1.27 1.49 1.92 3.58 2.09 3.54 2.44 3.51 3.24 3.00 2.95 2.81 2TC 6% 8% 14% 7% 23% 6% 9% 8% 8% 10% 9% 7% 1.28 1.52 1.98 3.63 2.15 3.62 2.53 3.61 3.32 3.08 3.03 2.84 MA1 7% 8% 13% 7% 24% 7% 10% 8% 8% 10% 10% 8% 11 11 *17 values for C-SA-4503 2TC estimation and 3 values for C-UCB-J 2TC estimation were determined as unidentifiable and excluded (based on VT of SE% > 10). THE JOURNAL OF NUCLEAR MEDICINE • Vol. 61• No. 1 • xxx 2019 Mansur et al. BST: Brainstem, SN: substantia nigra, THA: thalamus, VST: ventral striatum, CAU: caudate, PUT: putamen, HIP: hippocampus, INS: insular cortex, Tl; temporal lobe, PL: parietal lobe, FTCX: frontal cortex, CER: cerebellum THE JOURNAL OF NUCLEAR MEDICINE • Vol. 61• No. 1 • xxx 2019 Mansur et al. Supplemental Table 4. VT/fp estimates from 1TC, 2TC and MA1 Kinetic Regions of interest Radioligand model BST SN THA VST CAU PUT HIP INS TL PL FTCX CER CS 143 214 254 278 391 255 422 259 329 306 323 309 377 1TC 16% 17% 14% 21% 20% 35% 18% 18% 17% 17% 18% 18% 15% 157 232 277 302 418 271 451 286 351 328 343 327 405 18F-BCPP-EF 2TC 15% 18% 14% 20% 19% 35% 17% 17% 17% 17% 17% 18% 15% 157 232 277 303 419 271 450 287 352 329 344 329 405 MA1 16% 18% 14% 20% 20% 35% 17% 17% 17% 17% 18% 18% 15% 372 509 488 455 543 354 596 518 630 572 526 553 668 1TC 30% 27% 26% 27% 27% 37% 25% 24% 26% 26% 26% 29% 27% 456 611 544 520 605 476 698 608 736 664 598 628 765 11C-SA-5403 2TC 28% 30% 20% 27% 30% 27% 25% 24% 27% 26% 25% 29% 27% 465 588 553 508 604 405 671 590 714 647 584 614 747 MA1 36% 29% 29% 28% 27% 35% 25% 23% 26% 26% 26% 30% 27% 25 31 37 49 91 54 91 62 90 83 77 76 69 1TC 18% 13% 12% 15% 15% 28% 14% 12% 12% 11% 13% 13% 12% 11C-UCB-J 26 32 39 50 92 55 92 63 91 84 78 77 72 2TC 17% 13% 11% 14% 15% 27% 13% 12% 10% 11% 13% 13% 12% 25 32 38 50 92 54 91 64 91 84 78 76 72 MA1 17% 13% 11% 15% 15% 27% 13% 12% 10% 11% 13% 13% 12% 11 11 *17 values for C-SA-4503 2TC estimation and 3 values for C-UCB-J 2TC estimation were determined as unidentifiable and excluded (based on VT of SE%>10).
Load more

Recommended publications
  • Cerebral White Matter Lesions on Diffusion-Weighted Images
    diagnostics Article Cerebral White Matter Lesions on Diffusion-Weighted Images and Delayed Neurological Sequelae after Carbon Monoxide Poisoning: A Prospective Observational Study Sangun Nah 1 , Sungwoo Choi 1, Han Bit Kim 1, Jungbin Lee 2, Sun-Uk Lee 3 , Young Hwan Lee 1, Gi Woon Kim 1 and Sangsoo Han 1,* 1 Department of Emergency Medicine, Soonchunhyang University Bucheon Hospital, Bucheon 14584, Korea; [email protected] (S.N.); [email protected] (S.C.); [email protected] (H.B.K.); [email protected] (Y.H.L.); [email protected] (G.W.K.) 2 Department of Radiology, Soonchunhyang University Bucheon Hospital, Bucheon 14584, Korea; [email protected] 3 Department of Neurology, Korea University Medical Center, Seoul 02841, Korea; [email protected] * Correspondence: [email protected]; Tel.: +82-32-621-5116 Received: 29 August 2020; Accepted: 14 September 2020; Published: 16 September 2020 Abstract: Introduction: Carbon monoxide (CO) poisoning can result in delayed neurological sequelae (DNS). Factors predicting DNS are still controversial. This study aims to determine whether acute brain lesions observed using diffusion-weighted magnetic resonance imaging (MRI) following acute CO poisoning are related to the subsequent development of DNS. Methods: This prospective study was conducted on patients with CO poisoning treated at a university hospital in Bucheon, Korea. From August 2016 to July 2019, a total of 283 patients visited the hospital because of CO poisoning. Exclusion criteria included age under 18 years, refusing hyperbaric oxygen therapy, refusing MRI, being discharged against medical advice, being lost to follow-up, having persistent neurological symptoms at discharge, and being transferred from another hospital 24 h after exposure.
    [Show full text]
  • On-Line Table: MRI Imaging Recommendation and Summary Of
    On-line Table: MRI imaging recommendation and summary of key features Sequence Pathologies Visible Key Features T1 volumetric high-resolution Lewy body dementia Less consistent pattern of cerebral volume loss; a pattern of whole-brain reformatted in relatively focused atrophy of the midbrain, hypothalamus, axial, coronal, and sagittal planes and substantia innominata, with a relative sparing of the hippocampus and temporoparietal cortex; relatively little cortical atrophy Posterior cortical atrophy Bilateral parieto-occipital and temporo-occipital atrophy Pituitary region Pituitary macroadenoma: mass lesion intrinsic to pituitary Ͼ10 mm; T1 hypointense to gray matter (may be heterogeneous if hemorrhage present), T2 isointense, enhancing solid components; may extend into suprasellar region to distort optic chiasm; laterally may invade cavernous sinus FLAIR, volumetric whole-brain Focal cortical dysplasia T2 hyperintense cortical lesions Seizure (posterior cortical) Blurring of gray-white matter junction Focal white matter abnormal signal Transmantle increased signal and abnormal gyral pattern Mesial temporal sclerosis, possibly others Primary brain tumors Both low- and high-grade gliomas usually have associated FLAIR abnormality, involving cortex and white matter Enhancement, diffusion restriction, elevated cerebral blood volume in higher grade lesions Metastases Location at gray-white matter junction Multiplicity Heterogeneous, depending on primary lesion, hemorrhage Enhancement, variable pattern Edema out of proportion to size of lesion
    [Show full text]
  • Imaging of the Confused Patient: Toxic Metabolic Disorders Dara G
    Imaging of the Confused Patient: Toxic Metabolic Disorders Dara G. Jamieson, M.D. Weill Cornell Medicine, New York, NY The patient who presents with either acute or subacute confusion, in the absence of a clearly defined speech disorder and focality on neurological examination that would indicate an underlying mass lesion, needs to be evaluated for a multitude of neurological conditions. Many of the conditions that produce the recent onset of alteration in mental status, that ranges from mild confusion to florid delirium, may be due to infectious or inflammatory conditions that warrant acute intervention such as antimicrobial drugs, steroids or plasma exchange. However, some patients with recent onset of confusion have an underlying toxic-metabolic disorders indicating a specific diagnosis with need for appropriate treatment. The clinical presentations of some patients may indicate the diagnosis (e.g. hypoglycemia, chronic alcoholism) while the imaging patterns must be recognized to make the diagnosis in other patients. Toxic-metabolic disorders constitute a group of diseases and syndromes with diverse causes and clinical presentations. Many toxic-metabolic disorders have no specific neuroimaging correlates, either at early clinical stages or when florid symptoms develop. However, some toxic-metabolic disorders have characteristic abnormalities on neuroimaging, as certain areas of the central nervous system appear particularly vulnerable to specific toxins and metabolic perturbations. Areas of particular vulnerability in the brain include: 1) areas of high-oxygen demand (e.g. basal ganglia, cerebellum, hippocampus), 2) the cerebral white matter and 3) the mid-brain. Brain areas of high-oxygen demand are particularly vulnerable to toxins that interfere with cellular respiratory metabolism.
    [Show full text]
  • CT of Subinsular Infarction and Ischemia
    221 CT of Subinsular Infarction and Ischemia Steven R. Cobb 1 A number of CT head scans, covering a 2-year period and showing a variety of distinct C. Mark Mehringer1 curvilinear subinsular lucent lesions, were collected and reviewed. Variations in extent Hideo H. Itabashi2 of involvement, tendency toward bilateral symmetry, and clinical background allowed Henry Pribram3 the lesions to be grouped into four general patterns, most of which, to our knowledge, have not been specifically described in the radiologic literature. This project was undertaken first to bring to the attention of those involved in interpretation of cranial CT images several patterns of injury they may not heretofore have been aware of and second to attempt to derive a specific etiology for each of the patterns described. Pattern 1, which appears as a distinct curvilinear lesion (sometimes cystic) apparently limited to the lateral aspect of the putamen, is thought to represent the residua of previous lateral striatal hemorrhage. Pattern 2, occurring in a markedly younger age group appears as relatively symmetrical bilateral subinsular lucencies, which in one case completely resolved. A specific etiology for this pattern remains uncertain. Acute demyelination, either secondary to a variant of anoxic leukoencephalopathy or to a limited form of diffuse encephalomyelitis, is postulated. A third pattern, which extends from generalized deep frontal white-matter lucency across the anterior limb of the internal capsule and tapering posteriorly in the subinsular area is thought to be on the basis of chronic ischemia similar to subcortical arteriosclerotic encephalopathy. The fourth pattern, occurring as a broad band of lucency extending from the frontal horn of the lateral ventricle and also tapering posteriorly is due to relatively proximal occlusion of the lateral lenticulostriate arteries.
    [Show full text]
  • Features of the Cerebral Vascular Pattern That Predict Vulnerability to Perfusion Or Oxygenation Deficiency: an Anatomic Study
    431 Features of the Cerebral Vascular Pattern That Predict Vulnerability to Perfusion or Oxygenation Deficiency: An Anatomic Study D. M. Moody1 In an ongoing study of brain microvasculature in humans at autopsy, we had the 1 2 M.A. Bell · opportunity to analyze the overall scheme of this vascular supply. The native endothelial V. R. Challa3 membrane enzyme, alkaline phosphatase, is used to precipitate black lead sulfide salt in the vessel wall, rendering the brain microvasculature visible by both light microscopy and microradiography. There are six distinct patterns of intraparenchymal afferent blood supply to the supratentorial brain: short arterioles from a single source (e.g., those in the cortex); short- to intermediate-length arterioles, single source (anterior two-thirds of the corpus callosum); short- to intermediate-length arterioles and arteries, dual source (subcortical U fibers); intermediate-length arterioles and arteries, triple source (extreme/ external capsule and claustrum); long arteries and arterioles, single source (centrum semiovale); and large, long muscular arteries, single source (thalamus and basal ganglia). The nature of this arrangement offers some protection to certain regions of the cerebrum from circulatory challenges such as hypotension, while leaving other areas vulnerable. The distal arterioles supplying two of these protected regions, the U-fiber area and the extreme/external capsule and claustrum area, also exhibit the feature of interdigitation, which can offer additional collateral potential from one arteriolar territory to the next. Aging, hypertension, diabetes mellitus, and atherosclerosis can have a significant impact on brain microcirculation. The way in which vascular patterns dictate the distribution of these effects is discussed. The ability to stain the cerebral microvessels and demonstrate the finer points of their patterns in sections and microradiographs has enabled us to resolve some long-standing questions about vascular connections and directions.
    [Show full text]
  • Secondary Damage in Left-Sided Frontal White Matter Detected By
    Li et al. European Journal of Medical Research 2014, 19:44 http://www.eurjmedres.com/content/19/1/44 EUROPEAN JOURNAL OF MEDICAL RESEARCH RESEARCH Open Access Secondary damage in left-sided frontal white matter detected by diffusion tensor imaging is correlated with executive dysfunction in patients with acute infarction at the ipsilateral posterior corona radiata Chuo Li1*, Chao Dang2, Gang Liu2, Li Chen2, Jian Zhang2, Jingjing Li2, Zilin Ou2, Yusheng Zhang3 and Anding Xu3 Abstract Background: Executive dysfunction has been observed in patients with left-sided anterior corona radiata infarction. However, whether left-sided posterior corona radiata infarction could cause executive dysfunction is unclear. Also, whether secondary damage in the left frontal white matter following ipsilateral posterior corona radiata infarct is causal or not and contributes to the occurrence and development of executive dysfunction, is still uncertain. Methods: Twelve patients with posterior corona radiata infarction underwent diffusion tensor imaging (DTI) and an executive functional assessment at week 1 (W1), week 4 (W4), and week 12 (W12) after onset. Color duplex sonography and Transcranial Duplex Scanning (TCD) were performed at W1 and W12. Twelve healthy volunteers of similar ages and educational histories were examined as controls and assessed once. Results: In the patients, we observed an increased mean diffusivity (MD) and a decreased fractional anisotropy (FA) in the left frontal white matter from W1 to W12. There were no significant changes in cerebral blood flow in patients between W1 and W12 according to the result of Color duplex sonography and TCD. Patients showed progressively impaired executive function during 12 weeks.
    [Show full text]
  • Striatal Degeneration in Childhood
    Arch Dis Child: first published as 10.1136/adc.54.2.85 on 1 February 1979. Downloaded from Archives of Disease in Chlildhood, 1979, 54, 85-91 Striatal degeneration in childhood MAGDA ERDOHAZI AND P. MARSHALL Thze Hospital for Sick Children. London SUMMARY The clinical features, and the radiological and neuropathological findings of 3 unrelated children with striatal degeneration are presented. In one case the father had recently developed choreiform movements while in the other two the family history was negative for neurological dis- orders. Two patients had juvenile onset of psychiatric symptoms, seizures, and rigidity. The 3rd child presented with focal seizures at 9 weeks of age. The neuropathological findings are virtually identical in all 3 cases. The classification of striatal degeneration in childhood is discussed. Isolated degeneration of the striate body in child- occurred until a year later. Meanwhile, a slow hood is rare and constitutes a diagnostic problem. deterioration in her mental capacity became evident Patients with juvenile Huntington's disease demon- and at age 8 years her IQ had dropped to 54. strate striatal degeneration but the lesion is not She was first seen at The Hospital for Sick Children usually restricted to that structure. Cases with at age 9 years. During the previous year she had had striatal necrosis have also been described. Three increasingly severe generalised, akinetic, and ntyo- copyright. unrelated children with progressive degeneration of clonic seizures which responded poorly to a variety the striate body are reported. of anticonvulsant medications. On examination she was alert, co-operative, but obviously mentally Case reports retarded.
    [Show full text]
  • (EPVS): a Visual Rating Scale and User Guide
    Enlarged perivascular spaces (EPVS): a visual rating scale and user guide Gillian Potter, Zoe Morris & Joanna Wardlaw Section 1 Introduction Page 3 Section 2 EPVS on brain MRI A. Definition Page 4 B. Visualisation of EPVS on MRI Page 5 C. Location of EPVS Page 8 D. Description of EPVS in each anatomical area a. Basal ganglia (BG) Page 9 b. Centrum semiovale (CS) Page 12 c. Midbrain Page 14 Section 3 Potential difficulties in EPVS rating Page 15 A. Difficulties due to differences in EPVS visibility B. Difficulties rating due to white matter hyperintensities C. Varying number of EPVS on different slices D. ‘Double counting’ of linear EPVS E. Poor scan quality, including movement F. Asymmetry in background brain appearances G. Asymmetry in EPVS H. Focally dilated EPVS I. Differentiating between the most severe categories CS-EPVS 1 Guide prepared by Gillian Potter, Zoe Morris and Prof Joanna Wardlaw (University of Edinburgh) J. Variations in lesion load between cohorts Section 4: The EPVS rating scale A. Rating categories & descriptions Page 26 B. Imaging examples of rating categories a. Basal ganglia Page 27 b. Centrum semiovale Page 34 c. Midbrain Page 40 References Page 41 Conclusion Page 42 2 Guide prepared by Gillian Potter, Zoe Morris and Prof Joanna Wardlaw (University of Edinburgh) Section 1. Introduction Enlarged perivascular spaces (EPVS, sometimes called Virchow-Robin spaces) surround the walls of vessels as they course from the subarachnoid space through the brain parenchyma. 1 EPVS appear in all age groups, but are only visualised clearly on T2-weighted brain magnetic resonance imaging (MRI) when enlarged.
    [Show full text]
  • Blood Supply of Brain (Arteries) A205 (1)
    BLOOD SUPPLY OF BRAIN (ARTERIES) A205 (1) Blood Supply of BRAIN (arteries) Last updated: December 22, 2020 AORTIC ARCH .......................................................................................................................................... 2 Branching patterns ................................................................................................................. 2 Types ..................................................................................................................................... 4 Anomalies .............................................................................................................................. 4 Common carotid artery (CCA) .............................................................................................. 5 External carotid artery (ECA) ............................................................................................... 5 Subclavian artery ................................................................................................................... 8 ANTERIOR CIRCULATION (INTERNAL CAROTID SYSTEM) ..................................................................... 10 Internal carotid artery (ICA) ................................................................................................ 10 POSTERIOR CIRCULATION (VERTEBROBASILAR SYSTEM) .................................................................... 15 Vertebral artery (VA) ....................................................................................................................
    [Show full text]
  • Jnumed.119.228080.Full.Pdf
    Journal of Nuclear Medicine, published on July 19, 2019 as doi:10.2967/jnumed.119.228080 Characterization of 3 PET tracers for Quantification of Mitochondrial and Synaptic function in Healthy Human Brain: 18F-BCPP-EF, 11C-SA-4503, 11C-UCB-J 1,2,3 1,3,4 3,5 1.3 3,6 Ayla Mansur , Eugenii A. Rabiner , Robert A. Comley , Yvonne Lewis , Lefkos T. Middleton , 1,3 1,2,3 3,7 1,2,3 Mickael Huiban , Jan Passchier , Hideo Tsukada , Roger N. Gunn and MIND MAPS Consortium3 1Invicro LLC 2Division of Brain Sciences, Imperial College London, UK 3MIND MAPS Consortium: Laurent Martarello, Biogen; Robert A. Comley, AbbVie; Laigao Chen, Pfizer, Adam Schwarz, Takeda; Karl Schmidt, Celgene; Paul Matthews, Imperial College London; Marios Politis, King’s College London; Jonathan Rohrer, University College London; David Brooks, Newcastle University; James Rowe, University of Cambridge. 4King’s College London, UK 5Abbvie 6Neuroepidemiology and Ageing Research Unit, Imperial College London, UK 7Hamamatsu Photonics *Correspondence should be addressed to Ayla Mansur, PhD candidate, Imperial College London, Division of Brain Sciences, Hammersmith Hospital London, W12 0NN, UK. +442080086045 Email: [email protected] Short running title: Mitochondria and Synaptic PET Biomarkers Financial Support: The project was funded by the MIND MAPS consortium. Word Count: 5000 1 ABSTRACT Mitochondrial complex 1 (MC1) is involved in maintaining brain bioenergetics, the sigma 1 receptor (1R) responds to neuronal stress and synaptic vesicle protein 2A (SV2A) reflects synaptic integrity. Expression of each of these proteins is altered in neurodegenerative diseases. Here we characterise the kinetic behaviour of three positron emission tomography (PET) radioligands 18F-BCPP-EF, 11C-SA-4503 and 11C- UCB-J, for the measurement of MC1, 1R and SV2A, respectively, and determine appropriate analysis workflows for their application in future studies of the in vivo molecular pathology of these diseases.
    [Show full text]
  • Redalyc.Vascular Dementia and the Cholinergic Pathways
    Dementia & Neuropsychologia ISSN: 1980-5764 [email protected] Associação Neurologia Cognitiva e do Comportamento Brasil Engelhardt, Eliasz; Madeira Moreira, Denise; Laks, Jerson Vascular dementia and the cholinergic pathways Dementia & Neuropsychologia, vol. 1, núm. 1, enero-marzo, 2007, pp. 2-9 Associação Neurologia Cognitiva e do Comportamento São Paulo, Brasil Available in: http://www.redalyc.org/articulo.oa?id=339528997005 How to cite Complete issue Scientific Information System More information about this article Network of Scientific Journals from Latin America, the Caribbean, Spain and Portugal Journal's homepage in redalyc.org Non-profit academic project, developed under the open access initiative Materia 01 07.03.07 16:01 Page 2 Dementia & Neuropsychologia 2007;1:2-9 Vascular dementia and the cholinergic pathways Eliasz Engelhardt1, Denise Madeira Moreira2, Jerson Laks3 Abstract – Vascular cognitive impairment/vascular dementia have been the subject of a large number of stud- ies, due to their high prevalence and broad preventive and compensatory therapeutic potential. The knowledge of the cerebral anatomy correlated to the vascular territories of irrigation enables understanding of clinical manifestations, as well as classification into the several types of syndromic presentations. The central choliner- gic system exercises important neuromodulatory functions on cerebral circuits related to cognitive and behav- ioral integration, as well as on vasomotor control related to cerebral blood flow adjustments. The acquisition of data on the anatomy of the cholinergic pathways, including the localization of the nuclei of the basal prosen- cephalon and the routes of their projections, established an important milestone. The knowledge of the vascu- lar distribution and of the trajectories of the cholinergic pathways allows identification of the strategic points where a vascular lesion can cause interruption.
    [Show full text]
  • Panencephalopathic Type of Creutzfeldt-Jakob Disease: Primary Involvement of the Cerebral White Matter
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.44.2.103 on 1 February 1981. Downloaded from Journal of Neurology, Neurosurgery, and Psychiatry, 1981, 44, 103-115 Panencephalopathic type of Creutzfeldt-Jakob disease: primary involvement of the cerebral white matter TOSHIO MIZUTANI,* ATSUSHI OKUMURA,t MASAYA ODA,j AND HIROTSUGU SHIRAKI§ From the Clinical Neuropathology, Tokyo Metropolitan Institute for Neurosciences, Fuchu,* the Department of Psychiatry, School of Medicine, Osaka City University,t the Department of Neuropathology, Institute of Brain Research, School of Medicine, University of Tokyo,: and the Shir-aki Institute of Neuropathology, Tokyo, Japan§ S U M M A R Y Eight necropsy cases of a "panencephalopathic" type of Creutzfeldt-Jakob disease (CJD) in the Japanese are reported. The reasons why this type should be discussed separately from other types of CJD are that there is primary involvement of the cerebral white matter as guest. Protected by copyright. well as the cerebral cortex, and that the white matter lesion of one Japanese human brain with CJD similar to the present group has been successfully transmitted to experimental animals. Creutzfeldt-Jakob disease (CJD) is a diffuse de- 1000 g, irrespective of the duration of the clinical generation of the central nervous system usually course (5 to 30 months). This finding differs from occurring in middle age and fatal within two previous reports that the brain atrophy in CJD is years. Clinical variations are numerous, but the only mild to moderate in degree and increases with most common picture includes severe mental de- the duration of illness.5 terioration, rigidity of muscles and myoclonic jerks.
    [Show full text]