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NEUROIMAGES
Year : 2016  |  Volume : 64  |  Issue : 4  |  Page : 826-827

Integrated PET/MRI imaging of semantic dementia


1 Department of Molecular Imaging and Nuclear Medicine, Indraprastha Apollo Hospitals, New Delhi, India
2 Department of Neurology, Indraprastha Apollo Hospitals, New Delhi, India

Date of Web Publication5-Jul-2016

Correspondence Address:
Dr. Aashish Gambhir
Department of Molecular Imaging and Nuclear Medicine, Indraprastha Apollo Hospitals, Mathura Road, Sarita Vihar, New Delhi - 110 076
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.185365

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How to cite this article:
Jena A, Taneja S, Gambhir A, Renjen PN. Integrated PET/MRI imaging of semantic dementia. Neurol India 2016;64:826-7

How to cite this URL:
Jena A, Taneja S, Gambhir A, Renjen PN. Integrated PET/MRI imaging of semantic dementia. Neurol India [serial online] 2016 [cited 2019 Dec 5];64:826-7. Available from: http://www.neurologyindia.com/text.asp?2016/64/4/826/185365


A 61-year-old male patient presented to the Department of Neurology with gradually worsening single word comprehension, loss of semantic memory with well-maintained episodic memory, and preserved fluent speech with retained phonology and syntax. These findings were clinically suggestive of semantic dementia (SD). Patient underwent simultaneous integrated fluorine-18 fluorodeoxyglucose positron emission tomography/magnetic resonance imaging (18 F-FDG PET/MRI) using 7.65 mCi of 18 F-FDG with subsequent statistical parametric mapping performed using Scenium version 1 brain analysis software package (Siemens). MRI [Figure 1]a typically depicted the presence of bilateral asymmetrical (left > right) hippocampal atrophy, in addition to predominant anterior temporal cortical atrophy, with more inferior involvement than superior. Moreover, a relative sparing of the frontoparietal cortical volumes [Figure 1]d was noted.18 F-FDG PET and fused simultaneous PET/MRI simultaneously demonstrated matched bilateral asymmetrical hypometabolism, predominantly affecting the anterior temporal cortices [Figure 1]b and [Figure 1]c, more so on the left side (Scenium: SD: L, −10.4 to R, −7.7), with parietooccipital sparing [Figure 1]e and [Figure 1]f. Scenium-based parametric mapping of the brain [Figure 1]g, which compares a patient's scan with a normal database on a voxel-by-voxel basis for quantitative analysis, also demonstrated reduced tracer uptake in bilateral frontal areas (SD: L, −6.4 to R, −7.1). Bilateral, typically anterior and inferior, asymmetrical temporal lobe hypometabolism, combined with clinical features, are typical neuroimaging hallmarks of SD.
Figure 1: (a) Axial T1weighted three-dimensional anatomic magnetization prepared rapid acquisition gradient echo, (b) fluoro-2-deoxyglucose positron emission tomography, and (c) fused positron emission tomography/magnetic resonance imaging scans (top row) reveal bilateral hippocampal atrophy with predominantly left-sided anterior temporal cortical atrophy (white arrows) and corresponding anterior temporo-polar hypometabolism (white thick arrows). Similar images at a higher level (d-f) depict absence of any frontoparietal atrophy or hypometabolism (white arrowheads). Quantitative analysis (g) using scenium shows bilateral temporal antero-inferior hypometabolism more marked on the left side (white arrowhead) with bilateral frontal hypometabolism

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SD, a progressive neurodegenerative disorder characterized by loss of semantic memory in both the verbal and nonverbal domains, is one of the three canonical clinical syndromes associated with frontotemporal lobar degeneration (FTLD). First described by Arnold Pick in 1904, the clinical and neuropsychological features, as well as their association with temporal lobe atrophy were further described by Professor John Hodges and colleagues in 1992. It often presents with the complaints of word-finding difficulties, fluent aphasia, anomia, and associative visual agnosia. However, fluent aphasia is common in Alzheimer disease (AD)[1] and semantic deficits, usually considered basic to SD, also appear in AD. Hence, neuroimaging modalities such as MRI brain and FDG PET are often required to resolve this clinical dilemma. Atypically, both AD and FTLD have demonstrated significantly higher proportion of frontal lobe involvement in the Indian population, as compared to global literature.[2] Greater temporal atrophy on the left side rather than the right has been previously described as being characteristic of SD, and eventually, both temporal lobes and frontal areas become involved.[3] The combined structural and functional neuroimaging using MRI and FDG PET has been demonstrated to be a useful adjunct to clinical evaluation and can prove to be useful to differentiate FTLD from the other subtypes of frontotemporal lobar degeneration, frontotemporal dementia, and progressive nonfluent aphasia.[4] With the advent of simultaneous PET/MRI, such multimodal imaging techniques can have the potential role in the evaluation of neurodegenerative disorders. The shorter examination time, coupled with a higher patient comfort and compliance, makes this technique a readily acceptable one.

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Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Appell J, Kertesz A, Fisman M. A study of language functioning in Alzheimer patients. Brain Lang 1982;17:73-91.  Back to cited text no. 1
[PUBMED]    
2.
Das SK, Pal S, Ghosal MK. Dementia: Indian scenario. Neurol India 2012;60:618-24.  Back to cited text no. 2
[PUBMED]  Medknow Journal  
3.
Rohrer JD, McNaught E, Foster J, Clegg SL, Barnes J, Omar R, et al. Tracking progression in frontotemporal lobar degeneration: Serial MRI in semantic dementia. Neurology 2008;71:1445-51.  Back to cited text no. 3
    
4.
Schroeter ML, Raczka K, Neumann J, Von Cramon DY. Towards a nosology for frontotemporal lobar degenerations—A meta-analysis involving 267 subjects. Neuroimage 2007;36:497-510.  Back to cited text no. 4
    


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