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Year : 2020  |  Volume : 35  |  Issue : 1  |  Page : 72-73  

Posterior reversible encephalopathy syndrome: Pattern on18F-fluorodeoxyglucose positron emission tomography-computed tomography correlated with magnetic resonance imaging in pediatric hypertensive encephalopathy


1 Department of Nuclear Medicine, All India Institute of Medical Sciences, New Delhi, India
2 Department of Radiodiagnosis, All India Institute of Medical Sciences, New Delhi, India

Date of Submission18-Aug-2019
Date of Acceptance07-Sep-2019
Date of Web Publication31-Dec-2019

Correspondence Address:
Dr. Rakesh Kumar
Department of Nuclear Medicine, All India Institute of Medical Sciences, New Delhi 110 029
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijnm.IJNM_149_19

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   Abstract 


Posterior reversible encephalopathy syndrome (PRES) is characterized clinically by headache, seizures, vomiting, altered mental status, and blurred vision. However, with overlapping and atypical clinical symptoms, PRES becomes a diagnostic challenge. We describe the imaging findings of PRES in magnetic resonance imaging and18F-fluorodeoxyglucose positron emission tomography-computed tomography in an 11-year-old child who presented with features of hypertensive encephalopathy.

Keywords: 18F-fluorodeoxyglucose positron emission tomography-computed tomography, hypertensive encephalopathy, posterior reversible encephalopathy syndrome


How to cite this article:
Arora S, Passah A, Nalli H, Goyal H, Tripathi M, Shamim SA, Das CJ, Kumar R. Posterior reversible encephalopathy syndrome: Pattern on18F-fluorodeoxyglucose positron emission tomography-computed tomography correlated with magnetic resonance imaging in pediatric hypertensive encephalopathy. Indian J Nucl Med 2020;35:72-3

How to cite this URL:
Arora S, Passah A, Nalli H, Goyal H, Tripathi M, Shamim SA, Das CJ, Kumar R. Posterior reversible encephalopathy syndrome: Pattern on18F-fluorodeoxyglucose positron emission tomography-computed tomography correlated with magnetic resonance imaging in pediatric hypertensive encephalopathy. Indian J Nucl Med [serial online] 2020 [cited 2020 Jul 15];35:72-3. Available from: http://www.ijnm.in/text.asp?2020/35/1/72/274362



An 11-year-old female child presented to the pediatric emergency department with acute altered sensorium and multiple episodes of seizures for 1month. On evaluation, she was found to be hypertensive. Further investigations were done for workup of hypertension and associated seizure episodes. Ultrasound abdomen and renal Doppler study revealed normal left kidney and small right kidney with no definite evidence of renal artery stenosis. Computed tomography(CT) angiography revealed evidence of wall thickening and enhancement involving arch and descending aorta. For the evaluation of vasculitis and to look for any seizure foci, whole-body and brain18 F-fluorodeoxyglucose positron emission tomography-computed tomography (18 F-FDG PET-CT) was planned. Scan revealed hypometabolism in bilateral parieto-occipital region in the axial and sagittal sections [Figure 1]a, [Figure 1]b, [Figure 1]c, [Figure 1]d, [Figure 1]e, [Figure 1]f, white arrows]. Also noted was diffuse increased FDG uptake in the wall of ascending and arch of aorta and patchy mild FDG uptake in descending aorta. Coronal section showing increased FDG uptake in the ascending aorta is shown in [Figure 1]g (black arrow), correlating with wall thickening and enhancement in CT angiography (image not shown here), suggesting metabolically active inflammatory involvement in large vessels. To correlate these incidental brain hypometabolism changes, magnetic resonance imaging (MRI) brain was done which revealed edematous cortical gyri in bilateral parieto-occipital lobes in T1 [Figure 2]a, red arrow] showing hyperintensity on T2-weighted [Figure 2]b, yellow arrow] and fluid-attenuated inversion recovery sequences [Figure 2]c and [Figure 2]d, white arrows]. No significant restriction of diffusion was seen on diffusion-weighted images [Figure 2]e and [Figure 2]f. The overall findings suggested posterior reversible encephalopathy syndrome(PRES) secondary to acute hypertensive encephalopathy in the current clinical scenario.
Figure 1: Axial and sagittal sections of positron emission tomography and fused18F-fluorodeoxyglucose positron emission tomography-computed tomography images (a-f) of brain showing decreased fluorodeoxyglucose uptake in bilateral parietal and occipital lobes (white arrows). Coronal sections of whole-body18F-fluorodeoxyglucose positron emission tomography images (g) showing increased fluorodeoxyglucose uptake in relation to ascending and arch of aorta (black arrow), suggestive of metabolically active inflammatory involvement

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Figure 2: Axial T1-weighted image (a) showing edematous cortical gyri in bilateral parieto-occipital lobes (a, red arrow) showing hyperintensity on T2 (b, yellow arrow), and fluid-attenuated inversion recovery sequences (c and d, white arrow). There is no restriction of diffusion seen on diffusion-weighted image (e) and apparent diffusion coefficient map (f). These features are suggestive of posterior reversible encephalopathy syndrome

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PRES is a clinicoradiological entity presenting clinically with headache, visual disturbances, seizures, and altered mental status.[1],[2] Underlying causes include hypertension, cytotoxic medications, preeclampsia or eclampsia, autoimmune and systemic conditions, including thrombotic thrombocytopenic purpura, systemic lupus erythematosus, and sepsis.[3] It typically affects parieto-occipital region, but other regions can be involved.[4] Pathogenesis involves dysregulation of normal autoregulatory vasoconstriction, whenever there is sudden increase in systemic blood pressure causing endothelial damage, thrombotic microangiopathy, resulting in fluid leakage from the intravascular space to the interstitial compartment causing vasogenic edema.[5],[6],[7] It is usually a reversible phenomenon and resolves if underlying cause is corrected. Sometimes, it is a diagnostic challenge when it presents with overlapping and atypical symptoms. In the acute setting, CT helps for rapid assessment and also exclude other causes presenting with overlapping symptoms including, cerebral hemorrhage and space-occupying lesions, but CT can also be normal with no significant changes.[8] MRI typically shows bilateral white-matter abnormalities in vascular watershed areas in the posterior regions of cerebral hemispheres, most commonly involving parieto-occipital lobes. Atypical findings including hemorrhage and isolated involvement of the frontal lobes can be seen.[9] Based on these clinical and imaging features, diagnosis of PRES secondary to hypertensive encephalopathy was made. The patient was started on oral steroids and antihypertensive drugs and patient responded well to treatment. She is currently discharged from the hospital in stable condition.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient's parents have given consent for his images and other clinical information to be reported in the journal. The patient's parents understand that his names and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Lim MH, Kim DW, Cho HS, Lee HJ, Kim HJ, Park KJ, et al. Isolated cerebellar reversible leukoencephalopathy syndrome in a patient with end stage renal disease. Intern Med 2008;47:43-5.  Back to cited text no. 1
    
2.
Das CJ, Seith A. Posterior reversible encephalopathy syndrome (PRES). Indian Pediatr 2006;43:657-8.  Back to cited text no. 2
    
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Fugate JE, Claassen DO, Cloft HJ, Kallmes DF, Kozak OS, Rabinstein AA, et al. Posterior reversible encephalopathy syndrome: Associated clinical and radiologic findings. Mayo Clin Proc 2010;85:427-32.  Back to cited text no. 3
    
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McKinney AM, Short J, Truwit CL, McKinney ZJ, Kozak OS, SantaCruz KS, et al. Posterior reversible encephalopathy syndrome: Incidence of atypical regions of involvement and imaging findings. AJR Am J Roentgenol 2007;189:904-12.  Back to cited text no. 4
    
5.
Yano Y, Kario K, Fukunaga T, Ohshita T, Himeji D, Yano M, et al. Acase of reversible posterior leukoencephalopathy syndrome caused by transient hypercoagulable state induced by infection. Hypertens Res 2005;28:619-23.  Back to cited text no. 5
    
6.
Kapiteijn E, Brand A, Kroep J, Gelderblom H. Sunitinib induced hypertension, thrombotic microangiopathy and reversible posterior leukencephalopathy syndrome. Ann Oncol 2007;18:1745-7.  Back to cited text no. 6
    
7.
Cipolla MJ. Cerebrovascular function in pregnancy and eclampsia. Hypertension 2007;50:14-24.  Back to cited text no. 7
    
8.
Roth C, Ferbert A. The posterior reversible encephalopathy syndrome: What's certain, what's new? Pract Neurol 2011;11:136-44.  Back to cited text no. 8
    
9.
Bartynski WS. Posterior reversible encephalopathy syndrome, Part 1: Fundamental imaging and clinical features. AJNR Am J Neuroradiol 2008;29:1036-42.  Back to cited text no. 9
    


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