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INTERESTING IMAGE
Year : 2019  |  Volume : 34  |  Issue : 4  |  Page : 321-323  

FDG PET/CT with SPM analysis in early diagnosis of clinically suspected osmotic demyelination syndrome with non-contributory MRI


1 Department of Nuclear Medicine and PET/CT, Mahajan Imaging Center, Sir Ganga Ram Hospital, New Delhi, India
2 Department of Neurology, Sir Ganga Ram Hospital, New Delhi, India
3 Department of Nuclear Medicine and PET/CT, Institute of Nuclear Medicine and Allied sciences, New Delhi, India

Date of Web Publication23-Sep-2019

Correspondence Address:
Dr. Nikhil Seniaray
Department of Nuclear Medicine and PET/CT, Mahajan Imaging Centre, Sir Ganga Ram Hospital, Old Rajinder Nagar, New Delhi - 110 060
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijnm.IJNM_95_19

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   Abstract 


Early diagnosis is imperative for adequate management of patients with osmotic demyelination syndrome (ODS), which is usually a result of rapid shifts of osmolality secondary to rapid correction of hyponatremia. Magnetic resonance imaging (MRI) with its special sequences is the investigation of choice for early detection of the osmotic changes in the brain. We report a case of clinically suspected ODS with noncontributory MRI and positive fluoro-2-deoxy-d-glucose positron emission tomography (FDG PET) scan with statistical parametric mapping (SPM) analysis, which localized the focal hypermetabolism in the basal ganglia, thalamus, pons, and cerebellum.

Keywords: FDG PET, MRI, SPM


How to cite this article:
Seniaray N, Verma R, Ranjan R, Belho E, Malik D, Gupta V, Jaimini A, Mahajan H. FDG PET/CT with SPM analysis in early diagnosis of clinically suspected osmotic demyelination syndrome with non-contributory MRI. Indian J Nucl Med 2019;34:321-3

How to cite this URL:
Seniaray N, Verma R, Ranjan R, Belho E, Malik D, Gupta V, Jaimini A, Mahajan H. FDG PET/CT with SPM analysis in early diagnosis of clinically suspected osmotic demyelination syndrome with non-contributory MRI. Indian J Nucl Med [serial online] 2019 [cited 2019 Oct 22];34:321-3. Available from: http://www.ijnm.in/text.asp?2019/34/4/321/267520



We report a case of 66 year old lady, known case of hypertension and type-2 diabetes mellitus, who developed stiffness of limbs with associated slurring of speech and gait imbalance, since 4 days. On biochemical analysis, she was found to have hyponatremia (serum sodium 95 mmol/l) and was started on 3% saline therapy, following which the serum sodium level rose up to 120 mmol/l in the next 36 hours. Although her general condition showed improvement, she had deterioration in speech and bulbar function. On central nervous system examination, she was conscious and had bilateral gaze-evoked nystagmus without any restriction in ocular movements. She had relatively poor bilateral palatal movement with power IV+/V, increased generalized tone and equivocal plantar response. Gait ataxia and limb incoordination was also present. Suspecting osmotic demyelination syndrome (ODS), MRI brain was done, which was found to be normal [Figure 1]a, [Figure 1]b, [Figure 1]c, [Figure 1]d]. Her blood investigations, electroencephalogram, and autoimmune panel came out to be noncontributory. Fluoro-2-deoxy-d-glucose positron emission tomography/computed tomography (FDG-PET/CT) whole-body scan was done to rule out any precipitating factor. FDG-PET/CT scan was done [Figure 2] which revealed hypermetabolism in the basal ganglia, thalamus, pons, and cerebellum with no obvious abnormality on the corresponding CT images, which was in favor of pontine and extrapontine myelinolysis. SPM analysis [Figure 3] was done to validate the findings of FDG-PET. She was managed conservatively with serum sodium and potassium monitoring to keep the sodium levels around 130–134 mmol/l. She responded to the therapeutic interventions and stabilized gradually. Repeat MRI done 2 weeks later showed T2 hyperintensity in the pons, basal ganglia, and thalami with signal alteration in pons on diffusion-weighted (DW) imaging 'suggestive of ODS' [Figure 1]e, [Figure 1]f, [Figure 1]g, [Figure 1]h.
Figure 1: MRI scan showing T2-weighted and corresponding diffusion-weighted images. The images in the upper row (a-d) represent the initial MRI scan done at the time of presentation of symptoms of osmotic demyelination syndrome, which was unremarkable. Follow-up MRI (e-h) done 2 weeks after the initial MRI scan shows subtle hyperintensity in the basal ganglia, thalamus, and pons with restricted diffusion in the pons, consistent with the diagnosis of osmotic demyelination syndrome

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Figure 2: Fused axial FDG PET/CT images (a-c) showing hypermetabolism in the pons, basal ganglia, thalamus, and cerebellum with no obvious abnormality on the CT scan

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Figure 3: SPM analysis image showing areas of hyper-metabolism co-registered to a normal T1 weighted MRI for localization of region of involvement

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ODS, which encompasses both central and extrapontine myelinolysis, is a rare neurological complication attributed to rapid correction of hyponatremia or rapid shifts of osmolality in certain metabolic and toxic states.[1] It is characterized by destruction of the myelin sheath and oligodendrocytes in the pons, cerebellum, hippocampus, basal ganglia, brainstem, and thalamus without any inflammation with relative preservation of the axons.[1] The diagnosis is usually based on clinical suspicion and confirmed on MRI. Conventional MRI including T1-weighted, T2-weighted, fluid-attenuated inversion recovery (FLAIR), and DW imaging may show lesions in the form of signal alteration, days to weeks after the onset of symptoms, and may not be contributory to the diagnosis during the initial period.[2],[3],[4] FDG, a competitive glucose analog, demonstrates glucose metabolic activity at a given physiological or pathological site. Activated microglia and astrocytes in the brain, with their phagocytic properties, accumulate very rapidly at the site of demyelination in ODS and show increased glycolysis secondary to their accumulation; this results in focal hypermetabolism on FDG-PET images.[5] In our patient, in the clinical setting of complaints of dysarthria and ataxia with bulbar dysfunction and altered sensorium, in the background of rapid correction of hyponatremia, led to a clinical suspicion of ODS, which was strongly supported by the presence of focal hypermetabolism in pons and multiple extrapontine regions on FDG-PET/CT scan.[5] Thus, an FDG-PET/CT scan may act as a noninvasive confirmatory modality and contribute to the early diagnosis and management of patients with clinical suspicion of ODS and noncontributory/normal MRI.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understand that her name and intials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Martin RJ. Central pontine and extrapontine myelinolysis: The osmotic demyelination syndromes. J Neurol Neurosurg Psychiatry 2004;75 Suppl 3:iii22-8.  Back to cited text no. 1
    
2.
Ruzek KA, Campeau NG, Miller GM. Early diagnosis of central pontine myelinolysis with diffusion-weighted imaging. AJNR Am J Neuroradiol 2004;25:210-3.  Back to cited text no. 2
    
3.
Bekiesińska-Figatowska M, Bulski T, Rózyczka I, Furmanek M, Walecki J. MR imaging of seven presumed cases of central pontine and extrapontine myelinolysis. Acta Neurobiol Exp (Wars) 2001;61:141-4.  Back to cited text no. 3
    
4.
Miller GM, Baker HL Jr., Okazaki H, Whisnant JP. Central pontine myelinolysis and its imitators: MR findings. Radiology 1988;168:795-802.  Back to cited text no. 4
    
5.
Roh JK, Nam H, Lee MC. A case of central pontine and extrapontine myelinolysis with early hypermetabolism on 18FDG-PET scan. J Korean Med Sci 1998;13:99-102.  Back to cited text no. 5
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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