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Table of Contents    
Year : 2013  |  Volume : 61  |  Issue : 5  |  Page : 528-530

Magnetic resonance imaging features in seizures associated with nonketotic hyperglycemia

1 Department of Neurology, China-Japan Union Hospital, Jilin Univetsity, Changchun, China
2 Department of Radiology, China-Japan Union Hospital, Jilin Univetsity, Changchun, China
3 Department of Thoracic Surgery, China-Japan Union Hospital, Jilin Univetsity, Changchun, China

Date of Submission29-May-2013
Date of Decision11-Jun-2013
Date of Acceptance09-Oct-2013
Date of Web Publication22-Nov-2013

Correspondence Address:
Ying Chang
Department of Neurology, China-Japan Union Hospital, Jilin Univetsity, Changchun
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.121937

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How to cite this article:
Chang Y, Zhang MC, Wan HH, Xin H. Magnetic resonance imaging features in seizures associated with nonketotic hyperglycemia. Neurol India 2013;61:528-30

How to cite this URL:
Chang Y, Zhang MC, Wan HH, Xin H. Magnetic resonance imaging features in seizures associated with nonketotic hyperglycemia. Neurol India [serial online] 2013 [cited 2023 Dec 10];61:528-30. Available from:


A 57-year-old female was admitted for episodic clonic jerks affecting her right face and arm, each episode lasting for approximately 2′ of 10 days duration. There was no improvement of jerks with carbamazepine, instead there was increase in the frequency (every 5′) and also developed right upper limb weakness. Past medical history was negative. Neurological examination revealed right hemiparesia. Admission serum glucose was 29.8 mmol/L with no ketone bodies in the urine; serum sodium was 133.8 mmol/L and potassium was 3.5 mmol/L; blood urea nitrogen was 6.0 mmol/L and calculated serum osmolality was 310.4 mmol/L. Admission computed tomography was normal. Electroencephalography (EEG) revealed inter-ictal epileptiform discharges around the left central sulcus [Figure 1]a-c. Brain magnetic resonance imaging (MRI) [Figure 2] done on day 2 of admission showed subcortical hypointensity signal changes in the left parietal region on T2-weighted (T2-W), fluid attenuated inversion recovery (FLAIR) and diffusion-weighted imaging (DWI). Apparent diffusion coefficient (ADC) map showed isointensity in the corresponding region. Overlying cortical showed hyperintensity on FLAIR, DWI sequences and hypointensity on ADC map. The ADC values in cortical and subcortical lesions were lower than contralateral normal regions, especially in cortical lesions. T1-W sequences were normal. She was diagnosed as epileptia partialis continua (EPC) associated with nonketotic hyperglycemia (NKH). Carbamazepine was stopped and intravenous insulin therapy was started. She had good glycemic control and the jerking remitted completely within 72 h. Follow up MRI at 5 months showed complete resolution of cortical hyperintensity and subcortical hypointensity.
Figure 1: Ictal electroencephalography showing the presence of fast activity over the left central and parietal region with a frequency between 15 and 16 Hz, occasionally spreading to the left hemisphere with more theta waves

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Figure 2: The brain MRI at day 2 of admission showed subcortical hypointensity signal changes in the left parietal region on T2-W, FLAIR and DWI. ADC map showed isointensity in the corresponding region. Overlying cortical hyperintensity on FLAIR, DWI sequences and cortical hypointensity on ADC map were observed simultaneously. The ADC values in cortical and subcortical lesions were lower than contralateral normal regions, especially in cortical lesions (ADC value: The right parietal lobe: 708.1 mm 2/s; the left parietal cortex: 336 mm2/s; the left parietal white matter: 369.9 mm2/s)

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Epileptic seizures are common in hyperglycemia and are often presenting features, particularly in NKH with blood glucose levels more than 20 mmol/L. [1],[2],[3] NKH-related seizures are mostly focal motor, sometimes it can be EPC. In this patient, hyperglycemia was de novo. In patients presenting with EPC, NKH should be considered and ruled out. Seizures associated with NKH are resistant to antiepileptic drugs and remit with correction of hyperglycemic state. [4] The precise pathgenesis of EPC in patients with NKH is not yet clear. The proposed mechanisms include: Hyperglycemia induce vascular lesions; [5],[6] a decrease in brain gamma aminobutyric acid (GABA) level leading to a decrease in the seizure threshold. [7],[8] Intracellular acidosis may elevate GABA levels and lack of ketosis may be a trigger factor to induce seizures. [9]

Conventional computed tomography and MRI in patients with NKH and seizures are largely unremarkable. [10],[11] Recent reports have described transient, but typical changes with subcortical hypointensity on T2 and FLAIR images. [12],[13] Similar were the MRI findings in our patient. The exact mechanism for these transient subcortical hypointensity remains unclear. One possible mechanism could be subcortical free radical accumulation as a result of excitotoxic axonal damage during seizures. [14] But we suggest that hyperosmolar state in NKH may lead to these secondary pathological changes. DWI hyperintensity changes and low ADC values showed restricted diffusion in left parietal cortical region, which suggested "cytotoxic edema" induced by hyperosmolality. Hyperosmolality may also lead to dehydration of white matter. The existence of hyperosmolality was proved by magnetic resonance spectroscopy studies. [15] While hyperviscosity and the decline in carrying oxygen capacity of red blood cells caused hyperglycemia may be responsible for cortical cytotoxic edema. [16]

 » References Top

1.Lammouchi T, Zoghlami F, Ben Slamia L, Grira M, Harzallah MS, Benammou S. Epileptic seizures in non-ketotic hyperglycemia. Neurophysiol Clin 2004;34:183-7.  Back to cited text no. 1
2.Qi X, Yan YY, Gao Y, Zheng ZS, Chang Y. Hemichorea associated with non-ketotic hyperglycaemia: A case report. Diabetes Res Clin Pract 2012;95:e1-3.  Back to cited text no. 2
3.Scherer C. Seizures and non-ketotic hyperglycemia. Presse Med 2005;34:1084-6.  Back to cited text no. 3
4.Hennis A, Corbin D, Fraser H. Focal seizures and non-ketotic hyperglycaemia. J Neurol Neurosurg Psychiatry 1992;55:195-7.  Back to cited text no. 4
5.Taieb-Dogui T, Harzallah MS, Khlifa K, Dogui M, Ben Ammou S, Jallon P. Acute repetitive gyratory seizures as a manifestation of nonketotic hyperglycemia. Neurophysiol Clin 2002;32:254-7.  Back to cited text no. 5
6.Siddiqi ZA, VanLandingham KE, Husain AM. Reflex seizures and non-ketotic hyperglycemia: An unresolved issue. Seizure 2002;11:63-6.  Back to cited text no. 6
7.Moien-Afshari F, Téllez-Zenteno JF. Occipital seizures induced by hiperglycemia: A case report and review of literature. Seizure 2009;18:382-5.  Back to cited text no. 7
8.Schwechter EM, Velísková J, Velísek L. Correlation between extracellular glucose and seizure susceptibility in adult rats. Ann Neurol 2003;53:91-101.  Back to cited text no. 8
9.Likhodii SS, Serbanescu I, Cortez MA, Murphy P, Snead OC 3 rd , Burnham WM. Anticonvulsant properties of acetone, a brain ketone elevated by the ketogenic diet. Ann Neruol 2003;54:219-26.  Back to cited text no. 9
10.Freedman KA, Polepalle S. Transient homonymous hemianopia and positive visual phenomena in nonketotic hyperglycemic patients. Am J Ophthalmol 2004;137:1122-4.  Back to cited text no. 10
11.Ozer F, Mutlu A, Ozkayran T. Reflex epilepsy and non-ketotic hyperglycemia. Epileptic Disord 2003;5:165-8.  Back to cited text no. 11
12.Lavin PJ. Hyperglycemic hemianopia: A reversible complication of non-ketotic hyperglycemia. Neurology 2005;65:616-9.  Back to cited text no. 12
13.Kang SS, Keasey MP, Cai J, Hagg T. Loss of neuron-astroglial interaction rapidly induces protective CNTF expression after stroke in mice. J Neurosci 2012;32:9277-87.  Back to cited text no. 13
14.Benjelloun N, Renolleau S, Represa A, Ben-Ari Y, Charriaut-Marlangue C. Inflammatory responses in the cerebral cortex after ischemia in the P7 neonatal rat. Stroke 1999;30:1916-23.  Back to cited text no. 14
15.Guez A, Obadia M, Lafitte F, Tin SN, Héran F, Gout O. Magnetic resonance spectroscopy findings in a case of hyperglycaemic hemianopia. Rev Neurol (Paris) 2010;166:737-40.  Back to cited text no. 15
16.Chu K, Kang DW, Kim DE, Park SH, Roh JK. Diffusion-weighted and gradient echo magnetic resonance findings of hemichorea-hemiballismus associated with diabetic hyperglycemia: A hyperviscosity syndrome? Arch Neurol 2002;59:448-52.  Back to cited text no. 16


  [Figure 1], [Figure 2]

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[Pubmed] | [DOI]


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