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| LETTER TO EDITOR |
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| Year : 2013 | Volume
: 61
| Issue : 5 | Page : 528-530 |
Magnetic resonance imaging features in seizures associated with nonketotic hyperglycemia
Ying Chang1, Meng-Chao Zhang2, Huan-Huan Wan1, Hua Xin3
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 Submission | 29-May-2013 |
| Date of Decision | 11-Jun-2013 |
| Date of Acceptance | 09-Oct-2013 |
| Date of Web Publication | 22-Nov-2013 |
Correspondence Address:
Ying Chang
Department of Neurology, China-Japan Union Hospital, Jilin Univetsity, Changchun
China
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.121937
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 |
Sir,
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]
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[Figure 1], [Figure 2]
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