Hemichorea–Hemiballism after Diabetic Ketoacidosis  

Oleh:

Duker, A.P. ; Espay, A.J.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The New England Journal of Medicine (keterangan: ada di Proquest) vol. 363 no. 17 (Oct. 2010), page 363:e27.
Topik: DIABETES

Ketersediaan

Perpustakaan FK Nomor Panggil: N08.K.2010.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

A 37-year-old man with insulin-dependent diabetes who had undergone kidney transplantation 7 years earlier presented with delirium caused by diabetic ketoacidosis. His calculated serum osmolarity peaked at 304 mOsm per liter, and the serum glucose level reached 528 mg per deciliter (29.3 mmol per liter). The initial serum sodium level was 132 mmol per liter, which normalized to 139 mmol per liter over 18 hours. The patient's mental status normalized 2 days after the administration of insulin and intravenous hydration. Three weeks later, he noted that his right arm and right leg were “fidgety,” a symptom that rapidly increased in intensity. The physical examination revealed right hemichorea with a ballistic component (see video at NEJM.org). Magnetic resonance imaging (MRI) of the brain showed an area of T2-weighted hyperintensity in the pons (Panel A, arrowhead) with sparing of the corticospinal fibers, which was consistent with the osmotic demyelination syndrome. Also noted was a T1-weighted hyperintensity in the left putamen (Panel B, arrow). The osmotic demyelination syndrome refers to myelinolysis, typically in the central pontine region, which occurs as a result of osmotic derangements. Although the condition is typically associated with rapid correction of hyponatremia, diabetic ketoacidosis can also cause this syndrome as a result of osmotic shifts generated by rapid changes in serum glucose levels. The putaminal lesion that was seen on T1-weighted imaging probably resulted from a diverging response to the same hyperglycemia. The patient was given haloperidol, which resolved his symptoms. Haloperidol was discontinued after 1 month, without recurrence of hemichorea–hemiballism. At the 3-month follow-up visit, there were no abnormal movements on physical examination. Despite symptomatic resolution, repeat brain MRI showed the abnormalities that were seen on previous imaging.

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