局部神經症狀可能為非酮性高血糖患者最早出現的症狀，而且有時因此診斷出早已罹患但不自知的糖尿病。我們報告兩位非酮性高血糖患者，一位有一側肢體的舞蹈症，另一位則是有局部的運動型抽搐。這些疾患最佳的治療為胰島素及補充體液，當血糖控制之後，症狀通常很快緩解，若使用抗癲癎藥物來治療非酮性高血糖引起之抽搐，特別是二苯妥因(phenytoin)，常常無效，甚至使血糖更加升高。為何非酮性高血糖會導致局部神經症狀，原因仍不明，有一假說為當有非酮性高血糖時，腦部會以代謝伽馬氨基丁酸（Gamma-aminobutyric acid，簡稱GABA）來提供能量，GABA在腦部的作用為抑制性神經傳導物質，因GABA被代謝掉而不足，在基底核便產生舞蹈症，在大腦皮質便產生抽搐。另外有一假說認為高血糖會造成腦部血流灌注不足，使腦部暫時性局部缺血，因而產生症狀。所以遇到患者以局部神經症狀表現時，不可忽略掉非酮性高血糖這個原因，快速的診斷才能指引正確的治療。

Focal neurological symptoms may provide the first clinical clue to the presence of nonketotic hyperglycemia (NKH) and sometimes unveil previously undiagnosed diabetes. We report two patients with hemichorea-hemiballism (HC-HB) or partial motor seizures as the first manifestation of NKH. These disorders are best treated with insulin and rehydration. The neurological symptoms generally resolve with the correction of hyperglycemia. Antiepileptic treatment, especially phenytoin, is usually futile and even aggravates hyperglycemia. The exact mechanisms of how NKH causes focal neurological symptoms are unknown. One hypothesis is related to the depletion of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA), which is metabolized in the brain as an energy source in NKH. The deficiency of GABA in the basal ganglia may lead to HC-HB, while in the cerebral cortex it may lower the seizure threshold. Another hypothesis involves transient focal cerebral ischemia caused by hyperglycemia. Therefore we should not overlook NKH as a cause of focal neurological symptoms. Rapid recognition of their association will allow for prompt and correct treatment.