2013
DOI: 10.1590/0004-282x20130096
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Delayed hemichorea syndrome associated with nonketotic hyperglycemia

Abstract: A 69-year-old woman was admitted for investigation of an acute-onset right hemichorea 1. T1-weighted brain magnetic resonance imaging (MRI) showed hyperintensity in the left basal ganglia (Figs 1A and B). Although diabetic, she had no hyperglycemia. Interestingly, two weeks earlier, the patient was admitted due to nonketotic hyperglycemia. Brain computed tomography, previously reported as normal (Fig 1C), showed subtle

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“…The onset of the aberrant movements may be preceded by non-specific symptoms, such as numbness, weakness, gait imbalance, vertigo, and dizziness [4,25]. There is not always a close temporal correlation between diabetic decompensation and motor symptoms, and, to our knowledge, few case reports describe a delayed onset of chorea up to 3 months after the trigger (Table 2), and they seem to be similar to ours [25][26][27][28][29]. In general, these types of movements typically manifest during waking time and cease during sleep, and they tend to normalize after the correction of the glycemia and/or with the use of tetrabenazine and reserpine, which are dopamine-depleting agents; benzodiazepines, enhancing GABA signaling; and/or antipsychotics such as haloperidol (most used), chlorpromazine, sulpiride, tiapride, and pimozide, with variable outcomes [4,5,14,30,31].…”
Section: Case Report (Figure 1)supporting
confidence: 53%
“…The onset of the aberrant movements may be preceded by non-specific symptoms, such as numbness, weakness, gait imbalance, vertigo, and dizziness [4,25]. There is not always a close temporal correlation between diabetic decompensation and motor symptoms, and, to our knowledge, few case reports describe a delayed onset of chorea up to 3 months after the trigger (Table 2), and they seem to be similar to ours [25][26][27][28][29]. In general, these types of movements typically manifest during waking time and cease during sleep, and they tend to normalize after the correction of the glycemia and/or with the use of tetrabenazine and reserpine, which are dopamine-depleting agents; benzodiazepines, enhancing GABA signaling; and/or antipsychotics such as haloperidol (most used), chlorpromazine, sulpiride, tiapride, and pimozide, with variable outcomes [4,5,14,30,31].…”
Section: Case Report (Figure 1)supporting
confidence: 53%