Write Click: Editor’s Choice Section Editor Robert C. Griggs, MD Editors’ Note: In response to “Hemichorea-hemiballism associated with hyperglycemia and a developmental venous anomaly” by Kalia et al., Drs. Civardi and Collini describe their own case of putaminal CT hyperperfusion without the developmental venous anomaly (DVA), resulting in unilateral myoclonus. The authors describe possible explanations for the abnormal CT perfusion (CTP) findings in their own case study. Megan Alcauskas, MD, and Robert C. Griggs, MD HEMICHOREA-HEMIBALLISM ASSOCIATED WITH HYPERGLYCEMIA AND A DEVELOPMENTAL VENOUS ANOMALY Carlo Civardi, Alessandra Collini, Novara, Italy: Kalia et al. 1 described a case of a hyperglycemia- induced hemichorea-hemiballism with the typical high signal on T1-weighted images on MRI 2 in the puta- men contralateral to the movement. Additional neuro- imaging revealed a DVA adjacent to the affected putamen associated with increased cerebral blood flow and volume on CTP. The authors proposed that altered hemodynamics within the basal ganglia along with a metabolic distur- bance resulted in movement disorder. We reported a man with repetitive myoclonus of the left side of the body and contralateral putaminal CT hyperperfusion. Carbam- azepine completely controlled myoclonus and, concur- rently, CT showed normal perfusion. 3 Our patient did not have a DVA and there was no metabolic defect. As in other hyperkinetic disorders, CT hyperperfu- sion as observed in these patients 1,3 may indicate failed autoregulatory mechanisms in the basal ganglia vessels. 4 These 2 reports showed the same putaminal hyperper- fusion, albeit with a different etiology. The perfusional pattern may be related to hyperkinetic status and not to the etiology of the movement disorder. Moreover, this recent report confirms the utility of CTP in the assess- ment of hyperkinetic disorders. Author Response: Lorraine V. Kalia, Anthony E. Lang, Richard I. Aviv, Mario Masellis, Toronto: We thank Drs. Civardi and Collini for their thoughtful comments. We agree that there are several potential explanations for the abnormal CTP findings in our case. 1 As they suggested, one possibility is that the observed increases in cerebral blood flow and cerebral blood volume are a consequence and not a cause of the patient’s hemiballism-hemichorea. Another possibility is that this CTP pattern within the putamen was a result of the adjacent DVA. A similar pattern has been previously described with MRI perfusion (MRP) in 4 patients with a DVA. 5 Follow-up imaging in our patient after complete resolution of her hemiballism- hemichorea may have been useful in differentiating between these 2 possibilities (i.e., resolution of CTP abnormalities with the first possibility vs persistence with the second possibility). However, based on simi- larities between the MRP and CTP techniques, we anticipate that the latter would be more likely. While the CTP findings in our case 1 and those described by Civardi et al. 3 are interesting, further characterization of this type of imaging in hyperkinetic movement disorders is required before we can establish its utility in the assessment of patients with movement disorders. © 2013 American Academy of Neurology 1. Kalia LV, Mozessohn L, Aviv RI, et al. Hemichorea-hemiballism associated with hyperglycemia and a developmental venous anomaly. Neurology 2012;78:838–839. 2. Postuma RB, Lang AE. Hemiballism: revisiting a classic disorder. Lancet Neurol 2003;2:661–668. 3. Civardi C, Collini A, Stecco A, Carriero A, Monaco F. Neuro- logical picture: putamen hyperperfusion in subcortical-supraspinal myoclonus. J Neurol Neurosurg Psychiatry 2010;81:330. 4. Hsu JL, Wang HC, Hsu WC. Hyperglycemia-induced uni- lateral basal ganglion lesions with and without hemichorea: a PET study. J Neurol 2004;251:1486–1490. 5. Camacho DL, Smith JK, Grimme JD, Keyserling HF, Castillo M. Atypical MR imaging perfusion in developmen- tal venous anomalies. AJNR Am J Neuroradiol 2004;25: 1549–1552. DECREASED IRON LEVELS IN THE TEMPORAL CORTEX IN POSTMORTEM HUMAN BRAINS WITH PARKINSON DISEASE Osamu Kano, Ken Ikeda, Yasuo Iwasaki, Tokyo: Yu et al. 1 reported that iron levels in the temporal cortex were reduced in patients with Parkinson disease (PD) compared with age-matched controls. They also deter- mined that patients with Alzheimer disease (AD) had no change in iron levels in the temporal cortex. We Neurology 81 September 24, 2013 1181