Dear Sirs, Celiac disease (CD) may manifest only with neurological symptoms [5], even in advanced age [3]. No clear association has been reported to date between CD and Parkinson’s disease (PD). A 75-year-old man presented with a 1-year history of difficulty with walking, instability, and fatigability. Neurological examination showed facial hypomimia, bradykinesia, rigidity, and postural instability with a UPDRS/Part II score of 8 and a UPDRS/part III motor score of 19 (Table 1). The remaining neurological examination was unremarkable. The patient had never been treated with drugs acting on the central nervous system; in particular he had never received drugs causing parkinsonism such as neuroleptics. Brain MR revealed several nonspecific foci of hyperintensity in the frontal and parietal subcortical white matter but not in the basal ganglia. Few punctate calcifications were present in the globus pallidus bilaterally, a finding that is quite common in elderly subjects [6]. Singlephoton emission computed tomography (SPECT) after intravenous injection of 185 MBq of I-FP-CIT (DaTSCAN, G.E. Healthcare, UK) showed a pronounced decrease of radiotracer uptake in the left putamen and moderate decrease in the contralateral putamen (Fig. 1). Activity was clearly visible in the caudate nuclei of both hemispheres. Semi-quantitative analysis confirmed visual assessment of images: putamen-to-occipital cortex uptake ratios were lower than values obtained in healthy subjects, and the reduction was more pronounced on the left hemisphere. On the basis of clinical and SPECT data, a diagnosis of Parkinson’s disease was made. Laboratory studies revealed reduced serum folate level (2.8 ng/ml, n.v. 3–15) and hyperhomocysteinemia (23.4 lmol/l, n.v. 5–15), but vitamin B12 level was normal. The possibility of asymptomatic malabsortion due to a silent CD was explored. Serological screening revealed anti-gliadin antibodies, markedly elevated IgA (236 U/ml, n.v.\ 20) and IgG (86 U/ml; n.v. \ 20), anti-transglutaminase antibodies, and positive anti-endomysial antibodies. Duodenal histology was diagnostic of CD. The gastroenterologist prescribed a gluten-free diet. The patient came back to the neurological outpatient clinic only 3 months after the beginning of the gluten-free diet: during this period he had no pharmacological treatment for PD, but he reported an almost complete remission of symptoms. The improvement was confirmed by neurological evaluation, with a UPDRS/Part II score of 3 and a UPDRS/part III motor score of 8 (Table 1). Because of this improvement, we decided not to treat the patient at this stage. In order to define whether the gluten-free diet had modified striatum dopaminergic activity, we repeated the SPECT study 8 months after diet onset. SPECT confirmed the previous abnormalities and showed a further decrease in radiotracer uptake in the putamen bilaterally. Activity V. Di Lazzaro (&) F. Capone F. Ranieri Department of Neurosciences, Institute of Neurology, Campus Bio-Medico University, Via Alvaro del Portillo 200, 00128 Rome, Italy e-mail: v.dilazzaro@unicampus.it
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