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Authors = Gholam Ali Shahidi

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2 pages, 294 KiB  
Brief Report
Treatment of Levodopa-Induced Dyskinesia with Vitamin D: A Randomized, Double-Blind, Placebo-Controlled Trial
by Amir Hassan Habibi, Arezo Anamoradi, Gholam Ali Shahidi, Saeed Razmeh, Elham Alizadeh and Karim Moradian Kokhedan
Neurol. Int. 2018, 10(3), 7737; https://doi.org/10.4081/ni.2018.7737 - 1 Oct 2018
Cited by 13 | Viewed by 721
Abstract
Dyskinesia refers to any involuntary movement, such as chorea, dystonia, ballism that affect any part of the body. Levodopa-induced dyskinesia is a neurological disorder that afflicts many patients with Parkinson disease usually 5 years after the onset of levodopa therapy and can cause [...] Read more.
Dyskinesia refers to any involuntary movement, such as chorea, dystonia, ballism that affect any part of the body. Levodopa-induced dyskinesia is a neurological disorder that afflicts many patients with Parkinson disease usually 5 years after the onset of levodopa therapy and can cause severe disability. The pathophysiology of this dyskinesia is complex and not fully understood. However, the association between vitamin D and Parkinson disease is interesting. The present study was conducted to evaluate the effect of vitamin D on levodopa induced dyskinesia in patients with Parkinson’s disease .In this Double blind clinical trial, 120 patients with PD divided into two groups randomly, vitamin D and placebo group. A dose of 1000 IU/d was selected, Demographic information is registered. In the first visit, three variables have been measured which were the duration, severity of dyskinesia and unified Parkinson’s disease rating scale (UPDRS). These variables were measured again after 3 months and the data was analyzed using SPSS 22. There are no differences between two groups after 3 months. This study revealed, vitamin D has no effects on improvement of levodopa induced dyskinesia. Full article
3 pages, 452 KiB  
Brief Report
A Pilot Trial of Deferiprone in Pantothenate Kinase-Associated Neurodegeneration Patients
by Mohammad Rohani, Saeed Razmeh, Gholam Ali Shahidi and Maryam Orooji
Neurol. Int. 2017, 9(4), 7279; https://doi.org/10.4081/ni.2017.7279 - 15 Feb 2018
Cited by 21 | Viewed by 791
Abstract
Pantothenate kinase-associated neurodegeneration (PKAN) is the most common form of neurodegeneration with brain iron accumulation, it is an autosomal recessive disease due to mutation in PANK 2 on chromosome 20, which causes the accumulation of iron in basal ganglia and production of free [...] Read more.
Pantothenate kinase-associated neurodegeneration (PKAN) is the most common form of neurodegeneration with brain iron accumulation, it is an autosomal recessive disease due to mutation in PANK 2 on chromosome 20, which causes the accumulation of iron in basal ganglia and production of free radicals that cause degeneration of the cells. Deferiprone is an iron chelator that was used in treatment of thalassemia patients, it can cross the blood-brain barrier and reverse the iron deposition in the brain. Five patients with genetically confirmed PKAN received 15 mg/kg deferiprone twice daily. All patients were examined at baseline, 12 and 18 months and magnetic resonance imaging (MRI) was done at the baseline and after 18 months. In our study qualitative evaluation of MRI showed that deferiprone was able to reduce the iron load in globus pallidus of all the patients and the results of clinical rating scales show that in four patients, there is an improvement in the first 12 months. The results of our paper show that deferiprone can prevent the progression of the disease. Full article
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