scholarly journals Idiopathic Basal Ganglia Calcification Presented with Impulse Control Disorder

2015 ◽  
Vol 2015 ◽  
pp. 1-4
Author(s):  
Cem Sahin ◽  
Mustafa Levent ◽  
Gulhan Akbaba ◽  
Bilge Kara ◽  
Emine Nese Yeniceri ◽  
...  

Primary familial brain calcification (PFBC), also referred to as Idiopathic Basal Ganglia Calcification (IBGC) or “Fahr’s disease,” is a clinical condition characterized by symmetric and bilateral calcification of globus pallidus and also basal ganglions, cerebellar nuclei, and other deep cortical structures. It could be accompanied by parathyroid disorder and other metabolic disturbances. The clinical features are dysfunction of the calcified anatomic localization. IBGC most commonly presents with mental damage, convulsion, parkinson-like clinical picture, and neuropsychiatric behavior disorders; however, presentation with impulse control disorder is not a frequent presentation. In the current report, a 43-year-old male patient who has been admitted to psychiatry policlinic with the complaints of aggressive behavior episodes and who has been diagnosed with impulse control disorder and IBGC was evaluated in the light of the literature.

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kazuya Nishii ◽  
Ritsuko Shimogawa ◽  
Hisaka Kurita ◽  
Masatoshi Inden ◽  
Michio Kobayashi ◽  
...  

AbstractIdiopathic basal ganglia calcification (IBGC) is a rare intractable disease characterized by abnormal mineral deposits, including mostly calcium in the basal ganglia, thalamus, and cerebellum. SLC20A2 is encoding the phosphate transporter PiT-2 and was identified in 2012 as the causative gene of familial IBGC. In this study, we investigated functionally two novel SLC20A2 variants (c.680C > T, c.1487G > A) and two SLC20A2 variants (c.82G > A, c.358G > C) previously reported from patients with IBGC. We evaluated the function of variant PiT-2 using stable cell lines. While inorganic phosphate (Pi) transport activity was abolished in the cells with c.82G > A, c.358G > C, and c.1487G > A variants, activity was maintained at 27.8% of the reference level in cells with the c.680C > T variant. Surprisingly, the c.680C > T variant had been discovered by chance in healthy members of an IBGC family, suggesting that partial preservation of Pi transport activity may avoid the onset of IBGC. In addition, we confirmed that PiT-2 variants could be translocated into the cell membrane to the same extent as PiT-2 wild type. In conclusion, we investigated the PiT-2 dysfunction of four SLC20A2 variants and suggested that a partial reduced Pi transport function of PiT-2 might not be sufficient to induce brain calcification of IBGC.


2015 ◽  
Vol 2015 ◽  
pp. 1-3
Author(s):  
M. Abedini ◽  
N. Karimi ◽  
N. Tabrizi

Multiple sclerosis (MS) is a chronic inflammatory demyelinating and neurodegenerative disease of central nervous system that affects both white and gray matter. Idiopathic calcification of the basal ganglia is a rare neurodegenerative disorder of unknown cause that is characterized by sporadic or familial brain calcification. Concurrence of multiple sclerosis (MS) and idiopathic basal ganglia calcification (Fahr’s disease) is very rare event. In this study, we describe a cooccurrence of idiopathic basal ganglia calcification with multiple sclerosis. The association between this disease and MS is unclear and also maybe probably coincidental.


2014 ◽  
Vol 36 (9) ◽  
pp. 823-825 ◽  
Author(s):  
Makoto Ishitobi ◽  
Masao Kawatani ◽  
Mizuki Asano ◽  
Hirotaka Kosaka ◽  
Takashi Goto ◽  
...  

2019 ◽  
Vol 7 (12) ◽  
pp. 1483-1491
Author(s):  
Seiju Kobayashi ◽  
Kumiko Utsumi ◽  
Masaru Tateno ◽  
Tomo Iwamoto ◽  
Tomonori Murayama ◽  
...  

2018 ◽  
Vol 388 ◽  
pp. 150-154 ◽  
Author(s):  
Isao Hozumi ◽  
Hisaka Kurita ◽  
Kazuhiro Ozawa ◽  
Nobuyuki Furuta ◽  
Masatoshi Inden ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Shin-ichiro Sekine ◽  
Masayuki Kaneko ◽  
Masaki Tanaka ◽  
Yuhei Ninomiya ◽  
Hisaka Kurita ◽  
...  

2007 ◽  
Vol 22 (7) ◽  
pp. 1027-1030 ◽  
Author(s):  
Misuzu Saiki ◽  
Shinji Saiki ◽  
Koichiro Sakai ◽  
Ichiro Matsunari ◽  
Kotaro Higashi ◽  
...  

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