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      A case of psychosis due to Fahr's syndrome and response to behavioral disturbances with risperidone and oxcarbazepine

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          Abstract

          Calcification of basal ganglia or Fahr's syndrome is a rare disease characterized by bilateral and symmetrical intracranial deposition of calcium mainly in cerebral basal ganglia. Motor and neuropsychiatric symptoms are prominent features. We report a case presented with a few motor symptoms, features of delirium and prominent psychiatric symptoms (disorganized behavior) predominantly evident after the improvement in delirium. Radiological findings were suggestive of bilateral basal ganglia calcification. Parathyroid hormone levels were low with no significant findings in other investigations and negative family history. Patient showed significant improvement in behavioral disturbances with risperidone, low dose of lorazepam, oxcarbazepine, and memantine.

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          Long-term follow-up of patients with hypoparathyroidism.

          Deborah M Mitchell, M Cooley, Jürgen Becker … (2012)
          Despite tremendous interest in hypoparathyroidism, large cohort studies describing typical treatment patterns, laboratory parameters, and rates of complications are lacking. Our objective was to characterize the course of disease in a large cohort of hypoparathyroid patients. We conducted a chart review of patients with permanent hypoparathyroidism identified via a clinical patient data registry. Patients were seen at a Boston tertiary-care hospital system between 1988 and 2009. We identified 120 patients. Diagnosis was confirmed by documented hypocalcemia with a simultaneous low or inappropriately normal PTH level for at least 1 yr. Mean age at the end of the observation period was 52 ± 19 (range 2-87) yr, and the cohort was 73% female. We evaluated serum and urine laboratory results and renal and brain imaging. We calculated time-weighted average serum calcium measurements for all patients. The time-weighted average for calcium was between 7.5 and 9.5 mg/dl for the majority (88%) of patients. Using linear interpolation, we estimated the proportion of time within the target calcium range for each patient with a median of 86% (interquartile range 67-98%). Of those with a 24-h urine collection for calcium (n = 53), 38% had at least one measurement over 300 mg/d. Of those with renal imaging (n = 54), 31% had renal calcifications, and 52% of those with head imaging (n = 31) had basal ganglia calcifications. Rates of chronic kidney disease stage 3 or higher were 2- to 17-fold greater than age-appropriate norms. Hypoparathyroidism and its treatment carry a large burden of disease. Renal abnormalities are particularly common.
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            Prevalence and progression of basal ganglia calcification and its pathogenic mechanism in patients with idiopathic hypoparathyroidism.

            S. Das, Nandita Gupta, Raju Sharma … (2012)
            The pathogenesis of basal ganglia calcification (BGC) in hypoparathyroidism is not clear. Its occurrence in hypocalcaemic milieu of hypoparathyroidism is believed to be due to high serum calcium-phosphorus product and poor calcium control. To report details of BGC in patients with idiopathic hypoparathyroidism (IH) and factors determining its progression during follow-up. Clinical, biochemical characteristics and a meningioma-expressed antigen-6 (MGEA6) gene polymorphism were analysed in 145 patients with IH, recruited since 1998, to determine the factors associated with BGC. The progression of BGC and its relationship with metabolic control of serum calcium, phosphorus, serum 25(OH)D and 1,25(OH)(2) D were assessed after a mean of 6·9 ± 3·5 years in 49 of them. Basal ganglia calcification was present in 73·8% (95% CI: 66·6%-81·0%) of subjects affecting the globus pallidus (68·8%) putamen (55·9%) and caudate nucleus (54·8%). The other sites calcified were grey-white junction (39·8%), cerebellar parenchyma (31·2%), thalamus (29·0%) and dentate nuclei (24·7%). Parkinsonism and dystonic symptoms were present in three cases. The presence of BGC at presentation was associated with calcification of the choroid plexus, cataract and an increased risk of seizures but not tetany. The progression of BGC during follow-up was related to calcium/phosphorus ratio. For every 1% increase in this ratio, the odds of progression decreased by 5% (OR: 0·95, 95% CI: 0·93-0·99, P < 0·001). A MGEA6 polymorphism, serum 25(OH)D and 1,25(OH)(2)D did not affect progression of BGC. Basal ganglia calcification occurs in 73·8% of patients with IH and correlates with the duration of hypocalcaemia, choroid plexus calcification, seizures and cataract. The progression of BGC is related to the calcium/phosphorus ratio during follow-up. This brings forth the importance of adequate phosphorus control in the management of hypoparathyroidism. © 2012 Blackwell Publishing Ltd.
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              Subacute dementia and imaging correlates in a case of Fahr's disease.

              T Benke, E Karner, J Marksteiner … (2004)
              We report a case of idiopathic bilateral basal ganglia calcinosis, or Fahr's disease (FD) in a 50 year old patient who developed rapidly progressive behavioural abnormalities and severe neuropsychological impairments, but no movement disorder. Neuropsychological deficits included a severe dysexecutive syndrome, anterograde amnesia, and attentional impairment. Neuropsychiatric features comprised apathy with intermittent disinhibition, anxiety, irritability, frequent mood changes, ritualistic and antisocial behaviour, and psychosis. Fluorodeoxyglucose positron emission tomography showed a massive reduction of glucose metabolism in the basal ganglia and the frontal brain. The observed abnormalities possibly result from a disruption of frontostriatal circuits, presumably at the basal ganglia level. This case indicates that FD may cause exclusively behavioural alterations and that the associated hypometabolism in certain frontal areas is closely related to the clinical picture.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Indian J Psychiatry
                Journal ID (iso-abbrev): Indian J Psychiatry
                Journal ID (publisher-id): IJPsy
                Title: Indian Journal of Psychiatry
                Publisher: Medknow Publications & Media Pvt Ltd (India )
                ISSN (Print): 0019-5545
                ISSN (Electronic): 1998-3794
                Publication date (Print): Apr-Jun 2014
                Volume: 56
                Issue: 2
                Pages: 188-190
                Affiliations
                [1]Department of Psychiatry, NKP Salve Institute of Medical Sciences and Lata Mangeshkar Hospital, Nagpur, Maharashtra, India
                Author notes
                Address for correspondence: Dr. Abhijeet Dhawalram Faye, Department of Psychiatry (OPD-10), 2 nd Floor, OPD Building, NKP Salve Institute of Medical Sciences and Lata Mangeshkar Hospital, Digdoh Hills, Hingna Road, Nagpur - 440 019, Maharashtra, India. E-mail: dr.abhifaye@ 123456yahoo.co.in
                Article
                Publisher ID: IJPsy-56-188
                DOI: 10.4103/0019-5545.130506
                PMC ID: 4040070
                PubMed ID: 24891710
                SO-VID: d1515348-bdf1-4dd7-8990-a443a0a044f9
                Copyright © Copyright: © Indian Journal of Psychiatry
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Subject: Case Report

                ScienceOpen disciplines: Clinical Psychology & Psychiatry
                Keywords: basal ganglia,calcification,fahr's syndrome,parathyroid hormone,psychiatric symptoms
                Data availability:
                ScienceOpen disciplines: Clinical Psychology & Psychiatry
                Keywords: basal ganglia, calcification, fahr's syndrome, parathyroid hormone, psychiatric symptoms

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