Recurrent syncope and hypocalcaemic cardiomyopathy as manifestations of Fahr’s syndrome confirmed that these attacks had not occurred, exercise tolerance had improved, and oedema of the lower extremities was not present. However, the patient’s husband observed gradual deterioration of neurocognitive functions. Discussion In this case of BSPDC, attacks of unconscious- ness were the predominant neurological manifestation. Our patient also presented hypocalcaemic cardiomyopathy. There are case reports presenting cases of reversible hypocalcaemic cardiomyopathy [8-11]. Long-lasting hypocalcaemia may result in cardiac dysfunction. Having in mind that laboratory results disclosed hypothyroidism (caused by autoimmune processes – antithyroid antibodies) it may be possible that this condition is partially responsible for cardiomyopathy. Hypothyroidism may cause both systolic and diastolic dysfunction. In our patient only systolic dysfunction was noted, which seems to be connected with calcium deficiency. Restoration of a normal calcium level resulted in clinical and echocardiographic improvement in two weeks. We conclude that two weeks time was too short a period to restore hormonal balance although thyroxine was added to the treatment regimen. The patient did not consent to coronary angiography, so we cannot rule out atherosclerosis and ischaemic heart disease. However, the patient did not give a history of retrosternal pain or any other symptoms that could suggest coronary artery disease. The laboratory findings and massive intracranial calcifications suggesting long-standing hypocalcaemia confirm our theory. Calcium is necessary for myocardial contractile function. Parathormone has a positive inotropic effect on the heart muscle that is mediated by increasing the entry of calcium into myocardial cells and the release of endogenous myocardial norepinephrine [12]. Myocardial sarcoplasmic reticulum is not able to sequestrate a sufficient quantity of calcium to initiate contraction. The strength of myocardial contraction is associated with extracellular calcium influx. It has also been proposed that a decrease of calcium levels in renal tubular cells may increase renal sodium reabsorption and via this mechanism promote sodium retention and the development of cardiac failure [10]. The role of calcium in the therapy of cardiac failure should be kept in mind as loop diuretics such as furosemide or torasemide may induce hypocalcaemia even in patients with normal parathormone levels. If congestive heart failure does not respond to conventional anti-failure therapy, hypocalcaemia should be taken into consideration. Therefore, the idea of calcium level determination in all patients with heart failure suggested in previous reports [10, 11] is supported by us. It is possible that patients with asymptomatic hypocalcaemia and heart failure treated with high doses of loop diuretics may develop severe hypocalcaemia and their state may deteriorate. Such a case has been previously reported [9]. In conclusion, patients with BSPDC can present a variety of symptoms. BSPDC cases are reported mainly by psychiatrists or neurologists. Our patient demonstrated only mild neurological and psychiatric symptoms but developed hypocalcaemic heart failure. Having in mind that cardiomyopathy associated with hypocalcaemia is reversible, we should determine the calcium level in all subjects with heart failure. Acknowledgments Sincere thanks to Bogdan Błaszczyk, MD and Marek Kazanek, MD for help with the description of CT scans. R e f e r e n c e s 1. Geschwind DH, Loginov M, Stern JM. Identification of a locus on chromosome 14q for idiopathic basal ganglia calcification (Fahr disease). Am J Hum Genet 1990; 65: 764-72. 2. Kotan D, Aygul R. 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