A 69-year-old woman presented to our inpatient clinic to evaluate a 2-month history of widespread joint pain, muscle cramps, slowness of movements, tremor of the head, and difficulty in speech. She had suffered from arterial hypertension, secondary hypothyroidism, and hypoparathyroidism for 30 years, due to a papillary thyroid cancer for which she had undergone thyroparathyroidectomy and a radioactive iodine therapy (I-131). There was no history of preexisting neuropsychiatric manifestations, mood disturbances or seizure, and her family history was not contributory. Her drug treatment was amlodipine 10 mg/die, oral levo-tiroxin 125 lg/die, and calcitriol 0.25 lg/die, and she had discontinued the supplemental calcium salts intake for the 2 prior years, because of the findings of joint and kidney calcifications.At admission, she was conscious and oriented to the time and place, with a normal memory and intelligence. Vital signs were within normal limits, excepting a poor drug control of the blood pressure (181/103 mmHg). Neurological examination confirmed the intentional tremors of the head and the upper limbs, a gait disorder with mild impairment of balance and substantially normal coordination, and dysarthric speech with ''punctuated voice''. Otherwise, she had neither motor weakness nor cranial nerve involvement, presented only mild bradykinesia without rigidity or stooped posture, and absent primitive reflexes. Her remaining clinical examinations were unremarkable.Routine laboratory tests revealed normal hemogram, renal and liver function, serum electrolytes such as sodium, potassium, chloride and magnesium, protidogram, and standard urinalysis. Laboratory investigations of thyroid and parathyroid function and calcium-phosphorus metabolism showed hypocalcemia (total calcium 6.7 mg/dL, ionized calcium 3.03 mg/dL) and hyperphosphatemia (4.9 mg/dL), with normal values of thyroid-stimulating hormone (TSH, 0.83 lUI/mL), free thyroxine (fT4, 1.18 ng/dL), parathyroid hormone (PTH, 9.1 pg/mL) and vitamin D (22 ng/mL). Moreover, blood tests for rheumatic diseases such as rheumatoid factor, antinuclear antibody test, anti-cyclic citrullinate peptide antibody and extractable nuclear antigen panel were all unremarkable.To clarify the neurological involvement, an unenhanced brain magnetic resonance imaging (MRI) was performed, showing homogeneously altered signal intensity in the putamen, globus pallidus, caudate and cerebellar hemispheres (Fig. 1a). To rule out a chronic calcium deposition disease, an unenhanced brain computed tomography (CT) was carried out, confirming diffuse calcified concretions of basal ganglia and cerebellum (Fig. 1b, c). Based on these findings, a diagnosis of Fahr's syndrome was made.The patient's treatment was implemented with oral calcium and vitamin D3 supplements 1000 mg ? 880 UI/ die, levodopa and benserazide 100 ? 25 mg/die, and alprazolam 0.5 mg/die, observing an improvement in neurological signs and symptoms.Bilateral striatopallidodentate calcinosis (BSPDC), otherwise known as Fahr's synd...