Varied Neurological Manifestations Seijirou Abe, Katsuyoshi Tojo, Kimiyoshi Ichida, Takashi Shigematsu, Takashi Hasegawa, Masayo Morita and Osamusakai

CASE REPORT

A Rare Case of Idiopathic Hypoparathyroidism with Varied Neurological Manifestations Seijirou Abe, Katsuyoshi Tojo, Kimiyoshi Ichida, Takashi Shigematsu, Takashi Hasegawa, Masayo Morita and OsamuSakai

A 47-year-old man was admitted for evaluation of unsteady gait, postural instability, and dysarthria. Onadmission, neurological examinations revealed cerebellar ataxia, extrapyramidal signs including parkinsonism and positive Trousseau's sign. Laboratory findings revealed severe hypocalcemia and hyperphosphatemia, and serum intact parathyroid hormonewas not detectable. Brain computedtomography revealed severe calcification of basal ganglia and dentate nuclei. He was diagnosed as idiopathic hypoparathyroidism; treatment with la (OH) vitamin D3 brought markedimprovementof neurological manifestations. Wereport a rare case of idiopathic hypoparathyroidism presenting with extrapyramidal and cerebellar dysfunction with a review of literature. (Internal Medicine 35: 129-134, 1996) Key words: hypocalcemia, basal ganglia calcification, basal ganglia disease, parkinsonism, dysarthria

Introduction and standing position became unsteady. He was referred to the hospital for further evaluation and treatment. His past medical Varied neurological manifestations are observed in patients information, and past laboratory data including serum calcium with idiopathic hypoparathyroidism (1-6). Convulsions and levels were not available. He had never been treated with tetany are the most commonsymptoms.Extrapyramidal signs vitamin D before admission. including parkinsonism and cerebellar signs have rarely been On admission, he was 159.8 cm tall and weighed 64.0 kg. reported (7, 8). In this report, we describe a rare case of Body temperature was 36.6°C and his blood pressure was 88/60 idiopathic hypoparathyroidism associated with various types of mmHg.He had no subcutaneous calcification and no brachy- neurological manifestations including extrapyramidal and cer- dactylies. There were no abnormal findings on his chest and ebellar signs. abdomen.His consciousness wasalert and no mental retarda- tion was noted. The neurological examination revealed the Case Report following: He wasalert and had no obvious signs of intellectual deterioration. Trousseau's sign was positive. There was gaze- A 47-year-old manwas admitted to our hospital in June 1994 dependent nystagmusand his smootheye movementwas for the evaluation of unsteady gait, postural instability and dysmetric. His speech was slurred and slow. The limb and dysarthria. From his childhood he had sometimes suffered from truncal ataxia were observed. His muscle tonus was decreased, numbness of hands and sudden falling down. At the age of28, and there was slight muscle weakness. Although rigidity or he fell down when riding his bicycle and consulted a doctor. He involuntary movements were not noted, bradykinesia was present was diagnosed to have epilepsy and hypocalcemia and thereaf- and he showed a mask-like face with Myerson's sign. Deep ter he had taken antiepileptic drugs (Phenobarbital 1 00 mg/day, tendon reflexes were all decreased and no pathological reflexes Phenytoin 120 mg/day, Chlordiazepoxide 10 mg/day) and were detected. The laboratory data on admission (Table 1) calcium (calcium L-aspartate 2.4 g/day). At the age of 42, he showed mild anemia, severe hypocalcemia, hyperphosphatemia, was diagnosed as having cataracts. At the age of 47, his hypomagnesemiaand the elevation of serum lactate dehydro- movementand utterance becamevery slow and gait stability genase (LDH), alkaline phosphatase (ALP) and creatine phos- Fromthe Second Department of Internal Medicine, The Jikei University School of Medicine, Tokyo Received for publication February 16, 1995; Accepted for publication October 27, 1995 Reprint requests should be addressed to Dr. Seijirou Abe, the Second Department of Internal Medicine, Jikei University School of Medicine, 3-25-8 Nishi- shinbashi, Minato-ku, Tokyo 105

Internal Medicine Vol. 35, No. 2 (February 1996) 129 Abe et al

Table 1. Laboratory Data on Admission Peripheral blood Uric acid 3.8 mg/dl Wh i te bl oo d c el l s 5 ,9 0 0/ u l C hloride 100 meq// R e d b l o o d c e l l s 3 4 3 x l O > l S od iu m 143 meq// ' H e m o g l o b i n 1 1 . 1 g / d l P otassiu m 3.6 meq// * H e m a t o c r i t 3 2 . 6 % ^C alcium 4.2 mg/dl Pla te let s 2 1 . 1 x 1 04/ |l1 1 'P ho sp hate 6.6 mg/dl ^M agn esium 1.4 mg/dl Blood chemistry (1.9- 2 .8 ) Asparta te aminot ransfera se 1 9 m U/ml T o tal cho lestero l 167 mg/dl Alan ine amin otran sfer ase 1 2 mU/ ml T riglyceride 68 mg/dl 'L ac ta te d eh y dr og en as e 5 33 m U/ ml Hem ogl obi n A le 5.3 C h ol i n e s t e r a s e 6 0 6 m U / m l To t a l b i li r u bi n 0 . 3 m g /d l U rin aly sis ' Al k al in e ph os ph a ta se 46 9 m U/ ml P ro te in (- ) Y -Glu tamyl tran spep tidas e 4 1 m U/ml Su gar (- ) 'Crea tine phosphoki nase 1 ,01 1 mU/ml C a st (- ) A l d o l a s e 7 . 5 B u / m l *C alciu m 26.4 mg/day T o t a l p r o t e i n 6 . 9 g / d l Pho sphate 740 mg /day A l b u m i n 4 . 0 g / d l M ag ne siu m 64.6 mg/day Bl oo d u re a n it r og e n 18 mg / dl CA M P 1.8 umol/day C r e a t i n i n e 0 . 7 m g / d l (1.8- 6 .3)

*: abnormal findings

Table 2. Renal Function on Admission Table 3. Endocrinological Examinations on Admis- sion Creatinine clearance 1 08 ml/min *%TRP 94.4% *intact-PTH <3 pg/ml ( 1 5-50) *TmP/GFR 6.2 mg/dl (2.3-4.3) c-PTH 0.3 ng/ml (^0.5) *FECa 0.35% (2-4) c-PTHrP 40.4 pmol// (13.8-55.3) *FEMg 2.6% (3.5-7) calcitonin 20 pg/ml (^100) *1,25(OH)2 vitamin D3 16 pg/ml (20-76) *: abnormal findings, TRP: tubular reabsorption of phosphate, TmP/GFR:renal threshold phosphate concentra- *: abnormal findings, PTH: parathyroid hormone, c: c- tion, FECa: fractional excretion of calcium, FEMg:frac- terminal fragment, PTHrP: parathyroid hormone-related tional excretion of magnesium. peptide. phokinase (CK) levels. Renal function (Table 2) showed nor- with la(OH) vitamin D3 with monitoring of serum and urine mal creatinine clearance, low fractional excretion of calcium electrolyte levels (Fig. 2). During hospitalization his serum and fractional excretion of magnesiumlevels and a high per- calcium level gradually improved. His movement, utterance, centage of tubular reabsorption of phosphate and renal thresh- gait stability and standing position were markedly improved old phosphate concentration. Onendocrinological examina- following the correction of the serumcalciumlevel. Thecoor- tions (Table 3), serum intact-parathyroid hormone (PTH) level dination disturbance however, remained almost unchanged. On was not detectable and the serum 1,25(OH)2 vitamin D3 level laboratory data, serum LDH,ALPand CKlevels were com- was subnormal range and the serum parathyroid hormone- pletely normalized. related peptide level was normal. Brain computed tomography (CT) demonstrated severe cal- Discussion cification ofbasal ganglia and dentate nuclei (Fig. 1). Neck and abdominal CT and echography demonstrated no abnormal Varied neurological findings accompanied by hypoparathy- findings. Bone survey revealed the ectopic calcification in his roidism were observed in the present case. This patient had right shoulder. Electroencephalography demonstrated the slow suffered from convulsion and tetany since childhood and there- wave, basic rhythm and no abnormal spikes. after extrapyramidal signs with parkinsonism (mask-like face, Based on the clinical and laboratory findings, he was diag- akinesia and slow speech) and cerebellar signs (truncal ataxia, nosed as idiopathic hypoparathyroidism (IHP) and was treated slurred speech and disturbance of coordination) had developed.

130 Internal Medicine Vol. 35, No. 2 (February 1996) Hypoparathyroidism and Cerebellar Ataxia

Figure 1. Brain computed tomography revealed severe calcification of basal ganglia and dentate nuclei.

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Internal Medicine Vol. 35, No. 2 (February 1996) 131 Abe et al

It was difficult to diagnose cerebellar signs under the parkinson- ing chorea, athetosis, dystonia and oculogyric crisis (8). In ism and severe muscle weakness. In this case, the muscle Table 6 we summarized the reports, following these reviews, weakness was mild and disturbance of coordination had re- focusing on hypoparathyroidism with extrapyramidal and cer- mained almost unchanged. But there was a possibility that the ebellar dysfunctions. Wefound 3 1 cases: 1 1 cases ofidiopathic, cerebellar ataxia mayhave been enhanced by parkinsonism and 3 cases of familial idiopathic, 1 case of pseudo idiopathic muscle weakness. hypoparathyroidism and 13 cases of postoperative hypopar- Thereare several reports on the neurological manifestations athyroidism. The neurological complications were as follows: ofIHP in the world (1-3) (Table 4), and in Japan (4-6) (Table 17 cases ofparkinsonism, including suspicious cases, 16 cases 5). The incidence of extrapyramidal signs in IHP is about 4 to ofchorea or choreoathetosis, 4 cases ofcerebellar dysfunctions, 12.5%. But cerebellar dysfunctions accompanied with hy- 3 cases ofdysarthria, 2 cases of oral dyskinesia and hemiballis- poparathyroidism have rarely been described (7). McKinney mus. Calcification ofbasal ganglia was observed in all but a few reported patients with IHP who demonstrated both extrapy- cases (9, 15, 17). Chorea was the most frequent involuntary ramidal and cerebellar dysfunctions, and summarized rare movementnoted in the hypoparathyroidism reported by cases of hypoparathyroidism with abnormal movementinclud- McKinney(8). In our review, choreoathetosis was the most

Table 4. Neurological Manifestations of Idiopathic Hypoparathyroidism Outside Japan R e p o rter Ste inb erg et al (l ) B ro ns ky e t al ( 2) Le vi n et al ( 3) Y e a r 19 5 2 1 9 5 8 1 9 7 8 N o. of p at ie nt s 5 0 , * 5 2 , * * u n k n o w n 5 0 13

S y m p to m s T e ta n y 3 9 (7 8 % ) 3 6 (7 2 % ) 6 (4 6 % ) C o n v u ls io n s 2 6 (5 2 % ) 3 5 (7 0 % ) 6 (4 6 % ) M u s c l e c r a m p s 3 ( 6 % ) 2 3 (4 6 % ) Par est hes i a 2 ( 4 % ) 1 2 (2 4 % ) L a ry n g e a l sp a sm 3 ( 6 % ) 16 (3 2 % ) M e n ta l c h a n g e s 4 ( 8 % ) 1 2 (2 4 % ) 1 ( 8 % ) S u b n o rm al in te llig e n c e '4 ( 9 ( 1 8 % ) 2 (1 5 % ) E x tra p y ra m id a l sig n s P ark in so n ism 2 ( 4 % ) C h o re a 1 ( 2 % ) Cal ci fi cat io n of br ai n 2 (1 5 % ) B a sa l g a n g lia 蝣<* 7 1 4 (2 8 % ) O th e rs 4 ( 8 % )

Table 5. Neurological Manifestations of Idiopathic Hypoparathyroidism in Japan R e p o rte r F u ru k a w a (4 ) H ira i e t al (5 ) Y a m am o t o et a l (6 ) Y e a r 1 9 7 7 1 9 7 8 1 9 8 3 No . of p at ie nt s 1 6 6 4 , * u n k n o w n 8 8

S y m p to m s T e ta n y 1 0 0 % 9 3 .8 % 8 0 % C o n v u ls io n s 2 5 . 0 % 5 6 . 3 % 3 4 % M u s c l e c r a m p s 5 3 % P are sth esi a 6 2 . 5 % 8 2 % L a ry n g e a l sp a sm 1 0 . 9 % 9 % M en tal c h a n g e s 1 2 . 5 % 1 0 . 9 % S u b n o rm a l in te llig e n c e 3 1. 3 % 2 1. 9 % ¥6 % E x tra p y ra m id a l sig n s 1 2 . 5 % P a rk in so n ism 6 . 3 % B a llism u s 6 . 3 % M y o c lo n u s 3 .1 % Cal ci fi cat io n of br ai n 1 8 . 5 % B a sa l g a n g lia 1 2 . 5 % 3 8 %

132 Internal Medicine Vol. 35, No. 2 (February 1996) Hypoparathyroidism and Cerebellar Ataxia

Table 6. Case Reports of Hypoparathyroidism with Extrapyramidal and Cerebellar Dysfunctions

AAuthor. Year _, AAge/Sex,o TType NeurologicalZ f findings BGCReferenceNo P CA C OD H Others

Frame,B. 1965 68/F Postoperative + + (9) Frame,B. 1965 72/F Postoperative + - (9) Frame,B. 1965 57/F Postoperative + + (9) Fonseca, OA. 1967 65/F Postoperative + (10) Muenter, MD. 1 968 45/F Idiopathic + + ( 1 1 ) Hossain 1 970 54/M Idiopathic + + ( 1 2) Christiansen, N.J. 1972 28/M (Unknown) + + (13) Tabaee, ZM. 1 972 30/M Idiopathic + + ( 14) Rubenstein, A. 1974 56/F Postoperative + Dysarthria - (15) Klawans,HL. 1976 49/F Postoperative + + (16) Soffer, D. 1 977 1 8/F Idiopathic + - ( 1 7) Berendes,K. 1978 67/- Postoperative + + (18) Walters, RO. 1 979 1 2/M Idiopathic + + ( 19) Posen,S. 1979 73/F Postoperative T + (20) Berger,JR. 1981 62/F Postoperative + + (21) Kartin, P. 1982 74/M Postoperative + + + Cerebellarmanifestations + (22) Smits, M. 1982 25/M *Idiopathic + Ataxic gait and dysmetria + (23) Smits, M. 1982 59/M ^Idiopathic + Ataxic gait and dysmetria + (23) Salti, I. 1982 45/F Postoperative + + (24) Moriwaki, Y. 1 985 69/F Idiopathic Involuntary movement of the head + (25) Uncini,A. 1985 60/F Postoperative + + (26) Kawazawa, S. 1985 38/F Pseudoidiopathic + Dysmetria and truncal ataxia suspected + (27) Friedman, JH. 1987 53/F Idiopathic + + + (28) Kato, H. 1987 27/F **Idiopathic + + (29) Barabas, G. 1 988 1 2/M Idiopathic + + (30) Cheek, JC. 1 990 8 1/F (Unknown) + Dysarthria + (3 1 ) Okuda, S. 1990 29/F Idiopathic + + + + (32) Kashihara, K. 1 992 66/F Idiopathic + Dysarthria + (33 ) Baumert, T. 1993 29/F ***(Unknown) + + + (34) Tambyah,PA. 1993 69/F Postoperative + + (35) Goel, A. 1 994 1 7/M Idiopathic + + + (36)

*autosomal dominant, **familial, ***autoimmune polyglandular syndrome type I, P: parkinsonism, CA: choreoathetosis, C: chorea, OD: oral dyskinesia, H: hemiballismus, BGC:basal ganglia calcification, T: only parkinsonian tremor. frequent type of involuntary movementexcept for parkinson- ebellar signs of IHP remained unclear. One possible mecha- ism. From another point of view, 10 cases of chorea or nism may be calcification of basal ganglia and dentate nuclei. choreoathetosis were classified as having IHP, and only 3 cases But in these case reports, vitamin D orcalcium supplement were of them were diagnosed as postoperative hypoparathyroidism, effectiveforthose symptoms (10, 12, 14, 15, 17, 19, 21, 22, 24, suggesting that chorea and choreoathetosis tend to develop as 30, 35) exceptforsomecases (16, 18, 28). Inthepresentpatient, a complication in IHP rather than postoperatively. The sex the serum calcium level improved to the lower limit of the ratio, the age of onset, the duration of the hypoparathyroidism normal range, and the extrapyramidal and cerebellar signs were and the thyroid functions appear to differ between these two markedly improved, while the calcification of basal ganglia groups. But these factors remain inconclusive; further detailed and dentate nuclei were still noted. Therefore, it seems likely investigations are necessary for clarification. Amongthe neu- that the marked hypocalcemia was involved mainly in the cause rological manifestations, we found 3 1 cases associated with of parkinsonism and cerebellar signs in this case. extrapyramidal dysfunctions and only 4 cases with cerebellar It is well knownthat hypomagnesemiacauses hypocalcemia dysfunctions (22, 23, 27). This finding suggest, that cerebellar and peripheral resistance ofPTHactions. In this case, the serum dysfunctions were less frequent than extrapyramidal dysfunc- magnesium level was low normal. Thus, it seems unlikely that tions. magnesiumdeficiency was the cause of hypocalcemia in this The accurate mechanismsof extrapyramidal signs and cer- case.

Internal Medicine Vol. 35, No. 2 (February 1996) 133 Abe et al

The Ellsworth-Howard test maybe undertaken to assess the presenting symptom in idiopathic hypoparathyroidism. J Neurol Neurosurg Psychiatry 40: 692, 1977. function of PTHreceptor, but it was not performed for the 1 8) Berendes K, Dorstelmann D. Unsuccessful treatment with levodopa of a following two reasons: 1) the patient was allergic to PTH, and parkinsonian patient with calcification of the basal ganglia. J Neurol 218: 2) there is a report concerning the intact-PTH sensitivity for the 51,1978. diagnosis of IHP (37). In accordance with the development of 19) Walters RO. Idiopathic hypoparathyroidism with extrapyramidal and a PTHassay, the Ellsworth-Howard test is not always necessary myopathic features. Arch Dis Child 54: 236, 1979. 20) Posen S, Clifton BP, Cromer T. Computerized tomography of the brain to diagnose of IHP when repeatedly measured serum intact- in surgical hypoparathyroidism. Ann Intern Med 91: 415, 1979. PTHlevels are low. 21) Berger JR, Ross DB. Reversible Parkinson syndrome complicating Wereport a rare case of IHP associated with cerebellar postoperative hypoparathyroidism. Neurology 31: 88 1 , 198 1. ataxia, and extrapyramidal signs including parkinsonism and 22) Kartin P, Zupevc M, Pogacnik T, et al. Calcification of basal ganglia, severe calcification of basal ganglia and dentate nuclei. postoperative hypoparathyroidism and extrapyramidal, cerebellar, py- ramidal motor manifestations. J Neurol 227: 171 , 1982. 23) Smits M, Gabreels F, Froeling P, et al. Autosomal dominant idiopathic References hypoparathyroidism and nervous system dysfunction: report of three cases and review of the literature. J Neurol 228: 1 13, 1982. 1) Steinberg H, Waldron BR. Idiopathic hypoparathyroidism. An analysis 24) Salti I, Faris A, Tannir N, et al. Rapid correction by 1-alpha- of fifty-two cases, including the report of a new case. Medicine 31: 133, 1952. hydroxycholecalciferol of hemichorea in surgical hypoparathyroidism. J Neurol Neurosurg Psychiatry 45: 89, 1982. 2) Bronsky D, Kushner DS, Dubin A, et al. Idiopathic hypoparathyroidism 25) Moriwaki Y, Matsui K, Yamamoto T, et al. Cerebral subcortical calcifi- and pseudohypoparathyroidism. Case reports and review of the literature. cation andhypoparathyroidism- a case report and review of the literature. Medicine 37: 317, 1958. JpnJMed24: 53, 1985. 3) Levin IG, Papapoulos SE, Tomlinson S. Studies of hypoparathyroidism 26) Uncini A, Tartaro A, Di SE, et al. Parkinsonism, basal ganglia calcifica- and pseudohypoparathyroidism. Q J Med 47: 533, 1978. tion and epilepsy as late complications of postoperative hypoparathy- 4) Furukawa Y. Hypoparathyroidism. Endocrinology (Japan) 25: 33, 1977 roidism. J Neurol 232: 109, 1985. (in Japanese). 27) Kawazawa S, Nogaki H, Hara T, et al. Paroxysmal dystonic choreoathetosis 5) Hirai S, Morimatsu M, Eto F, et al. Someneurological observations on tetany. Rinsho Shinkeigaku 18: 670, 1978 (in Japanese, abstract in in a case of pseudoidiopathic hypoparathyroidism. Rinsho Shinkeigaku English). 25: 1 152, 1985 (in Japanese, abstract in English). 28) Friedman JH, Chiucchini I, Tucci JR. Idiopathic hypoparathyroidism 6) Yamamoto M, Takuwa Y, Shibata H, et al. The second report about with extensive brain calcification and persistent neurologic dysfunction. clinical aspects of the specific type of pseudohypoparathyroidismand its Neurology 37: 307, 1987. related disorders in Japan, in: The reports of the Japanese Research 29) Kato H, Kobayashi K, Kohari S, et al. Paroxysmal kinesigenic Committee for Abnormal Mechanisms of Hormonal Receptor. Japan choreoathetosis and paroxysmal dystonic choreoathetosis in a patient Ministry of Welfare, 1983, p.58 (in Japanese). with familial idiopathic hypoparathyroidism. Tohoku J Exp Med151: 7) Pleet AB, David JS. Neurological aspects of endocrine disturbance, in: 233, 1987. Clinical Neurology, Baker AB, BakerLH, Eds. (Revised ed), JB Lippincott Company, Philadelphia, 1993, Chap. 62: p.24. 30) Barabas G, Tucker SM. Idiopathic hypoparathyroidism and paroxysmal dystonic choreoathetosis [letter]. Ann Neurol 24: 585, 1988. 8) McKinney AS. Idiopathic hypoparathyroidism presenting chorea. Neu- rology (Minneap) 12: 485, 1962. 31) Cheek JC, Riggs JE, Lilly RL. Extensive brain calcification and progres- 9) Frame B. Parkinsonism in postoperative hypoparathyroidism. Arch In- sive dysarthria and dysphagia associated with chronic hypoparathy- tern Med 116: 424, 1965. roidism. Arch Neurol 47: 1038, 1990. 10) Fonseca OA, Calverley JR. Neurological manifestations ofhypoparathy- 32) Okuda S, Murakami N, Ito E, et al. A case of idiopathic hypoparathyroidism. Arch Intern Med 120: 202, 1967. roidism with extrapyramidal signs and insulin-dependent diabetes mellitus. Rinsho Shinkeigaku 30: 635, 1990 (in Japanese, abstract in English). 1 1) Muenter MD, Whisnant JP. Basal ganglia calcification, hypoparathy- 33) Kashihara K, Yabuki S. Unilateral choreic movements in idiopathic roidism, and extrapyramidal motor manifestations. Neurology (Minneap) 18: 1075, 1968. hypoparathyroidism. No To Shinkei 44: 477, 1992 (in Japanese, abstract in English). 12) Hossain M. Neurological and psychiatric manifestations in idiopathic 34) Baumert T, Kleber G, Schwarz J, et al. Reversible hyperkinesia in a hypoparathyroidism: response to treatment. J Neurol Neurosurg Psychia- patient with autoimmune polyglandular syndrome type I. Clin Invest 71: try 33: 153, 1970. 924, 1993. 13) Christiansen NJ, Hansen PF. Choreiform movements in hypoparathyroidism. N Engl J Med 287: 569, 1972. 35) Tambyah PA, Ong BK, Lee KO. Reversible parkinsonism and asympto- matic hypocalcemia with basal ganglia calcification from hypoparathy- 14) Tabaee ZM, Frame B, Kapphahn K. Kinesiogenic choreoathetosis and roidism 26 years after thyroid surgery. AmJ Med 94: 444, 1993. idiopathic hypoparathyroidism. N Engl J Med 286: 762, 1972. 36) Goel A, Bhatnagar MK, Vashishta A, et al. Hypoparathyroidism with 15) Rubenstein A, Brust JC. Parkinsonian syndromeas a complication of extensive intracranial calcification: acase report. Postgrad MedJ 70: 9 1 3, post-thyroidectomy hypoparathyroidism. N Y State J Med 74: 2029, 1994. 1974. 37) Mizunashi K, Furukawa Y, Abe K, Yoshinaga K. The relationship 16) Klawans HL, Lupton M, Simon L. Calcification of the basal ganglia as a between serum intact parathyroid hormone and calcium in idiopathic cause of levodopa-resistant parkinsonism. Neurology 26: 221 , 1976. hypoparathyroidism. Calcif Tissue Int 53: 378, 1993. 17) SofferD, Licht A, Yaar I, Abramsky O. Paroxysmal choreoathetosis as a

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