American Journal of Emergency Medicine xxx (2014) xxx–xxx
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
This is your brain on calcium: psychosis as the presentation of isolated hypoparathyroidism Abstract We report a case of long-standing isolated hypoparathyroidism that presented with psychosis and ataxia without other signs of hypocalcemia. A 56-year-old man presented to the emergency department with report of abnormal behavior. He had recently stopped attending work and was found moving all his furniture into his basement. Physical exam was remarkable for poor attention and cerebellar ataxia. Head computed tomography was remarkable for extensive and profound calcifications involving all regions of the brain; laboratory studies revealed hypocalcemia, hyperphosphatemia, and low parathyroid. Psychiatric symptoms remitted with normalization of parathyroid hormone and calcium levels, although his ataxia remained. Hypoparathyroidism is often caused by surgery, radiation, and autoimmune syndrome; however, it can develop spontaneously in isolation. Common presentations include seizure, tetany, and ataxia associated with calcification of the basal ganglia. Our case was remarkable for extensive intracranial calcifications and unusual neurological presentation. Neurological manifestations may be the only presenting symptom of hypoparathyroidism [1–6]. Hypoparathyroidism is a disorder of low serum calcium and inappropriately low parathyroid hormone (PTH), with varied symptoms and multiple etiologies. It may be triggered by surgery, radiation therapy, cancer, or infiltrative diseases [7,8]. It may be part of an autoimmune constellation such as a polyglandular autoimmune syndrome or may be isolated. Isolated hypoparathyroidism can be insidious, presenting in advanced stages with cataracts, skin changes, and neurological manifestations [6,8– 11]. We present a case of severe, chronic isolated hypoparathyroidism which presented as psychosis. A 56-year-old male was brought to the emergency department by his family for two weeks of confusion. The patient had often forgotten his name while remembering those of his family members, experienced staring spells (without evidence of tonic-clonic movements, bowel, or bladder incontinence), had missed work sporadically and had also attempted to leave for work at odd times. As per his family, he was a reliable employee at a packing plant prior to these changes. His family reported gait instability without witnessed falls. Three days prior to presentation, he was found moving all his furniture into the basement. Upon arrival to the emergency department, the patient complained intermittently of some mild right lower quadrant pain, endorsed falling out of bed recently. He denied headache, changes in vision, vertigo, bowel/bladder incontinence, fever, vomiting, diarrhea, flank pain, alcohol use or drug use. Vitals signs on admission were significant for blood pressure 129/ 68 mmHg, pulse of 77 beat/ min, temperature maximum 97.5°F, and
respirations 20 per minute with 94% saturation on room air. On physical exam, he was alert but confused to place and time. Extraocular movements were intact, visual fields were intact, sclera were anicteric, and pupils were equal and reactive. Cardiopulmonary exam was normal. Abdomen was soft, nontender, and non-distended with normal active bowel sounds. Muscle tone was slightly increased; reflexes were 2 + all. Patient was confused, occasionally mumbling in response to questions. Neurological exam revealed slightly ataxic gait, past-pointing on finger-to-nose; patient was unable to comply with heel shin or pronator exam. He did not have Trousseau or Chvostek signs. There was evidence of ecchymoses over bilateral shins but no evidence of vitiligo or surgical scars. Computed tomography (CT) head showed extensive bilateral basal ganglia calcifications extending to the white matter throughout the cerebral hemispheres. Calcification was most pronounced within the frontal and parietal lobes but also apparent within the occipital and temporal lobes as well as the cerebellar hemispheres. CT also showed mixed density acute/sub-acute subdural hemorrhage bilaterally, right
Fig. 1. CT head.
0735-6757/$ – see front matter © 2014 Elsevier Inc. All rights reserved.
Please cite this article as: Finan M, , This is your brain on calcium: psychosis as the presentation of isolated hypoparathyroidism, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.01.032
2
M. Finan & J. Axelband / American Journal of Emergency Medicine xxx (2014) xxx–xxx
Table Data Sodium 140 mmol/L Chloride 105 mmol/L BUN 23 mg/dL Glucose 112 mg/dL AST 27 U/L Total protein 7.5 g/d: Total bili 0.22 mg/dL WBC count 6.6.1 thousand/μL Hematocrit 32.3% Platelet 239 thousand U/L Calcium 5.7 mg/dL Magnesium 1.7 mg/dL vitD 125di OH 36.3 pg/mL PTH N term b5.5 pg/mL 24 h urine phop
Potassium 3.5 mmol/L Carbon dioxide 32 mmol/L Creatinine 1.07 mg/dL ALT 23 U/L Alk phosphatase 152 U/L Albumin 3.2 g/dL Hemoglobin 10.6 g/dL MCV 83 fl Calcium inonized 0.70 mmol/L phosphorus 6.5 mg/d vit D 25 OH 37.3 ng/mL Random urine calcium b5.0 mg/dL 24 h creatinine clearance 99 mL/min per 24 h TSH 0.650 μIU/ML
larger than left (Figs. 1-8). He was admitted to the surgical intensive care unit for further monitoring. Neurosurgery was consulted and determined to manage the patient conservatively. The patient’s laboratory results on admission were concerning for low calcium (Table). Ultrasound of the neck was unremarkable; electrocardiogram showed QT prolongation. He was admitted with the preliminary diagnosis of isolated hypoparathyroidism and started on calcitriol 0.5 mcg BID, calcium carbonate tablets TID, and levetiracetam 1000 mg BID. Electroencephalogram showed background slowing and disorganization without evidence of seizure activity. Eight days after admission, his confusion had entirely remitted. His gait still remained ataxic. Given his overall deconditioning he was discharged to a rehabilitation facility, without outpatient follow-up appointments with endocrinology and neurosurgery. PTH is one of the regulatory hormones of calcium homeostasis. Both insufficient PTH release and target cell resistance to appropriately elevated PTH may cause hypocalcemia [7]. Hypoparathyroidism refers to the former and may be caused by congenital defects such as
Fig. 2. Extensive calcification of the lenticular nuclei.
Fig. 3. Calcification extending throughout the cerebrum. Right subdural hematoma.
DiGeorge, infiltrative disease such as sarcoidosis, surgical removal of the parathyroid glands, and autoimmune causes. Autoimmune causes may present as a constellation or in isolation. Isolated hypoparathyroidism is the second most common form of hypoparathyroidism after post-surgical cases. Originally referred to as idiopathic hypoparathyroidism, isolated hypoparathyroidism has been linked to several genetic disorders. Several distinct genetic abnormalities including antibodies to external calcium sensing receptors, defects encoding PTH resulting in altered processing of the pre-pro-PTH molecule, defects of mRNA translation, and
Fig. 4. Cerebellar and temporal lobe calcification.
Please cite this article as: Finan M, , This is your brain on calcium: psychosis as the presentation of isolated hypoparathyroidism, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.01.032
M. Finan & J. Axelband / American Journal of Emergency Medicine xxx (2014) xxx–xxx
Fig. 5. Frontal lobe calcification.
3
Fig. 7. Coronal section demonstrating calcification and subdural hematoma.
mutations in the GCMP gene and Xq26-27 chromosome have all been linked to hypoparathyroidism [8,12]. Intracerebral calcifications have been linked to calcium deposition caused by hyperphosphatemia found in hypoparathyroid states [13]. Seventy-three percent of patients with isolated hypoparathyroidism exhibit basal ganglia calcification [14]. Basal ganglia calcifications are progressive, may occur secondary to the high metabolic rate of the lenticular nuclei and high mucopolysaccharide content, and are associated with low calcium/phosphorus ratio [14,15]. Proposed mechanisms for the neurological dysfunction seen with basal ganglia calcifications include increased neuronal excitability and tissue ischemia [16,17]. Fujita and Roztoczynska have both demonstrated that the duration of hypocalcemia and hyperphosphatemia are related to the development of intracerebral calcifications. The causal relationship between the presence of intracerebral calcifications and varied neurologic presentations ranging from tremor and seizure to dementia and parkinsonian symptoms has not been elucidated. Recent studies suggest multiple factors at work, including PTH mediated calcium exchange and PTH receptors in the basal ganglia. Several case reports have suggested a correlation between intracranial calcifications and neurological abnormalities [10,18,19]. Aggarwal et al [20] demonstrated correlation between duration of untreated hypopara-
thyroidism and neuropsychological symptoms but failed to find correlation with intracranial calcification in a study of 62 patients. Goswami found correlation between calcification of the lenticular nuclei and increased risk of seizures, although the risk of seizure is low and can be a common incidental finding in asymptomatic patients [21]. Seizure, chorea, hemiballismus, and dysarthria have been reported in longstanding untreated hypoparathyroidism [6]. Abe et al presented a case of gait instability and parkinsonian deficits in advanced hypoparathyroidism; however, that patient also exhibited cataracts, Trosseau’s sign, and decreased reflexes. Psychosis and delirium without seizure are rare [5]. Ang et al reported a case of hypoparathyroidism presented as auditory hallucinations, delusions, and deterioration of self care which responded to normalization of calcium levels. Our case was unusual in its presentation of altered mental status, delusions, and ataxia without Trousseau’s sign, decreased deep tendon reflexes, or other evidence of hypocalcemia. Our patient experienced complete remission of his psychiatric symptoms with appropriate treatment of his hypocalcemia. We report a case of long-standing isolated hypoparathyroidism which presented with psychosis and ataxia without other signs of
Fig. 6. Coronal section demonstrating lenticular nuclei calcification.
Fig. 8. Coronal section demonstration diffuse calcification.
Please cite this article as: Finan M, , This is your brain on calcium: psychosis as the presentation of isolated hypoparathyroidism, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.01.032
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M. Finan & J. Axelband / American Journal of Emergency Medicine xxx (2014) xxx–xxx
hypocalcemia. Head CT was remarkable for extensive and profound calcifications. After normalization of calcium levels, the patient returned to his baseline mental status. Although unusual, the only sign of severe hypocalcemia may be psychosis. Meaghen Finan MD Emergency Medicine Residency, St. Luke’s University Hospital Bethlehem, PA, USA E-mail address: meaghen.fi[email protected] Jennifer Axelband DO Emergency Medicine & Critical Care Medicine St Luke’s University Hospital, Bethlehem, PA, USA
References [1] Basak R. A case report of basal ganglia calcification - a rare finding of hypoparathyroidism. Oman Med J 2009;24(3):220–2. [2] Tabee-Zadeh MJ, Frame B, Kapphahn K. Kinesiogenic choreoathetosis and idiopathic hypoparathyroidism. N Engl J Med 1972;286:762–3. [3] Kumar G, Kaur D, Aggarwal P. Hypoparathyroidism presenting as cognitive dysfunction. BMJ Case Rep 2013. http://dx.doi.org/10.1136/bcr-2013-009220. [4] Rizvi I, Ansari N, Beg M, et al. Widespread intracranial calcification, seizures and extrapyramidal manifestation in a case of hypoparathyroidism. N Am J Med Sci 2012;4(8):369–72. [5] Ang A, Ko S, Tan C. Calcium, magnesium, and psychotic symptoms in a girl with idiopathic hypoparathyroidism. Psychosom Med 1995;57(3):299–302. [6] Abe S, Tojo K, Ichida K, et al. A rare case of idiopathic hypoparathyroidism with varied neurological manifestations. Intern Med 1996;35(2):129–34. [7] Maeda S, Fortes E, Oliveira U, et al. Hypoparathyroidism and pseudohypoparathyroidism. Arq Bra Endocrinol Metabol 2006;50(4):664–73.
[8] Bilezikian J, Khan A, Potts J, et al. Hypoparathyroidism in the adult: epidemiology, diagnosis, pathophysiology, target-organ involvement, treatment, and challenges for future research. JBMR 2011;26(10):2317–37. [9] Pumarino H, Contreras P, Michelsen H. Idiopathic hypoparathyroidism, a syndrome with various clinical expressions: analysis of 10 cases. Rev Med Chil 1989;117(6):647–52. [10] Adorni A, Lussignoli G, Geroldi C, et al. Extensive brain calcification and dementia in postsurgical hypoparathyroidism. Neurology 2005;65(9):1501. [11] Roztocynska D, Kroczka S, Kumorowicz-Czoch M, et al. Neurological disorders in patients with hypoparathyroidism. Przegl Lek 2010;67(11):1149–54. [12] Goswami R, Mohapatra T, Gupta N, et al. Parathyroid hormone gene polymorphism and sporadic idiopathic hypoparathyroidism. J Clin Endocrinol Metab 2004;89(10):4840–5. [13] Fujita T. Mechanism of intracerebral calcification in hypoparathyroidism. Clin Calcium 2004;14(6):55–7. [14] Goswami R, Sharma R, Sreenivas V, et al. Prevalence and progression of basal ganglia calcification and its pathogenic mechanism in patients with idiopathic hypoparathyroidism. Clin Endocrinol 2012;77(2):200–6. [15] Mendelsohn D, Hertzanu Y, Friedman L. Hypoparathyroidism with cerebral calcification extending beyond the extrapyramidal system. S Afr Med J 1984;65 (19):781–2. [16] McKinney A. Idiopathic hypoparathyroidism presenting as chorea. Neurology 1962;12:485–91. [17] Kurozumi A, Okada Y, Arao T, et al. Extrapyramidal symptoms and advanced calcification of the basal ganglia in a patient with autosomal dominant hypocalcemia. Intern Med 2013;52(18):2077–81. [18] Cheek J, Riggs J, Lilly R. Extensive brain calcification and progressive dysarthria and dysphagia associated with chronic hypoparathyroidism. Arch Neurol 1990;47(9):1038–9. [19] Koller W, Cochran J, Klawans H. Calcification of the basal ganglia: computerized tomography and clinical correlation. Neurology 1979;29(3):328–33. [20] Aggarwal S, Kailash S, Sagar R, et al. Neuropsychological dysfunction in idiopathic hypoparathyroidism and its relationship with intracranial calcification and serum total calcium. Eur J Endocrinol 2013;168(6):895–903. [21] Tedrus G, Fonseca L, Nogueira E. Basal ganglia calcification on computed tomography: clinical characteristics in 25 patients. Arq Neuropsiquiatr 2006;64 (1):104–7.
Please cite this article as: Finan M, , This is your brain on calcium: psychosis as the presentation of isolated hypoparathyroidism, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.01.032
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
This is your brain on calcium: psychosis as the presentation of isolated hypoparathyroidism Abstract We report a case of long-standing isolated hypoparathyroidism that presented with psychosis and ataxia without other signs of hypocalcemia. A 56-year-old man presented to the emergency department with report of abnormal behavior. He had recently stopped attending work and was found moving all his furniture into his basement. Physical exam was remarkable for poor attention and cerebellar ataxia. Head computed tomography was remarkable for extensive and profound calcifications involving all regions of the brain; laboratory studies revealed hypocalcemia, hyperphosphatemia, and low parathyroid. Psychiatric symptoms remitted with normalization of parathyroid hormone and calcium levels, although his ataxia remained. Hypoparathyroidism is often caused by surgery, radiation, and autoimmune syndrome; however, it can develop spontaneously in isolation. Common presentations include seizure, tetany, and ataxia associated with calcification of the basal ganglia. Our case was remarkable for extensive intracranial calcifications and unusual neurological presentation. Neurological manifestations may be the only presenting symptom of hypoparathyroidism [1–6]. Hypoparathyroidism is a disorder of low serum calcium and inappropriately low parathyroid hormone (PTH), with varied symptoms and multiple etiologies. It may be triggered by surgery, radiation therapy, cancer, or infiltrative diseases [7,8]. It may be part of an autoimmune constellation such as a polyglandular autoimmune syndrome or may be isolated. Isolated hypoparathyroidism can be insidious, presenting in advanced stages with cataracts, skin changes, and neurological manifestations [6,8– 11]. We present a case of severe, chronic isolated hypoparathyroidism which presented as psychosis. A 56-year-old male was brought to the emergency department by his family for two weeks of confusion. The patient had often forgotten his name while remembering those of his family members, experienced staring spells (without evidence of tonic-clonic movements, bowel, or bladder incontinence), had missed work sporadically and had also attempted to leave for work at odd times. As per his family, he was a reliable employee at a packing plant prior to these changes. His family reported gait instability without witnessed falls. Three days prior to presentation, he was found moving all his furniture into the basement. Upon arrival to the emergency department, the patient complained intermittently of some mild right lower quadrant pain, endorsed falling out of bed recently. He denied headache, changes in vision, vertigo, bowel/bladder incontinence, fever, vomiting, diarrhea, flank pain, alcohol use or drug use. Vitals signs on admission were significant for blood pressure 129/ 68 mmHg, pulse of 77 beat/ min, temperature maximum 97.5°F, and
respirations 20 per minute with 94% saturation on room air. On physical exam, he was alert but confused to place and time. Extraocular movements were intact, visual fields were intact, sclera were anicteric, and pupils were equal and reactive. Cardiopulmonary exam was normal. Abdomen was soft, nontender, and non-distended with normal active bowel sounds. Muscle tone was slightly increased; reflexes were 2 + all. Patient was confused, occasionally mumbling in response to questions. Neurological exam revealed slightly ataxic gait, past-pointing on finger-to-nose; patient was unable to comply with heel shin or pronator exam. He did not have Trousseau or Chvostek signs. There was evidence of ecchymoses over bilateral shins but no evidence of vitiligo or surgical scars. Computed tomography (CT) head showed extensive bilateral basal ganglia calcifications extending to the white matter throughout the cerebral hemispheres. Calcification was most pronounced within the frontal and parietal lobes but also apparent within the occipital and temporal lobes as well as the cerebellar hemispheres. CT also showed mixed density acute/sub-acute subdural hemorrhage bilaterally, right
Fig. 1. CT head.
0735-6757/$ – see front matter © 2014 Elsevier Inc. All rights reserved.
Please cite this article as: Finan M, , This is your brain on calcium: psychosis as the presentation of isolated hypoparathyroidism, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.01.032
2
M. Finan & J. Axelband / American Journal of Emergency Medicine xxx (2014) xxx–xxx
Table Data Sodium 140 mmol/L Chloride 105 mmol/L BUN 23 mg/dL Glucose 112 mg/dL AST 27 U/L Total protein 7.5 g/d: Total bili 0.22 mg/dL WBC count 6.6.1 thousand/μL Hematocrit 32.3% Platelet 239 thousand U/L Calcium 5.7 mg/dL Magnesium 1.7 mg/dL vitD 125di OH 36.3 pg/mL PTH N term b5.5 pg/mL 24 h urine phop
Potassium 3.5 mmol/L Carbon dioxide 32 mmol/L Creatinine 1.07 mg/dL ALT 23 U/L Alk phosphatase 152 U/L Albumin 3.2 g/dL Hemoglobin 10.6 g/dL MCV 83 fl Calcium inonized 0.70 mmol/L phosphorus 6.5 mg/d vit D 25 OH 37.3 ng/mL Random urine calcium b5.0 mg/dL 24 h creatinine clearance 99 mL/min per 24 h TSH 0.650 μIU/ML
larger than left (Figs. 1-8). He was admitted to the surgical intensive care unit for further monitoring. Neurosurgery was consulted and determined to manage the patient conservatively. The patient’s laboratory results on admission were concerning for low calcium (Table). Ultrasound of the neck was unremarkable; electrocardiogram showed QT prolongation. He was admitted with the preliminary diagnosis of isolated hypoparathyroidism and started on calcitriol 0.5 mcg BID, calcium carbonate tablets TID, and levetiracetam 1000 mg BID. Electroencephalogram showed background slowing and disorganization without evidence of seizure activity. Eight days after admission, his confusion had entirely remitted. His gait still remained ataxic. Given his overall deconditioning he was discharged to a rehabilitation facility, without outpatient follow-up appointments with endocrinology and neurosurgery. PTH is one of the regulatory hormones of calcium homeostasis. Both insufficient PTH release and target cell resistance to appropriately elevated PTH may cause hypocalcemia [7]. Hypoparathyroidism refers to the former and may be caused by congenital defects such as
Fig. 2. Extensive calcification of the lenticular nuclei.
Fig. 3. Calcification extending throughout the cerebrum. Right subdural hematoma.
DiGeorge, infiltrative disease such as sarcoidosis, surgical removal of the parathyroid glands, and autoimmune causes. Autoimmune causes may present as a constellation or in isolation. Isolated hypoparathyroidism is the second most common form of hypoparathyroidism after post-surgical cases. Originally referred to as idiopathic hypoparathyroidism, isolated hypoparathyroidism has been linked to several genetic disorders. Several distinct genetic abnormalities including antibodies to external calcium sensing receptors, defects encoding PTH resulting in altered processing of the pre-pro-PTH molecule, defects of mRNA translation, and
Fig. 4. Cerebellar and temporal lobe calcification.
Please cite this article as: Finan M, , This is your brain on calcium: psychosis as the presentation of isolated hypoparathyroidism, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.01.032
M. Finan & J. Axelband / American Journal of Emergency Medicine xxx (2014) xxx–xxx
Fig. 5. Frontal lobe calcification.
3
Fig. 7. Coronal section demonstrating calcification and subdural hematoma.
mutations in the GCMP gene and Xq26-27 chromosome have all been linked to hypoparathyroidism [8,12]. Intracerebral calcifications have been linked to calcium deposition caused by hyperphosphatemia found in hypoparathyroid states [13]. Seventy-three percent of patients with isolated hypoparathyroidism exhibit basal ganglia calcification [14]. Basal ganglia calcifications are progressive, may occur secondary to the high metabolic rate of the lenticular nuclei and high mucopolysaccharide content, and are associated with low calcium/phosphorus ratio [14,15]. Proposed mechanisms for the neurological dysfunction seen with basal ganglia calcifications include increased neuronal excitability and tissue ischemia [16,17]. Fujita and Roztoczynska have both demonstrated that the duration of hypocalcemia and hyperphosphatemia are related to the development of intracerebral calcifications. The causal relationship between the presence of intracerebral calcifications and varied neurologic presentations ranging from tremor and seizure to dementia and parkinsonian symptoms has not been elucidated. Recent studies suggest multiple factors at work, including PTH mediated calcium exchange and PTH receptors in the basal ganglia. Several case reports have suggested a correlation between intracranial calcifications and neurological abnormalities [10,18,19]. Aggarwal et al [20] demonstrated correlation between duration of untreated hypopara-
thyroidism and neuropsychological symptoms but failed to find correlation with intracranial calcification in a study of 62 patients. Goswami found correlation between calcification of the lenticular nuclei and increased risk of seizures, although the risk of seizure is low and can be a common incidental finding in asymptomatic patients [21]. Seizure, chorea, hemiballismus, and dysarthria have been reported in longstanding untreated hypoparathyroidism [6]. Abe et al presented a case of gait instability and parkinsonian deficits in advanced hypoparathyroidism; however, that patient also exhibited cataracts, Trosseau’s sign, and decreased reflexes. Psychosis and delirium without seizure are rare [5]. Ang et al reported a case of hypoparathyroidism presented as auditory hallucinations, delusions, and deterioration of self care which responded to normalization of calcium levels. Our case was unusual in its presentation of altered mental status, delusions, and ataxia without Trousseau’s sign, decreased deep tendon reflexes, or other evidence of hypocalcemia. Our patient experienced complete remission of his psychiatric symptoms with appropriate treatment of his hypocalcemia. We report a case of long-standing isolated hypoparathyroidism which presented with psychosis and ataxia without other signs of
Fig. 6. Coronal section demonstrating lenticular nuclei calcification.
Fig. 8. Coronal section demonstration diffuse calcification.
Please cite this article as: Finan M, , This is your brain on calcium: psychosis as the presentation of isolated hypoparathyroidism, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.01.032
4
M. Finan & J. Axelband / American Journal of Emergency Medicine xxx (2014) xxx–xxx
hypocalcemia. Head CT was remarkable for extensive and profound calcifications. After normalization of calcium levels, the patient returned to his baseline mental status. Although unusual, the only sign of severe hypocalcemia may be psychosis. Meaghen Finan MD Emergency Medicine Residency, St. Luke’s University Hospital Bethlehem, PA, USA E-mail address: meaghen.fi[email protected] Jennifer Axelband DO Emergency Medicine & Critical Care Medicine St Luke’s University Hospital, Bethlehem, PA, USA
References [1] Basak R. A case report of basal ganglia calcification - a rare finding of hypoparathyroidism. Oman Med J 2009;24(3):220–2. [2] Tabee-Zadeh MJ, Frame B, Kapphahn K. Kinesiogenic choreoathetosis and idiopathic hypoparathyroidism. N Engl J Med 1972;286:762–3. [3] Kumar G, Kaur D, Aggarwal P. Hypoparathyroidism presenting as cognitive dysfunction. BMJ Case Rep 2013. http://dx.doi.org/10.1136/bcr-2013-009220. [4] Rizvi I, Ansari N, Beg M, et al. Widespread intracranial calcification, seizures and extrapyramidal manifestation in a case of hypoparathyroidism. N Am J Med Sci 2012;4(8):369–72. [5] Ang A, Ko S, Tan C. Calcium, magnesium, and psychotic symptoms in a girl with idiopathic hypoparathyroidism. Psychosom Med 1995;57(3):299–302. [6] Abe S, Tojo K, Ichida K, et al. A rare case of idiopathic hypoparathyroidism with varied neurological manifestations. Intern Med 1996;35(2):129–34. [7] Maeda S, Fortes E, Oliveira U, et al. Hypoparathyroidism and pseudohypoparathyroidism. Arq Bra Endocrinol Metabol 2006;50(4):664–73.
[8] Bilezikian J, Khan A, Potts J, et al. Hypoparathyroidism in the adult: epidemiology, diagnosis, pathophysiology, target-organ involvement, treatment, and challenges for future research. JBMR 2011;26(10):2317–37. [9] Pumarino H, Contreras P, Michelsen H. Idiopathic hypoparathyroidism, a syndrome with various clinical expressions: analysis of 10 cases. Rev Med Chil 1989;117(6):647–52. [10] Adorni A, Lussignoli G, Geroldi C, et al. Extensive brain calcification and dementia in postsurgical hypoparathyroidism. Neurology 2005;65(9):1501. [11] Roztocynska D, Kroczka S, Kumorowicz-Czoch M, et al. Neurological disorders in patients with hypoparathyroidism. Przegl Lek 2010;67(11):1149–54. [12] Goswami R, Mohapatra T, Gupta N, et al. Parathyroid hormone gene polymorphism and sporadic idiopathic hypoparathyroidism. J Clin Endocrinol Metab 2004;89(10):4840–5. [13] Fujita T. Mechanism of intracerebral calcification in hypoparathyroidism. Clin Calcium 2004;14(6):55–7. [14] Goswami R, Sharma R, Sreenivas V, et al. Prevalence and progression of basal ganglia calcification and its pathogenic mechanism in patients with idiopathic hypoparathyroidism. Clin Endocrinol 2012;77(2):200–6. [15] Mendelsohn D, Hertzanu Y, Friedman L. Hypoparathyroidism with cerebral calcification extending beyond the extrapyramidal system. S Afr Med J 1984;65 (19):781–2. [16] McKinney A. Idiopathic hypoparathyroidism presenting as chorea. Neurology 1962;12:485–91. [17] Kurozumi A, Okada Y, Arao T, et al. Extrapyramidal symptoms and advanced calcification of the basal ganglia in a patient with autosomal dominant hypocalcemia. Intern Med 2013;52(18):2077–81. [18] Cheek J, Riggs J, Lilly R. Extensive brain calcification and progressive dysarthria and dysphagia associated with chronic hypoparathyroidism. Arch Neurol 1990;47(9):1038–9. [19] Koller W, Cochran J, Klawans H. Calcification of the basal ganglia: computerized tomography and clinical correlation. Neurology 1979;29(3):328–33. [20] Aggarwal S, Kailash S, Sagar R, et al. Neuropsychological dysfunction in idiopathic hypoparathyroidism and its relationship with intracranial calcification and serum total calcium. Eur J Endocrinol 2013;168(6):895–903. [21] Tedrus G, Fonseca L, Nogueira E. Basal ganglia calcification on computed tomography: clinical characteristics in 25 patients. Arq Neuropsiquiatr 2006;64 (1):104–7.
Please cite this article as: Finan M, , This is your brain on calcium: psychosis as the presentation of isolated hypoparathyroidism, Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.01.032
