Effect of basal ganglia calcification on its glucose metabolism and dopaminergic function in idiopathic hypoparathyroidism

Modi, Sagar; Arora, Geetanjali; Bal, Chandra Shekhar; Sreenivas, Vishnubhatla; Kailash, S.; Sagar, Rajesh; Goswami, Ravinder

doi:10.1111/cen.12649

Cited by 3 publications

(2 citation statements)

References 26 publications

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“…In an Indian cohort, the prevalence of seizures in IH was 64%, and just below 90% presented with a generalised tonic-clonic seizure, although partial complex seizures did also occur (4.4%) [ 14 ]. Basal ganglia calcification is easily seen on CT scan, as in our patient; however, nuclear imaging modalities such as 18 F-FDG may also be used to confirm basal ganglia calcification through reduced basal ganglia glucose uptake, which is directly proportional to the degree of basal ganglia calcification [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

Hypoparathyroidism Causing Seizures: When Epilepsy Does Not Fit

Seedat

Daya

Bhana

2018

Case Reports in Medicine

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A 24-year-old man presented to the Chris Hani Baragwanath Academic Hospital emergency department with recurrent seizures having previously been diagnosed with epilepsy from age 14. The biochemical investigations and brain imaging were suggestive of seizures secondary to hypocalcemia, and a diagnosis of idiopathic hypoparathyroidism was confirmed. After calcium and vitamin D replacement, the patient recovered well and is seizure free, and off antiepileptic therapy. This case highlights the occurrence of brain calcinosis in idiopathic hypoparathyroidism; the occurrence of acute symptomatic seizures due to provoking factors other than epilepsy; and the importance, in the correct clinical setting, of considering alternative, and sometimes treatable, causes of seizures other than epilepsy.

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Section: Discussionmentioning

confidence: 99%

Hypoparathyroidism Causing Seizures: When Epilepsy Does Not Fit

Seedat

Daya

Bhana

2018

Case Reports in Medicine

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“…( 152 ) Rarity of clinical parkinsonism and lack of correlation between cognitive disturbance and BGC could be explained by the presence of relatively intact glucose metabolism and dopaminergic transporters in calcified basal ganglia region in hypoparathyroidism. ( 153 ) These observations raise the possibility that mechanical destruction of the surfaces of the corticostriatal tracts where they pass through calcified basal ganglia or alteration in Ca 2+ ‐dependent enzymes might contribute to the pathogenesis of neuropsychological symptoms in hypoparathyroidism. ( 154 )…”

Section: Pathophysiology Of the Disease And Selected Complicationsmentioning

confidence: 99%

Etiology and Pathophysiology of Hypoparathyroidism: A Narrative Review

Pasieka

Wentworth

Yeo

et al. 2020

Journal of Bone and Mineral Research

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The approach utilized a systematic review of the medical literature executed with specifically designed criteria that focused on the etiologies and pathogenesis of hypoparathyroidism. Enhanced attention by endocrine surgeons to new knowledge about parathyroid gland viability are reviewed along with the role of intraoperative parathyroid hormone (ioPTH) monitoring during and after neck surgery. Nonsurgical etiologies account for a significant proportion of cases of hypoparathyroidism (~25%), and among them, genetic etiologies are key. Given the pervasive nature of PTH deficiency across multiple organ systems, a detailed review of the skeletal, renal, neuromuscular, and ocular complications is provided. The burden of illness on affected patients and their caregivers contributes to reduced quality of life and social costs for this chronic endocrinopathy. © 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).

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