Brief clinical observationReversible parkinsonism and asymptomatic hypocalcemia with basal ganglia calcification from hypoparathyroidism 26 years after thyroid surgery
References (5)
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Parkinsonism, basal ganglia calcification and epilepsy as late complications of postoperative hypoparathyroidism
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Computerised tomography of the brain in surgical hypoparathyroidism
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Cited by (40)
Fahr's syndrome due to hypoparathyroidism revisited: A case of parkinsonism and a review of all published cases
2021, Clinical Neurology and NeurosurgeryCitation Excerpt :Our patient presented with parkinsonism, which was the most common movement disorder among cases, with a moderate response to levodopa. Parkinsonism in Fahr’s syndrome generally does not respond to levodopa [13,47–51], whereas there is a significant response of parkinsonian signs to restoration of calcium levels using calcium and vitamin D [52–63] or both calcium/vitamin D and levodopa [64,65]. On the other hand, there have also been reported cases without any improvement despite treatment with calcium and vitamin D [66–68] or even worsening of symptoms and progression of BG calcifications [54,69].
Conventional Treatment of Hypoparathyroidism
2018, Endocrinology and Metabolism Clinics of North AmericaCitation Excerpt :Loop diuretics increase renal calcium excretion and should not be administered to patients with hypoparathyroidism.45,46 Extraskeletal calcifications (renal stones and calcifications, cataracts, and basal ganglia calcifications) are often present in patients with longstanding hypoparathyroidism.47–49 A high calcium-phosphate product likely increases the risk of extraskeletal calcifications, and it is, therefore, reasonable to decrease the serum phosphate level by prescribing and adhering to a low phosphate diet.50
Signs and Symptoms of Hypoparathyroidism
2018, Endocrinology and Metabolism Clinics of North AmericaCitation Excerpt :The prevalence of extrapyramidal symptoms in smaller case series of patients with hypoparathyroidism has been 4.0% to 12.5%.38 Whereas brain calcification may be responsible in part for the neuromotor symptoms described in hypoparathyroid patients, in various cases, neuromotor abnormalities were partially, if not completely, reversible with treatment for hypocalcemia.38,39,41,42 Aggarwal and colleagues43 systemically studied 62 patients with idiopathic hypoparathyroidism (age 37 ± 15 years, 44% women, duration 12 ± 9 years) and found that neurologic signs were present in 35.5% of patients with hypoparathyroidism, with extrapyramidal findings in 16.1% and cerebellar findings in 20.9%.
Epidemiology and Complications of Hypoparathyroidism
2018, Endocrinology and Metabolism Clinics of North AmericaCitation Excerpt :For every 1% increase in the calcium/phosphorus ratio during follow-up, the odds of progression decreased by 5% (OR 0.95; 95% CI 0.93–0.99). Intracranial calcifications have also been reported in longstanding postsurgical hypoparathyroidism, and may be associated with Parkinson-like symptoms,28 but these symptoms resolved with control of blood calcium. In a small case series of 9 patients with postsurgical hypoparathyroidism, calcifications were detected by CT imaging in 5 patients.29
Reborn after calcium infusion
2015, European Geriatric MedicineCitation Excerpt :Hypocalcemia may be associated with a spectrum of clinical manifestations, ranging from few if any symptoms if the hypocalcemia is mild, to life-threatening seizures, refractory heart failure, or laryngospasm if it is severe [2,3]. Extrapyramidal symptoms are seen in 4–12.5% of the patients with hypoparathyroidism [4,5]. The prevalence of hypothyroidism causing dementia is unknown.
Molecular and Clinical Aspects of Pseudohypoparathyroidism
2015, The Parathyroids: Basic and Clinical Concepts: Third Edition