Hypoparathyroidism With Brain Calcifications May Cause Movement Problems, Case Report Shows

Ana Pena, PhD avatar

by Ana Pena, PhD |

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Hypoparathyroidism may be the underlying cause of movement disorders, such as chorea, that are associated with calcium deposits in the brain, a case study reports.

In patients with such motor problems and brain calcifications but no other neurological signs, doctors should strongly consider hypoparathyroidism, the researchers said.

The study, “Adult-Onset Isolated Hemichorea Revealing Iatrogenic Hypoparathyroidism and Bilateral Basal Ganglia Calcification,” was published in the journal Annals of Indian Academy of Neurology.

Chorea is characterized by brief, irregular, and involuntary muscle contractions. Isolated hemichorea, which affects one side of the body without any other neurological features, is a distinctive clinical syndrome. In adults, it may be caused by hyperglycemia (high blood levels of glucose), toxoplasmosis infection in HIV patients, or immune-related conditions.

In the study, researchers described a rare case where hemichorea was caused by hypoparathyroidism and was its only symptom.

Hypoparathyroidism is caused by a deficiency in the parathyroid hormone (PTH) and marked by low levels of calcium (hypocalcemia) and high levels of phosphorus (hyperphosphatemia) in the blood.

Chronic hypocalcemia can lead to the accumulation of calcium (calcifications) in the basal ganglia, a group of small brain structures important for movement control.

Hypoparathyroidism-related calcification in the basal ganglia can potentially cause neurological problems such as chorea, and twisting movements of the hands and feet. However, these problems usually affect both sides of the body.

The study described the case of a 47-year-old woman in India, who had started experiencing involuntary movements on the left side of her body two years before she entered the clinic. The movements were initially intermittent, progressively causing greater clumsiness and difficulty in daily activities, speaking, and eating.

No other medical or cognitive issues were reported at the time. Laboratory analysis revealed severe hypocalcemia and hyperphosphatemia, as well as markedly low PTH levels, while all other parameters were normal.

This was consistent with a diagnosis of hypoparathyroidism, as was the fact that the woman had underwent a thyroidectomy (a surgery to remove the thyroid) 20 years earlier. Thyroidectomy may cause hypoparathyroidism because the parathyroid glands — where PTH is produced — may be inadvertently removed or injured during surgery.

Assessments of the patient for other possible causes of chorea, such as Wilson disease, were negative. Cognitive and neuropsychological scores were normal.

However, brain imaging by computer tomography scans revealed dense basal ganglia calcifications in both sides of her brain.

The patient was then prescribed oral calcium and vitamin D3 (cholecalciferol) supplements — the standard therapy for hypoparathyroidism — which significantly lessened hemichorea after two weeks. At a three-month follow-up, her movements had improved markedly.

Overall, one-sided (unilateral) muscle spasms were the only symptom found in this patient, unlike other cases of hypoparathyroidism-related brain calcifications, where movement disorders appear in combination with psychiatric syndromes, seizures, or cognitive decline.

“The case serves as a reminder that both metabolic conditions as well as bilateral symmetric structural lesions can present with a strictly unilateral neurological manifestation,” the researchers wrote.

Testing for hypoparathyroidism should be done on all patients with any movement disorder and basal ganglia calcifications so as not to miss this potentially treatable metabolic condition, the researchers said, before doctors consider idiopathic ‘Fahr’s disease,’ which is a rare genetic disorder with similar symptoms.