Postoperative hypoparathyroidism as a cause of neurologic symptoms mimicking an acute cerebrovascular accident: case report

Background. D. Hypoparathyroidism is a disorder caused by decreased secretion of parathyroid hormone and is characterized by hypocalcemia and hyperphosphatemia. Currently, up to 75-80% of hypoparathyroidism cases are postoperative. Transient hypoparathyroidism after thyroidectomy develops in 19-38% of patients, whereas permanent disease occurs in 1-7%. Russian clinical guidelines (2021) report comparable figures. Historically, clinical observations of tetany after thyroid surgery were first described by Ernest Gley in 1891, which contributed to the recognition of the parathyroid glands as an independent endocrine structure [1]. Hypocalcemia may cause a wide spectrum of neurological disturbances, including paresthesia, muscle cramps, tetany, seizures, cognitive impairment, QT interval prolongation, and transient focal neurological symptoms. The clinical presentation may closely resemble acute stroke, leading to inappropriate triage and delayed pathogenetic treatment. According to Goyal A. et al. (Frontiers in Neurology, 2021), up to 12% of episodes of severe hypocalcemia are misinterpreted as stroke.

Objective. To present a clinical case of chronic postoperative hypoparathyroidism manifesting as an acute focal neurological deficit initially suspected to be an acute cerebrovascular event, and to emphasize the diagnostic value of assessing calcium–phosphate metabolism and parathyroid hormone levels after thyroid surgery.

Materials and methods. We report a clinical case of a 28-year-old woman with Graves’ disease who underwent staged surgical treatment of the thyroid gland (hemithyroidectomy followed by total thyroidectomy), complicated by chronic hypoparathyroidism. A retrospective analysis of clinical manifestations, laboratory parameters (PTH, total and ionized calcium, serum phosphate, and 25(OH) vitamin D), and instrumental investigations was performed, including neuroimaging to exclude acute stroke. The patient’s clinical course and response to acute and maintenance therapy were evaluated.

Results. Severe hypocalcemia resulted in acute focal neurological symptoms, prompting emergency hospitalization with suspected stroke. Brain MRI revealed no ischemic lesions. Positive Chvostek and Trousseau signs, together with the rapid regression of neurological deficits after intravenous calcium gluconate administration, supported a metabolic origin of the presentation. Initiation of active vitamin D analogues (alfacalcidol) in combination with oral calcium supplementation led to clinical stabilization and prevention of recurrent episodes. This case highlights the need for routine postoperative monitoring of serum calcium and parathyroid hormone levels after thyroidectomy and for including hypocalcemia in the differential diagnosis of acute neurological conditions to avoid diagnostic errors and ensure timely pathogenetic treatment.

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