Síndrome de Fahr secundario a hipoparatiroidismo posquirúrgico 15 años después de tiroidectomía. Reporte de caso

Fahr’s syndrome secondary to postoperative hypoparathyroidism 15 years after thyroidectomy: A case report

Introducción. El síndrome de Fahr es un trastorno neurológico poco frecuente caracterizado por calcificaciones bilaterales simétricas en diferentes partes del cerebro. Cuando este síndrome es secundario a hipoparatiroidismo posquirúrgico, las manifestaciones clínicas suelen iniciar muchos años después de la tiroidectomía.

Presentación del caso. Mujer de 71 años que fue llevada al servicio de urgencias de un hospital de tercer nivel de atención de Pasto (Colombia) debido a la presencia de disartria progresiva, trismo, alteración de la marcha, alucinaciones visuales y cambios comportamentales durante la última semana. La paciente había sido sometida a una tiroidectomía total 15 años antes de la consulta y tenía hipotiroidismo en manejo con levotiroxina, pero no había sido valorada por endocrinología desde la cirugía. Los exámenes de laboratorio de ingreso mostraron hipocalcemia severa, hiperfosfatemia e hipoparatiroidismo. Una tomografía computarizada de cabeza mostró calcificaciones simétricas en ganglios basales y cerebelo. Teniendo en cuenta estos hallazgos, así como el antecedente de tiroidectomía, fue diagnosticada con síndrome de Fahr. Se instauró tratamiento intravenoso con gluconato de calcio, cloruro de potasio y sulfato de magnesio, el cual, luego de unos días, fue cambiado de forma gradual a administración oral de carbonato de calcio, calcitriol y cloruro de potasio. Ante la mejoría progresiva de los síntomas motores y neuropsiquiátricos, fue dada de alta cinco días después del ingreso con indicación de continuar el tratamiento farmacológico y asistir a controles periódicos. En cita de control tres semanas después del egreso, se observó una mejora considerable de la marcha, el estado mental y la conducta; los exámenes de control mostraron niveles normales de calcio y fósforo. El tratamiento oral se ha mantenido con ajustes periódicos y la paciente sigue asistiendo a controles regulares.

Conclusión. El diagnóstico del síndrome de Fahr en fases clínicas sintomáticas tardías exige una alta sospecha clínica. Este caso resalta la necesidad de seguimiento endocrinológico periódico y permanente tras tiroidectomía y evidencia que el tratamiento adecuado de las alteraciones bioquímicas puede mejorar significativamente la calidad de vida del paciente.

Introduction: Fahr’s syndrome is a rare neurological disorder characterized by symmetrical and bilateral calcifications in different brain regions. When this syndrome is secondary to postoperative hypoparathyroidism, clinical manifestations usually appear many years after thyroidectomy.

Case presentation: A 71-year-old female was admitted to the emergency department of a tertiary care hospital in Pasto (Colombia) due to progressive dysarthria, trismus, gait disturbance, visual hallucinations, and behavioral changes over the past week. The patient had undergone a total thyroidectomy 15 years prior to the consultation and was being treated for hypothyroidism with levothyroxine; however, she had not been evaluated by an endocrinologist since the surgery. Admission laboratory tests revealed severe hypocalcemia, hyperphosphatemia, and hypoparathyroidism. A head computed tomography (CT) scan showed symmetrical calcifications in the basal ganglia and cerebellum. Based on these findings and the history of thyroidectomy, she was diagnosed with Fahr’s syndrome. Intravenous treatment with calcium gluconate, potassium chloride, and magnesium sulfate was initiated, which, after a few days, was gradually switched to oral administration of calcium carbonate, calcitriol, and potassium chloride. As her motor and neuropsychiatric symptoms progressively improved, she was discharged five days after admission with instructions to continue the pharmacological treatment and attend periodic follow-up visits. At a follow-up appointment three weeks after discharge, a significant improvement in gait, mental status, and behavior was observed; follow-up tests showed normal calcium and phosphorus levels. Oral treatment has been maintained with periodic adjustments, and the patient continues to attend regular check-ups.

Conclusion: Diagnosing Fahr’s syndrome in late symptomatic clinical stages requires high clinical suspicion. This case highlights the need for periodic and ongoing endocrinology follow-up after thyroidectomy and demonstrates that appropriate treatment of biochemical abnormalities can significantly improve a patient’s quality of life.

Case report

José Leonel Zambrano-Urbano1,2,3 Leslie Yineth Guevara-Aroca4 Sara Gabriela Echeverry-Narváez4 Daniela Polo-Guerrero4 Nathalia Buitrago-Gómez1,5

1 Universidad Libre - Cali Campus - Faculty of Health Sciences - Santiago de Cali - Colombia.

2 Universidad de Nariño - Health Sciences Research Group (GICIENSA) - Pasto - Colombia.

3 Fundación Hospital San Pedro - Clinical Research and Public Health Group (CLISAP)- Pasto - Colombia.

4 Universidad de Nariño - Faculty of Health Sciences - Medicine Program - Pasto - Colombia.

5 Clínica de Occidente de Cali - Internal Medicine and Endocrinology Services - Santiago de Cali - Colombia.

Open access

Received: 26/05/2026

Accepted: 13/04/2026

Corresponding author: Sara Gabriela Echeverry-Narváez. Programa de Medicina, Universidad de Nariño, Facultad de Ciencias de la Salud. E-mail: gabuu1863@gmail.com.

Keywords: Calcium Metabolism Disorders; Hypoparathyroidism; Thyroidectomy; Hypocalcemia; Basal Ganglia (DeCS).

Palabras clave: Trastornos del Metabolismo del Calcio; Hipoparatiroidismo; Tiroidectomía; Hipocalcemia; ganglios basales (DeCS).

How to cite: Zambrano-Urbano JL, Guevara-Aroca LY, Echeverry-Narváez SG, Polo-Guerrero D, Buitrago-Gómez N. Fahr’s syndrome secondary to postoperative hypoparathyroidism 15 years after thyroidectomy: A case report. Rev. Fac. Med. 2026;74:e120606. English. doi: https://doi.org/10.15446/revfacmed.v74.120606.

Cómo citar: Zambrano-Urbano JL, Guevara-Aroca LY, Echeverry-Narváez SG, Polo-Guerrero D, Buitrago-Gómez N. [Síndrome de Fahr secundario a hipoparatiroidismo posquirúrgico 15 años después de tiroidectomía. Reporte de caso]. Rev. Fac. Med. 2026;74:e120606. English. doi: https://doi.org/10.15446/revfacmed.v74.120606.

Copyright: ©2026 The Author(s). This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium, as long as the original author and source are credited.

Abstract

Resumen

Introduction

Fahr’s syndrome is a rare neurological disorder, with an estimated prevalence of <1 case per 1 000 000 people,1-5 but, according to recent studies, the current estimated prevalence ranges from 2.1 to 6.6 cases per 1 000 people.2 This syndrome is characterized by symmetrical and bilateral calcifications in different brain regions that control movement, particularly the basal ganglia and subcortical white matter, although these abnormal calcium deposits may also occur in the thalamus, dentate nucleus, cerebral cortex, cerebellum, and hippocampus.1-8

In the literature, the terms “Fahr’s disease” and “Fahr’s syndrome” are generally used interchangeably.1,5,6 However, “Fahr’s disease” should be reserved for primary basal ganglia calcifications of unknown etiology (hereditary form, where autosomal dominant inheritance is the most common transmission pattern), while “Fahr’s syndrome” should be used for secondary basal ganglia calcifications with known causes (acquired form).1,3,4,6,8,9

In the acquired form, calcifications are typically caused by alterations in phosphocalcic metabolism or the blood-brain barrier,1,2 with hypoparathyroidism being one of the most common causes.3-5,7,9 Other etiologies include infectious diseases (especially intrauterine or perinatal), systemic diseases (e.g., systemic lupus erythematosus), and autoimmune brain tumors.4-6

Total or subtotal thyroidectomy is one of the most common etiologies of acquired or secondary hypoparathyroidism,3-5 with reports of immediate postoperative hypoparathyroidism in up to 18% of patients10 and permanent hypoparathyroidism in 0.9-5% of cases due to inadvertent damage or removal of the parathyroid glands.3,4,10,11 Regarding Fahr’s syndrome, idiopathic hypoparathyroidism is the most common cause, followed by post-thyroidectomy hypoparathyroidism.4,5,8

While some patients with Fahr’s syndrome are clinically asymptomatic, with incidental diagnoses on imaging tests (15-20% of cases),4,8 most present with movement disorders (tremors, ataxia, parkinsonism, dysarthria, and other extrapyramidal and cerebellar disorders), neuropsychiatric issues (behavioral changes, hallucinations, dementia, memory loss, depression, cognitive impairment, among others), and other nervous system disorders, including seizures, vertigo, and tetany.1-9

In this regard, a review of 223 cases of Fahr’s syndrome reported in the literature until 2021 found that 51.4%, 48.4%, 46.6%, and 40.4% of patients presented with tetany, movement disorders, seizures, and neuropsychiatric symptoms, respectively, while only 1.79% were asymptomatic.9 Furthermore, according to said review, this syndrome tends to affect women slightly more (56.6%), and the mean age at diagnosis is 44.6 years, with a mean time of 11.5 years between symptom onset and diagnosis.9

The mean time for diagnosing Fahr’s syndrome secondary to postoperative hypoparathyroidism is approximately 30 years after thyroidectomy,8,9 while the time between surgery and symptom onset ranges from 10 to 15 years, as described in recent case reports,4,7,12 but this period has been as long as 24 years in some cases.13

The literature on Fahr’s syndrome in Colombia is scarce and limited to case reports.14-20 Moreover, none of these reports describe the development of this syndrome following a thyroidectomy.

Case presentation

A 71-year-old woman was taken by her relatives to the emergency department of a tertiary care hospital in Pasto (Nariño, Colombia) due to the presence of the following clinical symptoms and signs over the last week: progressively worsening dysarthria, trismus, gait disturbance, weakness in the lower limbs, and progressive mental status deterioration characterized by episodes of aggressiveness, visual hallucinations—such as seeing cockroaches on the bed—and behavioral changes evidenced by disorganized behaviors such as “collecting rainwater with a bucket” when it was not raining.

According to her family, the patient had undergone a total thyroidectomy 15 years earlier due to an adenoma. She suffered from postoperative hypothyroidism under long-term treatment with levothyroxine (112 mcg/day), did not use psychoactive substances, and had not been evaluated by an endocrinologist since the surgery. No relevant family history was reported.

At the admission physical examination, the following findings were documented: blood pressure of 107/73 mmHg, heart rate of 98 bpm, and respiratory rate of 20bpm ; the patient was alert (Glasgow Coma Scale score of 14/15) but disoriented in time and place and, although she could speak fluently, she did so loudly and very rapidly (tachylalia) with frequent repetitions. Regarding the neurological and motor evaluation, the following were observed: active visual hallucinations, impaired short-term memory, and signs of cerebellar dysfunction (ataxia [positive Romberg test], dysmetria, and wide-based gait).

Admission laboratory tests showed severe hypocalcemia (4.08 mg/dL), hypokalemia (2.7 mEq/L), mild hypomagnesemia (1.5 mg/dL), hyperphosphatemia (7.5 mg/dL), decreased levels of intact parathyroid hormone (7.7 pg/mL), and slightly elevated levels of thyroid-stimulating hormone (4.08 mIU/L) (Table 1). In addition, the urine electrolyte test revealed low potassium (13.9 mEq/L) and high calcium (11.8 mEq/day) levels (Table 2). Tests for HIV, syphilis (VDRL), and hepatitis B and C were negative, ruling out an infectious etiology. A head CT scan was also requested, which showed symmetrical calcifications in the basal ganglia and cerebellum, as well as diffuse cortical atrophy, findings consistent with Fahr’s syndrome (Figure 1).

Table 1. Laboratory tests on admission.

Laboratory test	Result	Reference value
Complete blood count	Leucocytes: 11.23 x 103/μL Neutrophils: 73.2% Hemoglobin: 15.7 g/dL Hematocrit: 46% Platelets: 302 x 103/μL	4.5-11 x 103/μL 37-75% 11-18 g/dL 36-54% 150-400 x 103/μL
Glycemia	116 mg/dL	70-100 mg/dL
BUN	26 mg/dL	6-20 mg/dL
Blood creatinine	0.9 mg/dL	0.5-1.1 mg/dL
Sodium	136 mEq/L	135-145 mEq/L
Potassium	2.7 mEq/L	3.6-5 mEq/L
Chloride	93 mEq/L	95-108 mEq/L
Blood calcium	4.08 mg/dL	8.4-10.2 mg/dL
Serum magnesium	1.5 mg/dL	1.6-2.3 mg/dL
Serum phosphorus	7.5 mg/dL	2.5-4.5 mg/dL
Intact PTH	7.7 pg/ml	10-49 pg/ml
TSH	4.08 mUI/L	0.4-4.04 mUI/L

BUN: blood urea nitrogen; PTH: parathyroid hormone; TSH: thyroid-stimulating hormone.

Source: Own elaboration.

Table 2. Urine electrolytes.

Electrolytes	Result	Reference value
Urine potassium	13.9 mEq/L	25-100 mEq/L
Urine calcium	11.8 mEq/day	2.5-7.5 mEq/day
Urine sodium	137 mg/day	75-200 mg/day
Urine phosphorus	23.5 mEq/day	9.68-25.81 mEq/day

Source: Own elaboration.

Figure 1. Non-contrast computed tomography scan of the skull. Diffuse hyperintensities of the superficial and deep white matter are observed in the cerebral parenchyma; diffuse symmetrical calcifications are present in the basal ganglia, the infratentorial region, the brainstem, and the cerebellar hemispheres. Physiological calcification of the choroid plexuses and the pineal gland, as well parenchymal calcifications in the supratentorial and infratentorial regions with diffuse cortical atrophy, are also noted.

Source: Images taken while conducting the study.

Even though differential diagnoses such as metabolic encephalopathy, organic psychosis, secondary parkinsonism, and neurodegenerative dementia were initially considered, clinical, imaging, and laboratory findings—along with her history of thyroidectomy and the lack of endocrinological follow-up—led to the diagnosis of Fahr’s syndrome secondary to postoperative hypoparathyroidism.

Once diagnosed, she was started on intravenous calcium gluconate (slow infusion at 1g q8h), intravenous potassium chloride (20 mEq in saline solution/12 hours), and intravenous magnesium sulfate (1 g/day) on the first day of hospitalization. Furthermore, from the second day of hospitalization, a transition to oral treatment was made with calcium carbonate (1 1.5 g/day in three 500 mg doses of elemental calcium q8h), calcitriol (0.25 mcg q12h), and potassium chloride (40 mEq/day in divided doses of 4 mEq/hour). It should be noted that levothyroxine administration was maintained at the same dose (112 mcg/day), with adequate outpatient follow-up.

Since the patient tolerated the prescribed pharmacological therapy and showed progressive improvement in motor and neuropsychiatric symptoms, she was discharged five days after admission with instructions to continue treatment indefinitely and attend periodic follow-ups with the internal medicine and endocrinology services.

At the first follow-up visit, 3 weeks after discharge, the patient was alert and oriented, with no active hallucinations or speech disturbances; significant improvement in gait and behavior was also observed. Follow-up laboratory tests showed normal calcium (9.1 mg/dL) and phosphorus (3.8 mg/dL) levels, confirming an adequate biochemical response to treatment. Oral therapy has been maintained with periodic dose adjustments, and the patient continues under regular clinical follow-up by the internal medicine and endocrinology services.

Discussion

Fahr’s syndrome is a rare neurological disorder characterized by symmetrical and bilateral calcifications in various brain regions, primarily the basal ganglia1-8 These calcifications are frequently caused by alterations in phosphocalcic metabolism, with hypoparathyroidism being one of the most common causes.1-5,7,9 Furthermore, permanent postoperative hypoparathyroidism due to damage to or inadvertent resection of the parathyroid glands during thyroidectomy (total or partial) is the second most common cause of this syndrome.4,5,8,11

In this article, we report the case of a 71-year-old female patient with a history of total thyroidectomy performed 15 years prior due to a thyroid adenoma, who developed progressively worsening motor and neuropsychiatric symptoms in the context of severe hypocalcemia, hyperphosphatemia, and hypoparathyroidism, with diagnostic confirmation of Fahr’s syndrome via a head CT scan. The unusual nature of this case lies in the prolonged latency (more than a decade) between the surgical procedure and the onset of clinical symptoms.

The literature reports few cases with similar characteristics. For instance, Soares et al.21 described the case of a 53-year-old female who developed seizures and extensive cerebral calcifications following a thyroidectomy performed 22 years earlier, while Mahmood et al.13 reported the case of a 56-year-old woman who had undergone thyroidectomy 25 years earlier and presented with movement disorder and cognitive impairment secondary to hypoparathyroidism. These cases support the hypothesis that, even in the absence of early symptoms, postoperative endocrine damage may remain latent and manifest years or even decades later.

In addition to the cases mentioned above, Pons-Viñas et al.,4 described the case of a 46-year-old male diagnosed with acquired Fahr’s syndrome secondary to hypoparathyroidism 15 years after a total thyroidectomy. León Castellón et al.,12 also reported the case of a 57-year-old female patient with psychiatric disorders, seizures, involuntary movements, and brain calcifications who was diagnosed with Fahr’s syndrome due to hypoparathyroidism secondary to a thyroidectomy performed 25 years earlier. These reports recognize a pathophysiological mechanism similar to that observed in our case: a chronic alteration in phosphocalcic metabolism. However, there are clear differences in clinical presentation, as in the case reported by Pons-Viñas et al.4 motor-type neurological manifestations predominate, whereas León Castellón et al.12 describe greater neuropsychiatric involvement, which resembles what was observed in our patient, who presented with hallucinations, behavioral changes, and gait disturbance.

In our case, symptoms appeared approximately 15 years after the thyroidectomy, indicating a prolonged latency period between surgery and symptom onset, suggesting that Fahr’s syndrome was already present before it became apparent. Together, these findings strengthen the idea that, although they share a common pathophysiological mechanism, the clinical presentation of Fahr’s syndrome may be heterogeneous, which underscores the importance of long-term endocrinology follow-up in these patients.

The patient in this case presented with an atypical form of Fahr’s syndrome, with neuropsychiatric symptoms such as visual hallucinations, aggressive behavior, trismus, and cerebellar motor disturbances—all of which typically occur in areas affected by intracerebral calcifications. In this regard, it has been reported that up to 40% of patients with Fahr’s syndrome may initially present with psychiatric symptoms and that women are more likely to experience more severe clinical presentations.

In terms of diagnosis, the approach was both comprehensive and timely for our patient. A complete laboratory evaluation was performed, finding evidence of hypocalcemia and hypoparathyroidism, along with a non-contrast head CT scan showing typical radiological findings. According to the literature, CT remains the gold standard for confirming the diagnosis of this syndrome, as it allows for clear visualization of areas of hypercalcification, even in the early stages of neurological involvement.8

In our patient, treatment was aimed at correcting electrolyte imbalances through the administration of intravenous calcium, potassium, and magnesium, followed by outpatient management with oral calcium carbonate, calcitriol, and potassium. This approach achieved the normalization of these parameters and led to a notable clinical improvement, especially regarding the psychiatric symptoms. This strategy is consistent with that proposed by Saleem et al.,5 who emphasize that timely treatment can prevent the progression of neurological impairment and substantially improve patients’ quality of life.

This case report has some limitations that should be considered. First, the patient had not been followed up by an endocrinologist since her thyroidectomy, which is a key factor in the occurrence of this syndrome; such omission reflects not only a failure in postoperative follow-up but also a possible deficiency in patient education regarding the monitoring of potential long-term endocrine side effects. Second, periodic assessments of phosphocalcic metabolism were also lacking, and that could have enabled an early diagnosis of hypoparathyroidism and prevented the progression of neurological symptoms.

Nonetheless, the case reported here also has several strengths, including the timely recognition of the clinical and laboratory patterns consistent with Fahr’s syndrome and the prompt initiation of appropriate corrective treatment. Furthermore, the favorable clinical course, with symptom resolution and normalization of serum levels, underscores the importance of electrolyte replacement in this context.

Similarly, diagnosis in this case was based on established criteria, which made it possible to avoid more invasive studies—such as histopathology or genetic testing—that can be limited by cost and accessibility. Finally, the timely identification of hypoparathyroidism and its proper treatment allowed for a favorable outcome, highlighting the importance of long-term endocrinology follow-up in patients undergoing thyroid surgery to prevent potentially reversible neurological complications, as cases of asymptomatic hypoparathyroidism have been previously described in older adults.22

From a reflective perspective, this case report provides an opportunity to discuss the role of the healthcare system in the continuous follow-up of patients who undergo major surgical procedures, given that international guidelines recommend periodic monitoring of calcium, phosphorus, and parathyroid hormone levels following total thyroidectomy. Furthermore, it highlights the importance of considering Fahr’s syndrome in patients with a history of total thyroidectomy who develop neurological and/or psychiatric symptoms after the procedure, even many years later.

Conclusions

This case highlights the clinical diversity of Fahr’s syndrome, with multiple neurological and psychiatric manifestations that, combined with its low prevalence and the late onset of clinical manifestations when secondary to postoperative hypoparathyroidism, complicate an early diagnosis. This underscores the need to suspect this condition in patients with neurological symptoms and a history of thyroidectomy, as demonstrated in the present case, where, despite the symptoms appearing 15 years after the total thyroidectomy, a high clinical suspicion enabled a timely diagnosis, especially considering that the average time to diagnosis is 30 years after surgery.

This case also demonstrates the importance of performing a comprehensive metabolic panel, as the proper treatment of biochemical alterations can significantly improve these patients’ quality of life. Lastly, given that postoperative hypoparathyroidism is the second most common cause of Fahr’s syndrome, periodic and ongoing endocrinology follow-up after thyroidectomy (total or partial) is essential for an early diagnosis, thereby improving the prognosis of patients with this syndrome.

Ethical considerations

Written informed consent was obtained from the patient for the preparation of this case report.

Conflicts of interest

None stated by the authors.

Funding

None stated by the authors.

Acknowledgments

None stated by the authors.

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