|Year : 2020 | Volume
| Issue : 3 | Page : 181-184
Hyperparathyroidism: A rare cause of worsening of parkinsonism
Bhushan R Mishal1, Kartik J Kachhadiya1, Shaival H Chandalia2, Mehul S Bhansali3, Pettarusp M Wadia1
1 Department of Neurology, Jaslok Hospital and Research Centre, Mumbai, Maharashtra, India
2 Department of Endocrinology, Jaslok Hospital and Research Centre, Mumbai, Maharashtra, India
3 Department of Surgical Oncology, Jaslok Hospital and Research Centre, Mumbai, Maharashtra, India
|Date of Submission||13-May-2020|
|Date of Decision||17-Jun-2020|
|Date of Acceptance||07-Aug-2020|
|Date of Web Publication||07-Nov-2020|
Dr. Pettarusp M Wadia
Department of Neurology, Jaslok Hospital and Research Centre, Dr. Gopalrao Deshmukh Marg, Mumbai, Maharashtra.
Source of Support: None, Conflict of Interest: None
Parkinsonism secondary to hypoparathyroidism is well described. The association of hyperparathyroidism with parkinsonism is rare. We describe here a case of progressive supranuclear palsy (PSP) associated with hyperparathyroidism secondary to a parathyroid adenoma who improved significantly with surgical excision of the parathyroid adenoma.
Keywords: Hypercalcemia, hyperparathyroidism, parkinsonism, progressive supranuclear palsy (PSP), worsening of parkinsonism
|How to cite this article:|
Mishal BR, Kachhadiya KJ, Chandalia SH, Bhansali MS, Wadia PM. Hyperparathyroidism: A rare cause of worsening of parkinsonism. Ann Mov Disord 2020;3:181-4
|How to cite this URL:|
Mishal BR, Kachhadiya KJ, Chandalia SH, Bhansali MS, Wadia PM. Hyperparathyroidism: A rare cause of worsening of parkinsonism. Ann Mov Disord [serial online] 2020 [cited 2021 Mar 2];3:181-4. Available from: https://www.aomd.in/text.asp?2020/3/3/181/300260
Hyperparathyroidism associated with hypercalcemia can worsen underlying Parkinsonism More Details.
| Introduction|| |
Parkinsonism secondary to exposure to drugs and toxins, metabolic disorders, and cerebrovascular diseases has been described. Parkinsonism secondary to hypoparathyroidism is well described; however, the association of hyperparathyroidism with parkinsonism is rare. We describe here a case of progressive supranuclear palsy (PSP) associated with hyperparathyroidism secondary to a parathyroid adenoma who improved significantly with the treatment of the hyperparathyroidism.
| Case History|| |
A 70-year-old female presented with the complaints of repeated falls with imbalance when walking one and half years before the consultation. She also had complaints of dysphagia and hypophonia and history suggestive of rapid eye movement (REM) behavior disorder. In addition, she had urinary frequency, urgency, and urge incontinence. Her past history was notable for hypertension and hypothyroidism.
Examination revealed a hypophonic speech, and masked facial expressions. Examination of the extraocular movement revealed vertical supranuclear gaze palsy. There was significant bradykinesia (left > right) and rigidity (axial > limb) without any tremors. There was no limb apraxia. She walked with a short-stepped gait with and a reduced arm swing bilaterally. Tandem gait was normal. Pull test was positive where she fell into the examiner’s hands when pulled ([segment 1 of Video 1]). Rest of the examination was normal. Magnetic resonance imaging (MRI) done then had shown hummingbird sign consistent with the clinical diagnosis of PSP. She was put on increasing doses of Levodopa (L-Dopa) without significant symptomatic improvement.
She continued to have difficulty in walking, difficulty in swallowing, and continued to have repeated falls. She fell and had two fractures. While investigating for her fracture her calcium levels were found to be very high. Subsequently, her parathormone (PTH) levels were found to be elevated (302 pg/mL [N 15–65 pg/mL]). Her 99Tecnetium methoxyisobutylisonitrile (MIBI) scintigraphy showed increased ill-defined MIBI uptake in the lower pole of the left lobe of thyroid gland with complete washout pattern on delayed images suggestive of a thyroid adenoma and a high uptake in the superior mediastinum [Figure 1]A. The computed tomography (CT) scan of the neck and chest showed two well-defined solid heterogeneously enhancing lesions one at C7-D1 level and another at the D3 level [Figure 1]B. Based on the MIBI uptake, the superior mediastinum lesion was thought to be a parathyroid adenoma. The C7-D1 lesion was thought to be a thyroid adenoma. Her unified Parkinson’s disease rating score (UPDRS) part III score at this time was 36/108.
|Figure 1: (A) 99Tecnitium methoxyisobutylisonitrile (MIBI) Scintigraphy showing MIBI avid lesion of parathyroid adenoma in mediastinum (larger arrowhead). Another ill-defined MIBI uptake seen in the lower pole of the left lobe of thyroid gland (shorter arrowhead) with complete washout pattern on delayed images suggestive of a thyroid adenoma. (B) CT scan of the neck and chest showing two well-defined solid heterogeneously enhancing lesions at C7-D1 level (thick arrow) and D3 level (thin arrow), both representing functional parathyroid adenomas|
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She underwent surgical excision of the parathyroid adenoma in the superior mediastinum. Intraoperative PTH levels dropped to normal indicating adequate excision of the lesion. The C7-D1 lesion was hence not excised. Postsurgery, her PTH levels reduced and she started improving symptomatically [Figure 2]. The histopathology report confirmed a parathyroid adenoma. Her speech and gait improved considerably and the frequency of falling reduced. Her UPDRS III score that was 36 before surgery reduced to 24 in the postoperative period ([segment 2 of Video 1]) and was 18 when she followed up a month later [segment 3 of Video 1], and [Figure 2]. Her L-dopa requirement also drastically reduced [Figure 2].
|Figure 2: Temporal changes in UPDRS part III score, L-Dopa dose (mg), serum calcium (mg/dL), and PTH levels (mg/dL). The levodopa dose requirement reduced and the UPDRS III score reduced by 50% postoperatively and remained stable for up to 3 months postoperatively. The UPDRS increased gradually to reach 78% of the baseline score by 6 months reflecting a worsening of her Parkinsonism. The serum PTH levels continued to show a decreasing trend and the calcium level remained stable after an initial period of decline|
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Despite the initial improvement in her motor symptoms and signs at 1 month, she continued to have an imbalance when walking and sustained falls. Her postural instability and clinical state (UPDRS III 18/108) remained static at 3-month follow-up ([segment 4 of Video 1]). However, at 6 months postop follow-up, her UPDRS III score reached to 28/108. She continued to have vertical supranuclear palsy with significant bradykinesia and rigidity (axial more than appendicular). She had a short-stepped gait and significant postural instability on the pull test. There was posturing of the left arm without any apraxia or cortical sensory impairment ([segment 5 of Video 1]) The presence of vertical supranuclear gaze palsy and repeated unprovoked falls within 3 years of onset of the disease were suggestive of a diagnosis PSP-RS (Richardson Syndrome) as per the Movement Disorder Society Criteria.
| Discussion|| |
Although hypoparathyroidism is a recognized cause of Parkinsonism, only few case reports have described the association of parkinsonism secondary to hyperparathyroidism [Table 1].
|Table 1: Published literature of Parkinsonism associated with hyperparathyroidism|
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Berger and Ross have hypothesized that basal ganglia calcifications associated with these conditions damage postsynaptic dopamine receptors. Although our patient did not have basal ganglia calcifications, similar to the case described by Kovacs et al., it has been shown by Cogan et al. that total brain calcium content may be increased despite the absence of basal ganglia calcification. In few of the case reports available, some patients improved at least partially, to parathyroidectomy or cinacalcet (a calcimimetic agent). Thus, a high index of suspicion is required to suspect Parkinsonism secondary to hyperparathyroidism.
| Conclusion|| |
Hyperparathyroidism associated with hypercalcemia can cause or worsen underlying parkinsonism. Correction of hypercalcemia results in clinical improvement. In patients with parkinsonism having hypercalcemia it may be worthwhile testing parathormone levels.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]