Skip to content
Research Article Open access CC BY 3.0

Sub-acute Posterior Reversible Encephalopathy Associated with Extrapyramidal Signs Induced by Primary Hyperparathyroidism: A Case Report and a Revision of Literature

L. Giani, C. Lovati, C. Bana, I. Cova, F. De Angeli, C. Mariotti, D’Alessandro ., C. Mariani

International Neuropsychiatric Disease Journal · pp. 13–20 · Published 13 Nov 2013

10.9734/INDJ/2014/6366

Abstract

Aims: We present the case of a subacute psycho-motor deterioration in the context of a hypercalcemic state due to primary hyperparathyroidism inducing a posterior reversible encephalopathy. Presentation of Case: a 78 year-old man, affected by parkinsonism, developed a subacute psycho-motor deterioration in the course of a month and presented to our attention with generalized seizures. Biochemical analysis revealed hypercalcemia due to primary hyperparathyroidism. After the surgical removal of a hyperfunctioning parathyroid gland, we assisted to a dramatic improvement. Alongside with characteristic MRI findings, the picture was compatible with a posterior reversible encephalopathy syndrome (PRES). Discussion: To date, this is the third reported case of PRES caused by primary hyperparathyroidism. Our case appears peculiar because of the subacute onset of the syndrome, and of the accompanying progressive worsening of a pre-existing extrapyramidal syndrome. Also, the specific setting of radiologic findings and hormonal anomalies points to a prominent role of endothelial dysfunction in the still debated pathogenesis of PRES. Conclusion: Our case presents a rare combination of hyperparathyroidism, PRES and parkinsonism. We propose that the Blood-Brain barrier plays a central role in this setting.  

Posterior reversible encephalopathy syndrome hyperparathyroidism primary hypercalcemia parkinsonian disorders blood-brain barrier

References (16)

  1. 1 A Reversible Posterior Leukoencephalopathy Syndrome [DOI]
  2. 2 Posterior Reversible Encephalopathy Syndrome, Part 1: Fundamental Imaging and Clinical Features [DOI]
  3. 3 Posterior Reversible Encephalopathy Syndrome, Part 2: Controversies Surrounding Pathophysiology of Vasogenic Edema [DOI]
  4. 4 Blood–brain barrier disruption induces in vivo degeneration of nigral dopaminergic neurons [DOI]
  5. 5 Posterior reversible encephalopathy syndrome due to severe hypercalcemia [DOI]
  6. 6 Parathyroid hormone stimulates the endothelial nitric oxide synthase through protein kinase A and C pathways [DOI]
  7. 7 Parathyroid hormone stimulates the endothelial expression of vascular endothelial growth factor [DOI]
  8. 8 Posterior reversible encephalopathic syndrome due to severe hypercalcemia in AIDS [DOI]
  9. 9 Vasoconstriction as the Etiology of Hypercalcemia‐induced Seizures [DOI]
  10. 10 The detrimental role of inducible nitric oxide synthase in the pulmonary edema caused by hypercalcemia in conscious rats and isolated lungs [DOI]
  11. 11 Vasogenic Edema in a Case of Hypercalcemia-Induced Posterior Reversible Encephalopathy [DOI]
  12. 12 Treatment of Medically Refractory Hypercalcemic Crisis [DOI]
  13. 13 Reversible Parkinsonism Induced by Hypercalcemia and Primary Hyperparathyroidism [DOI]
  14. 14 Hypercalcemia and hypocalcemia.
  15. 15 Hyperparathyroidism Associated with Parkinsonism. [DOI]
  16. 16 Posterior encephalopathy: An uncommon manifestation of calcium toxicity [DOI]

Cited by 4

Showing 1 of 4 known citations — external sources report more than can currently be individually listed.

Article metrics

Real usage data collected on this platform.

35

Page views

0

PDF downloads

10

Outbound clicks

4

Citations

Views over time

Views by country

Approximate, from request IP at view time — not citizenship or institution. Countries with fewer than 5 views are grouped as "Other".

Traffic sources

Referring site, by host.

Views and downloads exclude known bots/crawlers. Citations combines this platform's own DOI-resolved index with each external source's own reported total — see Cited by above for individually listed citing works. Last refreshed 0 seconds ago.