P58. Primary hyperparathyroidism mimicking multiple sclerosis? A case report

Abstract

A 46-year-old Caucasian female patient was admitted to our hospital with suspected relapse of multiple sclerosis (MS). Diagnosis was made 2 years ago by unspecific white matter lesions, oligoclonal bands in the cerebrospinal fluid and a first episode with a slight hemiparesis left, which remitted in a few weeks. A treatment with interferon beta 1a was introduced. Since that there were no relapses noted. Since a few days she suffered fluctuating muscle weakness, dysarthria, fatigue and mood changes. Clinical examination revealed brisk tendon reflexes, no paresis but severe hypalgesia of both arms. After a 20 m walk she was not able to walk fast and she reported a feeling like a lead weight in her legs. A prednisolone pulse was given for 5 days. Brain MRI showed a new small single contrast enhancing lesion parieto-occipital. Patient shows a slight improvement, mainly concerning their fatigue. Few days after completed prednisolone treatment, the fluctuating muscle weakness progressed. She reported cognitive impairment and paroxysmal panic attacks. Repeated MRI (3 Tesla) oft he brain and cervical spine showed no new lesions. Prednisolone pulse was initiated repeatedly. Laboratory investigations revealed slight elevation of serum calcium. Therefore parathyroid hormone level was evaluated and showed 3-fold elevation. Further evaluations by endocrinologists showed a large adenoma oft he right caudal parathyroid gland. Surgery was planned. Retrospectively serum calcium showed elevated values 4 years ago, when patient was first admitted to a neurology department because of cerebral MRI white matter lesions without clinical symptoms. This case raises the question wether primary hyparathyroidism is a MS mimic? A recent study showed an association between plasma parathyroid hormone and white matter lesions (Hagstroem et al., 2014). Non focal muscle weakness is sometimes reported in primary hyperparathyroidism (pHPT), but severe sensory symptoms are not reported to our knowledge. In a series of pHPT patients subclinical changes of sensory nerve conduction velocity has been showed (Diniz ET, 2013). In our patient sensory electroneurography was normal, but hypalgesia was consistent in the quantitative sensory testing (QST). Our report present further neurophysiologic tests and will discuss possible underlying mechanisms oft he clinical symptoms in detail.