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Restless Legs Syndrome as a First Indicator of a Compression of Brainstem and Cervical Spinal Cord


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Restless Legs Syndrome as a First Indicator of a Meningioma-Induced Compression of Brainstem and Cervical Spinal Cord: A Case Report

Joachim Liepert1*, Elisabeth Kaiser2 and Marcos Tatagiba3
1Department of Neurorehabilitation, Kliniken Schmieder Allensbach, Germany 2Center of Excellence for Psychotraumatology/vivo International, University of Constance, Germany 3Department of Neurosurgery, University of Tübingen, Germany *Corresponding Author: Joachim Liepert,
Received: March 21, 2017; Published: April 12, 2017


We report on a patient who presented with a typical Restless Legs Syndrome (RLS) but, after a few months, developed additional symptoms suggesting a progressive spinal cord damage. Magnetic resonance imaging showed a large meningioma compressing lower brain stem and upper cervical spinal cord. Immediately after surgical removal, RLS symptoms disappeared completely and did not return during a follow-up

1016 Wolf in sheep skin: serious neurological condition presenting as refractory Restless Leg Syndrome

Pritam Neupane
Indiana University School of Medicine. 1Department of pulmonary critical care and sleep medicine

12 April 2019
, https://doi.org/10.1093/sleep/zsz069.1013

  • © 2019 Oxford University Press

    • Abstract
      Restless leg syndrome (RLS) is common in patients with known spinal cord injury but spinal cord disease presenting as RLS to our knowledge has not been reported. Here we present a case of progressive cervical spondylotic myelopathy who presented with refractory RLS.
      Report of case
      A 58 years old desperate man with history of obstructive sleep apnea, degenerative disc disease of lumbosacral and cervical spine, status post lumbosacral spine surgery in the remote past and RLS of 12 years duration presented with six months history of severe worsening of RLS symptoms. Review of systems was positive for several falls recently that he attributed to the extreme restlessness of his legs. He had been on pramipraxole for years but this was no longer effective. Another physician had switched him to ropinirole without clinical benefit. His physical examination demonstrated wide based gait with spasticity in the legs. He was given gabapentin and MRI of his cervical spine was obtained. While he had no response to gabapentin, his MRI showed severe cervical stenosis with multilevel spinal cord compression and cord signal change. He was urgently referred to neurosurgery for decompression and had complete resolution of RLS symptoms at one month post-operative follow up.

      While RLS is very common and is a clinical diagnosis, it is important to consider secondary causes of RLS and to perform a neurological examination. It was solely the history of falls and exam findings of myelopathy that led to the diagnosis of the serious spinal cord lesion in this patient. His failure to respond to usual treatments, chronic nature of RLS with acute worsening and complete resolution of his symptoms after spinal decompression all confirm that his RLS was the symptom of worsening cervical spondylotic myelopathy. It is important to consider these mimickers in the evaluation of patients with RLS.