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  • Severe parkinsonism associated with anti-CRMP5 antibody-positive paraneoplastic neurological syndrome and abnormal signal intensity in the bilateral basal ganglia

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Letter
Severe parkinsonism associated with anti-CRMP5 antibody-positive paraneoplastic neurological syndrome and abnormal signal intensity in the bilateral basal ganglia
  1. Satoru Tada1,2,
  2. Mitsuru Furuta3,
  3. Kei Fukada2,
  4. Daisuke Hirozawa4,
  5. Misa Matsui5,
  6. Futoshi Aoike6,
  7. Tatsusada Okuno3,
  8. Jin-ichi Sawada2,
  9. Hideki Mochizuki3,
  10. Takanori Hazama2
  1. 1 INSERM UMR1169 CEA/MIRCen, Fontenay aux Roses, France
  2. 2 Department of Neurology, Osaka General Medical Center, Osaka, Japan
  3. 3Department of Neurology, Osaka University Graduate School of Medicine, Suita, Japan
  4. 4Department of Neurology, Shizuoka Institute of Epilepsy and Neurological Disorders, National Hospital Organization, Shizuoka, Japan
  5. 5Department of Neurology, National Toneyama Hospital, National Hospital Organization, Toyonaka, Japan
  6. 6Department of Neurology, Tane General Hospital, Osaka, Japan
  1. Correspondence to Dr Kei Fukada, Department of Neurology, Osaka General Medical Center, 3-1-56, Bandaihigashi, Sumiyoshi-ku, Osaka 558-8558, Japan; fukada{at}gh.opho.jp

https://doi.org/10.1136/jnnp-2015-311569

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    Introduction

    Anticollapsin response mediator protein 5 antibody (anti-CRMP5 antibody, also known as anti-CV2 antibody) is usually associated with small-cell lung carcinoma (SCLC) or thymoma.1 Although optic neuropathy, cerebellar ataxia and chorea are considered typical clinical features of paraneoplastic neurological syndrome (PNS) associated with anti-CRMP5 antibody, the neurological involvement of anti-CRMP5 antibody is broader.1 We report the first known case with anti-CRMP5 antibody-associated PNS presenting with predominant parkinsonism and bilateral signal abnormalities in the caudate and putamen on brain MRI.

    Case report

    A 72-year-old man presented with a 6-month history of ambulatory disturbance. After the patient noticed sialorrhoea in September 2010, he began to develop a stooped posture, and short-stepped and propulsive gait. In January 2011, he noted gradual onset of dysarthria and constipation. His gait instability became severe, and by April 2011, he was only able to walk with assistance. He reported to our hospital in May 2011. On neurological examination, he was alert and communicative. His speech consisted of a low monotonous voice. Although he had marked bradykinesia and exhibited facial masking, no rigidity or tremor was observed. He shuffled when he walked with assistance, had a stooped posture and his arm swing was decreased bilaterally. Severe postural impairment was noted on the pulling test. Brain MRI showed bilateral lesions in the lenticular and caudate nuclei, which were hyperintense on T2-weighted images and fluid-attenuated inversion recovery images, and hypointense on T1-weighted images (figure 1A–C).

    Figure 1

    Axial T1-weighted, T2-weighted and fluid-attenuated inversion recovery image of the brain …

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