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Cerebellar ataxia associated with neuroendocrine thymic carcinoma and GAD antibodies
  1. L Bataller1,8,
  2. C Valero5,
  3. R Díaz2,
  4. A Froufe3,
  5. A Garcia-Zarza4,
  6. T Ribalta6,
  7. J J Vilchez1,8,
  8. A Saiz7
  1. 1
    Service of Neurology, Hospital Universitari La Fe, Valencia, Spain
  2. 2
    Service of Oncology, Hospital Universitari La Fe, Valencia, Spain
  3. 3
    Service of Pathology, Hospital Universitari La Fe, Valencia, Spain
  4. 4
    Service of Thoracic Surgery, Hospital Universitari La Fe, Valencia, Spain
  5. 5
    Section of Neurology, Hospital Arnau de Vilanova, Valencia, Spain
  6. 6
    Brain Tissue Bank, University of Barcelona, Hospital Clínic, Barcelona, Spain
  7. 7
    Service of Neurology, Hospital Clinic and Institut d’ Investigació Biomèdica August Pi i Sunyer (IDIBAPS), Barcelona, Spain
  8. 8
    Laboratory of Experimental Neurology, Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED)
  1. Dr L Bataller, Service of Neurology, Hospital Universitari la Fe, Avenida de Campanar 21, 46009 Valencia, Spain; l_bataller{at}yahoo.com

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Cerebellar ataxia may arise as a consequence of autoimmune damage of the cerebellum. Adult patients with autoimmunity against the cerebellum often have an underlying neoplasm (paraneoplastic cerebellar degeneration). These patients commonly develop rapidly evolving severe ataxia and harbour serum and CSF onconeuronal antibodies (mainly anti-Hu, Yo, Ri, Tr). By contrast, antibodies to neuronal glutamic acid decarboxylase (GAD-Abs) have been reported in patients with a less severe form of non-paraneoplastic cerebellar ataxia.1 The finding of GAD-Abs in patients with paraneoplastic neurological symptoms associated with malignant tumours is very rare. Here we report a patient with thymic neuroendocrine carcinoma who developed progressive cerebellar ataxia with GAD-Abs.

Case report

A 55-year-old man came to our attention in May 2007 because of gait instability. He smoked 40 cigarettes a day. There was no family history of neurological or autoimmune disorders. In December 2006 he started noticing imbalance that slowly progressed over months and prompted him to use a cane to walk. On examination he had mild scanning dysarthria, horizontal gaze evoked nystagmus and mild limb dysmetria and dysdiadochokinesia. His gait was …

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