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Unusual magnetic resonance imaging and cerebrospinal fluid findings in paraneoplastic cerebellar degeneration: a sequential study
  1. C de Andrés1,
  2. A Esquivel1,
  3. J G de Villoria2,
  4. F Graus3,
  5. S Sánchez-Ramón4
  1. 1Department of Neurology, Hospital General Universitario Gregorio Marañón, Madrid, Spain
  2. 2Department of Radiology, Hospital General Universitario Gregorio Marañón, Madrid, Spain
  3. 3Department of Neurology, Hospital Clinic, Barcelona, Spain
  4. 4Department of Immunology, Hospital General Universitario Gregorio Marañón, Madrid, Spain
  1. Correspondence to:
 Dr C de Andrés
 Department of Neurology, Hospital General Universitario “Gregorio Marañón”, C/Doctor Esquerdo 46, 28007, Madrid, Spain; claradeandres{at}

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Paraneoplastic cerebellar degeneration (PCD) is considered to be an autoimmune disorder, the clinical symptoms of which include dizziness, blurred or double vision, oscillopsia, and gait difficulties, which are not related to direct tumour invasion, adverse effects of chemotherapy, malnutrition, or infection.1 Some patients also develop multifocal neurological deficits through the evolution of the disease, involving multiple areas of the central nervous system (CNS), resulting in a miscellany of symptoms derived from limbic encephalitis, brainstem encephalitis, and myelitis, and known as paraneoplastic encephalomyelitis. The current pathogenic hypothesis is that the CNS lesions are immune mediated. The CSF may reveal no cells or pleocytosis and increased levels of proteins, and may exclude neoplastic cells and infections. Cranial magnetic resonance imaging (MRI) in PCD is usually normal or shows global cerebellar atrophy. Pathological studies show a diffuse loss of Purkinje cells throughout the cerebellar cortex. We describe a case of PCD with unusual findings.

A 51 year old woman was referred with a 1 month history of gait instability, personality and mood changes. Her medical history was remarkable for cigarette smoking (60 cigarettes/day) and depression. The clinical picture rapidly progressed to severe limb and truncal ataxia, dysarthria, and dysphagia that required nutritional support. She complained of double vision, difficulty in opening the eyes, and weight loss. General examination was significant for cachexia. Neurological examination revealed truncal ataxia, tremor affecting arms, head and, trunk, and she was unable to stand without aid. She had an apparently normal mental …

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