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Distinctions between critical illness polyneuropathy and axonal Guillain- Barré syndrome
  1. M A C J DE LETTER,
  2. LH VISSER
  1. Department of Neurology, St Elisabeth Hospital Tilburg, The Netherlands.
  2. Department of Neurology, University Hospital Rotterdam and Erasmus University Rotterdam, the Netherlands
  3. Department of Immunology
  1. M A C J de Letter, Department of Neurology, St Elisabeth Hospital Tilburg, PO box 90151, 5000 LC Tilburg, The Netherlands email megens-deletter{at}wxs.nl
  1. M A C J DE LETTER,
  2. W ANG,
  3. F G A VAN DER MECHÉ
  1. Department of Neurology, St Elisabeth Hospital Tilburg, The Netherlands.
  2. Department of Neurology, University Hospital Rotterdam and Erasmus University Rotterdam, the Netherlands
  3. Department of Immunology
  1. M A C J de Letter, Department of Neurology, St Elisabeth Hospital Tilburg, PO box 90151, 5000 LC Tilburg, The Netherlands email megens-deletter{at}wxs.nl
  1. W ANG,
  2. H F J SAVELKOUL
  1. Department of Neurology, St Elisabeth Hospital Tilburg, The Netherlands.
  2. Department of Neurology, University Hospital Rotterdam and Erasmus University Rotterdam, the Netherlands
  3. Department of Immunology
  1. M A C J de Letter, Department of Neurology, St Elisabeth Hospital Tilburg, PO box 90151, 5000 LC Tilburg, The Netherlands email megens-deletter{at}wxs.nl

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In this letter we comment on the publication of Yuki and Hirata who postulate a possible relation between critical illness polyneuropathy and axonal Guillain-Barré syndrome.1 The authors mentioned a nosological relation, which at that time still had to be demonstrated by the presence of antiganglioside antibodies in the serum of patients with critical illness polyneuropathy. Critical illness polyneuropathy is a neuromuscular disorder that has been recognised in critically ill patients.2 The clinical picture consists of difficulty in weaning from the artificial respirator, tetraparesis, and muscle wasting of the limbs. The tendon reflexes are mostly decreased or absent. The neurophysiological examination shows an axonal polyneuropathy and sometimes myopathic altered motor unit potentials. The morphological features in the nerve point to a primarily distal axonal degeneration of motor and sensory fibres. Muscle biopsy shows scattered atrophic fibres in acute denervation and grouped atrophy in chronic denervation. Also, necrotic muscle fibres can be found suggesting the contribution of a myopathy or a primary myopathy.3 On clinical …

Dr. Nobuhiro Yuki, Department of Neurology, Dokkyo University School of Medicine, Kitakobayashi 880, Mibu, Shimotsuga, Tochigi 321–0293, Japan.

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