The Japanese Journal of Rehabilitation Medicine
Online ISSN : 1881-8560
Print ISSN : 1881-3526
ISSN-L : 1881-3526
Volume 46, Issue 7
Displaying 1-5 of 5 articles from this issue
3rd Annual Meeting of the Japanese Board-certificated Physiatrist Association
Symposium
  • 2009 Volume 46 Issue 7 Pages 411-422
    Published: July 18, 2009
    Released on J-STAGE: July 30, 2009
    JOURNAL FREE ACCESS


    Hemiplegic Model of Cerebral Thrombosis : Functional Recovery and Neurotrophic Factors…Satoshi IKEDA 411

    Functional Neuroimaging Study into Functional Recovery after Stroke…Ichiro MIYAI, Masahito MIHARA, Megumi HATAKENAKA, Hajime YAGURA, Noriaki HATTORI 414

    Traumatic Brain Injury : Progress of Cognitive Rehabilitation…Keiji HASHIMOTO 418
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3rd Annual Meeting of the Japanese Board-certificated Physiatrist Association
Panel Discussion
3rd Annual Meeting of the Japanese Board-certificated Physiatrist Association
Educational Lecture
Case Report
  • Takashi KASAHARA, Mitsuhiko KODAMA, Yuji KOYAMA, Kozo HANAYAMA, Minoru ...
    2009 Volume 46 Issue 7 Pages 446-452
    Published: July 18, 2009
    Released on J-STAGE: July 30, 2009
    JOURNAL FREE ACCESS
    This report illustrates a case of chronic inflammatory demyelinating polyneuropathy (CIDP) masquerading as neurofibromatosis caused by multifocal enlargements of spinal nerve roots. At age 73, the patient reported a 6-year history of numbness, weakness and pain in the hands and legs, but he could but he could walk independently with a cane. And although tremor was present, he could still draw. T2-weighted magnetic resonance imaging (MRI) through the cervical spine demonstrated spinal cord compression bilaterally at C 6-7, caused by neurofibroma-like cervical root tumors and enlargement of the spinal nerve roots and the brachial and lumbosacral nerve plexuses. Nerve conduction studies showed very little evoked response, with the exception of the median nerve which demonstrated prolonged distal latency and reduced compound muscle action potential with temporal dispersion, suggesting a diagnosis of demyelinating neuropathy. Somatosensory evoked potentials of the median nerve revealed prolonged latency, and motor evoked potentials obtained from the abductor pollicis brevis and abductor digiti minimi by transcranial magnetic stimulation demonstrated prolonged latency and temporal dispersion. Sural nerve biopsies showed segmental demyelination, remyelination (onion-bulb formation), axonal loss, and lymphocyte infiltration suggesting CIDP. The patient did not have a positive family history and declined further genetic studies. We could therefore not rule out the possibility of a hereditary hypertrophic neuropathy such as Charcot-Marie-Tooth disease.
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