Guillain-Barré syndrome in Taiwan: a clinical study of 167 patients
Department of Neurology, Chang Gung
Memorial Hospital and Medical College, Taipei, Taiwan
Correspondence to: Dr Sien-Tsong Chen, Department of Neurology, Chang Gung Memorial Hospital, 199 Tung Hwa North Road, Taipei, Taiwan.
Received 24 February and in revised form 9 April 1997;
Accepted 21 April 1997
OBJECTIVE
To identify clinical characteristics of
various forms of Guillain-Barré syndrome in Taiwan.
METHODS
The clinical and electrophysiological
data of 167 consecutive patients with Guillain-Barré syndrome
admitted to Chang Gung Memorial Hospital, a general paediatric and
adult hospital in Taiwan, were reviewed.
RESULTS
Analysis of age distribution disclosed a
high incidence (21%) among patients under the age of 10 years.
Seasonal preponderance in Spring (March to May) was found. Utilising
clinical and electrophysiological data, these 167 patients with
Guillain-Barré syndrome were subclassified; 82 (49%) had acute
inflammatory demyelinating polyradiculoneuropathy (AIDP), 32 (19%) had
Fisher syndrome (FS), and six (4%) had axonal forms of
Guillain-Barré syndrome. The remaining 47 (28%) patients were
unclassified. Patients with AIDP and FS had many common clinical features, including seasonal distribution, history of preceding illness, sensory abnormalities, cranial nerve involvement except for
extraocular motor nerves, and albuminocytological dissociation on
examination of CSF. Follow up study on 145 patients disclosed that 127 (87%) recovered satisfactorily, 14 (10%) were persistently disabled,
and four (3%) died during admission to hospital. Clinical features
associated with poor outcome (persistent disability or death) were
requirement for mechanical ventilation, a low mean compound muscle
action potential amplitude (
10% of the lower limit of normal), and
age greater than 40 years.
CONCLUSION
Guillain-Barré syndrome in Taiwan
showed a peculiar age and seasonal distribution and a high frequency of
FS not seen in other series. Given that patients with AIDP and FS had
many common clinical features, AIDP and FS may have similar underlying
pathological mechanisms.
© 1997 by Journal of Neurology, Neurosurgery, and Psychiatry
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