Long-Term Disability After Guillain-Barré Syndrome
Long-Term Disability After Guillain-Barré Syndrome
Abstract & Commentary
By Michael Rubin, MD, Professor of Clinical Neurology, NewYork-Presbyterian Hospital, Cornell Campus. Dr. Rubin is on the speaker's bureau for Athena Diagnostics, and does research for Pfizer and Merck.
Synopsis: Treatment of GBS should not be only aimed at improving patients' disability but also at limiting the impact of the disease on their social life.
Source: Bersano A, et al. Long Term Disability and Social Status After Guillain-Barré Syndrome. J Neurol. 2006;253:214-218.
How do guillain-barré syndrome (gbs) patients fare years after their illness? Among 75 GBS patients enrolled in the Italian, multi-center, case-control study between 1996-1998 (Neurological Sciences. 2000:21:229-234), 70 were available for follow-up 3 to 5 years after disease onset. Diagnosis of GBS was made based on Asbury-Cornblath criteria (Ann Neurol. 1990;27:S21-S24), and outcome was classified using the World Health Organization (WHO) classification of impairments, disabilities, and handicaps, with disability graded, at initial contact, from 0 (healthy) to 6 (dead) and, additionally, at follow-up, by the modified Rankin scale (Scott Med. 1957:2;200-215). Handicap was measured using the 9-item Rotterdam scale that examines any social disadvantages in performing indoor and outdoor tasks (Muscle Nerve. 2002;25;370-377). Residual symptoms and job, daily activity, and social activity changes were addressed by a standard questionnaire. Clinical and laboratory features during the acute phase illness were assessed with respect to long-term prognostic significance, and statistical analysis of results was performed using STATA 8.0 software and chi square testing.
At follow-up (mean, 3.8 ± 0.6 years; median, 4 years), only 2 patients felt they were still improving, with the remainder unaware of any ongoing change following a recovery period varying from 12 days to 4 years (median, 6 months). Pain persisted in 33% (n = 23), limb weakness in 30% (n = 21), and sensory loss or paresthesiae in 27% (n = 19). None required nursing home care, artificial ventilation, or experienced autonomic instability at follow-up, but 14% (n = 10) demonstrated cranial nerve dysfunction. On direct questioning, 80% (n = 56) felt minor residual neuropathic symptoms or none at all, whereas 20% had functional impairment, with or without the need for ambulatory assistance (10% each). Minor limitations in daily life were present in 27% (n = 19), and 9% (n = 6) required home aid at least part of the day. Thirty percent (n = 21) noted an inability to perform their usual activities at their pre-morbid state, 20% (n = 14) had to stop or change jobs at least temporarily, and 7% (n = 5) were forced to modify or change their hobbies. Overall, a significant life change involving job, hobbies, or social activities was necessary in 27% (n = 19), while an additional 19% (n = 13) reduced their activities due to fatigue. No acute phase clinical or laboratory feature, including age, time to nadir or plateau, need for mechanical ventilation, cerebrospinal fluid protein level, ganglioside antibody positivity, or antecedent infection significantly correlated with long-term outcome, although patients treated with intravenous immunoglobulin (IVIG) tended to be less impaired at follow-up than those treated with plasma exchange (PE) or the combination of PE and IVIG. GBS significantly impacts daily life in the long term that goes beyond any residual impairment, and treatment of GBS should address these considerations as well.
Commentary
Almost 20% of recovered GBS patients experience fatigue to a degree that requires reduction of daily activities. Is this related to residual slowing of nerve conduction velocities that remains even in the long-term? To address this question, the distribution of median motor nerve conduction velocities was studied in 13 fatigued but well-recovered GBS patients, 2 fatigued but stable chronic inflammatory demyelinating polyneuropathy patients, and 19 healthy controls (Garssen MPJ, et al. Muscle Nerve. 2006;33;177-182). Diagnosis in all patients was based on standard criteria, and all patients were neurologically well recovered by study entry. Fatigue was measured using the Fatigue Severity Scale, and entry into the study required severe fatigue with a score of 5/7 (Arch Neurol. 1989;46;1121-1123). Exclusionary criteria included use of fatigue-inducing medication within the previous 4 weeks, underlying malignancy, infection, hypothyroidism, anemia, chronic fatigue syndrome, or diabetes. Measurement of maximal median motor nerve conduction velocity was determined in the conventional manner, and distribution of conduction velocities within the nerve was determined using Hopf's collision technique (Arch Neurol. 1963;30;307-312, Electroencephalogr Clin Neurophysiol. 1987;66;235-243). Results were analyzed using one-way analysis of variance with SPSS version 10.1.
No difference in maximal nerve conduction velocity was seen in GBS patients compared to normals, but the distribution of velocities within the nerve was narrowed in GBS, with loss of fastest and slowest conducting fibers. Paradoxically, those patients with the least fatigue demonstrated the most pronounced narrowing of the velocity distribution. Velocity changes do not appear to contribute to fatigue in following GBS.
Treatment of GBS should not be only aimed at improving patients' disability but also at limiting the impact of the disease on their social life.Subscribe Now for Access
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