QUANTITATIVE-ANALYSIS OF THE COMPOUND MUSCLE ACTION-POTENTIAL IN EARLY ACUTE INFLAMMATORY DEMYELINATING POLYNEUROPATHY

被引:37
作者
CLOUSTON, PD
KIERS, L
ZUNIGA, G
CROS, D
机构
[1] MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114
[2] MASSACHUSETTS GEN HOSP,ELECTROMYOG LAB,BOSTON,MA 02114
来源
ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY | 1994年 / 93卷 / 04期
关键词
COMPOUND MUSCLE ACTION POTENTIAL; DEMYELINATION; GUILLAIN-BARRE SYNDROME; POLYNEUROPATHY;
D O I
10.1016/0168-5597(94)90026-4
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
We quantitated the size and configuration of compound muscle action potentials (CMAPs) in 266 nerves (66 median, 67 ulnar, 71 tibial and 62 peroneal) of 72 patients with acute inflammatory demyelinating polyneuropathy (AIDP) initially studied within 19 days of symptom onset. Results were compared with criteria for CMAP abnormalities, including criteria for abnormal negative peak duration and desynchronisation, derived from a control population of 50 median, ulnar, tibial and peroneal nerves. Other motor conduction abnormalities including minimal F response latency were also examined. We also analysed patterns of CMAP abnormality, peak disability and outcome for AIDP patients who had at least 3 motor nerves evaluated at first electrophysiologic study. Amongst AIDP nerves, low-amplitude of the distal CMAP, usually with prolonged distal latency, was much more common than an abnormal fall in CMAP amplitude between stimulus sites. Using our CMAP criteria more than half of these low amplitude distal responses showed prolonged negative peak duration or desynchronisation or both, consistent with demyelination. Of the 47 AIDP patients who had 3 or more motor nerves initially studied, 37 (78.7%) had at least 1 motor nerve with a distal CMAP showing evidence of temporal dispersion. In addition, those with at least 75% of motor nerves showing a pattern of low amplitude of the distal CMAP without a further significant fall in amplitude between stimulus sites had greater peak disability and a poorer outcome. Assessment of temporal dispersion of the distal CMAP should be included in electrophysiologic criteria for acute demyelination. In addition, for some patients with AIDP patterns of CMAP amplitude abnormality amongst motor nerves are present early in the illness and may provide prognostic information.
引用
收藏
页码:245 / 254
页数:10
相关论文
共 32 条
[1]   SEQUENTIAL ELECTRODIAGNOSTIC ABNORMALITIES IN ACUTE INFLAMMATORY DEMYELINATING POLYRADICULONEUROPATHY [J].
ALBERS, JW ;
DONOFRIO, PD ;
MCGONAGLE, TK .
MUSCLE & NERVE, 1985, 8 (06) :528-539
[2]   ASSESSMENT OF CURRENT DIAGNOSTIC-CRITERIA FOR GUILLAIN-BARRE-SYNDROME [J].
ASBURY, AK ;
CORNBLATH, DR .
ANNALS OF NEUROLOGY, 1990, 27 :S21-S24
[3]   INFLAMMATORY LESION IN IDIOPATHIC POLYNEURITIS - ITS ROLE IN PATHOGENESIS [J].
ASBURY, AK ;
ARNASON, BG ;
ADAMS, RD .
MEDICINE, 1969, 48 (03) :173-&
[4]   REVERSIBLE PROXIMAL CONDUCTION BLOCK UNDERLIES RAPID RECOVERY IN GUILLAIN-BARRE-SYNDROME [J].
BERGER, AR ;
LOGIGIAN, EL ;
SHAHANI, BT .
MUSCLE & NERVE, 1988, 11 (10) :1039-1042
[5]   CONDUCTION BLOCK AND DENERVATION IN GUILLAIN-BARRE POLYNEUROPATHY [J].
BROWN, WF ;
FEASBY, TE .
BRAIN, 1984, 107 (MAR) :219-239
[6]   PATTERNS AND SEVERITY OF CONDUCTION ABNORMALITIES IN GUILLAIN-BARRE-SYNDROME [J].
BROWN, WF ;
SNOW, R .
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 1991, 54 (09) :768-774
[7]   MOTOR CONDUCTION STUDIES IN GUILLAIN-BARRE-SYNDROME - DESCRIPTION AND PROGNOSTIC VALUE [J].
CORNBLATH, DR ;
MELLITS, ED ;
GRIFFIN, JW ;
MCKHANN, GM ;
ALBERS, JW ;
MILLER, RG ;
FEASBY, TE ;
QUASKEY, SA .
ANNALS OF NEUROLOGY, 1988, 23 (04) :354-359
[8]   GUILLAIN-BARRE SYNDROME - CLINICAL AND ELECTRODIAGNOSTIC STUDY OF 25 CASES [J].
EISEN, A ;
HUMPHREYS, P .
ARCHIVES OF NEUROLOGY, 1974, 30 (06) :438-443
[9]   THE PATHOLOGICAL BASIS OF CONDUCTION BLOCK IN HUMAN NEUROPATHIES [J].
FEASBY, TE ;
BROWN, WF ;
GILBERT, JJ ;
HAHN, AF .
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 1985, 48 (03) :239-244
[10]   AN ACUTE AXONAL FORM OF GUILLAIN-BARRE POLYNEUROPATHY [J].
FEASBY, TE ;
GILBERT, JJ ;
BROWN, WF ;
BOLTON, CF ;
HAHN, AF ;
KOOPMAN, WF ;
ZOCHODNE, DW .
BRAIN, 1986, 109 :1115-1126