格林—巴利综合征呼吸肌麻痹病例报告
摘要
患者，男，60岁，因肢体无力进行性加重3天，伴麻木1天，于2001年1月6日入院：
患者于入院前3天因劳累后感头晕、流涕、打喷嚏，并觉双上肢无力，活动不灵活，
但尚能做家务活；自认为是劳累后所致，未加注意。入院前1天患者觉双上肢无力加重，
并同时感双下肢无力，行走困难，伴双手指及双足趾端麻木感。无头痛、呕吐、发热、
吞咽困难、胸闷、呼吸急促等症。饮食可，大小便正常。门诊以“肌无力原因待查”
收入院。
既往史：无类似发作史；否认高血压、糖尿病史。
入院查体：T：36．6℃，R：20次／分，P：80次／分，BP：130／80mmHg(17．3／10．7
kPa)，抬入病房，全身浅表淋巴结无肿大，咽部充血，甲状腺无肿大，心肺腹检查无
异常。
神经系统检查：神志清楚，言语流利；双侧眼裂对称，无眼睑下垂，双瞳孔等大
等圆，直径3mm，光反射存在，眼球各方向运动自如，眼底检查视乳头清晰。双侧鼻
唇沟对称，音叉试验听力正常，未见眼震；伸舌居中，双侧软腭活动好，咽反射存在，
耸肩及转颈有力；颈软，颈部动脉搏动对称；四肢肌肉无萎缩，双上肢肌力Ⅲ级，双
下肢肌力Ⅱ级：腹壁反射(+)、双侧肱二头肌反射、桡反射、膝反射、踝反射均消失，
四肢肌张力减低。全身深、浅感觉及共济运动检查未见明显异常；病理反射及脑膜刺
激征均未引出。植物神经系统检查未见异常。
辅助检查
1．实验室检查：血常规、尿常规、大便常规均正常，肝。肾功能正常，空腹血糖
6．02mmol／L，血K~+：3．90mmol／L，血清肌酶及甲状腺功能检查正常。血沉值在正常范围。
2．影像学检查：双肺X线片无异常；头颅CT检查未见异常。
3．心电图检查：正常窦性心律。
4．肌电图检查示：F波潜伏期延长、出现率减低(65％)；运动神经传导速度减慢，
感觉神经传导速度正常。
5．脑脊液检查：压力100mmH_2O，无色清亮，蛋白0.40g/L,细胞数4个/mm~3
糖4．2mmol／L.氯化物121mmol／L。于第入院第10天脑脊液检查压力110mmH_2O.无色
清亮，蛋白0。83g／L，细胞数2个／mm~3，糖3.8mmol／L，氯化物125mmol／L。
6．新斯的明试验结果阴性。
7．腓肠神经活检：神经纤维轻度肿胀，部分髓鞘斑片状脱失，少量炎性细胞浸润。
入院后给予激素、抗生素、VitBl、VitBl2营养神经等对症支持治疗．患者病情无
改善。入院第二同患者四肢肌力降至O级，并出现憋气，呼吸困难，心慌，意识模糊等
症状，立即气管插管后气管切丌，呼吸机辅助呼吸。
A 60-year-old male patient was admitted to the hospital beacause of progressive weakness of extremities for 3 days and accompany with numbness for 1 day.
About 2 days prior to his admission the patient felt dizziness snivel sneeze and experience weakness of bilateral upper extremities.Movement is not agility.He considered that was conduced by tied,so he had not pay attention to it.From this morning the patient feel the weakness of bilateral upper extremities exacerbation, and felt weakness of bilateral lower extremities.He was difficult to walk,and felt numbness of his fingers and toes.Without headache, vomiting, fever, felt oppressed dysphagia or shortness of breath.
Past history: He had not similar attacks, had not hypertension and diabetea.
Examination on admissim: T:36.6℃, P80 per min, R20 per min, P:15.0/9.3kpa. Common conditions were well, superfacial lymph nodes were impalpable. Posterior pharyngeal wall was congested.Thyroid was normal and trachea was in the center position.Examinations of lung,heart and abdomen were regular.
Neurological examination: He was conscious mind and specking was clear Palpebral fissures symmetrical without blepharoptosis.Pupils were round,symmetrical, dia 3.0 mm and reactive to light is normal and no nystagmus. The jundi showed no papilledema. The nasolabial groove was similarity . The fasciculatious of the tongue is in the midline. There was no atrophy of the tongue. The movement of soft palate were well.The gag reflex was intect .He shrugged his shoulders and turned his neck. The pulsation of the carotid arteries were symmetry. Muscles of all extremities had not atrophy. The upper extremities muscle force were III grade.and the lower extremities muscle force were II grade.The muscular tension were diminished. Abdominal refle(+),the bilaterally reflexes of biceps reflex, patellar reflex and ankle jerk extinction. His sensation were normal and no ataxia.There was no pathologic reflexes meningeal irriation and antagonistic system was normal.
Assisted examination
1.Laboratory examination:Routine examination of the blood urine and stool were normal. Liver and kindney serum founctions were regular. Fasting blood sugar:6.02 mmol L,K~+ 3.90mmol/L. serum myokinase, hyroid function and blood sedimentation rate were normal.
2. Image analysis: Lung x-ray slide; brain CT scan was normal.
3. Electrocardiogram examination was normal.
4.Electromyogram: F-wave latent period alongation and frequency of occurrence reduce, motor nerver condution velocity reduce,sensory nerver condution velocity was normal.
5. Examination of cerebrospinal fluid: The CSF was clear, pressure 100 mm H2O ,cell count 4 X 109/ L ,protein0.4 g/ L ,glucose 4.2 mmol/ L , CL+ 121mmol/L.
Lumbar examition was operation after 12 days, the CSF was clear, pressure:110 mmH2O,cell count2 X 109/ L ,protein0.83 g/ L ,glucose 3.8 mmol/ L , CL+125mmol/L
6. Prostigmine Test result was Negative.
7.Sural nerve Biopsy: Nerve fiber slightiy swelling, segment myelin losed a small inflammatory infiltrate
After related examination were taken, the patient received treatment with corticosteroid antibiotics VitB_1 and VitBj2. After patient was admitted 2 days,his extremities muscle force were descend to 0,and feel dyspnea palpitation obtundation , operate tracheostomy and intraacheal tube with ventilator was used.
患者于入院前3天因劳累后感头晕、流涕、打喷嚏，并觉双上肢无力，活动不灵活，
但尚能做家务活；自认为是劳累后所致，未加注意。入院前1天患者觉双上肢无力加重，
并同时感双下肢无力，行走困难，伴双手指及双足趾端麻木感。无头痛、呕吐、发热、
吞咽困难、胸闷、呼吸急促等症。饮食可，大小便正常。门诊以“肌无力原因待查”
收入院。
既往史：无类似发作史；否认高血压、糖尿病史。
入院查体：T：36．6℃，R：20次／分，P：80次／分，BP：130／80mmHg(17．3／10．7
kPa)，抬入病房，全身浅表淋巴结无肿大，咽部充血，甲状腺无肿大，心肺腹检查无
异常。
神经系统检查：神志清楚，言语流利；双侧眼裂对称，无眼睑下垂，双瞳孔等大
等圆，直径3mm，光反射存在，眼球各方向运动自如，眼底检查视乳头清晰。双侧鼻
唇沟对称，音叉试验听力正常，未见眼震；伸舌居中，双侧软腭活动好，咽反射存在，
耸肩及转颈有力；颈软，颈部动脉搏动对称；四肢肌肉无萎缩，双上肢肌力Ⅲ级，双
下肢肌力Ⅱ级：腹壁反射(+)、双侧肱二头肌反射、桡反射、膝反射、踝反射均消失，
四肢肌张力减低。全身深、浅感觉及共济运动检查未见明显异常；病理反射及脑膜刺
激征均未引出。植物神经系统检查未见异常。
辅助检查
1．实验室检查：血常规、尿常规、大便常规均正常，肝。肾功能正常，空腹血糖
6．02mmol／L，血K~+：3．90mmol／L，血清肌酶及甲状腺功能检查正常。血沉值在正常范围。
2．影像学检查：双肺X线片无异常；头颅CT检查未见异常。
3．心电图检查：正常窦性心律。
4．肌电图检查示：F波潜伏期延长、出现率减低(65％)；运动神经传导速度减慢，
感觉神经传导速度正常。
5．脑脊液检查：压力100mmH_2O，无色清亮，蛋白0.40g/L,细胞数4个/mm~3
糖4．2mmol／L.氯化物121mmol／L。于第入院第10天脑脊液检查压力110mmH_2O.无色
清亮，蛋白0。83g／L，细胞数2个／mm~3，糖3.8mmol／L，氯化物125mmol／L。
6．新斯的明试验结果阴性。
7．腓肠神经活检：神经纤维轻度肿胀，部分髓鞘斑片状脱失，少量炎性细胞浸润。
入院后给予激素、抗生素、VitBl、VitBl2营养神经等对症支持治疗．患者病情无
改善。入院第二同患者四肢肌力降至O级，并出现憋气，呼吸困难，心慌，意识模糊等
症状，立即气管插管后气管切丌，呼吸机辅助呼吸。
A 60-year-old male patient was admitted to the hospital beacause of progressive weakness of extremities for 3 days and accompany with numbness for 1 day.
About 2 days prior to his admission the patient felt dizziness snivel sneeze and experience weakness of bilateral upper extremities.Movement is not agility.He considered that was conduced by tied,so he had not pay attention to it.From this morning the patient feel the weakness of bilateral upper extremities exacerbation, and felt weakness of bilateral lower extremities.He was difficult to walk,and felt numbness of his fingers and toes.Without headache, vomiting, fever, felt oppressed dysphagia or shortness of breath.
Past history: He had not similar attacks, had not hypertension and diabetea.
Examination on admissim: T:36.6℃, P80 per min, R20 per min, P:15.0/9.3kpa. Common conditions were well, superfacial lymph nodes were impalpable. Posterior pharyngeal wall was congested.Thyroid was normal and trachea was in the center position.Examinations of lung,heart and abdomen were regular.
Neurological examination: He was conscious mind and specking was clear Palpebral fissures symmetrical without blepharoptosis.Pupils were round,symmetrical, dia 3.0 mm and reactive to light is normal and no nystagmus. The jundi showed no papilledema. The nasolabial groove was similarity . The fasciculatious of the tongue is in the midline. There was no atrophy of the tongue. The movement of soft palate were well.The gag reflex was intect .He shrugged his shoulders and turned his neck. The pulsation of the carotid arteries were symmetry. Muscles of all extremities had not atrophy. The upper extremities muscle force were III grade.and the lower extremities muscle force were II grade.The muscular tension were diminished. Abdominal refle(+),the bilaterally reflexes of biceps reflex, patellar reflex and ankle jerk extinction. His sensation were normal and no ataxia.There was no pathologic reflexes meningeal irriation and antagonistic system was normal.
Assisted examination
1.Laboratory examination:Routine examination of the blood urine and stool were normal. Liver and kindney serum founctions were regular. Fasting blood sugar:6.02 mmol L,K~+ 3.90mmol/L. serum myokinase, hyroid function and blood sedimentation rate were normal.
2. Image analysis: Lung x-ray slide; brain CT scan was normal.
3. Electrocardiogram examination was normal.
4.Electromyogram: F-wave latent period alongation and frequency of occurrence reduce, motor nerver condution velocity reduce,sensory nerver condution velocity was normal.
5. Examination of cerebrospinal fluid: The CSF was clear, pressure 100 mm H2O ,cell count 4 X 109/ L ,protein0.4 g/ L ,glucose 4.2 mmol/ L , CL+ 121mmol/L.
Lumbar examition was operation after 12 days, the CSF was clear, pressure:110 mmH2O,cell count2 X 109/ L ,protein0.83 g/ L ,glucose 3.8 mmol/ L , CL+125mmol/L
6. Prostigmine Test result was Negative.
7.Sural nerve Biopsy: Nerve fiber slightiy swelling, segment myelin losed a small inflammatory infiltrate
After related examination were taken, the patient received treatment with corticosteroid antibiotics VitB_1 and VitBj2. After patient was admitted 2 days,his extremities muscle force were descend to 0,and feel dyspnea palpitation obtundation , operate tracheostomy and intraacheal tube with ventilator was used.
引文
1. SedanoMJ, Calleja.Guillain-Barresyndromy in Canfabria, Spain, An epidemiological and clinical study. Acta Neurol Scand, 1994; 89(2): 287-292
2．蔡铨朗，李海桦．老年期及老年前期格林—巴利综合症的临床特征．中国神经精神疾病杂志，1997：23(3)：136-139
3．陈立山，张传玺，宋芝萍，等．格林—巴利综合征的心血管系统表现148例分析．中风与神经疾病杂志，1994；11(1)：109-210
4．白法毅，王维平，郭书英，等．格林—巴利综合征1287例临床分析．中华神经精神科杂志．1992，25；31-34
5. Visser LH. Cytomegalovirus infection and Guillain-Barre syndrome. Neurology, 1996; 47(3): 668-673
6. Jacobs BC. The spectrum of antecedent infections in Guillain-Barre syndrome. Neurology, 1998; 51(5): 1110-1115
7．张健．老年Guillain-Barre综合征的临床表现．中华实用医学，2002；(4)17：25-27
8．曾福昌 弓萃春．格林—巴利综合征并呼吸肌麻痹68例临床分析．河北医学，1998：4(2)：27-30
9. Sridharan CV, Tallis RC, Gautam PC. Guillain-Barre syndromy in the elderly: A ratro spective comparative study. Gerontology, 1993; 39(1): 170-175
10. The Italian Guillain-Barre Study Group. The prognosis and main prognostic indicators of Guillain-Barre syndrome: a multicentre prospective study of 297 patients. Brain, 1996; 119(7): 2053-2061
11. Ho TW, Li CY, Cornblath DR, et al. Guillain-Barre syndrome in northern Chine: relationship to Campylobecter jejuni infection and anti-glycolipid antibodies. Brain, 1995, 118(3): 597-605
12. Fletcher DD, Lawn ND, Wolter TD, et al. Long-term outcome in patients with
Guillain-Barre syndrome requiring mechanical ventilation. Neurology, 2000, 54(10): 2311-2315
13．张鸿民．简明内科临床新疗法．哈尔滨：黑龙江科学技术出版社，第一版，1995；192-194
14．蔡转，赵华．吉一巴(Guillain—Barre)综合征的强化治疗．德国医学，1995；12(2)：125-126
15. The French cooperative group on plasma exchange in Guillain-Barre syndrome. Ann Neurol, 1997; 41(2): 289-306
16. Asbury AK, McKhann GM. ChangingviewsofGuillain-Barre syndrome. Ann Neurol, 1997, 41(3): 287-288
17. Yeh JH, Chen WH, Chen JR, et al. Miller Fisher syndrome with central involvement: successful treatment with plasmapheresis. Ther Apher 1999, 3(1): 69-71
18．谈友芬，王志晔．血浆治疗格林-巴利综合征的疗效观察．中风与神经疾病杂志，1995，12(5)：308-309
19. Stangel M, Hartung HP, Marx P, et al. Intravenous immunoglobulin treatment of neurological autoimmune diseases. J Neurol Sci, 1998; 153(2): 203-214
20. Bril V, Lise W, Pearce R, et al. Pilot trial of immunoglobulin versus plasma exchange in patient with Guillain-Barre syndrome. Neurology, 1996; 46(1): 100-103
21. Van Der Meche, FGA, Schmitz PIM, et al. A randomized trial comparins intravenous、immune globulin and Plasma exchang in Guillain-Barre, syndrome. N Engl J Med 1992: 326: 1123-1134.
22．吴晓燕，王超．大剂量免疫球蛋白静脉注射治疗脑髓鞘疾病的临床观察．临床内科杂志，1999，6(3)：151-152
23．闻立斗．格林-巴利综合征的分型和重型处理．内科急危重症杂志，1998：4(1)：41-42
24. Guillain-Barre Study Group. Double-blind trial of intravenous ethyiprednisolone in Guillain-Barre syndrome. Lancet, 1993; 341(3): 586-590
25. KoskiCL.Inflammatory demyelinating poIyneuroPathy in Clinical Neuroimmunology.
course No 141, AAN 43rd Meetins 1991; 47-61
26．周盛年，刘黎青．大剂量甲基强的松龙冲击疗法对免疫疾病临床疗效的研究．临床神经病学杂志，1995，8(5)：292
27．周广福，王玲铃．大剂量甲基强的松龙治疗神经免疫疾病临床研究．中华新医学，2003；4(2)：111-112
28. Visser LH, Van der Mech FG, Van Doom PA, et al. Guillain-Barre syndrome without sensory loss (acute motor neuropathy). A subgroup with specific clinical, electrodiagnostie and laboratory features. DutchGuillain- BarreStudy Group. Brain, 1995, 118 (Pt 4): 841-847
29. Treatment of Guillain-Barre syndrome with high-dose immune globulins combined with methylprednisolone: apilot study. The Dutch Guillain-Barre Study Group. Ann Neurol 1994; 35(6): 749-752
30．张国兰，徐培锡，常伟荣，等．激素、血浆交换联合治疗巨症格林巴利综合征．江苏医药，1996，22(5)：345-345
31. Rees J. Guillain-Barre syndrome. Clinical manifestations and directions for treatment.Drugs, 1995; 49(6): 912-920
32．邓艳春，黄旌，赵钢．合并呼吸肌麻痹的格林—巴利综合征的救治．脑与神经疾病杂志，2000，8(3)：153-154
33．程显声．呼吸衰竭的诊断和治疗．新医学，1995，26(11)565-566
34. Simth AG, Bromberg MB. Treatment of inflammatrory Demyelinating neuropathies. J Clin Neuromusc Dis, 1999, 22(1): 21-31
35．马彩云，吴丽，耿香菊．格林-巴利综合征肢体瘫痪的康复治疗．实用儿科临床杂志，2003；18(3)：233-234
2．蔡铨朗，李海桦．老年期及老年前期格林—巴利综合症的临床特征．中国神经精神疾病杂志，1997：23(3)：136-139
3．陈立山，张传玺，宋芝萍，等．格林—巴利综合征的心血管系统表现148例分析．中风与神经疾病杂志，1994；11(1)：109-210
4．白法毅，王维平，郭书英，等．格林—巴利综合征1287例临床分析．中华神经精神科杂志．1992，25；31-34
5. Visser LH. Cytomegalovirus infection and Guillain-Barre syndrome. Neurology, 1996; 47(3): 668-673
6. Jacobs BC. The spectrum of antecedent infections in Guillain-Barre syndrome. Neurology, 1998; 51(5): 1110-1115
7．张健．老年Guillain-Barre综合征的临床表现．中华实用医学，2002；(4)17：25-27
8．曾福昌 弓萃春．格林—巴利综合征并呼吸肌麻痹68例临床分析．河北医学，1998：4(2)：27-30
9. Sridharan CV, Tallis RC, Gautam PC. Guillain-Barre syndromy in the elderly: A ratro spective comparative study. Gerontology, 1993; 39(1): 170-175
10. The Italian Guillain-Barre Study Group. The prognosis and main prognostic indicators of Guillain-Barre syndrome: a multicentre prospective study of 297 patients. Brain, 1996; 119(7): 2053-2061
11. Ho TW, Li CY, Cornblath DR, et al. Guillain-Barre syndrome in northern Chine: relationship to Campylobecter jejuni infection and anti-glycolipid antibodies. Brain, 1995, 118(3): 597-605
12. Fletcher DD, Lawn ND, Wolter TD, et al. Long-term outcome in patients with
Guillain-Barre syndrome requiring mechanical ventilation. Neurology, 2000, 54(10): 2311-2315
13．张鸿民．简明内科临床新疗法．哈尔滨：黑龙江科学技术出版社，第一版，1995；192-194
14．蔡转，赵华．吉一巴(Guillain—Barre)综合征的强化治疗．德国医学，1995；12(2)：125-126
15. The French cooperative group on plasma exchange in Guillain-Barre syndrome. Ann Neurol, 1997; 41(2): 289-306
16. Asbury AK, McKhann GM. ChangingviewsofGuillain-Barre syndrome. Ann Neurol, 1997, 41(3): 287-288
17. Yeh JH, Chen WH, Chen JR, et al. Miller Fisher syndrome with central involvement: successful treatment with plasmapheresis. Ther Apher 1999, 3(1): 69-71
18．谈友芬，王志晔．血浆治疗格林-巴利综合征的疗效观察．中风与神经疾病杂志，1995，12(5)：308-309
19. Stangel M, Hartung HP, Marx P, et al. Intravenous immunoglobulin treatment of neurological autoimmune diseases. J Neurol Sci, 1998; 153(2): 203-214
20. Bril V, Lise W, Pearce R, et al. Pilot trial of immunoglobulin versus plasma exchange in patient with Guillain-Barre syndrome. Neurology, 1996; 46(1): 100-103
21. Van Der Meche, FGA, Schmitz PIM, et al. A randomized trial comparins intravenous、immune globulin and Plasma exchang in Guillain-Barre, syndrome. N Engl J Med 1992: 326: 1123-1134.
22．吴晓燕，王超．大剂量免疫球蛋白静脉注射治疗脑髓鞘疾病的临床观察．临床内科杂志，1999，6(3)：151-152
23．闻立斗．格林-巴利综合征的分型和重型处理．内科急危重症杂志，1998：4(1)：41-42
24. Guillain-Barre Study Group. Double-blind trial of intravenous ethyiprednisolone in Guillain-Barre syndrome. Lancet, 1993; 341(3): 586-590
25. KoskiCL.Inflammatory demyelinating poIyneuroPathy in Clinical Neuroimmunology.
course No 141, AAN 43rd Meetins 1991; 47-61
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