格林－巴利综合征患者血清髓鞘脂抗体检测及其临床意义

应用ＥＬＩＳＡ方法对２８例格林－巴利综合征（ＧＢＳ）患者和３０例正常对照者、３０例疾病对照者进行血清抗髓鞘脂抗体检测，并对其中５例进行动态观察。结果发现：ＧＢＳ患者血清抗髓鞘脂抗体水平增高，与正常和疾病对照组相比有非常显著性差异（Ｐ＜０．０１）。ＧＢＳ患者髓鞘脂抗体出现的阳性率为２１．４％，ＧＢＳ患者髓鞘脂抗体水平下降与临床症状的改善相一致。     

格林—巴利综合征患者血清和脑脊液中的抗硫脂抗体

探讨抗硫脂抗体与格林－巴利综合征（ＧＢＳ）的关系。方法采用固相酶联免疫吸附法对急性期ＧＢＳ患者血清和脑脊液（ＣＳＦ）中抗硫脂ＩｇＧ和ＩｇＭ抗体进行检测。结果ＧＢＳ患者血清和ＣＳＦ中抗硫脂ＩｇＧ及ＩｇＭ抗体的阳性率均明显高于正常对照组；血清中抗硫脂ＩｇＭ抗体滴度与标本收集时患者发病天数呈负相关（Ｐ＜０．０５），而血清中抗硫脂ＩｇＧ抗体滴度与临床分级（Ｐ＜０．０１）、ＣＳＦ中抗硫脂ＩｇＧ抗体滴度（Ｐ＜０．０１）呈正相关；血清中抗硫脂ＩｇＧ或ＩｇＭ阳性的ＧＢＳ患者，体检时有不同程度的感觉障碍患者为５６％，而血清中抗硫脂抗体阴性患者仅为１６％，两者之间差异有显著意义（Ｐ＜０．０５）。结论抗硫脂抗体可能在ＧＢＳ的病理过程中起重要作用     

格林-巴利综合征中的抗神经节苷脂GM_1抗体

采用固相酶联免疫吸附法对３０例格林－巴利综合征患者，３２例其他神经系统疾病患者及９０例健康献血员的血清中抗ＧＭ＿１ＩｇＭ和ＩｇＧ抗体进行测定。结果表明：格林－巴利综合征患者抗ＧＭ＿１ＩｇＭ抗体的阳性率为４０％，明显高于其他两个对照组；提示抗ＧＭ＿１抗体可能在格林－巴利综合征的发病中起重要作用。     

37例格林－巴利综合征患者血清抗空肠弯曲菌脂多糖抗体检测

已有许多研究证实格林－巴利综合征（ＧＢＳ）与前驱空肠弯曲菌（Ｃｊ）感染有密切关系。但是，Ｃｊ诱发ＧＢＳ的病理机制仍不明确。作者试图探讨Ｃｊ菌体成份与ＧＢＳ发病的关系。以一株自ＧＢＳ患者分离得到的Ｃｊ之脂多糖（ＬＰＳ）为抗原，用酶联免疫吸附试验（ＥＬＩＳＡ）方法，检测了ＧＢＳ患者组（观察组）和健康成人组（对照组）的血清抗空肠弯曲菌脂多糖抗体。结果ＧＢＳ组血清呈阳性反应者为２０／３７（５４％）、对照组血清呈阳性反应的为１／３６（３％），差别具有统计学意义（Ｐ＜０．００１，ｘ２）。提示多数ＧＢＳ患者血清中存在着不同于健康人群的ＣｊＬＰＳ特异抗体．     

37例格林－巴利综合征患者血清抗空肠弯曲菌脂多糖抗体检测

已有许多研究证实格林－巴利综合征（ＧＢＳ）与前驱空肠弯曲菌（Ｃｊ）感染有密切关系。但是，Ｃｊ诱发ＧＢＳ的病理机制仍不明确。作者试图探讨Ｃｊ菌体成份与ＧＢＳ发病的关系。以一株自ＧＢＳ患者分离得到的Ｃｊ之脂多糖（ＬＰＳ）为抗原，用酶联免疫吸附试验（ＥＬＩＳＡ）方法，检测了ＧＢＳ患者组（观察组）和健康成人组（对照组）的血清抗空肠弯曲菌脂多糖抗体。结果ＧＢＳ组血清呈阳性反应者为２０／３７（５４％）、对照组血清呈阳性反应的为１／３６（３％），差别具有统计学意义（Ｐ＜０．００１，ｘ２）。提示多数ＧＢＳ患者血清中存在着不同于健康人群的ＣｊＬＰＳ特异抗体．     

格林-巴利综合征患者血清中抗神经节苷脂抗体的检测

目的 :探讨神经节苷脂抗体在格林 -巴利综合征 (Guillain- Barre syndrome GBS)发病中的作用。方法 :通过 EL ISA方法检测 85例 GBS病人血清中神经节苷脂 (GM1 、 M1 a、 GD1 b、 GA1 )的 Ig G、 Ig M、 Ig A抗体。结果 :anti-GD1 b Ig G抗体阳性在 AMAN中为 2 5 (2 5 / 5 3 47.2 % )例 ,在 AIDP中为 2 (2 / 32 6 .3% )例 ,正常对照组 2 (2 / 5 0 4% )例 ,其它神经科疾病组 1(1/ 5 0 2 % )例。AMAN与正常对照组相比 P=0 .0 0 1,OR=2 1.4;AIDP与正常对照组相比 P=0 .6 48。anti- GD1 b Ig G抗体阳性在 AMAN中为 2 7(2 7/ 5 3 5 0 .9% )例 ,在 AIDP中为 10 (10 / 32 31.3% )例 ,正常对照组4(4/ 5 0 8% )例 ,其它神经科疾病组 4(4/ 5 0 8% )例。AMAN与正常组相比 P=0 .0 0 1,OR=11.9;AIDP与正常对照组相比 P=0 .0 0 6 ,OR=5 .2 ;AMAN及 AIDP间 P=0 .0 76。结论 :GM1 Ig G抗体与 AMAN及 AIDP均相关 ,但 GD1 a抗体只与 AMAN相关。其它神经节苷脂抗体与 AMAN、AIDP不相关     

格林—巴利综合征合并颅内压,血清酶增高一例报告

l病例报告患者男，40岁，因发热4日，四肢无力伴呼吸困难互日人院。患者4日前发热，体温39C。两天后四肢无力，胸闷，吞咽困难，无心前区疼痛。一般查体：T39．SC，P84次／min，RZI次／min，BP18。12kPa。神清，言语欠流利，胸式呼吸减弱，双肺呼吸音低。神经系统：张口受限，软跨动度差，咽反射消失，转颈、耸肩无力。四肢肌肉无压病，双上肢肌力近端0级，远端且级，双下肢肌力IV级。肌张力低，腥反射消失，Babinski征（一）。诊断格林一巴利综合征。人院后气管切开，呼吸机辅助呼吸，同时给予抗生素等。发病第5d（日）体温正常，经…     

复发性格林-巴利综合征

报道３例复发性格林－巴利综合征病例，发现其具有明确的前驱因素，从发病到症状高峰少于１个月，易累及颅神经引起呼吸衰竭。发作期脑脊液蛋白质升高，神经传导速度减慢。１例病理上以周围神经脱髓鞘为主，伴有轻度炎性细胞浸润及轴索变性，此与慢性炎性脱髓鞘性多神经病相区别。其临床表现为数次急性炎性脱髓鞘所致。     

格林-巴利综合征与髓鞘抗体

格林-巴利综合征(Guillain-Barre Syndrome GBS)的病因及发病机理至今尚未完全清楚,近年来国外学者在GBS与髓鞘抗体的研究上已取得了一些进展,发现GBS病人血中抗髓鞘抗体水平升高,且抗体值的推移与临床症状的改善相一致。     

Atypical Miller Fisher syndrome with GQ1b antibodies

An atypical case of Miller Fisher syndrome is described in a patient with ophthalmoplegia and mild ataxia but no areflexia. High titres of acute phase antibodies to gangliosides asialo-GM1 and GQ1b were detected. Asialo-GM1 antibodies have not been previously reported in association with Miller Fisher syndrome. Considerable clinical recovery occurred in association with reduction in the ganglioside antibody titres. Ganglioside antibody assays may be helpful in the diagnosis of atypical cases of Miller Fisher syndrome. Detailed clinical, radiological and laboratory evaluation of suspected cases is warranted to improve our understanding of Miller Fisher syndrome. Such studies and the correlation with ganglioside antibody titres will also provide insights into the relationship between the classical and atypical cases of Miller Fisher syndrome, Guillain-Barré syndrome and Bickerstaff's brain stem encephalitis.     

Miller Fisher syndrome is associated with serum antibodies to GQ1b ganglioside.

A recent report described serum anti-GQ1b ganglioside antibodies in Miller Fisher syndrome (MFS), a clinical variant of Guillain-Barré syndrome (GBS). Four consecutive cases of MFS all had high titre anti-GQ1b antibodies which were absent from all control sera including those of patients with GBS.     

GD1b-specific antibodies may bind to complex of GQ1b and GM1, causing ataxia

Monospecific IgG antibodies to GD1b ganglioside (GD1b-specific antibodies) have been found in patients with acute ataxic neuropathy and Guillain–Barré syndrome, but the association of the GD1b-specific antibodies with specific neurological conditions has yet to be established. We tested sera from more than 10,000 patients with various neurological disorders, and found six sera, which contained IgG antibodies to GD1b, but not to LM1, GM1, GM1b, GD1a, GalNAc-GD1a, GT1a, GT1b and GQ1b. All six patients who carried GD1b-specific antibodies presented with acute onset of ataxia and monophasic course of the illness, of whom five demonstrated cerebellar-like ataxia. Four patients had antecedent symptoms of upper respiratory tract infection. The six patients demonstrated areflexia, and four complained of distal numbness. All the six patients who had the GD1b-specific antibodies carried IgG antibodies to complex of GQ1b/GM1 and GT1a/GM1. GD1b-specific antibodies were significantly absorbed by GQ1b/GM1 and GT1a/GM1 and anti-GQ1b/GM1 and -GT1a/GM1 antibodies were absorbed by GD1b. In conclusion, the GD1b-specific antibodies, which recognizes GQ1b/GM1 or GT1a/GM1 complex, are associated with acute ataxia.     

Severe Bickerstaff's encephalitis treated with Rituximab: Serum and CSF GQ1b antibodies

Bickerstaff's encephalitis is a syndrome of ophthalmoplegia, ataxia and impaired consciousness commonly associated with serum GQ1b antibodies. We describe a patient with seropositive Bickerstaff's encephalitis who did not respond either to plasma exchange or intravenous immunoglobulin but recovered following adjunct treatment with the anti-CD 20 monoclonal antibody, Rituximab. There was a concomitant reduction in serum GQ1b antibodies associated with improvement. Interestingly, GQ1b antibody was also detected in CSF. These findings have potentially significant clinical and immunopathological implications.     

Quantitative determination of 7 proteins in csf of patients with Guillain Barre syndrome]

Quantitative determinations were done for seven protein components namely albumin, IgG, transferrin, alpha-2 macroglobulin, IgA, IgM and ceruloplasmin in the CSF and sera from patients with Guillain Barré syndrome. The results showed that each of the protein significantly increased. All of these correlated remarkably with the increased values of total proteins in CSF. It seemed that the concentrations of the protein in CSF were influenced by those of the proteins in serum and the size of the corresponding protein molecule.     

Serum antibodies to GM1, GD1b,peripheral nerve myelin,and Campylobacter jejuni in patients with Guillain-Barré syndrome and controls: Correlation and prognosis

Serum antibodies to monosialoganglioside (GM1), disialoganglioside (GD1b), and Campylobacter jejuni, measured by enzyme-linked immunosorbent assay and serum antibodies to peripheral nerve myelin, measured by the C1 fixation and transfer assay, were studied in 58 acute-phase patients with Guillain-Barré syndrome (GBS), 42 disease controls, and 29 normal controls. Anti-peripheral nerve myelin antibodies were elevated in 57 of 58 patients with GBS compared with controls, whereas only 8.6% had increased antibody titers to GM1 and 10.3% to GD1b. Only low antibody titers (GM1) or no antibodies (GD1b) were found in controls. More GBS patients (17.2%) than controls (7%) had antibodies to C jejuni. Poor recovery with inability to walk at 1 year after onset of symptoms was seen in 3 (5%) of the patients with GBS. All 3 patients had serological evidence of recent C jejuni infection but no antibodies to GM1 or GD1b. GBS patients with antibodies to GM1 or GD1b had excellent recovery. Our data indicate that antibodies to GM1 or GD1b do not necessarily mediate the extensive axonal damage seen in these severely affected patients.     

A case report of Bickerstaff's brainstem encephalitis with positive anti GQ 1 b, GT 1 a, GM 1 ganglioside antibodies]

Patient was an 18-year-old female student. After she had symptoms of common cold for 3 days, she developed somnolence, diplopia, dysarthria, urinary disturbance and ataxia. On admission neurological examination revealed coma with mydriasis, ophthalmoplegia, ptosis and weakness of the upper limbs. Light reflex, corneal reflex and oculocephalic test were all negative. Deep tendon reflexes were brisk and extensor toe signs were positive bilaterally. She did not have nuchal rigidity. Laboratory test revealed normal cerebrospinal fluid with negative myelin basic protein. Brain MRI, brainstem evoked potentials presented no abnormality. EMG revealed normal conduction velocity and no conduction block. EEG had diffuse theta and delta slowing. Culture of the stool represented no Campylobacter jejuni. At the fifth day of admission consciousness level improved, and other neurological findings disappeared in about 6 weeks. She had anti GQ 1 b, GT 1 a(IgG, IgM) and anti GM 1(IgM) antibodies in the serum. We made a diagnosis of Bickerstaff's brainstem encephalitis from these neurological symptoms and clinical course. The main lesion was present in the brainstem from midbrain to medulla oblongata in the midline. High titer of anti GT 1a antibody may be related to the ophthalmoplegia as noted in Miller Fisher syndrome. As a result of EMG and stool culture, it denied the complication of Guillain-Barré syndrome. We had no proof of the reason of the presentation of anti GM 1 antibody.     

Serum IgG antibody to ganglioside GQ1b is a possible marker of Miller Fisher syndrome.

We studied serum anti-glycolipid antibodies by enzyme-linked immunosorbent assay and thin-layer chromatography-enzyme immunoassay in six consecutive patients with typical Miller Fisher syndrome. In all six, increased activity of IgG antibody against ganglioside GQ1b was present in the early phase and reduced with time, whereas such activity was not detected in normal control subjects and disease control subjects including those with Guillain-Barré syndrome. Anti-GQ1b IgG antibody is a new possible diagnostic marker of Miller Fisher syndrome and could well be related to the disease process itself.     

Acute oropharyngeal palsy is associated with antibodies to GQ1b and GT1a gangliosides.

Three patients with acute oropharyngeal palsy had high titre anti-GQ1b and anti-GT1a IgG antibodies. No patients had ophthalmoplegia or ptosis. In all patients limb ataxia or areflexia were present without notable limb weakness. These patients describe an oropharyngeal variant of Guillain-Barré syndrome in terms of anti-GQ1b antibody reactivity and show that high titre anti-GQ1b antibodies, serologically indistinguishable from those found in Miller Fisher syndrome, can occur in a clinical setting without ophthalmoplegia. The anti-GQ1b and anti-GT1a antibody assays may be helpful tests when considering the differential diagnosis of acute oropharyngeal palsy.