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N Yuki

Publications and source records attributed to N Yuki.

At least 145 records · Page 8Linked to original sources

Trochlear nerve enhancement on three-dimensional magnetic resonance imaging in Fisher syndrome.

PURPOSE: To examine the lesion associated with external ophthalmoplegia in Fisher syndrome using three-dimensional magnetic resonance imaging (3-D MRI). METHOD: Case report. A 65-year-old woman with Fisher syndrome was investigated by gadolinium-enhanced 3-D MRI. RESULT: The extramedullary portion of the left trochlear nerve was enhanced. CONCLUSION: Contrast-enhanced 3-D MRI revealed that the lesion responsible for the external ophthalmoplegia in Fisher syndrome is located in the extramedullary portion of the trochlear nerve.

Aged↗

Immunoadsorption therapy for Fisher syndrome associated with IgG anti-GQ1b antibody.

PURPOSE: To describe the effects of immunoadsorption therapy with a tryptophan-immobilized column on Fisher syndrome associated with IgG anti-GQ1b ganglioside antibody. METHODS: Three patients with Fisher syndrome and with a high serum IgG anti-GQ1b antibody titer underwent four to nine sessions of immunoadsorption therapy with a tryptophan-immobilized column. Using enzyme-linked immunosorbent assay (ELISA), we determined the differences in IgG anti-GQ1b antibody titers. RESULTS: ELISA disclosed that the IgG anti-GQ1b antibody titers of the serum samples collected from the inlet of the column were markedly higher than those collected from the outlet for all three patients. Moreover, after completion of the immunoadsorption therapy, the patients' serum IgG anti-GQ1b antibody titers were markedly lower than they were before the immunoadsorption therapy. The patients' ophthalmoparesis decreased in severity during the therapy. CONCLUSION: These findings suggest that immunoadsorption therapy with the tryptophan-immobilized column is an effective method for removing IgG anti-GQ1b antibody from serum.

Adolescent↗

Guillain-Barré syndrome associated with IgG anti-GM1b antibody subsequent to Mycoplasma pneumoniae infection.

Sera from patients with Guillain-Barré syndrome (GBS) frequently have antibodies to various gangliosides. We report a girl with GBS after Mycoplasma pneumoniae infection who had serum IgG antibody to GM1b ganglioside as well as the cold agglutinins. The cold agglutinins are polyclonal IgM autoantibodies to 'I' antigen on erythrocytes. Ganglioside GM1b contains the terminal moiety shared with sialylated I antigen, a main receptor for M. pneumoniae. In this patient, the anti-GM1b antibody may be elicited in a similar mechanism producing anti-I antibody, and functioned in the development of GBS.

Agglutinins↗

Fisher syndrome associated with IgG anti-GQ1b antibody following infection by a specific serotype of Campylobacter jejuni.

OBJECTIVE: The purpose of the study was to describe clinical and serologic features of Fisher syndrome associated with IgG anti-GQ1b ganglioside antibody following Campylobacter jejuni enteritis. DESIGN: A clinical trial. PARTICIPANTS: Four consecutive patients with Fisher syndrome were studied. INTERVENTION: Samples of sera from four patients were tested for reactivity to GQ1b ganglioside by enzyme-linked immunosorbent assay (ELISA). Campylobacter jejuni strains isolated from samples of stool from three patients were serotyped by the method of Penner and Hennessy and that of Lior. MAIN OUTCOME MEASURES: Serum IgG anti-GQ1b antibody titer and serotypes of C. jejuni. RESULTS: Diplopia occurred 8 to 14 days after the onset of diarrhea. Campylobacter jejuni was isolated from samples of stool from all of the patients. ELISA revealed a high serum IgG anti-GQ1b antibody titer for all four patients. Two patients had high serum titers of other antiganglioside antibodies frequently related to Guillain-Barré syndrome. These two patients developed limb weakness following the onset of ophthalmoplegia. The C. jejuni serotype was Penner's serotype 2 for all three of the patients tested. CONCLUSIONS: These findings suggest that C. jejuni, especially Penner's serotype 2, enteritis could trigger development of Fisher syndrome associated with IgG anti-GQ1b antibody.

Adolescent↗

Close association of IgA anti-ganglioside antibodies with antecedent Campylobacter jejuni infection in Guillain-Barré and Fisher's syndromes.

IgA has an important function in the gastrointestinal immune system. We investigated IgA anti-ganglioside antibodies in Guillain-Barré syndrome (GBS) and Fisher's syndrome (FS) subsequent to Campylobacter jejuni enteritis. In previous studies, serological diagnosis of C. jejuni infection was based on the detection of IgG, IgA, and IgM anti-C. jejuni antibodies. Our study, however, showed that the detection of IgG anti-C. jejuni antibody alone was sufficient for the serological diagnosis of antecedent C. jejuni enteritis in GBS and FS, when the cut-off level was defined for results of sera from C. jejuni-isolated patients. Serological evidence of C. jejuni infection was found in 62 (31%) of 201 GBS patients and 12 (18%) of 65 FS patients. IgA anti-GMI antibody was detected in sera from 33 (16%) of the GBS patients, 1 (2%) of the FS patients, and none of the 46 normal control subjects. IgA anti-GM1 antibody titers were significantly higher in the GBS patients with positive C. jejuni serology than in those with negative serology (P < 0.0001) or the FS patients with positive C. jejuni serology (P = 0.007). IgA anti-GQ1b antibody was detected in sera from 18 (28%) of the FS patients, 9 (4%) of the GBS patients, and none of the normal control subjects. FS patients with positive C. jejuni serology had significantly higher titers of IgA anti-GQ1b antibody than those with negative serology (P = 0.01) or the GBS patients with positive C. jejuni serology (P < 0.0001). We conclude that anti-GM1 and anti-GQ1b IgA antibodies are closely associated with antecedent C. jejuni enteritis in GBS and FS, respectively.

Antibodies, Bacterial↗

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Journal Article↗

Minimal number of plasma exchanges needed to reduce immunoglobulin in Guillain-Barré syndrome.

Plasma exchange (PE) in Guillain-Barré syndrome (GBS) probably removes pathogenic antibodies. Results of a recent clinical study by the French Cooperative Group suggest that at least two sessions of PE are required. As an alternative procedure, we examined the effect of the number of PEs on the reduction of immunoglobulins in 11 patients. A significant immunoglobulin decrease was obtained in the first two sessions but not in subsequent ones. Based on the French trial results and our findings, we conclude that at least two PEs are needed for treating GBS.

Gangliosides↗

Two patterns of clinical recovery in Guillain-Barré syndrome with IgG anti-GM1 antibody.

OBJECTIVE: To investigate the prognostic value of anti-GM1 antibody. BACKGROUND: Whether anti-GM1 antibody is a marker of poor prognosis due to axonal degeneration in Guillain-Barré syndrome (GBS) is a matter of controversy. METHODS: The clinical recovery of 41 consecutive GBS patients was analyzed. RESULTS: The Hughes functional grading scores were similar at the peak, and 1, 3, and 6 months after onset for the groups of patients with (n=19) and without (n=22) immunoglobulin (Ig) G anti-GM1 antibodies. However, the anti-GM1-positive group included significantly higher proportions of patients with poor recovery (inability to walk independently at 6 months, 5 of 19 versus 0 of 22; p=0.01) and those with a markedly rapid recovery (improvement by two or more Hughes grades within a month, 9 of 19 versus 4 of 22; p=0.05). The positivity of IgG anti-GM1 antibody correlated well with the electrodiagnosis of the acute motor axonal neuropathy pattern but was not always associated with poor prognosis. Anti-GM1-positive patients showed two different patterns of clinical recovery-their conditions improved slower or faster than those of the anti-GM1-negative patients, most of whom had acute inflammatory demyelinating polyneuropathy. CONCLUSIONS: Anti-GM1 antibody is not always a marker of poor prognosis and, besides axonal degeneration, early reversible effects other than demyelination could be part of the pathophysiology of Guillain-Barré syndrome with IgG anti-GM1 antibody.

Adult↗

Anti-ganglioside antibody and neuropathy: review of our research.

Some patients developed Guillain-Barré syndrome (GBS) after the administration of bovine gangliosides. Patients with GBS subsequent to Campylobacter jejuni enteritis frequently have IgG antibody to GM1 ganglioside. Fisher's syndrome (FS), a variant of GBS, is associated with IgG antibody to GQ1b ganglioside. We showed the existence of molecular mimicry between GM1 and lipopolysaccharide (LPS) of C. jejuni isolated from a GBS patient, and that between GQ1b and C. jejuni LPSs from FS patients. Several lines of evidence suggest a pathogenic role for anti-ganglioside antibodies. Some patients developed sensorimotor polyneuropathy after anti-GD2 antibody administration. Anti-GM1 antibody can block motor nerve conduction. The molecular mimicry between infectious agents and gangliosides may function in the production of anti-ganglioside antibodies and the development of GBS and FS. Anti-GQ1b IgG antibody is detected also in Bickerstaff's brainstem encephalitis and acute ophthalmoparesis, which suggests that these conditions are categorized as autoimmune diseases related to FS. Since a tryptophan-immobilized column effectively adsorb anti-GQ1b IgG antibody, immunoadsorption with the column should be considered as an alternative form of plasmapheresis for the anti-GQ1b IgG antibody syndrome.

Antibodies↗

[Usefulness of rapid examination method by test tape for cerebrospinal fluid].

We evaluated the usefulness of the test tape for cerebrospinal fluid (CSF), with which glucose and protein were examined, in aid of rapid diagnosis of various neurological diseases. Twenty-eight patients were examined to estimate the level of CSF glucose and protein using test tape. The data accuracy was confirmed with the data from standard measurements because the data from test tape correlated significantly with the data measured by standard method (glucose, p < 0.05; protein, p < 0.01). The test tape is useful for the rapid examination of CSF. We hope that more accurate test tape method will be developed for CSF glucose and protein determination.

Cerebrospinal Fluid↗

[Bickerstaff's brainstem encephalitis associated with nystagmus].

A 29-year-old man developed drowsiness, ophthalmoplegia and cerebellar ataxia following upper respiratory tract infection. We diagnosed the patient as having a Bickerstaff's brainstem encephalitis. There was upbeating nystagmus which appeared with upward gaze, and bilateral horizontal gaze-evoked nystagmus in both directions. On electronystagmography, eye-tracking test showed saccadic pattern with impaired smooth pursuit eye movement. The horizontal optokinetic nystagmus test showed diminution of response. These results suggested that brainstem and cerebellum were widely involved. Presence of nystagmus may help to speculate the lesion of Bickerstaff's brainstem encephalitis.

Adult↗

[A case of pharyngeal-cervical-branchial variant of Guillain-Barré syndrome with IgG anti-GT1a antibody].

A 36-year-old man with pharyngeal-cervical-brachial variant of Guillain-Barré syndrome (PCB) was described. Neurologic examination revealed total ophthalmoplegia, pharyngeal-cervical-brachial weakness and hyporeflexia in the upper limbs, sparing power and tendon reflexes in the lower limbs. Enzyme-linked immunosorbent assay showed that he had high titer of IgG antibody to GT1a (1:32,000), which did not cross-react with GQ1 b or GD1a. Thin-layer chromatography immunostaining confirmed that his serum IgG reacted with GT1a. These findings show that IgG anti-GT1a antibody without cross-reactivity with GQ1b plays a role in the development of PCB.

Adult↗

[Clinical utility of measurement for anti-GM1 and anti-GQ1b antibodies].

Gangliosides, important constituents of the plasma membrane, are particularly abundant in the nervous system. Some patients develop Guillain-Barré syndrome after the administration of bovine brain gangliosides. We previously showed existence of molecular mimicry between GM1 ganglioside and lipopolysaccharide of Campylobacter jejuni isolated from the patients with Guillain-Barré syndrome, and that between GQ1b and C. jejuni isolated from Fisher's syndrome patients. Moreover, the anti-ganglioside antibody can cause motor nerve dysfunction in vitro. These support the pathogenic significance of anti-ganglioside antibodies. To clarify clinical utility of measurement for anti-GM1 and anti-GQ1b antibodies, we investigated sera from 429 patients with immunoneurological diseases included Fisher's syndrome, Bickerstaff's brainstem encephalitis, acute ophthalmoparesis, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy, and controls by enzyme-linked immunosorbent assay. We found very high titers of IgM anti-GM1 antibody in serum from a patient who had been diagnosed as having motor neuron disease. By further electrophysiological study, the patient was diagnosed as having multifocal motor neuropathy. Presence of high IgG anti-GM1 antibody titers was useful for supporting diagnosis of Guillain-Barré syndrome, IgG anti-GQ1b antibody was detected in patients who had paresis of extraocular muscles in Fisher's syndrome, Guillain-Barré syndrome, Bickerstaff's brainstem encephalitis, and acute ophthalmoparesis. This study showed that the measurement for anti-GM1 and anti-GQ1b antibodies are very useful.

Adolescent↗

[A case of Guillain-Barré syndrome associated with bilateral ballism: an overlap between Fisher's syndrome and Guillain-Barré syndrome].

A 29-year-old woman developed diplopia and ataxic gait. Neurological examination revealed total ophthalmoplegia, cerebellar ataxia, and areflexia. Muscle weakness in four limbs was also noted. We diagnosed the patient as having an overlap between Fisher's syndrome and Guillain-Barré syndrome. On day 5, she suddenly had flinging involuntary movements affecting the face and four extremities. Surface EMG recording revealed 1.5- 2 Hz rhythmic grouping discharges. The involuntary movements were considered as ballism. Brain CT and MRI could not detect any abnormal findings in subthalamic nucleus, but, electrophysiological findings revealed CNS lesions. Therefore, the clinical diagnosis also were Bickerstaff's brainstem encephalitis. She had high titer of IgG antibody to GQ 1b (1:64,000). Sera taken from patients with Fisher's syndrome, Guillain-Barré syndrome with ophthalmoparesis and Bickerstaff's brainstem encephalitis during the acute phases of these syndromes frequently have IgG antibody to GQ 1b ganglioside. It is concluded that some cases of acute ophthalmoparesis subsequent to infection or immunization may be categorized as autoimmune diseases. Hence, such disease which show external ophthalmoparesis may be designated the "anti-GQ 1 b IgG antibody syndrome". This is the first report on the patient with Guillain-Barré syndrome and the related disorders who showed ballism.

Adult↗