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N Yuki

Publications and source records attributed to N Yuki.

At least 73 records · Page 4Linked to original sources
PubMed2001

[Pathophysiological diagnosis of facial paralysis using 3-D MRI].

Bilateral facial paralysis(facial diplesia) is often observed in Guillain-Barré syndrome(GBS) and Fisher's syndrome (FS). We tried to observe injured facial nerves using three-dimensional(3-D) MRI in facial diplesia due to GBS and its variants and examined function of blood nerve barrier and clinical use of 3-D MRI for detecting injured facial nerves. In the four patients with GBS and its variants(GBS three cases, FS one case), while routine brain MRI did not show any abnormal findings, contrast-enhanced 3-D MRI revealed Gd-enhancement of the facial nerves. On the other hand, only one case showed visualization using contrast-enhanced 3-D MRI in twelve cases of Bell's palsy. Therefore, it may be presumed that the reason why the significantly higher rate of visualization in facial paralysis in GBS and its variants than in Bell's palsy is attributable to a difference in the mechanism of injury or the extreme seriousness of the disease. In conclusion, the observation of facial nerve using 3-D MRI was very useful to know the condition of the facial diplesia in GBS and its variants.

Adult↗
PubMed2001

Animal model of axonal Guillain-Barré syndrome induced by sensitization with GM1 ganglioside.

Some humans develop the axonal form of Guillain-Barré syndrome after receiving bovine brain ganglioside. On sensitization with the ganglioside mixture, all of a group of rabbits injected developed high anti-GM1 IgG antibody titers, flaccid limb weakness of acute onset, and a monophasic illness course. Pathological findings for the peripheral nerves showed predominant Wallerian-like degeneration, with neither lymphocytic infiltration nor demyelination. IgG was deposited on the axons of the anterior roots, and GM1 was proved to be present on the axons of peripheral nerves. Sensitization with purified GM1 also induced axonal neuropathy, indicating that GM1 was the immunogen in the mixture. A model of human axonal Guillain-Barré syndrome has been established that uses inoculation with a bovine brain ganglioside mixture or isolated GM1. This model may help to clarify the molecular pathogenesis of the syndrome and to develop new treatments for it.

Animals↗
PubMed2001

[Pure dysarthria due to pontine infarction].

A 60-year-old man developed dysarthria in the morning. Neurological examination revealed no abnormality except for dysarthria. We diagnosed the patient as having a lacunar infarction. T2-weighted brain MRI revealed hyperintense lesion in the ventrolateral portion of the left upper pontine base. The clinical symptom completely disappeared on day 20. This is the first report on the MRI findings of the patient who showed pure dysarthria, which responsible lesion is in the pontine base. Involvement of corticopontine and corticobulbar tracts were considered to be responsible for the dysarthria in this case. This case may be useful for the somatotopy of corticopontine and corticobulbar tracts with articulation in the pontine base.

Cerebral Infarction↗
PubMed2001

[Atypical Fisher syndrome with optic nerve involvement].

We report a 38-year-old woman who developed what appeared to be Fisher syndrome associated with optic nerve involvement. One week after a common cold, she developed double vision and left facial palsy. Four days after the onset, she developed bilateral blurred vision, painful total ophthalmoplegia, and ataxic gait. Brain CT and MRI findings were normal. Her vision worsened but the optic fundi were normal. Serum anti-GQ 1 b antibody was elevated. She received steroid therapy at another hospital, and her vision, facial palsy and ocular pain improved. She was transferred to our hospital and we treated her by plasma exchange. She showed near complete recovery. Human optic and ocular nerves contain high amount of GQ 1 b. This may be a underlying mechanism for optic nerve involvement in Fisher syndrome. We thought that she had an atypical Fisher syndrome associated with optic nerve involvement.

Adult↗
PubMed2001

[Two-step interferon rebound therapy for refractory chronic hepatitis C].

In almost all patients in whom interferon(IFN) treatment dose not result in persistent negative findings for HCV-RNA, HCV-RNA levels show a rebound after discontinuing the administration. In most patients, HCV-RNA levels after administration are increased compared to pretreatment values. When a rapid increase in HCV-RNA levels causes transient exacerbation of transaminase levels, HCV-RNA levels then rapidly decrease. In two-step interferon rebound therapy(TIRT), IFN is additionally administered when HCV-RNA levels are decreased. We previously reported that TIRT was useful for treating type 1b patients with an HCV-RNA level of 1 Meq/ml or more who did not respond to IFN treatment. In the year 2000, health insurance covered the additional administration of IFN. The use of TIRT for additional administration may further improve treatment response in patients who do not respond to IFN treatment.

Adult↗
PubMed2001

[A case of brainstem encephalitis associated with Epstein-Barr virus infection: differentiation of acute disseminated encephalomyelitis and Bickerstaff's brainstem encephalitis].

A 28-year-old woman initially suffered high fever and headache (day 1). Aseptic meningitis was diagnosed on day 3. Limb ataxia, however, appeared on day 7, and external ophthalmoplegia and drowsiness were recognized on day 8. Urinary disturbance and orthostatic hypotension appeared on day 13. Cerebrospinal fluid showed moderately high cell counts(mononuclear cells, 51/microliter; polynuclear cells, 9/microliter). MRI T2-weighted images showed high intensity lesions in the pons and mesencephalon. No serum anti-GQ1b IgG antibody was detected on day 4. Epstein-Barr virus (EBV) viral capsid antigen-IgG antibody was positive, and EBV determined nuclear antigen antibody was seroconverted. EBV-DNA was detected in the CSF by PCR. These findings indicate prior infection by EBV. After intravenous dexamethasone therapy, these symptoms rapidly disappeared. Our patient showed external ophthalmoplegia, ataxia, and disturbance of consciousness, which are the cardinal signs in Bickerstaff's brainstem encephalitis. The time course of her neurological symptoms, the presence of meningitis, and the MRI findings, however, indicated the pathogenesis of acute disseminated encephalomyelitis rather than Bickerstaff's brainstem encephalitis. We diagnosed this patient as a brainstem encephalitis associated with EBV infection.

Adult↗
PubMed2001

[Ataxic form of Guillain-Barré syndrome associated with anti-GD1b IgG antibody].

A 28-year-old man was admitted after developing acute onset unstable gait following acute enteritis. Neurological examination revealed mild weakness in four limbs, areflexia and ataxia. Serum obtained from the patient during the acute stage contained a high titer of anti-GD1b IgG antibody. Because the patient showed obvious cerebellar ataxia unrelated to muscle weakness, without ophthalmoplegia or proprioceptive sensory disturbance, we concluded that he had ataxic form of Guillain-Barré syndrome (GBS) (Richter, 1962). Although ataxic GBS is not an established conception, one should pay attention to the possible existence of such a rare GBS variant. It is necessary to accumulate additional case reports to clarify the association between ataxic GBS and anti-ganglioside antibodies.

Adult↗
PubMed2001

[Anti-GQ1b IgG-negative case of overlapping Fisher's and Gullain-Barré syndromes after Campylobacter jejuni (PEN 19) enteritis].

We described a 70-year-old woman with overlapping Fisher's syndrome (FS) and Guillain-Barré syndrome (GBS), from whom Campylobacter jejuni had been isolated. In typical FS as well as GBS with ophthalmoplegia and acute ophthalmoparesis without ataxia, serum anti-GQ1b IgG antibody often is detected and ophthalmoplegia is characterized by the predominant abducens palsy. This patient, however, showed marked oculomotor nerve disturbance. Serum anti-GQ1b IgG antibody was negative and IgG antibodies against GM1, GM1b, and GD1a were strongly positive. Although FS and overlap of FS/GBS have been reported to be associated with PEN2 of C. jejuni, the isolate from our case belonged to PEN 19. C. jejuni serotype may be associated with clinical manifestations and anti-ganglioside antibody species.

Aged↗
PubMed2000

Ataxic Guillain-Barré syndrome with anti-GQ1b antibody: relation to Miller Fisher syndrome.

The authors reviewed the medical records of seven patients with anti-GQ1b immunoglobulin G (IgG) who had no or minimal external ophthalmoplegia but showed ataxia. The clinical features of the patients were consistent with the ataxic form of Guillain-Barré syndrome (GBS). Anti-GQ1b IgG antibodies from the patients, as well as from those with Miller Fisher syndrome (MFS), were absorbed by GT1a. The finding that ataxic GBS and MFS have in common an autoantibody with the same fine specificity suggests that they form a continuous spectrum.

Adult↗
PubMed2000

Antibodies to GM1(NeuGc) in Guillain-Barré syndrome after ganglioside therapy.

N-Glycolylneuraminic acid-containing GM1 [GM1(Gc)] is a molecule for serum antibodies in patients with Guillain-Barré syndrome (GBS). To clarify the pathogenesis of GBS after treatment with bovine brain ganglioside, we investigated the presence of anti-GM1(Gc) antibody in patients who developed GBS after ganglioside injection. Serum samples were taken from nine Italian patients with GBS after ganglioside therapy as well as from untreated Italian (n=30) and Japanese (n=131) GBS patients. Bovine brain gangliosides fractionated in a column were used as antigens, and binding of serum IgG or IgM was examined. An absorption study of IgG anti-GM1(Gc) antibody was made with GM1, asialo-GM1, GM2, GD1a, and GD1b. Four of the nine patients who developed GBS after being administered gangliosides had IgG anti-GM1(Gc) antibodies. Anti-GM1(Gc) IgG antibody frequencies were higher in patients with GBS after ganglioside therapy than in those who were untreated. Rates of absorption of IgG anti-GM1(Gc) antibodies by GM1 were significantly higher (except for asialo-GM1 and GD1b) than by GM2 and GD1a. The presence of GM1(Gc) was confirmed in bovine brain immunochemically using cholera toxin and Hanganutziu-Deicher antibody. Secondary ion mass spectra showed that the structure of the ganglioside was consistent with that of GM1(Gc). GM1(Gc) was recognized more frequently in sera from patients who developed GBS after ganglioside therapy than in sera from untreated GBS patients. Because N-glycolylneuraminic acid-containing gangliosides seem to be highly immunogenic in humans, GM1(Gc) may act as an immunogen in some patients who develop GBS following ganglioside therapy.

Animals↗
PubMed2000

Anti-SGPG antibody in CIDP: nosological position of IgM anti-MAG/SGPG antibody-associated neuropathy.

Polyneuropathy with monoclonal gammopathy usually is considered a nosological entity different from chronic inflammatory demyelinating polyneuropathy (CIDP). Criteria proposed by the American Academy of Neurology AIDS Task Force (1991), however, show monoclonal gammopathy to be a condition concurrent with CIDP. The purpose of this study was to clarify the nosological relationship between CIDP and IgM anti-myelin-associated glycoprotein (MAG)/sulfated glucuronyl paragloboside (SGPG)-associated polyneuropathy. We investigated IgM anti-MAG/SGPG antibody in 85 CIDP patients by various methods, then examined the relation of M-protein to the presence of IgM anti-MAG/SGPG antibody. In our large study, 17 (20%) of 85 CIDP patients had high IgM anti-SGPG antibody titers in the enzyme-linked immunosorbent assay. This was confirmed by thin-layer chromatography-immunostaining for IgM anti-SGPG antibody and immunoblotting for IgM anti-MAG antibody. Immunoelectrophoresis and immunofixation, respectively, detected IgM M-protein in 6 (35%) and 13 (76%) of the 17 CIDP patients. We conclude that some patients with IgM anti-MAG/SGPG antibody with or without monoclonal gammopathy may be diagnosed as having CIDP, when patients are diagnosed according to the current CIDP criteria.

Adult↗
PubMed2000

Current cases in which epitope mimicry is considered a component cause of autoimmune disease: Guillain-Barré syndrome.

Some patients develop 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. Miller Fisher syndrome (MFS), a variant of GBS, is associated with IgG antibody to GQ1b ganglioside. Molecular mimicry between GM1 and lipopolysaccharide of C. jejuni isolated from patients with GBS, and between GQ1b and C. jejuni lipopolysaccharides from patients with MFS have been demonstrated. The molecular mimicry between infectious agents and gangliosides may function in the production of anti-ganglioside antibodies. This sugar mimicry is one possible cause of the Guillain-Barré and Miller Fisher syndromes; however, unidentified host factors may contribute to the development of these syndromes.

Animals↗
PubMed2000

Is Campylobacter lipopolysaccharide bearing a GD3 epitope essential for the pathogenesis of Guillain-Barré syndrome?

The hypothesis has been proposed that the GD3 ganglioside-like lipopolysaccharide (LPS) is essential for and functions in the development of Guillain-Barré syndrome (GBS) and Miller Fisher syndrome (MFS) subsequent to Campylobacter jejuni enteritis. Our study showed that patients with GBS or MFS who had previously suffered diarrhea had anti-GD3 antibodies less often than those who had not had diarrhea. Sera from patients who showed GBS or MFS with the serologic evidence of prior C. jejuni infection had anti-GD3 antibodies less frequently than sera from those without evidence of infection. Statistical analysis showed that anti-GD3 antibodies were less frequent in patients with GBS or MFS from whom C. jejuni had been isolated than were other antiganglioside antibodies, such as anti-GM1 antibodies. These results could not support the above hypothesis.

Acute Disease↗
PubMed2000

Reappraisal of biochemical hepatitis C activity in hemodialysis patients.

We reappraised biochemical hepatitis C activity in hemodialysis patients in comparison with normal controls. A total of 111 hemodialysis patients and 66 healthy volunteer blood donors with hepatitis C virus (HCV) infection were consecutively enrolled. Serum alanine aminotransferase (ALT) levels were normal (< or =45 U/L) in 103 (93%) hemodialysis patients and 34 (52%) donors (p < 0.001). HCV viremic levels were lower in the hemodialysis group (p = 0.044), with no difference in the HCV genotype prevalence. During two-year follow-up, 60 (67%) of 90 hemodialysis patients and 13 (26%) of 50 donors showed persistently normal ALT levels (p < 0.001). For hemodialysis patients, however, the upper normal limit of ALT activity was reset at 25 U/L corresponding to the mean + 2 x SD for the normalized ALT distribution in 400 control patients. The adjusted ALT levels were initially normal in 73 (66%) hemodialysis patients and persistently normal in 19 (21%). Thus, ALT levels were the same for the two groups. GB virus C (GBV-C)/hepatitis G virus (HGV) coinfection found only in the hemodialysis group (10/111) had no influence on the disease. A relationship was noted between low disease activity and female gender in both groups. These findings indicate that biochemical hepatitis C activity in hemodialysis patients is similar to that in normal controls and should be monitored based on adjusted ALT levels.

Alanine Transaminase↗