1/31. miller fisher syndrome with central involvement: successful treatment with plasmapheresis.miller fisher syndrome is characterized by external ophthalmoplegia, ataxia, and areflexia. Most researchers favor a peripheral origin while others suggest a brainstem inflammatory lesion or a combination of central and peripheral demyelination. We report 2 cases of miller fisher syndrome with the typical triad of ataxia, areflexia, and ophthalmoplegia. Strong clinical evidence of central involvement included initial drowsiness, bilateral Babinski sign, and quadriparesis. Evoked potential studies showed prolongation of central conduction time. plasmapheresis was performed to relieve respiratory failure in Patient 1 and to shorten the duration of nasogastric tube feeding due to severe bulbar palsy in Patient 2. Significant improvement of electrophysiologic parameters was recorded after plasmapheresis. Abnormal evoked potentials, together with clinical evidence of central nervous system abnormalities, support the hypothesis that there is a combination of peripheral and central involvement in miller fisher syndrome in our patients. plasmapheresis is highly effective in relieving the profound neurological deficits of this atypical syndrome.- - - - - - - - - - ranking = 1keywords = ophthalmoplegia (Clic here for more details about this article) |
2/31. Bilateral ballism in a patient with overlapping Fisher's and Guillain-Barre syndromes.A 29 year old woman developed diplopia and ataxic gait. Neurological examination showed total ophthalmoplegia, cerebellar ataxia, and areflexia. Moreover, there was muscle weakness in all four limbs. An overlap of Fisher's and Guillain-Barre syndromes was dignosed. On day 5 she suddenly developed involuntary flinging movements that affected the face and four limbs. Surface EMG showed 1.5-2 Hz rhythmic grouping discharges. The involuntary movements were considered ballism. This is the first report of a patient with guillain-barre syndrome and a related disorder who showed ballism.- - - - - - - - - - ranking = 0.5keywords = ophthalmoplegia (Clic here for more details about this article) |
3/31. IgG anti-GQ1b positive acute ataxia without ophthalmoplegia.IgG anti-GQ1b antibody was present in a patient with acute ataxia and areflexia without ophthalmoplegia or elementary sensory loss. Sensory nerve conduction studies and somatosensory evoked potentials were normal, but postural body sway analysis showed dysfunction of the proprioceptive afferent system. The clinical presentation and laboratory results for this patient resemble those of miller fisher syndrome, except for the lack of ophthalmoplegia. This case may represent part of an IgG anti-GQ1b syndrome.- - - - - - - - - - ranking = 3keywords = ophthalmoplegia (Clic here for more details about this article) |
4/31. Acute onset of a bilateral areflexical mydriasis in Miller-Fisher syndrome: a rare neuro-ophthalmologic disease.Miller-Fisher syndrome (MFS) is characterized by variable ophthalmoplegia, ataxia, and tendon areflexia. It seems to be a variant of guillain-barre syndrome (GBS), but unlike in GBS, there is a primitive involvement of the ocular motor nerves, and in some cases there is brainstem or cerebellum direct damage. The unusual case of MFS in the current study started with a bilateral areflexical mydriasis and a slight failure of accommodative-convergence. Ocular-movement abnormalities developed progressively with a palsy of the upward gaze and a bilateral internuclear ophthalmoplegia to a complete ophthalmoplegia. In the serum of this patient, high titers of an IgG anti-GQ1b ganglioside and IgG anti-cerebellum. anti-purkinje cells in particular, were found. The former autoantibody has been connected to cases of MFS, of GBS with associated ophthalmoplegia, and with other acute ocular nerve palsies. The anti-cerebellum autoantibody could explain central nervous system involvement in MFS. The role of these findings and clinical implications in MFS and in other neuro-ophthalmologic diseases are discussed.- - - - - - - - - - ranking = 2.0004524827349keywords = ophthalmoplegia, ocular (Clic here for more details about this article) |
5/31. miller fisher syndrome: an uncommon acute neuropathy.The syndrome of ophthalmoplegia, ataxia, and areflexia was first described in 1956 by Miller Fisher. This syndrome has long been believed to be a variant of guillain-barre syndrome (GBS), mainly because of its areflexia, cerebrospinal fluid findings, and its postinfectious presentation. The case of an 11-year-old male with miller fisher syndrome (MFS) is described. MFS differs from GBS in several key clinical features and presents an extensive and challenging differential diagnosis. It is useful to recognize MFS as both a variant of GBS and a distinct entity with its own therapeutic considerations.- - - - - - - - - - ranking = 0.5keywords = ophthalmoplegia (Clic here for more details about this article) |
6/31. Features of sensory ataxic neuropathy associated with anti-GD1b IgM antibody.Some reports have called sensory ataxic neuropathy (SAN) associated with IgM antibody against b-series gangliosides a chronic form of miller fisher syndrome (MFS), but this has yet to be established. We examined five patients with SAN and eight patients with IgG anti-GQ1b-positive MFS. Only one patient with SAN complained of diplopia, whose ocular movement was not limited. The other four patients had neither diplopia nor limitation of ocular movement. All the SAN patients had severe deep sense impairment, whereas one patient with MFS showed only mild vibratory sense impairment. All sera from the SAN patients had remarkably high IgM antibody titers to the b-series gangliosides GD3, GD2, GD1b, GT1b, GQ1b, GQ1b alpha, fucosyl-GD1b, and alpha galactosyl [alpha fucosyl] GD1b. An absorption study confirmed that the anti-GQ1b antibodies cross-reacted with GD3, GD2, GD1b, and GT1b. In contrast, only two samples from the MFS patients had IgG antibody to GD3, and no sample reacted with GD2, GD1b, or GT1b. SAN has different clinical or serological features from MFS, and therefore is not a chronic form of it.- - - - - - - - - - ranking = 0.00045248273494772keywords = ocular (Clic here for more details about this article) |
7/31. Acute ophthalmoparesis (without ataxia) associated with anti-GQ1b IgG antibody: clinical features.OBJECTIVE: To examine the clinical features of acute ophthalmoparesis (AO) (without ataxia) associated with anti-GQ1b immunoglobulin g (IgG) antibody. DESIGN: Retrospective observational case series. PARTICIPANTS: Twenty-one subjects with AO (without ataxia) who had anti-GQ1b IgG. methods: Clinical features of 21 subjects with AO were analyzed. RESULTS: Seventeen had symptoms of antecedent infection. Gaze limitation was bilateral in 16 subjects and unilateral in five, indicative that laterality does not always negate AO. Nine subjects showed abducens paresis, and two limitation of abduction and adduction. Eight, who initially had bilateral abducens palsy, subsequently had impairment of adduction and vertical movement. These showed that bilateral abducens palsy followed by oculomotor nerve involvement is characteristic of AO. Muscle stretch reflexes were normal in nine subjects, hypoactive in eight, absent in three, and brisk in one. Distal paresthesias were present in seven subjects. Acellular cerebrospinal fluid (CSF) associated with raised protein concentration was detected in three. CONCLUSIONS: Antecedent infectious symptoms, characteristic limitation of ocular movement, areflexia, distal paresthesias, and CSF albuminocytologic dissociation are useful markers for diagnosing AO as well as anti-GQ1b IgG. AO can be considered a mild form of miller fisher syndrome or a regional variant of guillain-barre syndrome.- - - - - - - - - - ranking = 0.00022624136747386keywords = ocular (Clic here for more details about this article) |
8/31. The spectrum of IgG GQ1(b) syndrome: an unusual cluster.Four patients with IgG GQ1(b)antibodies were admitted to the gold Coast Hospital, a public hospital providing medical service to a population of approximately 400,000, over a 4-month period. This represents an unusual cluster of this syndrome, for which there is no apparent reason. Further, the four cases demonstrate the broad spectrum of the disorder from the benign ophthalmoplegia, ataxia and areflexia, miller fisher syndrome, to the severe form with encephalitis (Bickerstaff's brainstem encephalitis).- - - - - - - - - - ranking = 0.5keywords = ophthalmoplegia (Clic here for more details about this article) |
9/31. miller fisher syndrome with transient coma: comparison with Bickerstaff brainstem encephalitis.We herein report a 4-year-old boy with miller fisher syndrome (MFS) who presented with transient coma in addition to the typical triad of internal and external ophthalmoplegia, cerebellar ataxia and areflexia after an influenza type B infection. The electroencephalogram findings revealed intermittently generalized slow wave bursts. The cerebrospinal fluid revealed high protein and a lack of any cellular response. The serum anti-GQ1b IgG antibody was elevated in the acute phase and disappeared in the convalescent phase. The transient coma with the triad of MFS in this patient indicated an extended brainstem lesion including a reticular formation, which is also the responsible lesion of Bickerstaff brainstem encephalitis (BBE), but the magnetic resonance imaging repeatedly showed no abnormal finding. Our patient suggested the involvement of central nervous system in addition to the peripheral nerve injury in MFS. He also suggested that MFS and BBE may belong to the same group of disorders as syndrome of ophthalmoplegia, ataxia and areflexia (SOAA).- - - - - - - - - - ranking = 1keywords = ophthalmoplegia (Clic here for more details about this article) |
10/31. Benign intracranial hypertension: atypical presentation of miller fisher syndrome?Acute ocular paresis, nausea, vomiting, and headaches associated with high intracranial pressure without obvious intracranial pathology are typical features of benign intracranial hypertension. We describe two young children whose presentation, initially suggestive of idiopathic or benign intracranial hypertension, evolved to comprise ophthalmoplegia, ataxia, and areflexia. This triad characterizes miller fisher syndrome, a clinical variant of Guillain-Barre syndrome that occurs rarely among children. In both patients, this diagnosis was supported by the clinical course and neurophysiologic findings. Plasma serology was positive for campylobacter jejuni and anti-GQ1b antibodies in one patient and for antimyelin antibodies in the other. This report of two children with miller fisher syndrome presenting with intracranial hypertension adds to the findings for a similar patient treated previously, which raises the question concerning the possible role or contribution of benign intracranial hypertension in miller fisher syndrome.- - - - - - - - - - ranking = 0.50022624136747keywords = ophthalmoplegia, ocular (Clic here for more details about this article) |
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