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1.
Neurosciences (Riyadh) ; 26(3): 295-299, 2021 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-34230086

RESUMO

COVID-19 infection displays heterogeneity of clinical manifestations in symptomatic and asymptomatic patients. We report on a child with Miller Fischer syndrome (MFS) and posterior reversible encephalopathy syndrome (PRES) post-COVID-19 infection. An 11-year-old boy presented with vomiting, headache, blurred vision, dysarthria, dysphagia, respiratory failure, muscle weakness, and unsteadiness. He had been exposed to COVID-19 through an asymptomatic elder brother two months prior to his illness. The MRI brain showed findings consistent with PRES and the diagnosis with Miller Fischer variant of the Guillain-Barré syndrome was made. A cerebrospinal fluid analysis revealed cytoalbuminous dissociation, and a nerve conduction velocity study conclusively showed polyneuropathy. A fluoroscopy of the diaphragms found that there was limited movement in both. Although children seem to be less affected by COVID-19 infection, this report highlights on an important neurological complications that can develop in children and its presence should be taken into consideration when diagnosing different forms of Guillain-Barré.


Assuntos
COVID-19/complicações , COVID-19/diagnóstico por imagem , Síndrome de Miller Fisher/diagnóstico por imagem , Síndrome de Miller Fisher/etiologia , Síndrome da Leucoencefalopatia Posterior/diagnóstico por imagem , Síndrome da Leucoencefalopatia Posterior/etiologia , Criança , Seguimentos , Humanos , Imunoglobulinas Intravenosas/administração & dosagem , Masculino , Síndrome de Miller Fisher/tratamento farmacológico , Síndrome da Leucoencefalopatia Posterior/tratamento farmacológico , Tratamento Farmacológico da COVID-19
2.
Neurol Clin ; 38(3): 711-735, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-32703478

RESUMO

The immune-mediated neuropathies are a broad category of diseases differentiated by time course, affected nerve fibers, and disease associations. This article spans the common, well-defined inflammatory demyelinating polyradiculoneuropathies (Guillain-Barré syndrome and chronic inflammatory demyelinating polyradiculoneuropathy) to the rarer, acquired demyelinating neuropathy variants (Miller-Fisher syndrome and multifocal motor neuropathy), vasculitic neuropathies, and sensory neuronopathies (dorsal root ganglionopathies). These case studies illustrate the characteristic clinical patterns of the immune-mediated neuropathies encountered in neurologic practice. Recommendations for diagnostic evaluation and treatment approach accompany each case. Prompt recognition of these disorders is imperative; delays in treatment may result in prolonged morbidity and permanent disability.


Assuntos
Síndrome de Guillain-Barré/diagnóstico por imagem , Síndrome de Guillain-Barré/imunologia , Síndrome de Miller Fisher/diagnóstico por imagem , Síndrome de Miller Fisher/imunologia , Polineuropatias/diagnóstico por imagem , Polineuropatias/imunologia , Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/diagnóstico por imagem , Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/imunologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Síndrome de Guillain-Barré/terapia , Humanos , Masculino , Pessoa de Meia-Idade , Síndrome de Miller Fisher/terapia , Polineuropatias/terapia , Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/terapia
5.
J Neuroimmunol ; 330: 170-173, 2019 05 15.
Artigo em Inglês | MEDLINE | ID: mdl-30642576

RESUMO

Anti-GQ1b antibody syndrome encompasses Miller Fisher syndrome and its related disorders. We retrospectively identified 11 pediatric patients (5.4-18 years old) with anti-GQ1b antibody syndrome. Diagnoses of patients included acute ophthalmoparesis (n = 6), classical Miller Fisher syndrome (n = 2), Miller Fisher syndrome/Guillain-Barré syndrome (n = 1), acute ataxic neuropathy (n = 1), and pharyngeal-cervical-brachial weakness (n = 1). Nine patients (81.8%) fully recovered. Maturational change in GQ1b antigen expression and the accessibility of anti-GQ1b antibodies might be the cause of the difference of clinical manifestations in children with anti-GQ1b antibody syndrome.


Assuntos
Autoanticorpos/sangue , Gangliosídeos/sangue , Síndrome de Miller Fisher/sangue , Síndrome de Miller Fisher/epidemiologia , Oftalmoplegia/sangue , Oftalmoplegia/epidemiologia , Adolescente , Criança , Pré-Escolar , Feminino , Humanos , Masculino , Síndrome de Miller Fisher/diagnóstico por imagem , Oftalmoplegia/diagnóstico por imagem , República da Coreia/epidemiologia , Estudos Retrospectivos , Síndrome
6.
Neurol Sci ; 39(2): 305-311, 2018 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-29124441

RESUMO

The study aimed to determine the incidence and the onset time of bulbar paralysis (BP) associated with Miller-Fisher syndrome (MFS) and its overlaps, to better understand the clinical characteristics among patients with MFS and its overlaps. Medical records from 48 patients with MFS and its overlaps were divided into two groups based on the presence (MFS-BP+) or absence (MFS-BP-) of BP. Their clinical features, laboratory and electrophysiological findings, neuroimaging data, and treatment plan were analyzed and compared between two groups. The incidence of BP associated with MFS and its overlaps was 48%. Eighty-two percent of the patients developed BP within 1 week after the onset of MFS and its overlaps. The cerebrospinal fluid (CSF) protein level in patients was higher in MFS-BP+ than in MFS-BP- group (67.69 ± 26.59 vs. 50.15 ± 20.44 mg/dl; P < 0.05). Frequencies of severe limb weakness, hypoglossal paralysis, disturbance of consciousness, and tracheal intubation required were also significantly higher in MFS-BP+ than in MFS-BP- group. Positive results of anti-GQ1b and anti-GT1b antibodies were all found in MFS-BP+ group. The prevalence of BP in MFS and its overlap was higher, the majority of BP occurred within 7 days after the onset of the disease, and early diagnosis of BP concurrence is helpful to decide the treatment plan.


Assuntos
Paralisia Bulbar Progressiva/complicações , Paralisia Bulbar Progressiva/epidemiologia , Síndrome de Miller Fisher/complicações , Síndrome de Miller Fisher/epidemiologia , Adulto , Idoso , Povo Asiático , Paralisia Bulbar Progressiva/diagnóstico por imagem , Eletrofisiologia , Feminino , Gangliosídeos/imunologia , Humanos , Imunoglobulina G/sangue , Incidência , Masculino , Pessoa de Meia-Idade , Síndrome de Miller Fisher/diagnóstico por imagem , Neuroimagem , Estudos Retrospectivos
7.
Rinsho Shinkeigaku ; 57(5): 234-237, 2017 05 27.
Artigo em Japonês | MEDLINE | ID: mdl-28450686

RESUMO

The patient was a 47-year-old man who presented with diplopia and gait instability with a gradual onset over the course of three days. Neurological examinations showed ophthalmoplegia, diminished tendon reflexes, and truncal ataxia. Tests for anti-GQ1b antibodies and several other antibodies to ganglioside complex were positive. We made a diagnosis of Fisher syndrome. After administration of intravenous immunoglobulin, the patient's symptoms gradually improved. However, bilateral facial palsy appeared during the recovery phase. Brain MRI showed intensive contrast enhancement of bilateral facial nerves. During the onset phase of facial palsy, the amplitude of the compound muscle action potential (CMAP) in the facial nerves was preserved. During the peak phase, the facial CMAP amplitude was within the lower limit of normal values, or mildly decreased. During the recovery phase, the CMAP amplitude was normalized, and the R1 and R2 responses of the blink reflex were prolonged. The delayed facial nerve palsy improved spontaneously, and the enhancement on brain MRI disappeared. Serial neurophysiological and neuroradiological examinations suggested that the main lesions existed in the proximal part of the facial nerves and the mild lesions existed in the facial nerve terminals, probably due to reversible conduction failure.


Assuntos
Nervo Facial/diagnóstico por imagem , Paralisia Facial/diagnóstico , Paralisia Facial/etiologia , Síndrome de Miller Fisher/complicações , Síndrome de Miller Fisher/diagnóstico , Potenciais de Ação , Autoanticorpos , Biomarcadores/sangue , Encéfalo/diagnóstico por imagem , Nervo Facial/patologia , Nervo Facial/fisiopatologia , Paralisia Facial/diagnóstico por imagem , Paralisia Facial/fisiopatologia , Gangliosídeos , Humanos , Imunoglobulinas Intravenosas/uso terapêutico , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Síndrome de Miller Fisher/diagnóstico por imagem , Síndrome de Miller Fisher/fisiopatologia , Exame Neurológico , Fatores de Tempo
8.
J Clin Neurosci ; 39: 63-67, 2017 May.
Artigo em Inglês | MEDLINE | ID: mdl-28209311

RESUMO

BACKGROUND: Miller Fisher syndrome (MFS) is a rare demyelinating condition which may have involvement of cranial nerves. There are a few case reports of optic pathway involvement in children. We describe 3 patients with optic pathway enhancement in pediatric patients with MFS. CASE SERIES: We retrospectively reviewed brain imaging findings in 17 pediatric patients with of Guillain-Barré syndrome (GBS) meeting Brighton criteria who had brain MRIs performed during their acute illness. Cranial nerve enhancement was seen in 6/17 patients and optic nerve/chiasm enhancement was seen in 3 patients. CONCLUSION: Cranial nerve enhancement and optic pathway in particular, can be seen in patients with MFS. Imaging findings do not always correlate with clinical manifestations of cranial nerve involvement.


Assuntos
Imageamento por Ressonância Magnética , Síndrome de Miller Fisher/diagnóstico por imagem , Quiasma Óptico/diagnóstico por imagem , Adolescente , Tronco Encefálico/diagnóstico por imagem , Criança , Pré-Escolar , Nervos Cranianos/diagnóstico por imagem , Feminino , Síndrome de Guillain-Barré/diagnóstico por imagem , Síndrome de Guillain-Barré/terapia , Humanos , Imageamento por Ressonância Magnética/métodos , Masculino , Síndrome de Miller Fisher/terapia , Neuroimagem/métodos , Estudos Retrospectivos
10.
Muscle Nerve ; 52(6): 1106-10, 2015 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-26123539

RESUMO

INTRODUCTION: Focal enlargement of the peripheral and spinal nerves, visualized using high-resolution ultrasound (HRUS), has been reported in early Guillain-Barré syndrome, but not in the Miller Fisher variant. We report the use of HRUS in 2 patients who presented with acute ataxic neuropathy, areflexia, and ophthalmoparesis. METHODS: Ultrasound and/or nerve conduction studies (NCS) of peripheral nerves, the vagus, and spinal nerves C5/6 were performed at onset and 2 weeks after immunoglobulin therapy. RESULTS: Both patients fulfilled criteria for diagnosis of Miller Fisher syndrome (MFS). Laboratory findings revealed elevated ganglioside Q1b antibodies in both and an albuminolocytologic dissociation in 1 patient. In addition, 1 patient had NCS evidence for demyelinating neuropathy. However, ultrasound showed focal enlargement in the vagus, the spinal nerves, and/or in the peripheral nerves in both patients. After therapy, nerve enlargement decreased in parallel with clinical improvement. CONCLUSION: Spinal and/or peripheral nerve enlargement supports the diagnosis of MFS in early phases of the disease.


Assuntos
Síndrome de Miller Fisher/diagnóstico por imagem , Síndrome de Miller Fisher/patologia , Nervos Periféricos/diagnóstico por imagem , Adolescente , Anticorpos/sangue , Gangliosídeos/imunologia , Humanos , Masculino , Pessoa de Meia-Idade , Condução Nervosa/fisiologia , Nervos Periféricos/fisiopatologia , Ultrassonografia
13.
J Neurol Neurosurg Psychiatry ; 80(5): 512-7, 2009 May.
Artigo em Inglês | MEDLINE | ID: mdl-19066195

RESUMO

BACKGROUND: Fisher syndrome (FS) is characterised by a triad of ophthalmoplegia, ataxia and areflexia. The lesion sites responsible for ataxia and ophthalmoplegia in FS require further exploration. The aim of this study was to determine the involvement of the central nervous system in FS using (18)F-fluorodeoxyglucose-positron emission tomography (FDG-PET). METHODS: Cerebral glucose metabolism in 10 patients with FS was compared with that of 60 age and sex matched normal controls using PET. For individual analyses, 15 age and sex matched controls were selected from the control group. Patients also underwent MRI of the brain and measurement of serum anti-GQ1b antibody. RESULTS: Group analyses revealed increased metabolism in the cerebellar vermis and hemispheres, pontine tegmentum, midbrain tectum, left thalamus and right inferior frontal cortex (p<0.001, uncorrected). In contrast, the visual association cortices (Brodmann areas 18 and 19) showed decreased metabolism bilaterally. Individual analyses disclosed hypermetabolism in the cerebellar vermis or hemispheres (n = 7), inferior frontal cortex (n = 5) and brainstem (n = 4, p<0.005, uncorrected). A negative correlation between the cerebellar hypermetabolism and the interval from symptom onset to PET (r = -0.745, p = 0.013) was also found. Hypermetabolism was normalised on follow-up PET with an improvement in ophthalmoplegia and ataxia in one patient. CONCLUSIONS: These findings indicate involvement of the central nervous system in FS, and the hypermetabolism in the cerebellum and brainstem suggests an antibody associated acute inflammatory process as a mechanism of this autoimmune disorder.


Assuntos
Química Encefálica/fisiologia , Glucose/metabolismo , Síndrome de Miller Fisher/diagnóstico por imagem , Síndrome de Miller Fisher/metabolismo , Adulto , Idoso , Encéfalo/diagnóstico por imagem , Feminino , Fluordesoxiglucose F18 , Gangliosídeos/imunologia , Síndrome de Guillain-Barré/genética , Humanos , Processamento de Imagem Assistida por Computador , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Tomografia por Emissão de Pósitrons , Compostos Radiofarmacêuticos
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