At 2 weeks after hospital discharge, the bilateral facial paralysis had recovered, ataxia was eliminated, walking was obviously improved and the movement of the eyeballs had partially recovered. type, anti-GM1 antibody and MFS remains Valnoctamide unclear and requires further research. strong class=”kwd-title” Keywords: Miller Fisher syndrome, intracranial hypertension, facial nerve palsy, treatment Introduction Miller Fisher Rabbit Polyclonal to AML1 (phospho-Ser435) syndrome (MFS) is considered to be a variant of GuillainCBarr syndrome (GBS).1 Its clinical symptoms include external ophthalmoplegia, ataxia Valnoctamide and hyporeflexia or areflexia of the tendons of the four limbs.1 The anti-ganglioside Q1b (anti-GQ1b) antibodies are always positive.2 MFS rarely manifests as intracranial hypertension and delayed bilateral facial nerve palsy. The present case report explains a man with MFS with early intracranial hypertension and delayed bilateral simultaneous facial nerve palsy, without anti-GQ1b antibodies but with anti-ganglioside M1-immunoglobulin M (anti-GM1-IgM) antibodies. Case report A 40-year-old unmarried male presented to the Department of Neurology, Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China in April 2017 with a 3-day history of unsteady walking and numbness on both hands, and a 2-day history of seeing double images and unclear articulation. He had a cold for the 2 2 weeks prior to presentation. He did not have any relevant medical history. The symptoms gradually worsened and on the 4th day he was admitted to the hospital. On admission, the general medical examination was normal. A neurological examination revealed the following: unclear articulation, velar nasal, the movement of the bilateral eyeballs was slightly limited, the pharyngeal reflex was obtuse, areflexia with no limb muscle weakness and an ataxic gait. The remainder of the neurological examination was normal. Brain computed tomography and magnetic resonance imaging revealed no abnormalities. Routine laboratory examinations were normal, including blood cell count, blood biochemistry, cancer index and immunological examinations. Various antiviral antibodies were unfavorable. Lumbar puncture was performed on day 4 and revealed an opening pressure of 260 mm H2O (the patient had no headache), cerebrospinal fluid protein content 290?mg/l and a cell count of 12??106/l. Lumbar puncture was conducted again after 1 week when the pressure had spontaneously returned to normal levels, protein levels improved and the separation of proteins and cells occurred. Serum anti-GM1-IgM was found to be positive, but anti-GQ1b and the remaining antibodies were all unfavorable. Nerve conduction examinations were normal. Valnoctamide The patient was diagnosed with MFS and was treated with 0.4?g/kg per day of intravenous immunoglobulin (IVIG) for 5 days. Around the 4th day of treatment with IVIG (i.e. 9 days after the onset of symptoms), his ataxia and unsteady walking improved, but his bilateral eyeballs were fixed, and over the next few days he developed consecutive bilateral peripheral facial paralysis. After IVIG treatment, the patient was given 3 days of 1000 mg/day methylprednisolone via intravenous drip. The dose was halved every 3 days until the dose reached 60?mg/day methylprednisolone via intravenous drip. Then the drug was taken orally and the dose was gradually decreased. Around the 18th day after onset of symptoms, facial paralysis, dysarthria, dysphagia and ataxia further improved. Around the 19th day after onset of symptoms, the patient was discharged from hospital. At 2 weeks after hospital discharge, the bilateral facial paralysis had recovered, ataxia was eliminated, walking was obviously improved and the movement of the eyeballs had partially recovered. On the 3rd week after discharge, the movement of the eyeballs had obviously improved, mild diplopia remained, speaking Valnoctamide with a twang had disappeared and coughing while drinking had been eliminated. One month after discharge, the patients eyeballs moved freely and the diplopia had disappeared. This study was conducted in accordance with the declaration of Helsinki. This study was conducted with approval from the Ethics Committee of the Third Affiliated Hospital of Guangzhou Medical University. Written.
At 2 weeks after hospital discharge, the bilateral facial paralysis had recovered, ataxia was eliminated, walking was obviously improved and the movement of the eyeballs had partially recovered
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