Make a FDAR GUILLAIN BARRE SYNDROME   A 53-year-old man was admitted to the hospital with a 3-h history of left-arm weakness, glossolalia, and right eyelid droop. After admission, his condition suddenly worsened, with quadriplegia, bilateral peripheral facial palsy, bilateral ophthalmoplegia, and other neurological symptoms. Based on the findings from a neurological examination, MRI, cerebrospinal fluid analysis, and nerve conduction study, a diagnosis of GBS was made. He received intravenous immunoglobulin (0.4 kg/day) for 5 days. After 20 days of systematic therapy, his dysphagia, dyspnea, facial paralysis, ocular movement disorder, and leg weakness recovered almost completely, but his arms were still moderately impaired, with a power of 4/5. Fortunately, the patient recovered well without any sequelae after 2 years of follow-up. Conclusions: In patients with an atypical presentation, the diagnosis of GBS is often delayed. With this case report, we intend to highlight the fact that some symptoms mimicking stroke may be a feature of GBS at onset; close observation and timely diagnosis are crucial for clinicians. Neuroimaging is a valuable diagnostic tool in differentiating stroke from GBS.   A 53-year-old man presented with left-arm weakness, glossolalia, and right eyelid droop for a duration of 3 h. He had a sore throat and stuffy nose 10 days earlier. Other than having hypertension and gout, his medical history was unremarkable. None of his family members had experienced similar symptoms. On admission, his vital signs were normal, and his higher mental functions were appropriate for his age. Neurological examination showed dysarthria, right eyelid droop, left facial droop, and a left-held tongue. No nystagmus, ophthalmoplegia, ataxia, or hearing loss was noticed. His muscle strength was 4/5 in the left upper limb (in both the proximal and distal muscles). There was no sensory function deficit. Deep tendon reflexes were present and symmetrical. The results of coordination tests and gait tests were normal, and plantar responses were normal bilaterally. The results of the rest of his physical examination were normal. The results of his brain CT examination were normal. In summary, he was managed as having a posterior circulation infarct. The patient and his family did not agree to intravenous thrombolysis because of the risk of bleeding. Eight hours after he was admitted, his condition deteriorated, with quadriplegia and bilateral peripheral facial palsy. Immediately, cranial MRI with magnetic resonance angiography was performed, but no abnormal manifestations were found Cervical and thoracic spinal MRI were also performed, and the results were normal. Because of his unremarkable neuroimaging results, GBS became the primary working diagnosis. The following day, he developed bilateral ophthalmoplegia, dysphagia, dyspnea, and numbness in all extremities, and he underwent tracheotomy to prevent a worsening of his acute respiratory failure. Lumbar puncture was performed, and cerebrospinal fluid (CSF) analysis showed that the protein level was 0.87 g/L (normal values: 0.25–0.47 g/L), while the white blood cell count was 5 × 106/L (normal values: 0–8 × 106/L). Anti-ganglioside antibody analysis of the serum and CSF revealed high levels of anti-GQ1b. The blots for other anti-gangliosides (anti-GM1, anti-GM2, anti-GM3, anti-GD1a, anti-GD1b, and anti-GT1b) were negative. Nerve conduction study (NCS) results showed that the amplitudes of the bilateral facial, median, ulnar, and right peroneal (fibular) motor nerves were reduced; the occurrence rates of the F wave in the left median nerve and ulnar nerve were reduced; the F wave was absent in the right median nerve; and the rest of the testing revealed normal results Figure 2). Unfortunately, the H wave could not be detected in either leg due to the limitations of the patient's posture. According to the NCS results, mild to moderate damage to multiple motor nerves was considered. The patient received intravenous immunoglobulin (0.4 kg/day) for 5 days. Three weeks after admission, at discharge, his dysphagia, dyspnea, facial paralysis, ocular movement disorder, and leg weakness had recovered almost completely, but his arms were still moderately impaired, with a power of 4/5 (in both the proximal and the distal muscles). When the patient was discharged, he no longer needed a ventilator and could breathe normally. The patient had to be flown home, and due to safety concerns, the patient was discharged with a tracheotomy. Fortunately, the patient recovered well without any sequelae after 2 years of follow-up.

Make a FDAR GUILLAIN BARRE SYNDROME   A 53-year-old man was admitted to the hospital with a 3-h history of left-arm weakness, glossolalia, and right eyelid droop. After admission, his condition suddenly worsened, with quadriplegia, bilateral peripheral facial palsy, bilateral ophthalmoplegia, and other neurological symptoms. Based on the findings from a neurological examination, MRI, cerebrospinal fluid analysis, and nerve conduction study, a diagnosis of GBS was made. He received intravenous immunoglobulin (0.4 kg/day) for 5 days. After 20 days of systematic therapy, his dysphagia, dyspnea, facial paralysis, ocular movement disorder, and leg weakness recovered almost completely, but his arms were still moderately impaired, with a power of 4/5. Fortunately, the patient recovered well without any sequelae after 2 years of follow-up. Conclusions: In patients with an atypical presentation, the diagnosis of GBS is often delayed. With this case report, we intend to highlight the fact that some symptoms mimicking stroke may be a feature of GBS at onset; close observation and timely diagnosis are crucial for clinicians. Neuroimaging is a valuable diagnostic tool in differentiating stroke from GBS.   A 53-year-old man presented with left-arm weakness, glossolalia, and right eyelid droop for a duration of 3 h. He had a sore throat and stuffy nose 10 days earlier. Other than having hypertension and gout, his medical history was unremarkable. None of his family members had experienced similar symptoms. On admission, his vital signs were normal, and his higher mental functions were appropriate for his age. Neurological examination showed dysarthria, right eyelid droop, left facial droop, and a left-held tongue. No nystagmus, ophthalmoplegia, ataxia, or hearing loss was noticed. His muscle strength was 4/5 in the left upper limb (in both the proximal and distal muscles). There was no sensory function deficit. Deep tendon reflexes were present and symmetrical. The results of coordination tests and gait tests were normal, and plantar responses were normal bilaterally. The results of the rest of his physical examination were normal. The results of his brain CT examination were normal. In summary, he was managed as having a posterior circulation infarct. The patient and his family did not agree to intravenous thrombolysis because of the risk of bleeding. Eight hours after he was admitted, his condition deteriorated, with quadriplegia and bilateral peripheral facial palsy. Immediately, cranial MRI with magnetic resonance angiography was performed, but no abnormal manifestations were found Cervical and thoracic spinal MRI were also performed, and the results were normal. Because of his unremarkable neuroimaging results, GBS became the primary working diagnosis. The following day, he developed bilateral ophthalmoplegia, dysphagia, dyspnea, and numbness in all extremities, and he underwent tracheotomy to prevent a worsening of his acute respiratory failure. Lumbar puncture was performed, and cerebrospinal fluid (CSF) analysis showed that the protein level was 0.87 g/L (normal values: 0.25–0.47 g/L), while the white blood cell count was 5 × 106/L (normal values: 0–8 × 106/L). Anti-ganglioside antibody analysis of the serum and CSF revealed high levels of anti-GQ1b. The blots for other anti-gangliosides (anti-GM1, anti-GM2, anti-GM3, anti-GD1a, anti-GD1b, and anti-GT1b) were negative. Nerve conduction study (NCS) results showed that the amplitudes of the bilateral facial, median, ulnar, and right peroneal (fibular) motor nerves were reduced; the occurrence rates of the F wave in the left median nerve and ulnar nerve were reduced; the F wave was absent in the right median nerve; and the rest of the testing revealed normal results Figure 2). Unfortunately, the H wave could not be detected in either leg due to the limitations of the patient's posture. According to the NCS results, mild to moderate damage to multiple motor nerves was considered. The patient received intravenous immunoglobulin (0.4 kg/day) for 5 days. Three weeks after admission, at discharge, his dysphagia, dyspnea, facial paralysis, ocular movement disorder, and leg weakness had recovered almost completely, but his arms were still moderately impaired, with a power of 4/5 (in both the proximal and the distal muscles). When the patient was discharged, he no longer needed a ventilator and could breathe normally. The patient had to be flown home, and due to safety concerns, the patient was discharged with a tracheotomy. Fortunately, the patient recovered well without any sequelae after 2 years of follow-up.