To identify the factors that could predict the functional outcome in patients with the axonal type of Guillain-Barre syndrome (GBS).
Two hundred and two GBS patients admitted to our university hospital between 2003 and 2014 were reviewed retrospectively. We defined a good outcome as being "able to walk independently at 1 month after onset" and a poor outcome as being "unable to walk independently at 1 month after onset". We evaluated the factors that differed between the good and poor outcome groups.
Twenty-four patients were classified into the acute motor axonal neuropathy type. There was a statistically significant difference between the good and poor outcome groups in terms of the GBS disability score at admission, and GBS disability score and Medical Research Council sum score at 1 month after admission. In an electrophysiologic analysis, the good outcome group showed greater amplitude of median, ulnar, deep peroneal, and posterior tibial nerve compound muscle action potentials (CMAP) and greater amplitude of median, ulnar, and superficial peroneal sensory nerve action potentials (SNAP) than the poor outcome group.
A lower GBS disability score at admission, high amplitude of median, ulnar, deep peroneal, and posterior tibial CMAPs, and high amplitude of median, ulnar, and superficial peroneal SNAPs were associated with being able to walk at 1 month in patients with axonal GBS.
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Guillain-Barre syndrome (GBS) and syringomyelia are diseases of different entities. GBS is an acute post-infectious autoimmune disease which is mediated by autoantibodies against the myelin of peripheral nerves. Syringomyelia is a chronic disease characterized by a cavity extending longitudinally inside the spinal cord. A 67-year-old man is being hospitalized due to severe numbness and ascending weakness in all limbs. On neurological examination, the motor power of all limbs are decreased and show absence of deep tendon reflexes (DTRs). The patient is being diagnosed with GBS on the basis of the acute clinical course, nerve conduction studies of segmental demyelinating polyneuropathy, and a finding of albuminocytologic dissociation in the cerebrospinal fluid. The patient is presented with a new set of symptoms thereafter, which composes of sensory changes in the upper extremities, the urinary dysfunction including frequency and residual urine, spastic bilateral lower extremities, and increased reflexes of the knee and the biceps at follow-up examinations. The spinal magnetic resonance imaging in the sagittal section revealed a syrinx cavity between the fifth cervical and the first thoracic vertebral segment in the cord. The somatosensory evoked potential show sensory pathway defects between both the brachial plexus and the brain stem. Thus, this patient is being diagnosed with both GBS and syringomyelia. We report a case of symptomatic syringomyelia coexisting with GBS. Since the GBS is presented with a progressive muscle weakness and reduced DTRs, the muscle weakness and stiffness in the extremities suggests a concurrent syringomyelia might be easily overlooked.
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Acute multiple cranial neuropathies are considered as variant of Guillain-Barre syndrome, which are immune-mediated diseases triggered by various cases. It is a rare disease which is related to infectious, inflammatory or systemic diseases. According to previous case reports, those affected can exhibit almost bilateral facial nerve palsy, then followed by bulbar dysfunctions (cranial nerves IX and X) accompanied by limb weakness and walking difficulties due to motor and/or sensory dysfunctions. Furthermore, reported cases of the acute multiple cranial neuropathies show electrophysiological abnormalities compatible with the typical Guillain-Barre syndromes (GBS). We recently experienced a patient with a benign infectious disease who subsequently developed symptoms of variant GBS. Here, we describe the case of a 48-year-old male patient who developed multiple symptoms of cranial neuropathy without limb weakness. His laboratory findings showed a positive result for anti-GQ1b IgG antibody. As compared with previously described variants of GBS, the patient exhibited widespread cranial neuropathy, which included neuropathies of cranial nerves III-XII, without limb involvement or ataxia.
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A 24-year-old male developed bulbar palsy, ophthalmoplegia, ptosis, and shoulder weakness bilaterally 2 weeks after he had experienced an upper respiratory infection. The electrodiagnostic study demonstrated axonal polyradiculoneuropathy. The repetitive nerve stimulation study (RNS) showed no significant decrement of the compound muscle action potentials (CMAPs). The videofluoroscopic swallowing study (VFSS) showed severe impairment of the pharyngeal phase of swallowing. He was diagnosed as having the pharyngeal-cervical-brachial variant of Guillain-Barré syndrome. The patient's dysphagia was not improved for 3 months. A follow up RNS showed a significant decrement of the CMAPs. Pyridostigmine bromide was tried to improve the dysphagia. The patient showed immediate improvement of his dysphagia on the VFSS after the trial with pyridostigmine bromide. Pyridostigmine bromide was given before each meal for 8 days and he showed continuous improvement of his dysphagia. The follow up VFSS after 3 months showed complete recovery of dysphagia.
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