This case was reported in a literature article and described the occurrence of chronic inflammatory demyelinating polyradiculoneuropathy in a 62-year-old male subject who received FLUARIX. On an unknown date, less than a month after receiving FLUARIX, the subject developed chronic inflammatory demyelinating polyradiculoneuropathy. Serious criteria included disability and GSK medically significant. Additional event(s) included common cold, leg cramps, lower extremities weakness of, paraparesis with serious criteria of GSK medically significant, sensory loss, mild - grade 1 numbness in hand, weakness generalized, areflexia, difficulty in standing, unable to walk with serious criteria of GSK medically significant, walker user and foot drop. The subject was treated with Immunoglobulin, mycophenolate mofetil and azathioprine. the outcome of chronic inflammatory demyelinating polyradiculoneuropathy was recovering/resolving. The outcome(s) of the additional event(s) included common cold (recovering/resolving), leg cramps (recovering/resolving), lower extremities weakness of (recovering/resolving), paraparesis (recovering/resolving), sensory loss (recovering/resolving), numbness in hand (recovering/resolving), weakness generalized (recovering/resolving), areflexia (recovering/resolving), difficulty in standing (recovering/resolving), unable to walk (recovering/resolving), walker user (recovering/resolving) and foot drop (recovering/resolving). It was unknown if the investigator considered the chronic inflammatory demyelinating polyradiculoneuropathy, common cold, leg cramps, lower extremities weakness of, paraparesis, sensory loss, numbness in hand, weakness generalized, areflexia, difficulty in standing, unable to walk, walker user and foot drop to be related to FLUARIX. Diagnostic results (unless otherwise stated, normal values were not provided): On an unknown date, CSF protein result was 700 mg/dL. On an unknown date, Nerve conduction studies result was Abnormal absent. On an unknown date, Physical examination result was generalized weakness absent. On an unknown date, Reflex test abnormal result was Areflexia absent. Additional information received: This case was reported in a literature article and it described the occurrence of acute-onset chronic inflammatory demyelinating polyneuropathy in a 62-year-old male patient who had received an unspecified influenza vaccine (manufacturer unspecified). No information on the patient's concurrent medical conditions, medical and family history or concomitant medication was provided. On an unspecified date, the patient received an unspecified influenza vaccine (dosage unknown; administration route and site unspecified, batch numbers not provided). On an unspecified date, within 4 weeks of the vaccination, the patient had a common cold that presented with leg cramps and lower extremity weakness that progressed to severe paraparesis. He also developed sensory loss in his lower extremities that ascended to his abdomen with mild numbness in the hands. Upon clinical examination he was found to have generalised weakness in his proximal and distal muscles (3/5) as well as areflexia. He was unable to stand or walk and the results of his electrodiagnostic studies were consistent with an acquired demyelinating neuropathy. After the initial treatment the patient's muscle strength improved slowly, and he was able to walk with a walker within 4 months but had bilateral flail feet. His neuromuscular score at this point improved from 20/100 at nadir to 65/100, but his improvement plateaued during the following 3-4 months. The findings in electrodiagnostic studies performed 7 months after onset changed the diagnosis from Guillain-Barre syndrome to acute-onset chronic inflammatory demyelinating polyneuropathy and he was started on a prolonged intravenous immunoglobulin treatment. He improved rapidly after this and his neuromuscular score was 90/100 after 5 pulse therapies. He was able to walk with a walker but with a residual bilateral foot drop. He continued to improve slowly with the treatment. This was a serious case as the events were disabling. His cerebrospinal fluid protein level was 700 mg/dl with no pleocytosis during his first presentation. A nerve conduction study performed 4 weeks after onset showed absent sural, superficial fibular, median and ulnar sensory nerve action potentials, with low amplitude radial sensory nerve action potentials (7 mV) and absent fibular and tibial compound muscle action potential. Median and ulnar motor conduction studies showed marked slowing of conduction velocities (median: 19, ulnar 29/29), borderline compound muscle action potential amplitudes [median distal amplitude (wrist) 4.4; median proximal amplitude (elbow) 1.6 (normal range not provided; ulnar distal amplitude (wrist) 5.2; ulnal proximal amplitude (below elbow) 2.6 and ulnar proximal amplitude (above elbow) 2.8 (no normal range provided)], median conduction block in the forearm (median conduction velocity 19), and markedly prolonged F-wave latencies (median F-waves latency 38.3; ulnar F-wave minimal latency 63.1). An electrodiagnostic study showed absent sensory nerve action potentials and worsening ulnar and median compound muscle action potential amplitudes, conduction blocks in the forearms bilaterally, and marked slowing of velocities 7 months after onset. Right median motor recording abductor pollicis brevis: distal amplitude (wrist) 2.6; proximal amplitude (elbow): 0.2; distal latency 11.3 and conduction velocity 13. Right ulnar motor recording abductor digiti minimi: distal amplitude (wrist) 1.9; proximal amplitude (below elbow) 1.0 (normal range no provided); proximal amplitude (above elbow) 0.9 (normal range no provided); distal latency 7.4; conduction velocities (in the forearm/across the elbow) 14/20 and F-wave minimal latency not recordable. Left median motor recording abductor pollicis brevis: distal amplitude (wrist) 3.0; proximal amplitude (elbow): 0.1 (no normal range provided); distal latency 8.9 and conduction velocity 12. Left ulnar motor recording abductor digiti minimi: distal amplitude (wrist) 2.8; proximal amplitude (below elbow) 0.9 (normal range no provided); proximal amplitude (above elbow) 0.3 (normal range no provided); distal latency 7.5 and conduction velocities (in the forearm/across the elbow) 14/18. An electrodiagnostic study 3 years after onset showed significant improvement in compound muscle action potential amplitudes of the upper extremities with partial left median conduction block and persisting slowing of velocities. Sensory nerve action potential and lower extremity compound muscle action potentials remained absent. Right median motor recording abductor pollicis brevis: distal amplitude (wrist) 6.8; proximal amplitude (elbow); 3.7 (no normal range provided); distal latency 6.4; conduction velocity 21 and F-wave minimal latency 68.6. Right ulnar motor recording abductor digiti minimi: distal amplitude (above elbow) 2.6; distal latency 5.1 and conduction velocities (in the forearm/across the elbow) 19/23. Left median motor recording abductor pollicis brevis: distal amplitude (wrist) 7.0; proximal amplitude (elbow): 3.8 (normal range no provided); proximal amplitude (above elbow) 2.6 (normal range no provided); distal latency 5.4 and conduction velocity 19. Left ulnar motor recording abductor digiti minimi: distal amplitude (wrist) 2.5; proximal amplitude 2.1 (normal range no provided); proximal amplitude (above elbow) 1.9 (normal range no provided); distal latency 5.1 and conduction velocities (in the forearm/across the elbow) 20/21. Initial treatment consisted of a course of intravenous immunoglobulin (2 g/kg). After the definitive diagnosis he was placed on a prolonged course of immunoglobulin 2 g/kg every 4 weeks. Mycophenolate mofetil (dosages unspecified) was added instead of azathioprine due to pancytopenia. One year later, he was walking independently with bilateral ankle-foot orthoses, so the immunoglobulin infusion intervals were increased slowly to every 12 weeks and were discontinued 2 years later. The patient was maintained on mycophenolate. The outcome of the event was recovering as the authors commented that the patient was walking independently but required bilateral ankle-foot orthoses 1 year after commencing the periodic immunoglobulin infusions, but that he continued improving after that. The authors did not comment on any possible causal link between the vaccine and this particular case. The authors concluded that "close observation of patients with severe Guillain-Barre syndrome beyond the acute illness phase and well into the rehabilitation phase is needed to identify this subgroup of acute-onset chronic inflammatory demyelinating polyneuropathy patients and to start immunotherapy. Repeat electrodiagnostic studies should be performed, perhaps more frequently, to distinguish patients with acute-onset chronic inflammatory demyelinating polyneuropathy from Guillain-Barre syndrome. Acute-onset chronic inflammatory demyelinating polyneuropathy patients will show signs of demyelisation on electrodiagnostic studies, whereas Guillain-Barre syndrome patients reveal signs of residual axonal loss. Prospective studies are needed to confirm our clinical and electrodiagnostic studies observations in patients with Guillain-Barre syndrome and acute-onset chronic inflammatory demyelinating polyneuropathy." This case is 1 of the 2 valid cases reported in the same literature article (see case US2015GSK150913).