This case was reported in a literature article and described the occurrence of chronic inflammatory demyelinating polyradiculoneuropathy in a 71-year-old male subject who received FLUARIX. On an unknown date, 10 days after receiving FLUARIX, the subject developed chronic inflammatory demyelinating polyradiculoneuropathy. Series criteria included hospitalization, disability and GSK medically significant. Additional event(s) included numbness of extremities, severe - grade 3 weakness generalized, urinary retention with serious criteria of GSK medically significant, incontinence, facial palsy, dyspnea, orthopnea, difficulty in standing, walker user, sensory abnormality of lower extremities and mild - grade 1 sensory ataxia. The subject was treated with Immunoglobulin. The outcome of chronic inflammatory demyelinating polyradiculoneuropathy was resolved with sequelae. The outcome(s) of the additional event(s) included numbness of extremities (recovered/resolved), weakness generalized (recovered/resolved), urinary retention (recovered/resolved), incontinence (recovered/resolved), facial palsy (recovered/resolved), dyspnea (recovered/resolved), orthopnea (recovered/resolved), difficulty in standing (recovered/resolved), walker user (recovered/resolved), sensory abnormality of lower extremities (not recovered/not resolved) and sensory ataxia (not recovered/not resolved). It was unknown if the investigator considered the chronic inflammatory demyelinating polyradiculoneuropathy, numbness of extremities, weakness generalized, urinary retention, incontinence, facial palsy, dyspnea, orthopnea, difficulty in standing, walker user, sensory abnormality of lower extremities and sensory ataxia to be related to FLUARIX. Diagnostic results (unless otherwise stated, normal values were not provided): On an unknown date, Blood sodium result was 127 mmol/L. On an unknown date, CSF protein result was 82 mg/dL. On an unknown date, Nerve conduction studies result was Abnormal 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 71-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, 10 days after the vaccination, the patient developed numbness in his hands and feet followed by severe generalized weakness, urinary retention and incontinence that required the placement of a Foley catheter. On admission he was noted to have elevated cerebrospinal fluid protein level and hyponatremia. His arms improved significantly after receiving a 5-day course of intravenous immunoglobulin; but the weakness worsened 6 weeks later and he developed bilateral facial palsy accompanied by dyspnoea and orthopnoea. The dyspnoea and arm/facial strength improved after receiving a second course of immunoglobulin but he remained non-ambulatory. He underwent rehabilitation but his condition failed to improve for 10 months during which he could only stand assisted by 2 people. An electrodiagnostic test repeated at this point showed demyelinating signs so diagnosis was changed from Guillain-Barre syndrome to acute-onset chronic inflammatory demyelinating polyneuropathy and he was commenced on a prolonged course of immunoglobulin. The patient was able to stand on his own, walked independently with a walker and had normal strength in the upper extremities after 5 cycles. This was a serious case as the events were disabling and the patient required hospitalization. His cerebrospinal fluid protein level was elevated at 82 mg/dl with no pleocytosis during his first presentation. He also noted to have hyponatremia (sodium 127 mEq/L, normal ranges not provided) on admission. A nerve conduction study performed 5 days after onset on his right side showed the following results: for median motor recording abductor pollicis brevis: distal amplitude (wrist) 2.1; proximal amplitude (elbow): 2.0 (no normal range provided); distal latency 5.3; conduction velocity 52 and F-wave minimal latency 41.8. Ulnar motor recording abductor digiti minimi: distal amplitude (wrist) 8.4; proximal amplitude (below elbow) 5.4 (normal range no provided): proximal amplitude (above elbow) 5.3 (normal range no provided); distal latency 2.7; conduction velocities (in the forearm/across the elbow) 56/50 and F-wave minimal latency 32.1. A nerve conduction studies performed on his right sight 6 weeks after onset showed conduction blocks in the forearms with slowing and absent F-waves. Median motor recording abductor pollicis brevis: distal amplitude (wrist) 1.4; proximal amplitude (elbow): 0.4 (no normal range provided); distal latency 8.5; conduction velocity 31 and F-wave minimal latency not recordable. Ulnar motor recording abductor digiti minimi: distal amplitude (wrist) 2.5; proximal amplitude (below elbow) 1.1 (normal range not provided); proximal amplitude (above elbow) 1.1 (normal range not provided); distal latency 5.2; conduction velocities (in the forearm/across the elbow) 50/54 and F-wave minimal latency not recordable. A repeated electrodiagnostic test performed at 9 months after onset in view of his lack of progress showed markedly decreased motor conduction velocities in the upper extremities bilaterally (10-14 m/s), prolonged distal latencies, and prolonged F-wave latencies. Right site median motor recording abductor pollicis brevis: distal amplitude (wrist) 1.5; proximal amplitude (elbow); 0.7 (no normal range provided); distal latency 15.9; conduction velocity 17 and F-wave minimal latency 66.6. Right site ulnar motor recording abductor digiti minimi: distal amplitude (wrist) 1.2; proximal amplitude (below elbow) 0.2; proximal amplitude (above elbow) 0.1 (normal range not provided); distal latency 12.1; conduction velocities (in the forearm/across the elbow) 14/14 and F-wave minimal latency not recordable. Left side median motor recording abductor pollicis brevis: distal amplitude (wrist) 0.7; proximal amplitude (elbow): 0.6 (no normal range provided); distal latency 15.1; conduction velocity 10 and F-wave minimal latency 75.1. Left ulnar motor recording abductor digiti minimi: distal amplitude (wrist) 1.1; proximal amplitude (below elbow) 0.1 (normal range no provided); proximal amplitude (above elbow) not recordable (normal range no provided); distal latency 12.4; conduction velocities (in the forearm/across the elbow) 12/15 and F-wave minimal latency 55.8. This was repeated again at 16 months of onset and it showed remarkable improvement of compound muscle action potential amplitudes in the upper extremities. Right median motor recording abductor pollicis brevis: distal amplitude (wrist) 2.3; proximal amplitude (elbow): 2.2; distal latency 5.6; conduction velocity 33 and F-wave minimal latency 34.8. Right ulnar motor recording abductor digiti minimi: distal amplitude (wrist) 7.2; proximal amplitude (below elbow) 4.9 (normal range no provided); proximal amplitude (above elbow) 4.9 (normal range no provided); distal latency 3.8; conduction velocities (in the forearm/across the elbow) 32/15 and F-wave minimal latency 31.3. Left median motor recording abductor pollicis brevis: distal amplitude (wrist) 4.0; proximal amplitude (elbow): 2.4 (no normal range provided); distal latency 6.4; conduction velocity 33 and F-wave minimal latency not recordable. Left ulnar motor recording abductor digiti minimi: distal amplitude (wrist) 6.4; proximal amplitude (below elbow) 4.9 (normal range no provided); proximal amplitude (above elbow) 4.7 (normal range no provided); distal latency 3.3; conduction velocities (in the forearm/across the elbow) 35/56 and F-wave minimal latency not recordable. Initial treatment consisted of a 5-day course of intravenous immunoglobulin (dosage unspecified). The patient received a second course (dose unspecified) after he developed the facial palsy, dyspnoea and orthopnoea. He was finally placed on a prolonged course of immunoglobulin 2 g/kg every 4 weeks to which he responded dramatically. The infusion intervals were extended gradually during the following 26 months to every 8 weeks after he had at least 5 cycles. The outcome of the event was resolution with sequelae as the authors commented that the patient walked independently without weakness but had reduced sensation in the legs with mild sensory ataxia at a 2-year follow-up. 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 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 US2015GSK150919).