Chronic Inflammatory Demyelinating Polyneuropathy (CIDP); This literature case was received on 22-Feb-2021, concerning 46-year old, male patient.  This short study was conducted at the neuromuscular clinic from 2001 to 2005.   The patient had no relevant medical history. The patient was in good health prior to the onset of chronic inflammatory demyelinating polyneuropathy (CIDP), did not have any acute illness, systemic infections, diabetes mellitus, history of alcohol abuse, or exposure any known neurotoxins, and there was no family history of neuropathy. The patient's concomitant medications were not reported.  On an unknown date, the patient was vaccinated influenza virus vaccine polyvalent (brand not specified; dose, anatomical location, indication and route of administration: not reported). The batch number was not reported.   On an unspecified date, seven days after receiving influenza virus vaccine polyvalent, the patient experienced sensation of burning, tingling, and itching over the trunk. The patient underwent detailed history, general and neurological examinations, electrodiagnostic and laboratory studies, including spinal fluid, complete blood count, metabolic panel, serology for autoimmune disorders, Lyme serology, venereal disease research laboratory (VDRL), serum immune fixation, thyroid studies, glucose and HbA1C, and magnetic resonance imaging (MRI) of the brain and spine.  On an unspecified date, over the next ten days, the patient developed difficulty chewing, bilateral facial weakness and diplopia, along with tingling and numbness in feet and hands, mild weakness in limbs, and gait difficulty. All tendon reflexes were absent, and sensations were normal. The cerebral spinal fluid (CSF) analysis revealed elevated protein (142 mg/dl) with two lymphocytes and normal glucose and cell count. Other laboratory and imaging studies were normal. Electrodiagnostic studies were unremarkable except for mild impersistence of median nerve F waves (four of ten) with normal latencies. Needle electromyogram (EMG) testing of distal lower extremity muscles was unremarkable. Blink reflex showed absent R1 and R2 responses bilaterally and normal response with direct facial stimulation, suggesting a proximal conduction block. Cranial magnetic resonance imaging (MRI) showed subtle enhancement of facial nerves.   On an unspecified date, he was treated with a 5-day course of immunoglobulin (IVIG) at a dose of 0.4 g/kg per day.   On an unspecified date, the patient improved.   On an unspecified date, four weeks later, the patient noted increasing numbness in toes and hands as well as increasing weakness in ankles with decreased balance and gait difficulty. Examination showed weakness with grade four medical research council (MRC) strength in intrinsic hand muscles, hip flexors, and ankle dorsiflexion. Muscle stretch reflexes were diminished in the arms and absent at knees and ankles. Vibration and pin sensation were diminished in feet with preserved proprioception. Electrodiagnostic findings for median motor were: distal motor latency (DL) (ms): 5.3, amplitude (amp): 3.5, conduction velocity (CV) (m/s): 34.21 and F wave latency (ms): 59; for peroneal motor: right (rt): DL (ms): 7.5, amp: 0.8, CV (m/s): 41.22 and F wave latency (ms): No response (NR), left (lt): DL (ms): 6.4, amp: 1.1, CV (m/s): 30.42 and F wave latency (ms): NR; for tibial motor: rt: DL (ms): 6.6, Amp: 3.7, CV (m/s): 34, F wave latency (ms): 84, lt: DL (ms): 5.8, amp: 5.6, CV (m/s): 30 and F wave latency (ms): 78; and for ulnar motor: DL (ms): 3.8, amp: 8.6, CV (m/s): 48, 43, 60, F wave latency (ms): 38. Sural amplitude for lt was 13 µV and rt: 11 µV, median sensory amplitude and ulnar sensory amplitude were: NR. Electrodiagnostic studies showed widespread abnormalities, indicating a demyelinating polyneuropathy. Median and ulnar sensory potentials were absent, and sural sensory potentials were preserved.   On an unspecified date, the patient was treated with intravenous Gammaglobulin (immunoglobulin g human) (IVIG) at a dose of 1 g/kg monthly for four months.  On an unspecified date, the patient improved promptly.   On an unspecified date, he experienced another relapse, which responded to pulse intravenous methylprednisolone at a dose of 1000 mg per week (mg/wk) and developed gastrointestinal side effects. Thereafter, he was treated with monthly immunoglobulin (IVIG), and oral Mycophenolate (mycophenolate mofetil) at a dose of 1 g two times a day (bid).   On an unspecified date, at the 36-month follow-up, the patient showed no deficit. He had not required IVIG for one year and remained free of relapses.  At the time of initial reporting, the patient recovered from event.  The reporter assessed the event as related to influenza virus vaccine polyvalent. Physician reported that the patient who was otherwise healthy, developed CIDP with rapid onset in close proximity to influenza vaccination, suggesting a plausible relationship between the immunization and the induction of CIDP, however the plausible relationship was not clear.  In conclusion, the relationship between immunization, particularly influenza vaccination, and the development of acquired demyelinating neuropathies has been discussed in the literature, mostly in the context of Guillain-Barre syndrome (GBS). Although the concern that CIDP might follow influenza vaccination similar to Guillain-Barre syndrome (GBS) might seem intuitive, there were no clearly documented cases in the literature of CIDP with abrupt onset within a few days after influenza vaccination. Our patient, who was otherwise healthy, developed CIDP with rapid onset in close proximity to influenza vaccination, suggesting a plausible relationship between the immunization and the induction of CIDP. Rapid onset resembling GBS occurs in about 15 percent to 20 percent of cases of CIDP. It was possible that antecedent events such as immunization are more likely in such patients, but that has not been systematically evaluated. In contrast to GBS, which was a monophasic illness, how a single event such as immunization may trigger induction of a relapsing or chronic immune-mediated disorder such as CIDP is not known.   This case is linked to cases 202101474 and 202101475 (the same literature article).  Company comment: A 46-year-old male patient developed chronic inflammatory demyelinating polyradiculoneuropathy after vaccination with the suspect product, influenza virus vaccine polyvalent. Chronology is plausible. The patient was in good health prior to the onset of chronic inflammatory demyelinating polyneuropathy (CIDP) and did not have any acute illness or systemic infections, diabetes mellitus, history of alcohol abuse, or exposure to any known neurotoxins. As reported, the patient had multiple relapses with varying diagnostic findings. Information regarding the concomitant medications have not been provided. Based on plausible time relationship, causality for the reported event cannot be totally excluded and is assessed as possibly related.; Reporter's Comments: Physician reported that the patient who was otherwise healthy, developed CIDP with rapid onset in close proximity to influenza vaccination, suggesting a plausible relationship between the immunization and the induction of CIDP, however the plausible relationship was not clear.; Sender's Comments: A 46-year-old male patient developed chronic inflammatory demyelinating polyradiculoneuropathy after vaccination with the suspect product, influenza virus vaccine polyvalent. Chronology is plausible. The patient was in good health prior to the onset of chronic inflammatory demyelinating polyneuropathy (CIDP) and did not have any acute illness or systemic infections, diabetes mellitus, history of alcohol abuse, or exposure to any known neurotoxins. As reported, the patient had multiple relapses with varying diagnostic findings. Information regarding the concomitant medications have not been provided. Based on plausible time relationship, causality for the reported event cannot be totally excluded and is assessed as possibly related.