Sex: M
Vaccine: VARZOS
Symptoms: Areflexia, CSF protein increased, CSF white blood cell count negative, Demyelinating polyneuropathy, Fall
Clinical narrative: Guillain-Barre syndrome; demyelinating polyneuropathy; tingling and numbness in his feet; numbness in his feet/PINPRICK SENSATION DIMINISHED; areflexia at biceps, brachioradialis, patella, and Achilles despite Jendrassik maneuver; diminished vibration bilaterally from the toes to the knees; weakness with foot dorsiflexion; Fall; This case was reported in a literature article and described the occurrence of guillain barre syndrome in a 79-year-old male patient who received Herpes zoster (Shingrix) for prophylaxis.  Concurrent medical conditions included neuropathy.   On an unknown date, the patient received Shingrix. On an unknown date, 10 days after receiving Shingrix, the patient experienced guillain barre syndrome (serious criteria GSK medically significant), demyelinating polyneuropathy (serious criteria GSK medically significant), tingling of extremity, hypoesthesia, areflexia, loss of sensation, joint range of motion decreased and fall. The patient was treated with doxycycline and immunoglobulins nos (Ivig). On an unknown date, the outcome of the guillain barre syndrome, demyelinating polyneuropathy, tingling of extremity, hypoesthesia, areflexia, loss of sensation, joint range of motion decreased and fall were unknown.   The reporter considered the guillain barre syndrome, demyelinating polyneuropathy, tingling of extremity, hypoesthesia, areflexia, loss of sensation, joint range of motion decreased and fall to be possibly related to Shingrix.  Additional details were provided as follows: This case was reported in a literature article and described the occurrence of Guillain-Barre syndrome (GBS), in a 79-year-old male patient, who was vaccinated with Shingrix (GlaxoSmithKline) for prophylaxis.  The patient had a history of clinically diagnosed neuropathy by his primary care physician (PCP). No information on patient family history or concurrent condition or concomitant medication was reported. n an unknown date, the patient was vaccinated with Shingrix (administration route and site unspecified, dosage unknown; batch number not provided). The age at vaccination was not reported but it could be between 78 or 79 years old at the time of vaccination. On an unspecified date, 10 days after vaccination, the patient had onset of symptoms. The patient initially presented with symptoms of progressive tingling and numbness in his feet for over a week to the urgent care clinic. At the baseline, the patient was very active, and the history was negative for any other relevant symptoms. The neurological examination at the urgent care was reported unremarkable (no further details available). Due to the patient's history of outdoor activities, the patient got empirically treated with doxycycline, and blood drawn for tick-borne serologies came back negative. The patient returned with worsening paresthesia and weakness in his legs, which culminated in a fall. A neurological examination done on this visit showed diminished pinprick and vibration bilaterally from the toes to the knees with areflexia at biceps, brachioradialis, patella, and Achilles despite Jendrassik maneuver. Romberg was positive, with no dysmetria on finger to nose test. The patient gait was broad-based. There was no loss of sensation in the upper limbs. Motor examination showed a weakness with foot dorsiflexion and medical research council- MRC grading of 4/5 for bilateral hip flexion and knee extension. Lumbar puncture showed elevated cerebrospinal fluid (CSF) Protein: 195 mg/dl, with a normal corrected white blood cell (WBC) count. Electrodiagnostic study (Nerve conduction study (NCS)) revealed demyelinating polyneuropathy was done. The motor NCS shows prolonged latency and slowed conduction velocity in addition to reduced compound muscle action potential amplitudes in some nerves due to pre-existing neuropathy. The results of NCS were: Left median: nerve site was wrist showing latency 7.7 m/s (reference: less than 4.2 m/s) and compound muscle action potential (CMAP) amplitude was 4.0 mV (reference: more than 4.0 mV). Nerve site was elbow showing latency 14.3 m/s, CMAP amplitude was 3.6 mV and conduction velocity was 37.5 m/s (reference: 50 m/s). Right Ulnar: nerve site was wrist showing latency 4.2 m/s (reference: less than 3.6 m/s) and CMAP amplitude was 7.2 mV (reference: more than 5.0 mV). Nerve site was below elbow showing latency 10.3 m/s, CMAP amplitude was 6.0 mV and conduction velocity was 41.3 m/s. Nerve site was above elbow showing latency 13.0 m/s, CMAP amplitude 5.7 mV and conduction velocity was 36.6 m/s (reference: 50.0 m/s). Left/Right Peroneal: nerve site was ankle and results were not recordable for both left and right (reference for latency less than 6.0 m/s; reference for CMPA amplitude more than 2.5 mV). Left tibial: nerve site was ankle showing latency 15.6 m/s (reference: less than 6.6 m/s) and CMAP amplitude was 0.9 mV (reference: more than 2.0 mV). Nerve site was knee showing latency 32.2 m/s, CMAP amplitude was 0.3 mV and conduction velocity was 27.1 m/s. Right tibial: nerve site was wrist showing latency 9.1 m/s (reference: less than 6.6 m/s) and CMAP amplitude was 1.9 mV (reference: more than 2.0 mV). Nerve site was knee showing latency 27.1 m/s, CMAP amplitude was 1.1 mV and conduction velocity was 25.2 m/s (reference: 40 m/s). Left Peroneal Tibialis Anterior: nerve site was fibular head showing latency 4.0 m/s (reference: less than 4.0 m/s) and CMAP amplitude was 4.0 mV (reference: more than 4.0 mV). Nerve site was knee showing latency 6.9 m/s, CMAP amplitude was 3.9 mV and conduction velocity was 33.7 m/s (reference: 40 m/s). Right Peroneal Tibialis Anterior: nerve site was fibular head showing latency 12.4 m/s (reference: less than 4.0 m/s) and CMAP amplitude was 2.5 mV (reference: more than 4.0 mV). Nerve site was knee showing latency 14.4 m/s, CMAP amplitude was 2.2 mV and conduction velocity was 48.3 m/s (reference: 40 m/s). Magnetic resonance imaging (MRI) of the lumbar spine with contrast showed enlarged and enhancing nerve roots involving L1 through S1. The patient was diagnosed with GBS. The patient was started on intravenous immunoglobulins (IVIg) (2g/kg body weight over 5 days), resulting in improvement of strength with residual pinprick sensation deficit only in the toes and reduced vibration in his feet from his previous neuropathy two months after treatment. Outcome was not reported. The authors commented, The temporal association of the development of autoimmune neuromuscular disorders and vaccine administration is well documented. Several vaccines, although beneficial, have proposed to be implicated in the development of autoimmune disorders, especially GBS. The precise mechanism is unknown, but one probable cause could be the vaccine components eliciting an exaggerated immune response. As stated earlier, the Shingrix vaccine consists of the glycoprotein E and adjuvant AS01B. Adjuvants, by definition, are substances that augment antigen-specific immune response. However, studies reported the role of adjuvants in causing autoimmunity by molecular mimicry and simulating an immune reaction in animal models or humans similar to the bacterial or viral infections. Although hypothesized that the Shingrix vaccine may have led to GBS in our patient, the exact pathogenesis is still not clear. In addition to the adjuvants, immune responses directed against the Glycoprotein E can also result in autoantibodies or T-cell activation that cross-react with ganglioside GM1 in the myelin resulting in immunological damage to the peripheral nerve sheaths. Further in vitro studies will be required to assess this relationship.   Following review below correction was done for the date received on 3rd December 2020: The patient country was updated.