a subsequent non-traumatic fall; Paresthesias/tingling and electrical shock sensations; numbness on the dorsal region of her right lower extremity; difficulty lifting both legs; bilateral proximal lower extremity weakness; initially started with inability to ascend stairs; difficulty with standing; Guillain-Barre syndrome; acute inflammatory demyelinating polyneuropathy (GBS); endorse microvascular ischemic disease involving the white matter; nondisplaced spiral fracture; Inappropriate antidiuretic hormone secretion; bilateral absent Patellar and Achilles tendon reflexes; degenerative antegrade spondylolisthesis deformity at L5-S1; neuropathic pain in bilateral lower extremities; burning sensation; difficulties with swallowing; esophageal dysmotility; hyponatremic; Blood pressure fluctuation; unfortunately feels; Weakness/muscular strength continued to decline; large ankle joint effusion; lower extremity pain; Dysautonomia; This case was reported in a literature article and described the occurrence of guillain barre syndrome in a 76-year-old female patient who received Herpes zoster (Shingrix) for prophylaxis.   The patient's past medical history included hyperlipidemia, asthma, macular degeneration, pancreatitis (two previous episodes of unknown origin) and upper respiratory tract infection (mild, ten weeks prior to admission).   On an unknown date, the patient received Shingrix (intramuscular). On an unknown date, 8 days after receiving Shingrix, the patient experienced guillain barre syndrome (serious criteria hospitalization and GSK medically significant), demyelinating polyneuropathy (serious criteria GSK medically significant), weakness in extremity (serious criteria hospitalization), gait disturbance (serious criteria hospitalization), difficulty in standing (serious criteria hospitalization), cerebral small vessel ischemic disease (serious criteria GSK medically significant), fall (serious criteria hospitalization), paresthesia (serious criteria hospitalization), numbness of lower extremities (serious criteria hospitalization), movement disorder (serious criteria hospitalization), femur fracture (serious criteria GSK medically significant), absent ankle jerk, spondylolisthesis, neuropathic pain, burning sensation, swallowing difficult, dyskinesia of esophagus, hyponatremia, blood pressure fluctuation, feeling sad, weakness, joint effusion, pain of lower extremities, inappropriate antidiuretic hormone secretion (serious criteria GSK medically significant) and dysautonomia. The patient was treated with immunoglobulins nos (Immunoglobulin), gabapentin and amitriptyline. On an unknown date, the outcome of the guillain barre syndrome, demyelinating polyneuropathy, weakness in extremity, gait disturbance, difficulty in standing, cerebral small vessel ischemic disease, fall, paresthesia, numbness of lower extremities, movement disorder, absent ankle jerk, spondylolisthesis, neuropathic pain, burning sensation, swallowing difficult, dyskinesia of esophagus, hyponatremia, blood pressure fluctuation, feeling sad, weakness, joint effusion, pain of lower extremities and inappropriate antidiuretic hormone secretion were recovered/resolved and the outcome of the femur fracture and dysautonomia were unknown.   The reporter considered the guillain barre syndrome, demyelinating polyneuropathy, weakness in extremity, gait disturbance, difficulty in standing, cerebral small vessel ischemic disease, fall, paresthesia, numbness of lower extremities, movement disorder, absent ankle jerk, spondylolisthesis, neuropathic pain, burning sensation, swallowing difficult, dyskinesia of esophagus, hyponatremia, weakness, pain of lower extremities,blood pressure fluctuation, feeling sad, joint effusion, inappropriate antidiuretic hormone secretion and dysautonomia to be related to Shingrix. It was unknown if the reporter considered the femur fracture to be 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 76-year-old female patient, who was vaccinated with Shingrix (GlaxoSmithKline) for prophylaxis. The patient had past medical history of hyperlipidemia, asthma, macular degeneration, and two previous episodes of pancreatitis of unknown origin. The patient denied recent camping, hiking, insect bites, and prior neuropathy/myopathy. However, the patient did report a mild upper respiratory tract infection ten weeks prior to admission. No information on patient's family history, concurrent condition or concomitant medication was provided. On an unspecified date, 10 (ten) days before hospitalization, the patient received Shingrix (administration route and site unspecified, dosage unknown; batch number not provided). The age of vaccination was not provided but it could be 75 years or 76 years. [The Patient stated that she had received the new Shingrix (Recombinant Zoster) vaccine ten days before hospitalization]. On an unspecified date, 10 days after vaccination, the patient presented with a two-day history of bilateral proximal lower extremity weakness. The patient reported that the patient had progressive weakness that initially started with inability to ascend stairs. This progressed to difficulty with standing and a subsequent non-traumatic fall. These described symptoms deviated significantly from her baseline. The Patient's baseline consisted of independence with mobility and activities of daily living. The patient did not require any assistive devices. On presentation, the patient was afebrile (98.4 degree Fahrenheit), had a normal respiratory rate (17 breaths/minute), had an oxygen saturation of 98% on room air, and was normotensive (136/76 mmHg). The patient reported paresthesias and numbness on the dorsal region of her right lower extremity and difficulty lifting both legs. On examination, the patient was alert and oriented, cranial nerves II-XII were intact, there was 5/5 bilateral upper extremity strength, and 5/5 bilateral lower extremity strength with dorsiflexion. The patient had normal sensation bilaterally in upper and lower extremities. However, the patient had 3/5 lower bilateral extremity strength with hip flexion. Furthermore, that patient had bilateral absent Patellar and Achilles tendon reflexes. On further assessment, the patient's labs were unremarkable. A computed tomography scan of the brain was performed, which revealed no evidence of acute intracranial abnormalities. The report did endorse microvascular ischemic disease involving the white matter. These results were found to be secondary to aging. Magnetic resonance imaging scan of the brain and lumbar spinal cord was only positive for degenerative antegrade spondylolisthesis deformity at L5-S1. Over the next 24 hours, the patient reported worsening lower extremity paresthesias and weakness. The patient could no longer stand without assistance. The patient also stated that having neuropathic pain in bilateral lower extremities; burning, tingling, and electrical shock sensations. Furthermore, the patient described new difficulties with swallowing. An endoscopy was performed, and the patient was described to have esophageal dysmotility because the patient was unable to pass the barium pill during the examination. Consequently, a lumbar puncture was performed due to concern for disease progression. Lumbar cerebral spinal fluid studies revealed an elevated protein level (61 mg/dL), a normal white blood cell count (0 CUMM), and a cytoalbuminogenic dissociation. These results indicated acute inflammatory demyelinating polyneuropathy (GBS). Neurologic consultation was obtained. No electrodiagnostic studies were performed. The patient was diagnosed with Guillen Barre Syndrome likely secondary to Shingrix vaccine. Treatment with intravenous immunoglobulin (2 g/kg divided over five days) was initiated. The patient showed gradual improvements with five days of treatment and was transferred to an acute rehabilitation facility (Hospital day 5). At discharge, the patient's bilateral Patellar and Achilles tendon reflexes remained absent. However, the patient was able to stand and ambulate with a walker. Five days after discharge to the rehab facility, the patient reported worsening of bilateral lower extremity pain (per patient, this pain was worse than her prior admission). The patient was therefore readmitted to the hospital. On examination, the patient had 5/5 bilateral upper extremity strength, 5/5 bilateral strength on lower extremity dorsiflexion, normal bilateral sensation in upper and lower extremities, and 3/5 bilateral lower extremity hip flexion strength. This strength assessment was consistent with the patient's previous presentation. Furthermore, light touch sensation was intact in all four extremities. There was no apparent sensory loss. Bilateral Achilles and Patellar tendon reflexes remained absent. However, the patient could no longer stand with and without assistance and therefore could no longer ambulate. This presentation significantly deviated from her prior discharge appearance. Initially the patient described neuropathic pain and therefore, the patient was treated with Gabapentin and amitriptyline. However, the patient became hyponatremic (133 mmol/L on admission to 122 mmol/L after treatment) and had significant fluctuations in her blood pressure (ranging from 110/67 mmHg to 182/88 mmHg). Additionally, the patient unfortunately feels due to weakness while attempting to walk with assistance. The patient suffered a nondisplaced spiral fracture through the distal fibular metaphysis and had a large ankle joint effusion. The patient was seen by Orthopedic Surgery and was placed in a CAM boot. Plasma exchange was initiated because the patient's muscular strength continued to decline, and her lower extremity pain was increasing. After undergoing three plasma exchange treatments, the patient showed remarkable improvement with lower extremity strength and power. The patient was then able to ambulate the hospital halls with the use of a walker and some assistance after five treatments of plasma exchange. Additionally, the patient's neuropathic pain improved. The patient was then discharged to an acute rehabilitation center with scheduled physical therapy. This case has been considered as serious due to hospitalization.  The author commented, "We present a case of Guillian-Barre syndrome that occurred 10 days after Shingrix vaccine administration. We identified no other possible etiology of the patient's symptoms. The patient displayed several key features of GBS established by the Brighton Criteria of weakness; paresthesias, diminished Patellar and Achilles deep tendon reflexes, hyponatremia secondary to Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH), dysautonomia, and cytoalbuminological dissociation on cerebral spinal fluid analysis. We believe that this is an example of post-vaccine related Guillain-Barre Syndrome, given the timing of the presentation and when she received her vaccine. While electrodiagnostic studies have been used to help diagnose GBS secondary to bacterial, viral, and vaccination origins, these results are not necessary. The diagnosis of GBS is confirmed with the elevated CSF protein level and absence of deep tendon reflexes (found in 90% of GBS affected patients). Additionally, it can take up to four weeks before electrodiagnostic studies show loss of motor and sensory response secondary to GBS. There have been numerous vaccines connected to GBS, including the H1N1 swine flu vaccine and the pneumococcal vaccine. However, the newly release Shingrix vaccine has yet to be reported to be associated with this potentially life threatening polyradiculoneuropathy. Documented adverse reactions to the Shingrix vaccination from eight high quality randomized control trials, include local injection site rash or irritation, disseminated rash, herpes zoster infection in immunocompetent patients, and life-threatening complications in immunocompromised recipients. However, none of these studies demonstrated a relationship between Shingrix, nor the previous Zoster vaccine, to GBS. As a result, GBS likely secondary to the Shingrix vaccine could not have been expected in this patient after receiving this immunization. In summary, the bacterial lipopolysaccharide epitope acts as a molecular mimicker. The precise nature by which this occurs is still unclear. Therefore, the mechanism by which GBS may result from Shingrix vaccine remains unknown. If further cases reveal a similar association, this should be further explored. Per this case report and prior documentation of GBS secondary to herpes zoster, there is now evidence to state that antibodies generated in a lab against herpes zoster and then given intramuscularly via vaccination (Shingrix) may be a sufficient nidus for Guillain-Barre syndrome." The author concluded, "In summary, we present a case of GBS that occurred shortly after Shingrix vaccination. Our case is consistent with other vaccine and herpes zoster related cases of GBS. Clinicians should be cognizant of the possible association between Guillain-Barre syndrome and the new Shingrix vaccine." This article corresponding to this case is not available for regulatory submission due to copyright restriction.   Upon internal review following correction was done for the date received on 3rd December 2020: The patient country updated.