Guillain-Barre Syndrome and COVID-19 Vaccine: A Report of Nine Patients

Background: Guillain-Barre syndrome (GBS) is an autoimmune acute inflammatory demyelinating polyneuropathy usually elicited by an upper respiratory tract infection. Several studies reported GBS associated with coronavirus-2019 (COVID-19) infection. In this study, we describe nine GBS patients following the COVID-19 vaccine. Methods: In this study, nine patients introduce from six referral centers of neuromuscular disorder in Iran between April 8 and June 20, 2021. Four patients received the Sputnik V, three patients administrated the Sinopharm, and two patients received the AstraZeneca vaccine. All patients were diagnosed with GBS, including nerve conduction studies and/or cerebrospinal fluid analysis. Results: The median age of the patients was 54.22 years (range, 26-87 years), and seven patients were male. The patients were treated with intravenous immunoglobulin (IVIg) or plasma exchange (PLEX). All patients were discharged with some improvement. Conclusion: The link between the COVID-19 vaccine and GBS is not well understood. Given the prevalence of GBS in the general population, this association may be coincidental. Therefore, more studies are needed to investigate a causal relationship.

Use of pacemaker in GBS dysautonomia

Autonomic dysfunction in Guillain-Barrè syndrome (GBS) involves labile hypotension, hypertension, resting tachycardia and sweating. While autonomic involvement affects 66% of patients with GBS, the changes are usually transient and reversible. We hereby delineate a case of a female who presented to our medical centre with flaccid, painless progressive quadriparesis with features of dysautonomia. She had resting tachycardia, was tachypneic with reduced chest expansion and required immediate invasive mechanical ventilation. After pertinent laboratory evaluation, nerve conduction studies were promptly performed at the bedside and findings were concordant with acquired acute inflammatory demyelinating polyneuropathy. The diagnosis of GBS was made on the standard set of investigations and plasmapheresis was initiated on the same day. Her intensive care unit stay was complicated by the multiple episodes of asystole. Even though a temporary transvenous pacemaker was inserted, she, unfortunately, succumbed to a sudden episode of asystole. This paper illustrates that GBS-associated autonomic dysfunction can be severe and close cardiac monitoring is imperative in these patients.

Case Report on Guillain Barre Syndrome: Acute Inflammatory Demyelinating Polyneuropathy

Guillain Barre Syndrome (GBS) is an autoimmune disorder which affects the peripheral nervous system. It is a rare disorder affects in 1 per million people in year. It is characterized by symmetrical, progressive limb weakness and tingling. Case Report: A 53 year old male patient was presented with insidious onset of difficulty in moving right upper and lower limbs as well as gradual weakness of left limbs, and breathing difficulty, known case of diabetics’ mellitus and hypertension. Nerve conduction study shows suggest axonopathy; Acute Inflammatory Demyelinating Polyneuropathy (AIDP) is identified, which is a subtype of Guillain Barre Syndrome. Patient gradually develops areflexia, bifacial weakness, and quadriparesis. Patient was treated with IV immunoglobulin and intranasal oxygen therapy. Patient shows slight improvement in his medical condition, shows improvement in the power of lower limbs after one week of therapy. Physiotherapy was suggested. Keywords: Guillain Barre Syndrome, GBS, Acute Inflammatory Demyelinating Polyneuropathy, AIDP.

NEUROMUSCULAR MANIFESTATIONS AND COMPLICATIONS OF COVID-19 INFECTION

In this paper, various neuromuscular manifestations of coronavirus infection are considered and methods of damage to the nervous system are highlighted. These include the "cytokine storm", impaired hemostasis, neurotropicity and neurovirulence of SARS-CoV-2. The persistence of the virus in the body affects the course of comorbid diseases, which requires a systematic approach to patient treatment. In this paper we discuss the data from modern research papers and clinical cases both from updated international literature and from our own clinical practice: it is the most frequently met condition - Guillain-Barré syndrome – acute inflammatory demyelinating polyneuropathy. We present both rare and common neuro-muscular conditions, their clinical onset, possible pathogenesis, variants of manifestation. According to the data from current publications, the evaluation and management of patients suffering from Guillain-Barré syndrome associated with new coronaviral infection SARS-CoV-2 is does not have major differences with the classical ones, that are not associated with the pandemic. Our patient that we present as our own case, was hospitalized, and observed as an in-patient. She was treated using plasma exchange in the algorithm of management. The outcome of this case was positive. We conclude that neuromuscular manifestation of new coronaviral infection SARS-CoV-2 could be new and possibly associated with this disease, but also could be described as worsening of the premorbid disorders. For instance, inherited neuromuscular diseases could have different variants during the period of pandemic caused by novel coronavirus SARS-CoV-2 infection.

Acute Inflammatory Demyelinating Polyneuropathy (AIDP) Masked by Autoimmune Thyroiditis

Hashimoto’s thyroiditis and Guillain-Barre syndrome (GBS) are autoimmune disorders that are both well-known in their own right. Hashimoto’s is one of the most common causes of primary hypothyroidism, and GBS involves immune mediated damage to the peripheral nervous system. The association between the two is a rare clinical entity. This case demonstrates that these entities can occur together and could be related in similar pathophysiology. A 37 year old male presented with complaints of bilateral hand and feet numbness for one month. The numbness started in the hands, then involved the feet, and was mostly felt in tips of extremities. He also complained of weakness in arms and legs. Neurology exam showed bilateral patellar, ankle, and biceps hyporeflexia. Muscle strength was 5/5 in all extremities, but decreased grip strength was noted in the hands. Initial lab work including complete blood count, comprehensive metabolic profile and urinalysis were all in normal range. Computerized tomographic scan (CT) head was normal while CT abdomen/pelvis showed hepatic fatty infiltration. Other lab tests including HIV, syphilis, Hepatitis B, Hepatitis C, glycosylated hemoglobin A1c, lipid panel, anti-nuclear antibody, anti-neutrophil cytoplasmic antibodies, serum/urine protein electrophoresis, alcohol level, vitamin B1, B6, folate, copper, and creatine kinase were all negative or within normal range. Lab abnormalities included elevated thyroid stimulating hormone (TSH) of 20.2 mIU/l and low normal B12 level of 289 pg/ml. His triiodothyronine (T3) and thyroxine (T4) hormone levels were in normal range. A thyroid peroxidase antibody level came back as high as 966 IU/ml. A diagnosis of Hashimoto’s thyroiditis leading to subclinical hypothyroidism was made. Patient was discharged on vitamin B12 and 112mcg of Synthroid. Instead of getting better, he returned 1 week later with worsening numbness and tingling which was now ascending upward to bilateral knees and elbows. Meanwhile TSH improved to 10 mIU/l and vitamin B12 increased to 1162 pg/ml. A magnetic resonance imaging (MRI) of the cervical/thoracic spine was unremarkable. A lumbar puncture showed negative xanthochromia, 0 WBC, 0 RBC, 0 neutrophils, 0 lymphocytes, 0 monocytes, glucose 63 mg/dl, elevated protein of 57 mg/dl, and culture was negative. Guillain-Barre syndrome was then the working diagnosis, more specifically its most common subtype, acute inflammatory demyelinating polyneuropathy (AIDP). Patient received five days of intravenous immunoglobulins and his symptoms improved. He was then discharged to follow up with endocrinologist. This subtle presentation of GBS/AIDP masked by Hashimoto’s thyroiditis and vitamin B12 deficiency suggests a close association of autoimmune etiology between these disorders. Although rare, endocrinologists should consider this rare association in cases of paresthesias with unexplained symptoms.