Shoulder Weakness Following Intramuscular COVID- 19 Vaccine

History: Transient and generalized adverse effects are common following COVID-19 vaccination;among other adverse effects, shoulder injuries related to vaccine administration (SIRVA) have been known to occur. In this case, a previously healthy right-hand dominant 62-year-old male presented with left shoulder pain and weakness 3 months after receiving a COVID-19 intramuscular vaccine in the left deltoid. Approximately 2 weeks after the injection, he started experiencing pain and numbness around the injection site along with ipsilateral shoulder weakness. Despite conservative management with Motrin, Medrol Dosepak, gabapentin and physical therapy (PT), the pain and weakness persisted. Physical Exam: Left Shoulder-No calor or erythema;significant atrophy of the anterior and middle deltoid muscle relative to right side;abduction 4/5;external rotation with shoulder adducted 4/5;range of motion for active forward flexion was 150 degrees and passive was 170 degrees;passive range of motion for external rotation was 70 degrees;internal rotation to the level of L5;sensation to light touch was intact. Right Shoulder-Range of motion, strength, and sensation were intact. Cervical Spine-Full ROM;no cervical paraspinal tenderness noted. Negative Spurling's and Lhermitte's tests. Differential Diagnosis: 161. Axillary Nerve Palsy 2/2 Chemical Neurotoxicity 162. Brachial Neuritis 163. Mechanical Axillary Nerve Palsy 2/2 Vaccination 164. Partial-Tear of Left Supraspinatus Tendon 165. Acromioclavicular Osteoarthritis Test Results: Left Shoulder-XR:Mild pseudo-subluxation;MRI w/o contrast: 8x9mmpartial-thickness articular surface tear of the distal supraspinatus tendon (<50%fiber thickness). Minimal subacromial bursitis. Mild acromioclavicular joint osteoarthritis. EMG/NCV: Left and Right Axillary Motor Nerves: prolonged distal onset latency;Left Deltoid: increased insertion activity, moderately increased spontaneous activity, reduced recruitment;Remaining LUE muscles without evidence of electrical instability Final Diagnosis: Axillary Nerve Palsy Secondary To Chemical Neurotoxicity from Intramuscular COVID-19 Vaccine. Discussion(s): We postulate that the neurologic deficits presented in our case may be attributed to chemical neurotoxicity to the axillary nerve following vaccination as the delayed onset of pain and weakness are most consistent with this differential. There are several cases of brachial neuritis following vaccination for the prevention of COVID- 19, however, EMG/NCV results in our patient were not consistent with brachial plexopathy. Additionally, while there have been a handful of reported cases of bursitis following COVID-19 vaccines falling under the SIRVA classification of injuries, this is the first case of reported axillary nerve neurapraxia. Outcome(s): The patient's left shoulder numbness and pain improved with PT and medical management. While mild improvement in strength was noted, weakness and atrophy persisted even on the third follow up visit 6 months after the initial appointment. He was counseled on his injury and was recommended to undergo repeat EMG testing to document recovery after his 6-month follow-up appointment. Follow-Up: The patient did not follow-up for a repeatEMG after his 6-month follow-up appointment. At that time, the patient was clinically stable, tolerating PT, and expecting recovery of his deltoid function.

Physiotherapy results of a patient with critical illness polyneuropathy due to COVID-19: A case report

The aim of this study is to examine the results of physiotherapy in a patient with critical illness polyneuropathy (CIP) due to coronavirus disease 2019 (CO-VID-19). The 48-year-old male patient with CIP due to COVID-19 was enrolled in a physiotherapy program for 3 months with 5 sessions/week. Pain intensity, motor skills, daily living activities, fatigue level, cognitive status, and decubitus ulcer were evaluated with a visual analogue scale, the Medical Research Coun-cil-Sum Score, the Functional Independence Scale, the Fatigue Severity Scale, the Standardized Mini-Mental Test, and pressure wound staging, respectively. Positive improvements were achieved in functional level, fatigue, pain, and pressure sores with the physiotherapy program for this patient with CIP due to COVID-19. This report provides an idea about the effects of physiotherapy programs for COVID-19-related CIP to academics and clinicians working in this field.Copyright © 2022, Derman Medical Publishing. All rights reserved.

WE-159. Critical Illness Neuropathy in Severe COVID-19: a case series

Introduction: Neurological complications of SARS-CoV-2 disease have received growing attention, but only few studies have described to date clinical and neurophysiological findings in COVID patients during their stay in intensive care units (ICUs). Here, we assessed the presence of either critical illness neuropathy (CIP) or myopathy (CIM) in ICU patients. Method(s): Patients underwent a neurophysiological assessment, including bilateral examination of the median, ulnar, deep peroneal and tibial motor nerves and of the median, ulnar, radial, and sural sensory nerves. Needle electromyography (EMG) was performed for both distal and proximal muscles of the lower and upper limbs. The technique of Direct Muscle Stimulation (DMS) was applied either to the deltoid or tibialis anterior muscles. Peak to peak amplitudes and onset latencies of the responses evoked by DMS (DMSamp, DMSlat) or by motor nerve stimulation (MNSamp, MNSlat) were compared. The ratio MNSamp to DMSamp (NMR) and the MNSlat to DMSlat difference (NMD: MNSlat-DMSlat) were also evaluated. Result(s): Nerve conduction studies showed a sensory-motor polyneuropathy with axonal neurogenic pattern, as confirmed by needle EMG. Both MNSamp and NMR were significantly reduced when compared to controls (p < 0.0001), whereas MNSlat and NMD were markedly increased (p = 0.0049). Conclusion(s): We have described COVID patients in the ICU with critical illness neuropathy (CIP). The predominance of CIP as compared to critical illness myopathy (CIM) has implications for the functional recovery and rehabilitation strategies in severe COVID-19. Copyright © 2022

Quadriparesis after COVID-19 Vaccination: Two Cases with Different Diagnosis

Aim and objective: During the recent COVID-19 pandemic various vaccines have been developed and approved for emergency use, including adenovirus vector-based ChAdOx1 nCov-19. There are few reports of serious adverse events following immunization (AEFI). Materials and methods: Here, we report two cases of serious AEFI who required ICU admission. Results: Case 1: A 55-y-m hospitalized with complaints of giddiness for 4 days and onset of weakness of all four limbs with altered sensorium for 1 day. He had no history of any comorbidity, non-smoker and non-alcoholic, and no previous episodes of transient ischemic attacks. He was vaccinated with a second dose of adenoviral vector-based ChAdOx1 nCov-19 vaccine (8 days before the onset of first symptoms). After hospitalization, immediate intubation was done for airway protection. His neurological examination revealed blinking of eyes spontaneously, motor power of 0/5 in all four limbs, deep tendon reflex of +2, and mute plantar. MRI Brain was done on the next day (day of illness, DOI-4), which revealed acute infarct in the pons and bilateral cerebellar hemisphere. He was referred to our ICU on DOI-12. Repeat MRI Brain on DOI-16 showed subacute infarcts in the pons, bilateral middle cerebellar peduncles, and left cerebral hemisphere with thrombosed basilar artery. Lipid profile, homocysteine levels, auto-immune work-up were normal. Echocardiography showed normal LV function with no evidence of LA clot. Carotid Doppler showed normal carotid vessels. In view of ischemic stroke and basilar artery thrombosis anti-platelet agent and therapeutic anticoagulation continued. Over the next 3 weeks, he showed gradual improvement in motor power (3/5 in upper limbs and 2/5 in lower limbs) and weaned off from mechanical ventilation. Case 2: A 19-y-m hospitalized with complaints of acute onset paraesthesia and progressive weakness in both lower limbs for 4 days and difficulty in speech and swallowing for 1 day. He had no history of any comorbidity, and no history of preceding viral/bacterial infection except that he had received the first dose of the adenoviral vector-based ChAdOx1 nCov-19 vaccine (16 days before the onset of first symptoms). After hospitalization, he required intubation in view of pooling of oral secretions and respiratory distress. Clinical examination revealed bifacial weakness, severe neck muscle weakness, and flaccid areflexic quadriparesis with prominent proximal upper and lower limb weakness. Pin-prick sensation was distally reduced in both lower limbs with associated autonomic instability in the form of tachycardia and hypertension. MRI Brain was normal in the study. In further work, Guillain-Barré syndrome (GBS) was diagnosed. CSF showed albumin-cytologic dissociation (protein 1.14 g/L and nil cell), and bilateral motor nerve axonal neuropathy on nerve conduction study. Immunoglobulin (IVIG) therapy was started on DOI-6. He did not show significant improvement and was referred to our ICU for further management. During the 5th week of illness, the IVIG dose was repeated without any improvement and continuing requirement of mechanical ventilation. Conclusion: Though vaccination is one of the important public health interventions implemented to tackle the COVID-19 pandemic, there are known and unknown serious AEFI being reported. Both cases presented quadriparesis with different diagnoses, who received vaccination for COVID-19.

Super Slow Conduction Velocitiesin Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)

Objective: NA Background: Chronic inflammatory demyelinating polyneuropathy (CIDP) is characterized on nerve conduction study (NCS) by prolonged distal latencies, slowed conduction velocities, prolonged late responses, conduction blocks, and temporal dispersion. Unmyelinated fibers typically conduct action potentials at speeds of 0.5-10 m/s;myelinated fibers conduct an order of magnitude faster, e.g. 50-70 m/s. While very slow conduction velocities < 25 m/s are typically associated with the genetic neuropathies as in the Charcot-Marie Tooth neuropathies, CIDP can manifest with slow conduction velocities. Prompt recognition of CIDP is crucial for the timely initiation of immunotherapy. Design/Methods: NA Results: This case series of three CIDP patients demonstrates very slow conduction velocities and prolonged distal latencies. An 81-year-old woman with history of multiple sclerosis and chronic myelogenous leukemia presented with inability to walk over a few months with diffuse sensory loss. NCS showed absent motor responses in the leg, partial conduction blocks in the arm, prolonged ulnar motor distal latency 7.9 ms (normal ≤3.4ms), and very slow conduction velocities < 15 m/s. A 50-year-old woman with prior history of COVID-19 presented with diffuse weakness. NCS showed ulnar motor distal latency of 23.2 ms, slowed motor conduction velocities < 30 m/s. After treatment initiation with intravenous immunoglobulin, sensory responses improved, and conduction velocities increased to > 30 m/s. A 49-year-old woman presented with 3 months of bilateral weakness and sensory symptoms two weeks after a COVID-19 vaccination. NCS showed ulnar motor distal latency of 14 ms and slowed motor conduction velocities < 30 m/s. Conclusions: Very slow conduction velocities are a feature not just of the genetic neuropathies but also of acquired demyelination as seen in CIDP, and the latter is distinguished by abnormal temporal dispersion and conduction blocks. Astute electrophysiologists should modify sweep speed and gain to increase sensitivity for delayed or dispersed responses.

COVID-19 associated myositis with severe proximal and bulbar weakness

Objective: NA Background: Here we report a patient with COVID-19 associated inflammatory myopathy, presenting with facial, bulbar and proximal limb weakness. A 58-year-old woman presented with cough, dyspnea, and myalgia. Vital signs and her physical exam was unremarkable. Initial PCR testing for SARS-CoV-2 was negative and the patient was discharged home. She returned three weeks later with more severe dyspnea, cough, dysarthria, dysphagia, odynophagia and severe generalized weakness with inability to ambulate. She had no sensory symptoms or bowel or bladder dysfunction. Physical examination was significant for tachycardia and oxygen saturation of 88% on room air. She had bilateral ptosis, facial weakness, hypernasal dysarthria and profound symmetric proximal limb weakness. Reflexes were symmetrically diminished. Repeated SARS-CoV-2 PCR was positive. MRI of the entire neuroaxis showed no central or peripheral nervous system involvement, but demonstrated diffuse muscle edema and enhancement, with a region of myonecrosis Motor nerve conduction studies were unremarkable, needle electromyography revealed sparse fibrillation potentials;On admission, CK was elevated to 700 U/L. Anti-Sjögren's-syndrome-related antigen and anti-small ubiquitinlike modifier-1 activating enzyme antibodies were both strongly positive and Ku antibody was weakly positive. Muscle biopsy showed perivascular inflammatory infiltration with endomysial extension, regenerating fibers and upregulation of HLA Class ABC expression on non-necrotic fibers. Our presumptive diagnosis was COVID-19 associated myositis and a five-day course of 1000 mg intravenous methylprednisolone was administered. Over two weeks, her CK levels normalized and she recovered the ability to raise her arms and legs from the bed and showed slow improvement in bulbar function. Design/Methods: NA Results: Viral infection is a well-known cause of myositis. The severe immune activation known to occur in COVID-19 patients likely plays a major pathophysiologic role. The finding of multiple serologic autoimmune antibodies is intriguing suggesting an epiphenomenon rather than activation or unmasking of a specific immune response directed to the muscles. Conclusions: NA.

Atypical Pharyngo-Cervico-Brachial Variant of GBS Associated with Covid-19 Antibodies

Objective: Neurological manifestations are common with Covid-19 illness. Many unusual neurological manifestations have been described and we herewith report one such case. Background: COVID-19 is predominantly a respiratory pathogen but can cause multi system involvement. Many studies have shown significant neurological manifestations associated with Covid-19 infection. Some of these neurological manifestations are quite specific like GuillainBarre syndrome. But, many uncommon manifestations have been described like the following case. Design/Methods: A 35-year old woman with no prior history of fever or any other illness presented with insidious onset, gradually progressive weakness of bulbar and bilateral facial weakness along with asymmetrical weakness of both upper limbs of one and half months duration. She was evaluated and investigated accordingly. Results: On neurological examination, the patient had dysphonia, dysphagia, bilateral lower motor neuron facial palsy. Along with weakness of neck flexors and grossly asymmetrical weakness of upper limbs. The motor power on right is MRC 2/5 and MRC 4/5 in left upper limb with diffuse hypotonia. Motor power was normal in lower limbs. There was diffuse hyporeflexia in all the four limbs. Nerve conduction studies showed absent SNAPS with decreased motor nerve conduction velocities and increased CMAP latencies in both upper and lower limbs. CSF examination showed albumin-cytological dissociation. MRI Brain and Cervical Spine were normal. Serum ANA and Serum Ganglioside antibodies were negative. She was tested for total Covid-19 antibodies which was significantly positive with 55.25 COI. Patient was treated initially with IV Methylprednisolone with no significant response. So, followed with intravenous immunoglobulins and showed some improvement. Conclusions: Atypical Pharyngo-cervico-brachial variant of GB Syndrome with gross asymmetrical upper limb weakness and progressed over six weeks associated with positive SARS Cov-2 antibodies. During the pandemic, unusual neurological manifestations should be evaluated for possibility of SARS-CoV-2 associated antibodies as neuropathogenesis has shown both vascular and post infectious demyelinating disorders.