Leg paralysis after AstraZeneca COVID-19 vaccination diagnosed as neuralgic amyotrophy of the lumbosacral plexus: a case report.

The ongoing global administration of vaccines for coronavirus disease 2019 (COVID-19) means that increasing numbers of patients are likely to present with post-vaccination complications. We describe the first reported case of neuralgic amyotrophy (NA) involving the lumbosacral plexus occurring after AstraZeneca COVID-19 vaccination. The patient presented with acute-onset leg paralysis following administration of the vaccine. Based on the clinical, electrodiagnostic, and radiologic findings, the patient was diagnosed with post-vaccination NA. We speculate that the COVID-19 vaccine elicited an immune-mediated inflammatory response to the injected antigen due to inflammatory immunity in a patient with predisposed susceptibility to NA.

Parsonage-Turner syndrome following post-exposure prophylaxis.

BACKGROUND: The 'Parsonage-Turner syndrome' (PTS) is a rare but distinct disorder with an abrupt onset of shoulder pain, followed by weakness and atrophy of the upper extremity musculature, and a slow recovery requiring months to years. To our best knowledge, this is the first case describing symptoms and signs of PTS following the administration of a post-exposure prophylaxis (PEP) regimen against possible human immunodeficiency virus (HIV) and hepatitis B virus (HBV) infection. CASE PRESENTATION: A 25-year-old Caucasian man presented with pain and unilateral scapular winging following PEP against possible HIV and HBV infection. Although atrophy and weakness were observed for the right supraspinatus muscle, a full range of motion was achievable. Neurological examination, plain radiography of the right shoulder and electromyography showed no additional abnormalities. The patient was diagnosed with post-vaccination PTS and treated non-operatively. During the following 15 months the scapular winging receded and full muscle strength was regained. CONCLUSION: Parsonage-Turner syndrome is a rare clinical diagnosis. The precise pathophysiological mechanism of PTS remains unclear, but it seems to involve an interaction between genetic predisposition, mechanical vulnerability and an autoimmune trigger. An immunological event, such as - in this case - a vaccination as part of PEP treatment, can trigger the onset of PTS. The clinical presentation is distinctive with acute severe pain followed by patchy paresis, atrophy and sensory symptoms that persist for months to years. No currently available tests can provide a definite confirmation or exclusion of PTS. Routine blood examination, electromyography (EMG), and computed tomography (CT) or magnetic resonance imaging (MRI) serve mainly to exclude other disorders. The recovery can be quite lengthy, non-operative treatment is the accepted practice. Supplementary administration of oral prednisolone could shorten the duration of pain. Although the outcome is typically preferable, a substantial amount of patients are left with some residual paresis and functional impairment.

Brachial neuritis following a corticosteroid injection.

This report presents a case of brachial neuritis following a subacromial corticosteroid injection. The patient developed an anterior interosseous neuropathy shortly after the injection, with no other trigger being identified. This neuropathy has unfortunately not shown any sign of recovery at 2 years. The authors propose that corticosteroid injection be added to the list of possible triggering events of brachial neuritis and highlight the frequent use of oral corticosteroids in its treatment. (1) The injection of local anaesthetic and corticosteroid should be considered as a potential trigger for brachial neuritis. (2) Brachial neuritis should be considered in the differential diagnosis for patients presenting with severe arm pain and weakness. (3) The nerves originating from the upper trunk of the brachial plexus are most commonly affected. (4) The anterior interosseous nerve is involved in one-third of cases.

Unusual association of epidemic dropsy with brachial neuritis and palatal palsy.

Epidemic dropsy (ED) results from accidental ingestion of adulterated mustard oil with argemone oil. Chief organs involved in this disease are heart, subcutaneous tissue, eyes and kidneys. Nervous system involvement is very rare. Objective manifestation of neurological involvement is even rarer. The authors report two cases from the same family, who were victims of epidemic dropsy along with their parents. One of them showed objective neurologic involvement in the form of brachial neuritis and another showed palatal palsy.

Neuralgic amyotrophy associated with antibiotic therapy.

OBJECTIVE: To report a case of neuralgic amyotrophy associated with antibiotic therapy. CASE SUMMARY: A 22-year-old male with cystic fibrosis had been nonadherent to treatment for 4 years; when he returned to the clinic with symptoms, his forced expiratory volume in 1 second dropped from 84% predicted to 43% predicted. He was admitted to the hospital for treatment after failing to improve on oral ciprofloxacin and inhaled tobramycin. Treatment was initiated with intravenous tobramycin 560 mg daily and piperacillin/tazobactam 4.5 g infused every 6 hours. He continued inhaled tobramycin 300 mg twice daily, his home doses of pancreatic replacement enzymes and vitamins, albuterol 2.5 mg by high flow nebulizer (HFN) 4 times daily, and dornase alpha 2.5 by HFN daily. Sputum cultures were positive for methicillin-resistant Staphylococcus aureus, and intravenous vancomycin 1 g every 8 hours was added to the treatment regimen on hospital day 7. The patient developed bilateral shoulder pain followed by decreased function of his upper extremities 2 days later. He was treated with oral ibuprofen 600 mg every 6 h and oral cyclobenzaprine 5 mg daily, which improved his pain, but the shoulder stiffness remained throughout his hospital stay and persisted for 2 months following discharge. These symptoms resolved but recurred rapidly (within 24 h) and were more debilitating following a second exposure to the same antibiotics at the same doses 8 months later when the patient was readmitted for treatment of another cystic fibrosis-related pulmonary exacerbation. DISCUSSION: To our knowledge, this is the first case report illustrating neuralgic amyotrophy triggered by exposure to the antibiotics vancomycin, tobramycin, and piperacillin/tazobactam. After analysis of the case, ruling out other possibilities and using the Naranjo probability scale, we found that there is a highly probable likelihood that the symptoms presented by our patient were secondary to his drug therapy. Neuralgic amyotrophy is a rare condition of unknown etiology that has never before been associated with administration of these antibiotics, individually or in combination. Because of the specifics of the clinical history, we were unable to ascertain whether this complication was due to a single antibiotic or to the combination. It is quite possible that vancomycin was the only culprit, but impossible to ensure with the available evidence. CONCLUSIONS: Clinicians should be aware of this adverse reaction when facing similar complex neurologic symptoms in patients who are receiving the antibiotic treatment described here, especially vancomycin.

Neuritis braquial idiopática tras una anestesia general / Idiopathic brachial neuritis following general anesthesia

Mujer de 25 años que, horas después de una anestesiageneral para mamoplastia de aumento, presentó dolorintenso en el hombro izquierdo seguido de un marcadodéficit motor y sensitivo en la misma extremidad. Trasdescartar las principales causas de daño neurológicointraoperatorio, se hizo un diagnóstico de presunción deneuritis braquial idiopática. A las 3 semanas de postoperatorioel dolor del hombro había cedido pero no habíacambios en la afectación motora y sensitiva. A la cuartasemana se realizó un estudio electrofisiológico que evidencióalteraciones compatibles con edema o inflamacióny ausencia de signos de denervación. Estos resultadosy la evolución clínica favorable confirmaron eldiagnóstico de neuritis braquial idiopática. A los 3 mesessólo persistía debilidad y anestesia leves en el área deltoidea.El origen de la mayoría de neuropatías postquirúrgicases yatrogénico. Sin embargo, cuando no se halleuna causa evidente debe incluirse la neuritis braquialidiopática en el diagnóstico diferencial. Se trata de unsíndrome raro de buen pronóstico que puede aparecerespontáneamente en el periodo postoperatorio con independenciadel tipo de cirugía y de la técnica anestésica.La sintomatología, las pruebas de imagen y el estudioelectrofisiológico nos permitirán confirmar el diagnóstico.Esto resulta importante tanto desde el punto de vistaclínico como a la hora de establecer posibles responsabilidadesmedicolegales (au)

A 25-year-old woman complained of intense pain in herleft shoulder several hours after augmentationmammaplasty under general anesthetic; pain was followedby marked sensory and motor deficit in the same arm. Adiagnosis of idiopathic brachial neuritis was made afterthe main causes of intraoperative nerve damage had beenruled out. The shoulder pain resolved after 3 weeks but thesensory and motor deficit remained unchanged. Anelectrophysiological study performed at 4 weeks revealedabnormalities suggestive of edema or inflammation and anabsence of signs of denervation. These findings and thefavorable clinical course confirmed the diagnosis ofidiopathic brachial neuritis. After 3 months, only mildweakness and numbness in the deltoid region persisted.Although most postoperative neuropathies are iatrogenic,idiopathic brachial neuritis should be included in thedifferential diagnosis when no evident cause is found. Thissyndrome is rare but may appear spontaneously after anytype of surgery or anesthetic technique; the prognosis isgood. Diagnosis, which can be based on symptoms,imaging and electrophysiological studies, is importantboth for clinical management and for establishing medicaland legal liability (AU)

[Brachial plexitis and myelitis and herpes-zoster lumbar plexus disorder in patient treated with infliximab]. / Plexitis lumbar por herpes zoster, mielitis y plexitis braquial en paciente tratada con infliximab.

Infliximab, a chimeric monoclonal antibody, is a TNF-a inhibitor approved for use in refractory rheumatoid arthritis and Crohn s disease. We present the case of a patient affected by severe rheumatoid arthritis who was successfully treated with infliximab. She suffered diverse neurological complications: brachial plexitis, asymptomatic thoracic myelitis with extensive lesions in MRI study, and herpes zoster lumbar plexitis. We review the neurological adverse effects of infliximab (aseptic meningitis, opportunistic germs infections, disseminated herpes zoster) and focus in their potential adverse effect to induce central and peripheral nervous system demyelination.

Plexitis lumbar por herpes zoster, mielitis y plexitis braquial en paciente tratada con infliximab / Brachial plexitis and myelitis and herpes-zoster lumbar plexus disorder in patient treated with infliximab

El infliximab es un anticuerpo monoclonal quimérico con acción anti-TNF-alfa que se utiliza eficazmente en el tratamiento de la artritis reumatoide agresiva y de la enfermedad de Crohn fistulosa. Se presenta el caso de una paciente con artritis reumatoide agresiva, tratada satisfactoriamente con infliximab, que sufrió complicaciones neurológicas de diversa índole: plexitis braquial idiopática, mielitis dorsal paucisintomática, aunque con lesiones extensas en la resonancia magnética, y plexitis lumbar por herpes zoster. Se revisan las complicaciones neurológicas del infliximab (meningitis aséptica, infecciones por gérmenes oportunistas, herpes zoster diseminado) y en particular su efecto desencadenante de procesos desmielinizantes, tanto del sistema nervioso central como periférico

Infliximab, a chimeric monodonal antibody, is a TNF-alfa inhibitor approved for use in refractory rheumatoid arthritis and Crohn's disease. We present the case of a patient affected by severe rheumatoid arthritis who was successfully treated with infliximab. She suffered diverse neurological complications: brachial plexitis, asymptomatic thoracic myelitis with extensive lesions in MRI study, and herpes zoster lumbar plexitis. We review the neurological adverse effects of infliximab (aseptic meningitis, opportunistic germs infections, disseminated herpes zoster) and focus in their potential adverse effect to induce central and peripheral nervous system demyelination

Focal rhabdomyolysis and brachial plexopathy: an association with heroin and chronic ethanol use.

A 22-year-old man presented with acute swelling of the left neck and associated weakness of the left arm upon awakening after having snorted heroin. He had consumed large amounts of ethanol regularly for 7 years. Serum creatine kinase was greater than 19,000 units/l. A diagnosis of focal rhabdomyolysis and left brachial plexopathy was made. Focal rhabdomyolysis with associated plexopathy is an uncommon but recognized complication of acute heroin use. Chronic ethanol use may have a "sensitizing" role in the pathogenesis of this syndrome.

[Neuralgic amyotrophy (Parsonage-Turner syndrome) following streptokinase thrombolytic therapy]. / Neuralgische Amyotrophie (Parsonage-Turner-Syndrom) nach Streptokinase-Lysetherapie.

HISTORY AND CLINICAL FINDINGS: A 61-year-old man was given short-term thrombolytic treatment with streptokinase (1.5 million IU) 6 hours after the onset of anginal symptoms. Ten days later he complained of severe pain in the right upper arm and right shoulder, and also on the left 3 days later. Simultaneously there occurred severe atrophic pareses of the supra- and infraspinatus, deltoid and rhomboid muscles bilaterally, without sensory component. TESTS: When admitted to the neurological department 3 weeks later laboratory tests, immunological parameters, electrophoresis and cerebrospinal fluid were unremarkable. Radiological examinations of the cervical and thoracic vertebrae demonstrated moderate degenerative changes. Computed tomography and magnetic resonance imaging of the cervical vertebrae showed small disc protrusion and narrowing of the intervertebral foramina, but they could not explain the clinical picture. Electromyography demonstrated a bilateral peripheral neurogenic lesion without evidence of radicular distribution or any lesion of individual peripheral nerves. These findings led to the diagnosis of neuralgic amyotrophy (Parsonage-Turner syndrome). TREATMENT AND COURSE: With analgesics and physiotherapy the pareses slowly regressed over the following months. CONCLUSIONS: The infusion of streptokinase was the only probable cause found to explain the neuralgic amyotrophy, a connection that has never been reported until now.

Neurotoxic treatment in a patient with brachial neuritis associated with Hodgkin's disease.

Brachial neuritis is a rare form of neuropathy associated with Hodgkin's disease. In the patient we describe, a brachial neuritis occurred during chemotherapy for Hodgkin's disease. He later developed a marked sensory peripheral neuropathy with vincristine. Lhermitte's sign also developed following modest doses of radiotherapy (35 Gy in 20 fractions to the whole cervical cord). We suggest that neurotoxic treatment must be given with extra care to patients with non-metastatic tumour induced neuropathies.