We report a 12-year-old male patient with relapsing-remitting multiple sclerosis who showed a strong response to allopurinol with no safety concern. Researchers should further evaluate this drug option in multiple sclerosis.
We report a 12-year-old male patient with relapsing-remitting multiple sclerosis who showed a strong response to allopurinol with no safety concern. Researchers should further evaluate this drug option in multiple sclerosis.
In December 2019, the World Health Organization declared COVID-19 a pandemic; an unprecedented health crisis has rocked the world. Enormous efforts by governments, the pharmaceutical industry, and health professionals, including a new mRNA vaccine technology against SARS-CoV-2, have been massively employed to control the COVID-19 pandemic. The vaccine's primary mechanism is based on S glycoprotein, the leading viral surface antigen, which induces protective neutralizing antibodies.
This project aims to present two cases of demyelinating syndromes in previously asymptomatic patients. The triggering factor in both cases was vaccination against COVID-19 with mRNA vaccines.
The first case is a young female, 25 years old, previously asymptomatic, one week after the ChAdOx1 Vaccine developed right hemiparesis. Brain MRI and MRI of the spinal cord demonstrated multiple hyperintense lesions, acute and chronic. The second case is an 8-year-old Caucasian male; 12 days after the double dose of the Pfizer-BioNTech vaccine, the patient complained of bilateral visual blurring. The patient was pulsed with methylprednisolone one g/day/5 days with complete recovery.
Rarely can vaccines trigger multiple sclerosis or optic neuritis. This report demonstrated two demyelinating syndromes triggered by the m-RNA COVID-19 vaccine.
Guillain-Barré syndrome (GBS) is an immuno-mediated disorder of the peripheral nervous system with an acute onset of 2–4 weeks, and a monophasic course. In the subacute variant the symtpoms nadir is reached in 4–8 weeks. However, in sporadic cases the onset and the evolution of the disease may be different than expected, leading to significant diagnostic difficulties.
Case report: A 78-yrs old man presented at our Hospital with a 4-month history of progressive, diffuse motor and sensory deficit. He had previously undergone two electrophysiological examinations with uncertain findings. At hospitalization the nerve conduction study (NCS) and the cerebrospinal fluid examination were consistent with inflammatory demyelinating polyradiculoneuropathy. While a 5-day high-dose of intravenous methylprednisolone proved to be ineffective, a single intravenous immunoglobulin cycle risulted in a significant clinical improvement without relapse after an 18-month follow-up. Based on clinical and neurophysiological findings, a diagnosis of atypical subacute GBS was finally made.
Conclusion: Although generally accepted that GBS has an acute onset within a few weeks, with a maximum of 8 weeks in the subacute variant, this case report shows that it may initially present with a very slow clinical progression and inconsistent NCS findings. However, its recognition and differentiation from the chronic inflammatory nerve disorders, which have a chronic, long-term evolution, is mandatory to provide the correct therapy protocol.
We present a case of a preschool boy admitted to the pediatric intensive care unit with generalized weakness and encephalopathy that progressed to coma and spastic paralysis over the next few weeks. Extensive evaluation of a wide range of possible diagnoses, including infectious, post-infectious, autoimmune, and paraneoplastic disorders, proved unrevealing. Owing to concerns regarding autoimmune encephalitis, the patient received plasmapheresis, intravenous immunoglobulin, high-dose glucocorticoids, anakinra, rituximab, and empirical botulinum antitoxin. Despite these treatments, the patient's neurological condition continued to deteriorate, requiring endotracheal intubation. The patient developed repeated tremors and dystonic events, which progressed to hypertonia with gaze deviation. His-EEG in the third week of admission showed Radermecker complexes most consistent with SSPE. Because of his history of travel to Afghanistan at 8 months of age, before he was vaccinated for measles, and after a measles-like illness upon return, we checked the measles IgG titer in the CSF from the initial lumbar puncture and found it to be elevated. Global coverage with the first dose of the measles vaccine has dropped to 81 % by 2021, the lowest rate since 2008. This decline raises the concern of a possible increase in the incidence of measles and its fatal complications such as SSPE.
Neuromyelitis optica spectrum disorder (NMOSD) is a rare autoimmune disease causing axonal damage with corresponding functional deficits. In this case report, we prospectively tracked walking recovery and corticospinal excitability of a female diagnosed with NMOSD through six months after her inpatient rehabilitation (IPR) stay. She recovered independent walking function in home and community settings. Neurophysiological measures acquired using transcranial magnetic stimulation showed two temporal evolution patterns. There was a remarkably reduced intra-cortical inhibition and increased intra-cortical facilitation at the early recovery phase whereas increased corticospinal pathway excitability was noted at 6 months after IPR discharge.
Multiple sclerosis (MS) is a chronic autoimmune inflammatory disease affecting the central nervous system. Injectable disease-modifying therapies such as interferon-beta have had longstanding and widespread use in MS treatment. We report the case of a 54-year-old woman with relapsing-remitting MS, who developed multiple bilateral subcutaneous granulomata and calcifications on both hips 11 years after a 9-year course of treatment with interferon-beta-1a (IFN-β-1a). We highlight the potential for delayed severe skin responses with subcutaneous IFN-β-1a injections, outline preventative measures, and discuss treatment options for this treatment complication.
Tumefactive multiple sclerosis (TMS) is a rare subtype of multiple sclerosis (MS) that poses a diagnostic and therapeutic challenge, with relatively little available published data. Though studies have demonstrated similar disease course in TMS with non-tumefactive disease, refractory cases requiring early escalation of therapy are noted and risk factors are unclear. Furthermore, no studies have presented data specifically on adult African American patients with TMS.
We present a case of TMS refractory to steroids and plasma exchange in an African-American woman. Disease progression was halted after treatment with cyclophosphamide. The patient was later transitioned to rituximab maintenance therapy.
This case contributes to the limited data on disease course and treatment response of this rare disease process in a population that is under-represented in the literature. We note the importance of further studies to identify risk factors for refractory disease requiring early initiation of high-efficacy disease modifying treatment (DMT).
Anti-Muscle-specific tyrosine kinase – Myasthenia gravis (MuSK-MG) is a rare neuromuscular junction (NMJ) disease subtype with variable clinical presentation and often atypical electromyography findings. While amyotrophic lateral sclerosis (ALS) can present with respiratory failure, its median respiratory insufficiency onset is estimated at six months from the onset of diagnosis, with variability predicted by baseline functional vital capacity (FVC) and bulbar onset-ALS. Anti-MuSK-MG presentation with the predominately irritable myopathic diaphragm is rarely reported.
We report a case of Anti-MuSK-MG presenting with persistent respiratory insufficiency and bulbar dysfunction initially misdiagnosed as bulbar-type ALS due to bulbar findings and tongue atrophy. Electromyography (EMG) and single fiber EMG (SFEMG) defied former diagnosis (ALS) with findings of asymmetrical right ulnar and spinal accessory decrements on slow rate repetitive nerve stimulation (RNS), abnormal jitter on SFEMG, and irritable myopathy pattern of the diaphragm and proximal muscles. The serology marker is positive for Anti-MuSK Antibody, and negative AhCR anti-body. With supportive care and Rituximab, the patient's bulbar and respiratory function gradually improved.
Anti-MusK-MG presenting with persistent respiratory insufficiency has been reported with atypical electromyography findings of myopathy and denervation. We report an intriguing case of MuSK-MG with irritable diaphragm myopathy pattern presenting with myasthenic crisis mimicking bulbar subtype ALS.
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