A 62-Year-Old Man Presenting with Bilateral Tremor of the Upper Limb After a Diagnosis of COVID-19 with Confirmed Volumetric Brain Loss.

BACKGROUND The SARS-CoV-2 viral infection is associated with respiratory and multi-organ systemic disease. It has been shown to affect the central nervous system and produce varied neurological symptoms, including ischemic strokes, seizures, and encephalitis. Neurological manifestations of this viral infection are thought to be due to neurotropic reactions on the central nervous system or post-infectious immune-mediated damage. This report presents a case of bilateral tremor of the upper limbs more than 6 weeks after a diagnosis of COVID-19, with confirmed volumetric brain loss shown by follow-up brain magnetic resonance imaging (MRI) combined with 3-dimensional volumetric NeuroQuant image analysis. CASE REPORT We report a case of new-onset tremors in a 62-year-old man after SARS-CoV-2 infection. MRI of the brain was performed shortly after the onset of tremors, and a follow-up MRI after 2 months showed evidence of rapid parenchymal volume, loss of midbrain substance, and increased cerebrospinal fluid volume within 2 months of the initial examination. CONCLUSIONS This case report shows central neurological effects of COVID-19, which can be evaluated by quantitative volumetric MRI analysis, although further studies are warranted to determine how this type of brain imaging can be used to evaluate the effects of SARS-CoV-2 infection over time.

Current and Upcoming Treatment Modalities in Myasthenia Gravis.

ABSTRACT: Myasthenia gravis (MG) is one of the extensively studied autoimmune disorder. There has been a dramatic increase in research to further understand molecular pathogenesis of MG and clinical trials for new drugs in MG treatment in the past decade. This review article is to consolidate the available information in simple terms with students, residents, and fellows as target audience for easy learning and help application of this knowledge to clinical practice.

Brachial plexopathy with Sjögren syndrome.

This report will explain an unusual presentation of brachial plexopathy associated with manifestation of Sjögrens and will emphasize that Sjögrens may also present initially with neurological involvement only.

Recurrent Opportunistic Infections in a Thymectomised Patient with Myasthenia Gravis and Good's Syndrome.

We report the case of a 65-year-old man with myasthenia gravis, who developed recurrent opportunistic infections following thymectomy and immunosuppressive therapy. Subsequent evaluation including immunological studies, flow cytometry, and bone marrow studies confirmed the diagnosis of Good's syndrome. The patient was successfully treated with intravenous immunoglobulin (IVIG) and has remained stable with a monthly IVIG regimen. Good's syndrome should be strongly suspected when patients with myasthenia gravis develop recurrent opportunistic infections, especially after discontinuation of immunosuppressive therapy. Any delay in diagnosis can be life-threatening in such patients. Serum immunoglobulin levels and flow cytometry should be considered part of the initial diagnostic evaluation in patients with myasthenia gravis and an anterior mediastinal mass prior to the initiation of immunosuppressive therapy.

Mast Cell Activation in Brain Injury, Stress, and Post-traumatic Stress Disorder and Alzheimer's Disease Pathogenesis.

Mast cells are localized throughout the body and mediate allergic, immune, and inflammatory reactions. They are heterogeneous, tissue-resident, long-lived, and granulated cells. Mast cells increase their numbers in specific site in the body by proliferation, increased recruitment, increased survival, and increased rate of maturation from its progenitors. Mast cells are implicated in brain injuries, neuropsychiatric disorders, stress, neuroinflammation, and neurodegeneration. Brain mast cells are the first responders before microglia in the brain injuries since mast cells can release prestored mediators. Mast cells also can detect amyloid plaque formation during Alzheimer's disease (AD) pathogenesis. Stress conditions activate mast cells to release prestored and newly synthesized inflammatory mediators and induce increased blood-brain barrier permeability, recruitment of immune and inflammatory cells into the brain and neuroinflammation. Stress induces the release of corticotropin-releasing hormone (CRH) from paraventricular nucleus of hypothalamus and mast cells. CRH activates glial cells and mast cells through CRH receptors and releases neuroinflammatory mediators. Stress also increases proinflammatory mediator release in the peripheral systems that can induce and augment neuroinflammation. Post-traumatic stress disorder (PTSD) is a traumatic-chronic stress related mental dysfunction. Currently there is no specific therapy to treat PTSD since its disease mechanisms are not yet clearly understood. Moreover, recent reports indicate that PTSD could induce and augment neuroinflammation and neurodegeneration in the pathogenesis of neurodegenerative diseases. Mast cells play a crucial role in the peripheral inflammation as well as in neuroinflammation due to brain injuries, stress, depression, and PTSD. Therefore, mast cells activation in brain injury, stress, and PTSD may accelerate the pathogenesis of neuroinflammatory and neurodegenerative diseases including AD. This review focusses on how mast cells in brain injuries, stress, and PTSD may promote the pathogenesis of AD. We suggest that inhibition of mast cells activation and brain cells associated inflammatory pathways in the brain injuries, stress, and PTSD can be explored as a new therapeutic target to delay or prevent the pathogenesis and severity of AD.