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Coronavirus disease 19 (COVID-19) is caused by severe acute respiratory coronavirus 2 (SARS-CoV-2). Apart from respiratory manifestations, COVID-19 can affect the nervous system due to its neurotropic features. Neurological manifestations and complications include headache, polyneuropathies, cerebrovascular accidents, seizures, encephalopathy, and demyelinating disease. We describe a case of multiple sclerosis, a demyelinating disease following COVID-19 infection, rarely reported in the literature. A 47-year-old female presented with fatigue, blurry vision, numbness, and signs of upper motor neuron lesions that had occurred three weeks after COVID-19 infection. Magnetic resonance imaging of the brain revealed demyelinating lesions in the periventricular area of both hemispheres, suggesting a demyelinating disease. A provisional diagnosis of multiple sclerosis was made. Her condition improved after the commencement of methylprednisolone.

Coronavirus disease 19 (COVID-19) is a respiratory disease, has a variable presentation, and neurological involvement in COVID-19 is not widely reported. We report a rare case of acute encephalitis in a COVID-19 patient presented with fever, dry cough, and dyspnea. She had a fever, tachypnea, and tachycardia. On auscultation, she had scattered wheezing in both lung fiends. Chest X-ray revealed small infiltrates in the lower lobe of both lungs. A nasopharyngeal swab for the COVID-19 polymerase chain reaction was positive. Later on, she developed sudden onset confusion accompanied by restlessness and visual hallucinations. Neurological examination revealed an altered level of consciousness, slight trembling of the limbs, psychomotor restlessness, and poor speech with no signs of meningeal irritation. Magnetic resonance imaging of the brain revealed diffuse hyperintense signals. A possible diagnosis of acute encephalitis was made due to concurrent COVID-19 infection and lack of other findings suggesting a diagnosis other than COVID-19. She was treated with azithromycin, tocilizumab, and methylprednisolone. Her condition started improving gradually.

Amyloidosis is a rare multisystem disease due to deposition of abnormal protein fragments, and cardiac amyloidosis is progressive and difficult to diagnose due to its subtle and non-specific symptoms unless the physician maintains a high degree of suspicion. This case report focuses on amyloid deposition in the heart of an 84-year-old woman who presented with symptoms of uncompensated heart failure.

Posterior reversible encephalopathy syndrome (PRES) is an entity which is characterized by acute to subacute onset of neurological symptoms like altered mental status, seizures, headaches and other focal neurological deficits. It is diagnosed with the help of MRI findings which typically involve the subcortical white matter of parieto-occipital lobes. In this review, we will discuss the various etiologies and risk factors including some of the most common chemotherapeutic agents and immunosuppressant agents associated with this disorder. We will discuss the mechanism of actions and side effect profiles of a few drugs and their role in causation of PRES. This review article discusses if there is any difference in presentation and imaging findings of PRES caused by cytotoxic agents versus caused by other etiologies. It also highlights the difficulty in management of PRES caused by cytotoxic agents as the discontinuation of these drugs could be life-threatening due to graft rejections or graft versus host disease.

Atrial fibrillation (AF) is a common arrhythmia, and gastroesophageal reflux disease (GERD) is a common gastroenterology disease; both are highly encountered daily in clinical practice. Since both share common predisposing factors, we can conclude that there is a link between them. To date, the precise mechanism of reflux disease as a possible cause of atrial fibrillation remains uncertain. However, some possibilities can be postulated, such as the inflammation process, and sympathovagal imbalance represents the main factors for how GERD can initiate AF. Vigorous aerobic exercise in healthy people can bring about acidic esophageal reflux, which is a common risk factor for AF. Various inflammatory markers such as C-reaction protein (CRP) and interleukins have been a central role in initiating AF. A large hiatal hernia (HH) can cause direct compression on the left atrium that is possibly predisposing to atrial arrhythmogenesis. It has been sporadically reported that using a proton pump inhibitor to treat GERD in patients with coexisting AF has a noticeable effect on decreasing symptoms of AF and recurrence with less cost and side effects.

Fibromyalgia is a complex syndrome characterized by widespread chronic pain, without any obvious etiology, and it is often accompanied by a constellation of symptoms such as fatigue, sleep disturbances and cognitive dysfunction, to name a few. The syndrome may be associated with a variety of autoimmune and psychiatric conditions. Fibromyalgia can occur with other musculoskeletal pathologies and its symptoms can overlap with other chronic painful conditions such as chronic myofascial pain syndromes seen in cervical and lumbar spinal osteoarthritis and degenerative disc disease. Gene polymorphisms have been related to a decreased pain threshold and an increased susceptibility to disorders associated with chronic pain. Some of those genetic variants might trigger the onset of fibromyalgia. Researchers are looking into the possible factors that might contribute to its pathophysiology. It is important to study the connections between pro-inflammatory cytokines and genetic variants in pain-related genes and their roles in predisposition and development of fibromyalgia. The objective of this review article is to provide a brief overview of the pro-inflammatory cytokines commonly associated with fibromyalgia, as well as to look into the genes that have shown some level of involvement in the development of fibromyalgia and its symptomatology.

Cardiac involvement in amyloidosis and sarcoidosis is poorly understood, and is associated with high morbidity and mortality. Atrial and ventricular arrhythmias, along with conduction defects, are frequent in cardiac amyloidosis and sarcoidosis. Atrial dysfunction in cardiac amyloidosis may result in atrial fibrillation and increases the risk of stroke, making anticoagulation significant and challenging. Ventricular arrhythmia and conduction defects are more common in AL amyloidosis and cardiac sarcoidosis. Premature ventricular contractions (PVCs) from Purkinje fibers trigger ventricular arrhythmias in cardiac amyloidosis, while the inflammation and scarring leading to the reentrant process is the cause in cardiac sarcoidosis. The typical treatment modalities include Class II and III antiarrhythmic drugs and ablation techniques, while corticosteroids and immunosuppressants are indicated in cardiac sarcoidosis to reduce the burden of the disease and arrhythmias. Sudden cardiac death can be a manifestation of both disorders that can be prevented by the Implantable cardioverter-defibrillator (ICD), although the predictive risk factors for primary prevention remain uncertain. In this review, we addressed the current understanding of the pathways involved in inducing arrhythmias in cardiac amyloidosis and sarcoidosis-also, the complications including sudden death and stroke associated with arrhythmia in both diseases. We have discussed other preventive steps needed to minimize arrhythmias to provide symptomatic relief and palliation to patients.

Atypical hemolytic uremic syndrome (aHUS), defines as non-Shiga toxin HUS, is thrombotic microangiopathy characterized by microangiopathic hemolytic anemia, consumptive thrombocytopenia, and renal impairment. aHUS is associated with high morbidity and mortality, necessitating the need for an early diagnosis to limit target organ damage. Mutations or autoantibodies against specific complement factors over-activate the complement system forming microthrombi. aHUS has the potential to cause multi-organ system dysfunction, but it predominantly affects the kidneys. aHUS is treated with eculizumab, a terminal blocker of the complement system. Clostridium difficile infection is a rare precipitant of aHUS. We present a case of aHUS associated with Clostridium difficile infection in a 60-year-old female patient that was successfully treated with eculizumab.