Severe Headache as an Early Manifestation of Brain Involvement in a Patient with Covid-19 Infection

Purpose of study COVID-19 primarily affects the respiratory system from flu-like syndrome to acute hypoxic respiratory failure. Neurological manifestations are uncommon and can result in serious complications. We report a unique case of sudden onset of rapidly progressive encephalopathy in the setting of COVID-19. Methods used Reviewed the manifestations, clinical course, and outcome for a patient presenting with altered mental status secondary to COVID-19. Summary of results A 48-year-old with no significant past medical history presented to the emergency department complaining of severe headache for four days. His vital signs on presentation showed a blood pressure of 154/90, pulse of 114 bpm, temperature of 99.6 degreeF, and oxygen saturation of 97% on room air. Physical exam was unremarkable. Lab work showed elevated D-dimer 8,500 ng/L, Elevated ESR:42, LDH:340 and Ferritin:692. White blood count: 7.59 uL, Platelets 50 x 103 uL. Computer tomography angiography (CTA) of the chest showed bilateral multifocal pneumonia. CT Head was performed and was negative for an acute hemorrhage, hydrocephalus or territorial infarcts. Patient spiked a fever shortly after admission 103degreeF. Patient was started on Ceftriaxone and Azithromycin. Blood and urine cultures were positive for Klebsiella pneumonia. Patient was re-evaluated in the morning and was found altered with associated neck stiffness. Antibiotics were switched to cover for suspected meningitis. Neurology was consulted and recommended lumbar puncture. Within a few hours, the patient's mental status deteriorated and was found to be hypertensive with a blood pressure of 220/110. Repeat CT Head was negative. The patient was tested and found to be positive for COVID-19. Patient further decompensated within a few hours and became unresponsive, pulseless. ACLS was performed and the patient was transferred to the intensive care unit. Conclusions This case report highlights the heterogenous presentation in patients with COVID-19 and the importance of recognizing a new onset, severe headache as the only initial presentation. Headaches in some cases may precede the respiratory symptoms or may be the only manifestations in COVID-19 patients and it is crucial to be aware of the neurological complications and the rapid decompensation these patients may undergo if not recognized early.

Reversible parkinsonism post combined infection with COVID- 19 and typhoid

Objective: To describe a case of levo-dopa responsive parkinsonism secondary to combined COVID-19 and Enteric fever in a patient Background: The first link between viruses and parkinsonism comes from the possible relationship between lethargic encephalitis and the Spanish flu of 1918.In addition, other viruses, including West Nile virus, herpes viruses, influenza A virus, and human immunodeficiency virus (HIV), have been associated with parkinsonism Methods: A 31 years old presented with fever ,headache for 5 days followed by altered sensorium. At presentation he had neck rigidity ,was localizing to pain ,not fully oriented and not following verbal command but he had hypoxia and need nasal oxygen support.He had D-Dimer 12506,COVID-19 RTPCR positive and was treated with Remdesivir,ceftriaxone ,dexamethasone after which he had improvement in sensorium.At day 6 of illness he had generalized rigidity,bradykinesia with slow hypophonic speech and was needing support to sit and walk . A provisional diagnosis of infection related parkinsonism was considered and Cerebrospinal fluid study,MRI Brain and spine ,Blood culture were done .His Cerebrospinal fluid study has normal protein , glucose,cells, stains and culture and negative autoimmune and paraneoplastic plane . His urine culture,blood culture was positive for salmonella typhi and serum widal titre was 1:640.MRI Brain and spine does not show any new abnormalities except old trauma sequalae. He was treated with Levo-dopa carbidopa and titrated to a dose of 675 mg/day and had sustained improvement with levo-dopa carbidopa .There are 6 other case of COVID-19 associated parkinsonism in literature .There are also few case of typhoid associated case of parkinsonism described in literature . Our patient had combined infection of both COVID-19 and typhoid associated parkinsonism. Result(s): We report a case of Infection related parkinsonism secondary to combined COVID-19 plus typhoid infection Conclusion(s): Exploring the potential relationship of co-infection SARS-CoV-2 and Salmonella typhi infection with development of parkinsonism is essential because of the epidemiological implications,as well as to gain a better understanding of the pathophysiological aspects of these disorders.

Guillain-Barre syndrome: An autoimmune disorder post-COVID-19 vaccination?

SARS-CoV-2 causes Coronavirus Disease 2019 (COVID-19), an infectious condition that can present none or one or more of these symptoms: fever, cough, headache, sore throat, loss of taste and smell, aches, fatigue and musculoskeletal pain. For the prevention of COVID-19, there are vaccines available including those developed by Pfizer, Moderna, Sinovac, Janssen, and AstraZeneca. Recent evidence has shown that some COVID-19-vaccinated individuals can occasionally develop as a potential side effect Guillain-Barre syndrome (GBS), a severe neurological autoimmune condition in which the immune response against the peripheral nerve system (PNS) can result in significant morbidity. GBS had been linked previously to several viral or bacterial infections, and the finding of GBS after vaccination with certain COVID-19, while rare, should alert medical practitioners for an early diagnosis and targeted treatment. Here we review five cases of GBS that developed in different countries after COVID-19 vaccination.Copyright © 2021

SLE After SARS-COV-2 Infection

SARS-COV-2 infection is often associated with exaggerated immune response, also referred to as a ‘cytokine storm’. There is growing concern that it may be linked to autoimmunity, with many cases of autoimmune diseases either triggered by or related to SARS-COV-2 having been reported, ranging from Guillain-Barre syndrome, Graves’ disease, multiple sclerosis, Kawasaki-like disease. Our patient was a 20-year-old female with a history of hidradenitis who presented with malaise, feet and ankle swelling, asthenia, anorexia, weight loss of 50 Ibs of 4 months. She had COVID pneumonia 7 months prior and was also seen in the ER thrice afterwards for ankle pain and fatigue managed with antibiotics and analgesics. Exam findings included tender bilateral lower extremity edema, diffuse hyperkeratotic and hyperpigmented purpuric rashes and bilateral suppurative axillary swellings. She was admitted for protein-energy malnutrition. Blood work showed WBC 13.5, low Hb 9.3, AST 509, ALT 104, BUN 29, Creatinine 0.9, Protein 7.5, albumin 1.5 (globulin gap of 6). Urine assay showed 3+ proteinuria Hb 3+ with RBC 3-10/hpf, absent nitrite, LE 1+, protein/creatinine ratio was 2949 mg/g. Blood cultures returned negative. US showed trace pericardial effusion and normal kidneys. Infectious workup returned negative for anti-streptolysin O, HIV, hepatitis B and C. Two days after, she developed AMS, fever, tachycardia and neck stiffness concerning for possible meningoencephalitis. CT head was normal. Lumbar puncture was performed. IV vancomycin and piperacillin-tazobactam was started. CSF fluid analysis revealed total protein of 125mg/dl, elevated IgG 79.8, concerning for an underlying inflammatory pathology. EEG was unremarkable. She became oliguric with creatinine and BUN both peaking at 2.6 and 58 respectively. Renal ultrasound revealed medical renal disease. Urine microscopy showed granular cast and no dysmorphic RBCs. ANA, anti-smith SSA, SSB, DS-DNA, RF, smooth muscle, anti-histone, anti-centromere, JO-1 and RNP antibodies were markedly elevated. She was unstable for CT trocar biopsy of the kidney. She subsequently went into cardiac arrest multiple times about a week into admission, before eventually expiring. Though causation was not established in our patient, SARS-COV-2 infection causing exaggerated immune response may unmask SLE or be associated with SLE.

Atypical presentation of a neuroinvasive west nile fever

Background West Nile Virus is the most common cause of arboviral diseases and is endemic in the US. It can cause clinical presentation ranging from asymptomatic infection to neuroinvasive disease. Factors like old age, hematologic malignancies, and organ transplantation result in more severe disease. Case presentation An 85-year-old male farmer with coronary artery disease, congestive heart failure (CHF) and diabetes presented with sore throat, cough and shortness of breath. He was treated for CHF exacerbation and discharged but returned with fatigue, headache, Nausea, and vomiting. Imaging of the head and chest, inflammatory markers, COVID-19 PCR,and metabolic panel were all negative, . Then he became febrile, lethargic, and had altered mentation. He exhibited asymmetric weakness, bilateral positive Babinski and neck rigidity. Intravenous ceftriaxone, vancomycin, bactrim, and acyclovir were all initiated for meningoencephalitis of unclear etiology. CSF analysis showed 51 WBC, 0 RBC, 49% granulocytes, 55 glucose and 74 proteins. He was transferred to ICU with a glasgow coma score of 6-7 but was on a 'DO NOT INTUBATE' status. He developed acute anuric kidney injury which prompted emergent hemodialysis and vasopressor support had to be initiated. Family elected for palliative care, and he passed away shortly after. A day later, West Nile serology was reported positive as IGM in CSF. Also, both IgG and IgM were positive in serum Discussion This case demonstrates a rare, severe presentation of West Nile infection. Most persons infected with West Nile (WNV) virus are asymptomatic;symptoms are seen in only about 20 to 40 percent of infected patients [1] Serologic surveys and extrapolations from blood donor screening data indicate that neuroinvasive disease following infection is infrequent, with estimates ranging from 1 in 140 to 1 in 256 infections resulting in meningitis or encephalitis [2] The patient's risk factors for severe infection include elderly age and male sex. Age in particular is the most important risk factor for neurologic progression of disease.[3] The diagnosis can be suspected in patients who have altered mental status, signs of meningitis, unexplained fever, and focal neurologic deficit, especially when it presents in late summer months and has no obvious etiology. The CSF West Nile IgM antibody detection via ELISA is diagnostic as was in our case. The treatment is mainly supportive. The preventive measures including mosquito control, personal protective devices are of substantial importance. Vaccines are not available. [4 5 6] Conclusion The high index of suspicion is necessary to diagnose WNV neuroinvasive diseases especially in patients with atypical presentation. Seasonal clues must be considered.