A case of Guillain-Barre syndrome following Pfizer COVID-19 vaccine.

Since the first-reported case of Severe Acute Respiratory Distress Syndrome-Coronavirus 2 in December 2019, COVID-19 has caused a global pandemic associated with significant morbidity and mortality. After a year of advances in vaccine research and development, three vaccines for the prevention of COVID-19 (manufactured by Pfizer, Moderna and Johnson & Johnson's Janssen Biotech) are approved for use in the USA. We report the first case of Guillain-Barre Syndrome after receiving the second dose of the Pfizer COVID-19 vaccine, in a 42-year-old woman presenting with progressive ascending weakness and paresthesias. Diagnostic workup demonstrated cytoalbuminologic dissociation on cerebrospinal fluid analysis with confirmatory evidence of early demyelinating electrodiagnostic features on nerve conduction study and an extensive serological workup being negative for other viral or autoimmune disease triggers. Management included administration of intravenous immunoglobulin (total of 2 gm/kg), with frequent monitoring of forced vital capacity and negative inspiratory force. A longitudinal risk profile of neurologic complications caused from COVID-19 vaccines remains limited, and prompt recognition of potential neurological complications from the COVID-19 vaccine is of interest to public health.

Leading with inclusion during the COVID-19 pandemic: Stronger together.

Inclusion is the deliberate practice of ensuring that each individual is heard, all personal traits are respected, and all can make meaningful contributions to achieve their full potential. As coronavirus disease 2019 spreads globally and across the United States, we have viewed this pandemic through the lens of equity and inclusion. Here, we discuss how this pandemic has magnified preexisting health and social disparities and will summarize why inclusion is an essential tool to traverse this uncertain terrain and discuss strategies that can be implemented at organizational and individual levels to improve inclusion and address inequities moving forward.

De novo formation of a carotid web: case report.

A carotid web is a shelf-like intraluminal filling defect typically arising from the posterolateral wall of the proximal internal carotid artery. It is recognized as a possible cause of ischemic stroke in young adults. However, its etiopathogenesis is controversial and remains to be fully elucidated. The authors report de novo formation of a carotid web from an intimal dissection documented on serial imaging studies. The findings in this case suggest that a focal intimal dissection could be the underlying cause of a carotid web. Lower shear stress at the posterolateral wall of the proximal internal carotid artery is hypothesized to be a predisposing factor and explains the predilection of a carotid web for this specific location.

Heterozygous genotype at codon 129 correlates with prolonged disease course in Heidenhain variant sporadic CJD: case report.

Sporadic Creutzfeldt-Jakob disease (sCJD) is a rapid and fatal neurodegenerative disease defined by misfolded prion proteins accumulating in the brain. A minority of cases initially present with posterior cortical atrophy (PCA) phenotype, also known as Heidenhain variant or visual variant CJD. This case provides further evidence of sCJD presenting as PCA. The case also provides evidence for early DWI changes and cortical atrophy over 30 months before neurologic decline and subsequent death. The prolonged disease course correlates with prion protein codon 129 heterozygosity and coexistence of multiple prion strains.

Headache, TIA and subarachnoid haemorrhage: dissecting an unusual cause for stroke-like symptoms.

We present a case of supraclinoid internal carotid artery dissection. Eleven months prior, the patient developed isolated periorbital pain and was diagnosed with giant-cell arteritis with iritis. The patient experienced recurrent spells concerning for transient ischaemic attacks and was transferred to our institution for endovascular intervention after head CT revealed an embolic infarct with a 'dense middle cerebral artery sign.' Digital subtraction angiography was negative for occlusion, instead demonstrating luminal stenosis and poststenotic dilatation. He subsequently experienced acute neurological decline secondary to massive subarachnoid haemorrhage. Non-invasive vascular imaging revealed an intimal flap and a pseudoaneurysm at the site of luminal stenosis, confirming our suspicion for intracranial carotid artery dissection. Given the moribund clinical state, the family opted to withdraw care, and he quickly expired.

Neurologic Complications of Commonly Used Drugs in the Hospital Setting.

This chapter reviews the neurologic complications of medications administered in the hospital setting, by class, introducing both common and less common side effects. Detail is devoted to the interaction between pain, analgesia, sedation, and their residual consequences. Antimicrobials are given in nearly every hospital setting, and we review their capacity to produce neurologic sequelae with special devotion to cefepime and the antiviral treatment of human immunodeficiency virus. The management of hemorrhagic stroke has become more complex with the introduction of novel oral anticoagulants, and we provide an update on what is known about reversal of the new oral anticoagulants. Both central and peripheral nervous system complications of immunosuppressants and chemotherapies are reviewed. Because diagnosis is generally based on clinical acumen, alone, neurotoxic syndromes resulting from psychotropic medications may be easily overlooked until severe dysautonomia develops. We include a practical approach to the diagnosis of serotonin syndrome and neuroleptic malignant syndrome.

Expanding the spectrum of subacute diencephalic angioencephalopathy.

We present a patient with subacute diencephalic angioencephalopathy (SDAE), a poorly understood syndrome of progressive confusion, disorientation, and dementia that rapidly deteriorates to severe encephalopathy and death. This is the seventh and most thoroughly investigated report of this exceedingly rare diagnosis to date, and we present the first evidence of a potential sentinel syndrome that may allow for earlier diagnosis and therapeutic intervention. We also review the relevant literature, and highlight new evidence that suggests that SDAE and the related disorder, subacute brainstem angioencephalopathy (SBAE), represent severe and terminal variants of posterior reversible encephalopathy syndrome (PRES). Taken together, we suggest a new understanding of SDAE/SBAE and PRES as a spectrum of hypertension-associated non-inflammatory vascular encephalopathies that are mediated by a loss of venous autoregulation, marked by cytotoxic edema, and that ultimately produce subacute-to-acute diencephalic, brainstem, and posterior fossa injuries with devastating neurologic consequences.