Parainfluenza virus infection associated with posterior reversible encephalopathy syndrome: a case report

Abstract

IntroductionPosterior reversible encephalopathy syndrome is a clinical and radiological entity. The most accepted theory of posterior reversible encephalopathy syndrome is a loss of autoregulation in cerebral blood flow with a subsequent increase in vascular permeability and leakage of blood plasma and erythrocytes, producing vasogenic edema. In infection-associated posterior reversible encephalopathy syndrome, a clinical pattern consistent with systemic inflammatory response syndrome develops. Parainfluenza virus has not been reported in the medical literature to be associated with posterior reversible encephalopathy syndrome.Case presentationWe report herein the case of a 54-year-old Caucasian woman with posterior reversible encephalopathy syndrome associated with parainfluenza virus infection who presented with generalized headache, blurring of vision, new-onset seizure and flu-like symptoms.ConclusionInfection-associated posterior reversible encephalopathy syndrome as well as hypertension-associated posterior reversible encephalopathy syndrome favor the contribution of endothelial dysfunction to the pathophysiology of this clinicoradiological syndrome. In view of the reversible nature of this clinical entity, it is important that all physicians are well aware of posterior reversible encephalopathy syndrome in patients presenting with headache and seizure activity. A detailed clinical assessment leading to the recognition of precipitant factors in posterior reversible encephalopathy syndrome is paramount.

Etiologies, Cerebral Vasomotion, and Endothelial Dysfunction in the Pathophysiology of Posterior Reversible Encephalopathy Syndrome in Pediatric Patients

“…7 Chemotherapeutic agents may accordingly contribute to the pathogenesis of PRES by directly effecting osmotic injury, necrosis or apoptosis of endothelial cells, 14,47,50,52,58,105,115,122,125 or inducing axonal swelling. 14,58 Sans direct cytotoxic injury, a variety of etiologies may converge on augmenting infectious 11,[126][127][128][129][130][131][132][133][134][135][136][137][138][139][140] or autoimmune [141][142][143][144][145][146][147][148][149][150] mediated activation of cellular adaptive immune mechanisms and pathways, effecting the activation of macrophages and consequent elaboration of cytokines, including tumor necrosis factor α, interleukin-1, interleukin-6, interleukin-8, and interleukin-12. 151,152 Collectively, these molecules generate fever by promoting the synthesis of pyrogenic prostaglandins in the thermoregulatory nuclei of the hypothalamus and upregulate the expression of vascular cell adhesion molecule 1 (VCAM-1) and intracellular adhesion molecule 1 (ICAM-1) in the endothelium.…”

Posterior Reversible Encephalopathy Syndrome Associated with FOLFOX Chemotherapy

“…Other possible etiologies are eclampsia, transplantation, neoplasia and chemotherapy treatment, systemic infections, and a renal disease, acute or chronic [1, 5]. …”

Rotavirus Infection-Associated Posterior Reversible Encephalopathy Syndrome

“…Convulsive symptoms related to rotavirus infection may occur as PRES without definite fluctuation of blood pressures. Approximately one-third of patients with PRES have normal or only mildly increased blood pressure, though most are hypertensive [4,5]. PRES is an increasingly recognized disorder readily diagnosed via brain MRI in clinical practice.…”

“…However, as mentioned earlier, a significant proportion of patients do not demonstrate hypertension. An alternative theory is that systemic inflammation causes endothelial dysfunction [4]. In a systemic inflammatory process such as sepsis, eclampsia, transplantation, and autoimmune disease, the vasoconstriction that occurs during autoregulation could exacerbate pre-existing inflammatory endothelial dysfunction, causing hypoxia and subsequent vasogenic edema [5].…”

“…However, we are not sure whether age affected the patient's symptoms. There have been only two cases reported so far: parainfluenza virus infection in an adult and rotavirus infection in an infant [4,5]. In other words, infection-associated PRES, as well as hypertension-associated PRES, contribute endothelial dysfunction to the pathophysiology of this clinical-radiological syndrome.…”