Posterior Reversible Encephalopathy Syndrome (PRES): Pathophysiology and Neuro-Imaging

Abstract

Posterior reversible encephalopathy syndrome (PRES) represents a unique clinical entity with non-specific clinical symptoms and unique neuroradiological findings. This syndrome may present with a broad range of clinical symptoms from headache and visual disturbances to seizure and altered mentation. Typical imaging findings include posterior-circulation predominant vasogenic edema. Although there are many well-documented diseases associated with PRES, the exact pathophysiologic mechanism has yet to be fully elucidated. Generally accepted theories revolve around disruption of the blood-brain barrier secondary to elevated intracranial pressures or endothelial injury. In this article, we will review the clinical, typical, and atypical radiological features of PRES, as well as the most common theories behind the pathophysiology of PRES. Additionally, we will discuss some of the treatment strategies for PRES related to the underlying disease state.

Neurological symptoms, manifestations, and complications associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and coronavirus disease 19 (COVID-19)

“…PRES may result from elevated inflammatory markers and cytokines leading to changes in endothelial morphology, impairment of the blood–brain barrier and consecutive increased vascular permeability [ 112 ]. MRI of the brain typically indicates cerebral vasogenic edema in the parietal and occipital regions bilaterally, occasionally associated with hemorrhagic lesions [ 113 ]. Patients with severe SARS-CoV-2 infection have a drastic inflammatory reaction, provoking a cytokine storm which damages the blood brain barrier and resulting in PRES.…”

Unilateral posterior reversible encephalopathy syndrome characterized with a long and gradually exacerbating course over 3 years and that presented propofol infusion syndrome – A case report

“…[ 5 , 7 ] Both theories are related to dysfunction of the cerebrovascular autoregulation, leading to cerebral edema with various symptoms. [ 1 , 5 ] Our case did not have hypertension, and her blood pressure on admission was within the optimal range of 124/77 mmHg. Therefore, endothelial dysfunction seemed to play a key role in this case.…”

“…Furthermore, PRES incidence may be higher in women,[ 12 ] but the actual gender difference associated with the PRES development is still unknown. [ 1 , 2 , 7 , 13 ] Although it is unknown whether favorable or adverse effect ovarian dysfunction and Kaufmann’s treatment had on the cerebral vascular function and endothelial cells, our patient’s pathophysiology may be associated with those female hormonal dynamics, which attenuated endothelial functioning.…”

“…The neuroimaging typically reveals that patchy areas of vasogenic edema generally occurring bilaterally in the posterior parietal and occipital lobes. [ 1 , 2 , 7 , 8 ] Its prognosis is usually favorable, and most patients wholly recover. [ 22 ] However, about 40% of PRES patients require intensive care monitoring and treatment due to severe complications such as status epilepticus, cerebral ischemia, intracerebral hemorrhage, or intracranial hypertension.…”

Tacrolimus-induced posterior reversible encephalopathy syndrome presenting as left upper limb monoplegia, convulsions, and sudden blindness: case report

“…These symptoms were found in combination with neuroradiographic findings of edema of the posterior cerebral white matter. Although the exact pathophysiological mechanism is still unclear, numerous etiologies have been reported and include use of immunosuppressant medications, hypertensive encephalopathy, and eclampsia [8]; that is supposed to cause disruption in the BBB results in picture similar to that of vasogenic edema vs. cytotoxic edema [10].…”