Clinically, PRES can cause visual disturbances, headache, nausea, altered consciousness, seizures and, in some cases, focal neurological disorders [1], [5], [6], [7], [8]. The most frequently observed symptom is seizures, which occur in approximately 90% of reported cases [9]. While seizures are typically generalized, some cases have shown focal onset [10]. Visual problems may range from blurring of vision to cortical blindness [10]. The onset of symptoms is gradual, spanning hours, and their duration can extend from days to weeks, contingent on the severity and the promptness of congenial treatment [11].
Although elevated blood pressure (BP) is often associated with PRES, it is not a mandatory criterion for diagnosis, and its level of elevation varies. Normal or lower normal BP has been documented in some cases [7], [11], [12]. A quick increase in blood pressure, rather than the absolute standard, is considered a more critical factor for risk [13], [14]. Clinical and radiographic signs of PRES have not been linked to an increase in absolute blood pressure according to previous studies [4].
Radiologically, PRES is identified by T2 hyperintensities that symmetrically affect the posterior portion of the brain, specifically the occipital lobe and parietal lobes [1]. While this description is generally applicable, there are instances of asymmetric presentations involving the deep gray matter, temporal lobes and frontal lobe as well [8]. The introduction of diffusion weighted imaging (DWI) clarified that the MRI findings changes in PRES are attributable to vasogenic edema rather than ischemia or cytotoxic edema [15]. However, diffusion restriction can be observed in some cases, indicating that ischemic changes can be a complication of PRES [15].
Case studies have shown that PRES affects people of any age group, with young and middle-aged individuals having the highest occurrence and that women are more likely than men to be affected by it [16], [17]. In an individual study, 635 patients with PRES as the initial diagnosis were selected from the National Inpatient Sample. The patients' mean age was 57 years, and 72% of them were female [18]. Underlying comorbidities often play a role in contributing to acute hypertension, endothelial dysfunction or both. A retrospective analysis of the PRES performed in German hospitals revealed several commonly associated comorbidities, such as infection, immunosuppression, organ transplantation, acute renal failure and autoimmune disorders [19].
The diagnostic challenge for PRES arises from its nonspecific clinical features, necessitating differentiation from other causes of headache, confusion, and seizures. In the differential diagnosis of posterior circulation stroke, encephalitis, cerebral venous sinus thrombosis, reversible cerebral vasoconstriction syndrome, and ictal or postictal states must be included, although their presentations are similar. If patients present with an acute confusional state with increased blood pressure or underlying endothelial dysfunction, PRES should be considered.
There are no proper data or studies conducted that have reported the detailed outcomes of patients with PRES. However, our results revealed one complete recovery within 6 months, one with repeat convulsion after the cessation of medication, and another with significant improvement and residual visual impairment.
Common complications of PRES include seizures, which occur acutely in patients. Following recovery, very few patients may develop unprovoked seizures. However, if a precipitating factor is present, it may provoke a seizure attack many days following the resolution of PRES. Recurrent PRES, systemic infection/sepsis, benzodiazepine withdrawal, alcohol withdrawal, subdural hemorrhage, intracerebral hemorrhage, and electrolyte imbalance can all lead to a seizure attack in a patient who has recovered from PRES. In a study conducted on 127 patients, 66% had seizures at presentation. Patients were followed up for 3 years. Fifteen patients had provoked seizures during the follow-up period; among them, 8 had seizures due to recurrent PRES [20]. Periodic lateralized epileptiform discharges are also found in very few patients during the acute phase of PRES [21]. EEGs obtained during follow-up may provide a clearer picture of patients who develop seizures even after neuroimaging changes resolve.
It is advised to withdraw antiepileptic medication following recovery after confirming that risk factors are minimized and that any factor that may reduce the seizure threshold is removed. Although we could not identify a risk factor or provoking factor, one of our patients experienced a seizure attack eight months after diagnosis and five months after recovery and discontinuation of antiepileptic medication. She needed to start medication again for an indefinite period. We planned to perform another MRI and EEG session during her next visit, but we could not reach her.
In a study conducted by Alexander M. McKinney and his colleagues involving 76 patients, brain area involvement was reported as follows: parieto-occipital at 98.7%, temporal at 68.4%, thalamic at 30.3%, cerebellar at 34.2%, brainstem at 18.4%, and basal ganglia at 11%. Less common manifestations included enhancement at 37.7%, restricted diffusion at 17.3%, hemorrhage at 17.1%, and a newly described unilateral variant at 2.6% [22]. In our investigation, the parieto-occipital region was the most frequently affected location. This region was observed in all three patients (100%) and involved the frontal lobe in two patients (66.67%), the temporal lobe in one patient (33.33%) and the cerebellum in one patient (33.33%).