From the Guidelines
PRES predominantly occurs in the posterior circulation due to the region's unique anatomy and less pronounced sympathetic innervation, making it more susceptible to sudden changes in blood pressure and perfusion. The posterior circulation, which includes the vertebrobasilar system and supplies the occipital lobes, brainstem, and cerebellum, has a distinct autoregulatory mechanism compared to the anterior circulation. According to the European Heart Journal study 1, when blood pressure is markedly elevated, cerebral autoregulation cannot prevent a rise in intracranial pressure, leading to cerebral edema, especially in the posterior areas of the brain. This is because the posterior circulation has less sympathetic innervation, resulting in less effective damping of blood pressure oscillations.
Some key factors that contribute to the development of PRES in the posterior circulation include:
- Less sympathetic innervation, making it more prone to vasodilation and increased permeability of the blood-brain barrier
- Increased susceptibility to sudden changes in blood pressure and perfusion
- Unique anatomy of the vertebrobasilar system, which supplies the occipital lobes, brainstem, and cerebellum
- Failure of autoregulation of blood flow in the posterior circulation, leading to vasogenic edema and characteristic symptoms of PRES
The study 1 highlights the importance of timely recognition and management of hypertensive encephalopathy, which is one of the causes of PRES. Magnetic resonance imaging (MRI) with fluid attenuated inversion recovery (FLAIR)-imaging can confirm the diagnosis, while computerized tomography (CT) is useful to exclude intra-cerebral hemorrhage. Prompt identification and treatment of the underlying cause, such as controlling blood pressure, are crucial to prevent permanent neurological damage and ensure reversibility of PRES.
From the Research
Pathophysiology of PRES
The pathophysiology of Posterior Reversible Encephalopathy Syndrome (PRES) is not yet fully understood, but several factors are thought to contribute to its development, including:
- Endothelial dysfunction and breakdown of the blood-brain barrier with subsequent vasogenic edema 2
- Abrupt hypertension, which has been identified as one of the risk factors for PRES 3
- Cerebral hyperperfusion due to acute hypertension and cerebral hypoperfusion related to endothelial dysfunction 2
Predominance of Posterior Circulation Involvement
PRES predominantly occurs in the posterior circulation, which may be due to several factors, including:
- Lower sympathetic innervation of the posterior circulation, making it more vulnerable to vasodilatation caused by certain substances 4
- Larger number of autonomic receptors in the carotid artery compared to the vertebral-basilar system, which may contribute to the clinical-radiological differences between anterior and posterior circulation PRES 5
- The parieto-occipital region is more susceptible to vasogenic edema, which is a characteristic feature of PRES 2
Clinical and Radiological Features
PRES is characterized by nonspecific symptomatology, including:
- Headache
- Visual disturbances
- Encephalopathy
- Seizures
- Classically, cortical and subcortical vasogenic edema predominantly affecting the parieto-occipital region 2 The clinical and radiological features of PRES can vary, and atypical cases have been reported, including involvement of the frontal and temporal lobes, basal ganglia, brainstem, and cerebellum 6