Neuroimaging reveals the posterior parts of the cerebrum, especially the parieto-occipital regions, to be generally involved, with relative sparing of the occipital cortical gray matter.

The term reversible posterior leukoencephalopathy syndrome (RPLS) describes a syndrome of headaches, confusion, seizures, and visual disturbances associated with transient, predominantly posterior cerebral lesions revealed by neuroimaging. Because MR imaging (in particular, fluid-attenuated inversion recovery MR imaging) has shown that lesions can occur in both gray and white matter, the term posterior reversible encephalopathy syndrome has also been suggested.

Etiology
RPLS occurs in association with hypertension and/or immunosuppression, and known triggers include acute renal failure, eclampsia (especially puerperal).Hypertension is commonly associated with RPLS but may be relatively mild and is not universally present, especially in the setting of immunosuppression.

Pathology

The underlying pathophysiology of RPLS is not well understood, but two main mechanisms have been suggested. One hypothesis is that cerebral vasospasm results in ischemia and subsequent development of T2 hyperintensity. Alternatively, it has been suggested that there is a temporary failure of the autoregulatory capabilities of the cerebral vessels, leading to hyperperfusion, breakdown of the blood-brain barrier, and consequent vasogenic edema.
 Presumably, this hyperperfusion is triggered by hypertension. Drugs have been postulated to contribute to this physiological effect, by cytotoxic effects on the vascular endothelium or by inducing or exacerbating hypertension.

Location

The preferential involvement of the parietal and occipital lobes is thought to be related to the relatively poor sympathetic innervation of the posterior circulation .