INTRODUCTION Reversible Posterior Leukoencephalopathy Syndrome was introduced into clinical practice in 1996 in order to describe unique syndrome, clinically expressed during hypertensive and uremic encephalopathy, eclampsia and during immunosuppressive therapy [1 ]. First clinical investigations showed that leucoencephalopathy is major characteristic of the syndrome, but further investigations showed no significant destruction in white cerebral tissue [2, 3,4]. In majority of cases changes are localize in posterior irrigation area of the brain and in the most severe cases anterior region is also involved. Taking into consideration all above mentioned facts, the suggested term was Posterior Reversible Encephalopathy Syndrome (PRES) for the syndrome clinically expressed by neurological manifestations derived from cortical and subcortical changes localized in posterior regions of cerebral hemispheres cerebral trunk and cerebellum [5]. CASE REPORT Patient, aged 53 years, was re-hospitalized in Cardiovascular Institute "Dedinje" two months after succesfull aorto-coronary bypass performed in June 2001 due to the chest bone infection. During the treatment of the infection (according to the antibiogram) in September 2001, patient in evening hours developed headache and blurred vision. The recorded blood pressure was 210/120 mmHg so antihypertensive treatment was applied (Nifedipin and Furosemid). After this therapy there was no improvement and intensive headache with fatigue and loss of vision developed. Neurological examination revealed cortical blindness and left hemiparesis. Manitol (20%, 60 ccm every 3 hours) and iv. Nytroglicerin (high blood pressure). Brain CT revealed oedema of parieto-occipital regions of both hemispheres, more emphasized on the right. (Figure 1 a, b, c). There was no sign of focal ischemia even in deeper sections (Figure 1d, e, f). Following three days enormous high blood pressure values were registered. On the fourth day the significant clinical improvement occurred with lowering of blood pressure, better mental state and better vision. There was no sign of left hemiparesis on the 7th day. On the 9th day there were no symptoms or sign of disease. Control brain CT (15th day) was normal. ETHIOPATHOGENESIS Most common causes of PRES are hypertensive encephalopathy [6-8], pre-eclampsia/eclampsia [9-12] cyklosporin A administration [13-22] and uremic encephalopathy [23]. There are several theories about the mechanism for PRES in hypertensive encephalopathy (reversible vasospasm and hyperperfusion) and administration of cyclosporin A (neurotoxic effect). CLINICAL PICTURE Most common symptoms are headache, nausea, vomiting, confusion, behavioural changes, changes of conciousnes (from somnolencia to stupor), vision disturbances (blurred vision, haemianopsia, cortical blindness) and epileptic manifestations (mostly focal attacs with secondary generalization). Mental functions are characterised with decreased activity and reactivity, confusion, loss of concentration and mild type of amnesia. Lethargy is often initial sign, sometimes accompanied with phases of agitation. Stupor and coma rarely occurred. DIAGNOSIS In patients with hypertensive ecephalopathy and eclampsia high blood pressure is registered. Neurological examination revealed vision changes and damages of mental function as well as increased reflex activity. Today, brain MRI and CT are considered the most important diagnostic method for the diagnosis and follow-up of patients with PRES [6]. Brain MRI better detects smaller focal parenhim abnormalities than brain CT.The most often neuroradiological finding is relatively symetrical oedema of white cerebral tissue in parieto-occipital regions of both cerebral hemispheres. Gray cerebral tissue is sometimes involved, usually in mild form of disease. Diagnosis of this "cortical" form of PRES is possible by MR FLAIR (Fluid-Attenuated Inversion Recovery) technique [5]. TREATMENT Therapeutic strategy depends on the cause of PRES and clinical picture. Most important are blood pressure regulation (labetalol, nitroprusid, diuretici), control of epileptic attacs (phenytoin), anti-oedema therapy. (Manitol), induction of vaginal delivery in eclampsia and discontinuation of cyclosporin therapy. In most cases there are no neurological manifestations after the 7th day but some studies showed normalization of clinical finding after one year and more.
Methomyl poisoning presenting with decorticate posture and cortical blindness