Hypertensive encephalopathy

Eclampsia 2

Renal failure with hypertension

Immunosuppressive agents3 and cytotoxic drugs:-Cyclosporin A, Interferon alfa, Intravenous immunoglobulins, Cisplatin, , Cytarabine Erythropoietin, Tacrolimus

Collagen vascular disorders-e.g. Systemic lupus erythematosus4 etc

Others :- hypercalcemia5, Postdural puncuture and spinal anaesthesia678

Aetiopathogenesis

The exact pathogenesis of the condition is not known. A rapid rise in blood pressure leads to altered autoregulation of cerebral blood flow producing dilatation of cerebral arterioles with opening up of endothelial tight junctions and leakage of plasma and red cells into the extracellular space, producing cerebral oedema. The cerebral white matter is composed of myelinated fibre tracts in a cellular matrix of glial cells, arterioles, and capillaries that makes this structure more susceptible to accumulation of fluid in the extracellular spaces (vasogenic oedema). The posterior circulation is thought to be more susceptible to this type of damage, because there is less sympathetic innervation of the vertebrobasilar vasculature to protect the parenchyma from rapid increases in arterial blood pressure 910. According to another hypothesis, patients with PRES develop vasospasm secondary to sudden and severe rises in blood pressure and ischaemia of brain tissue. Ischaemic damage to brain tissue first produces cytotoxic oedema and then extracellular oedema. However, the reversibility of imaging abnormalities with immediate treatment is not consistent with the hypothesis of vasospasm and cerebral ischaemia.

Most common symptoms are headache, nausea, vomiting, confusion, behavioural changes, changes of conciousness (from somnolencia to stupor), vision disturbances (blurred vision, haemianopsia, cortical blindness) and epileptic manifestations (mostly focal attacks with secondary generalisation). Mental functions are characterised with decreased activity and reactivity, confusion, loss of concentration and mild type of amnesia. Stupor and coma rarely occurred. Multiple seizures are more common than single events. Recently few cases reported in postpartum woman who, developed posterior reversible encephalopathy syndrome after spinal anesthesia and/or complicated by postdural puncture headache678

Brain MRI better detects smaller focal abnormalities than brain CT. The most often neuroradiological finding is relatively symmetrical 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. 11

One of the important differential diagnoses of PRES in pregnancy and post-partum period is cerebral venous thrombosis12 (CVT). Onset of CVT is acute and evolved in days. Usually presented as headaches, seizures, focal neurological deficits (hemiparesis or monoporesis), papilloedema, stupor or coma, evidence of venous thrombosis elsewhere and infrequently hypertensive

The posterior encephalopathy syndrome needs to be recognized promptly. The syndrome is usually reversible within 7days, after controlling the blood pressure. Offending immunosuppressive agents should either be discontinued or the dose should be reduced. Delay in initiating the appropriate treatment may result in permanent damage to the brain. Patients experiencing seizures become seizure free after resolution of imaging abnormalities and do not require chronic antiepileptic treatment. Therapeutic strategy depends on the cause of PRES and clinical picture. Most important are blood pressure regulation (labetalol, nitropruside, diureticis), control of epileptic attacks (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 normalisation of clinical finding after one year and more.