The rationale behind our reporting this case lies in the sequence and unusual nature of events whereby clinically, at the beginning of Posterior Reversible Encephalopathy Syndrome (PRES) there is cortical blindness, radiological finding of bilateral occipital hematoma at the acute phase then its evolution to cortical atrophy in the chronic phase and subsequently the occurrence of late symptomatic occipital lobe epilepsy secondary to vascular sequelae.
Despite the high incidence of eclampsia in Africa [2
], we did not find in the literature any reference on symptomatic occipital lobe epilepsy secondary to this disease which is well described in our context.
In this case, evidence for a PRES were: postpartum eclampsia with encephalopathy and seizures, occipital localization of the lesions on CT-scan and reversibility of the disorders [6
Cortical blindness presented by our patient has been reported in the literature. Cunningham and collaborators have reported 15 women with a reversible cortical blindness related to eclampsia during 14 years [11
], and in the series by Hinchey and collaborators, out of 15 women, 3 had eclampsia, and 9 patients had visual disturbances [6
]. It is unusual that this blindness has an excellent prognosis, with full recovery of visual acuity. From a pathophysiology perspective, the blindness is linked to vasogenic edema and not vasospasm and so its reversibility is linked to the resolution of edema [12
The occipital lobe epilepsy secondary to eclampsia that we found is exceptional. Till date, two patients with occipital lobe epilepsy post eclampsia have been reported [8
] but contrary to our observation, initial brain CT imaging was normal in these two patients as reported by Plazzi and collaborators [8
The pathophysiologic mechanism of irreversible tissue damage during PRES syndrome is not clear in the literature. The irreversible damage that we found in our patient could result from a combination of events including: delay in early treatment, inadequate anti-hypertensive drugs that could worsen the brain damage by hypoperfusion, inadequate or delayed treatment for seizures or status epilepticus [7
The anticonvulsant treatment of choice for the management of PRES secondary to eclampsia, is magnesium sulfate. Indeed, a multicenter trial [15
], including 1680 eclamptic patients showed clearly the superiority of magnesium sulfate compared to diazepam and phenytoin in the prevention of seizures. In addition, its anti-edematous effect, higher than that of mannitol during PRES is known [16
]. Also, a rapid decrease in serum magnesium seems to contemporarily trigger PRES. In the absence of controlled trial, treatment with magnesium sulfate is still elective and in the course of this treatment serum monitoring should be systematically done in cases of PRES. However, the effectiveness of magnesium sulfate in preventing eclampsia in patients with preeclampsia remains controversial [17
The use of magnesium sulfate, however, raises the problem of the choice of antihypertensive drugs. Their association with injectable calcium channel blockers, generally accepted as the treatment of choice for the management of high blood pressure at the acute phase of stroke [18
], involves a risk of aggravation: the effect of calcium channel blockers may be potentiated by magnesium sulfate, then causing a drop in blood pressure with an increase risk of acute brain damage thus, a risk of irreversible sequelae [8
In this case report, an analysis of different stages of the management shows a significant drop in blood pressure (BP) during the acute phase. Indeed, the association of maximum doses of magnesium sulfate and nicardipine resulted in a sharp fall in BP to less than 50% the original figures in less than 6 hours. This potentially damaging attitude is known to aggravate brain lesions, with onset of irreversible damage which potentially could be epileptogenic [7
According to his initial description, PRES classically causes reversible damage. However, patient care is not accurate (delayed diagnosis, inappropriate management of BP and or seizures), irreversible sequelae may alter the course of the disease.
The relationship between hypertensive encephalopathy, PRES and symptomatic epilepsy must be confirmed by longitudinal studies [7