neurology

128Neurology India, 50, June 2002

The Neurology of Eclampsia : Some Observations

A. Chakravarty, S.D. Chakrabarti*

Department of NeurologyVivekananda Institute of Medical Sciences and Medical College*

Calcutta -700 006, India

Summary

Nineteen patients admitted with diagnosis of eclampsia in a large general hospital between1996 - 1999, were analyzed. Eight patients were referred to neurologists for assessment andmanagement. All these patients had recurrent generalized seizures. Five patients developedvisual disturbance. Neuroimaging (CT and/or MRI) revealed symmetrical occipital lesionsin all. One patient had a large pontine lesion. Seizure control was achieved in all withintravenous phenytoin. All patients recovered fully without any residual neurologicaldeficit and their radiological brain lesions resolved completely, in all except one case. Theneurological manifestations and neuroimaging features in cases of eclampsia have beenreviewed. A brief note on the pathogenesis of the cerebral lesions is included and thecontroversial aspect of seizure control in eclampsia highlighted.

Key words : Eclampsia, Neurologic manifestations, Visual loss, Seizure control.

Neurol India, 2002; 50 : 128-135

Introduction

Pre-eclampsia is a complex disorder characterized bypregnancy induced hypertension, proteinuria andedema occurring after twenty weeks of pregnancy.The clinical presentation varies in severity andmultiorgan involvement is common. Themanifestations may include pulmonary edema,oliguria, disseminated intravascular coagulopathy andhepatic hemorrhages. Neurologic manifestations ofpre-eclampsia include headache, confusion,hyperreflexia, visual hallucinations and blindness.Eclampsia has been defined as the occurrence ofconvulsion, not caused by any coincidental neurologicdisease (e.g. epilepsy) in a woman whose condition

also meets the criteria for pre-eclampsia.1 Pre-eclampsia, in effect, becomes eclampsia with theadvent of a seizure or coma and would be brieflyhighlighted later. The cerebral lesions causingneurologic features, including seizures, presumablyoccur as a result of cerebral circulatory dysregulationand neuropathologic studies support this conjecture.To the best of the authors knowledge, nocomprehensive study on the neurological andneuroradiological aspect of eclampsia has beenpublished in the current neurologic literature in India.Only a solitary case report highlighting reversible MRimaging features was reported in 1997.2 The presentreport describes the principal authors (AC)experience with eight patients of eclampsia,highlighting clinical neurologic aspects, neuro-radiological features and seizure control measuresadopted, along with a brief review of the subject.

Correspondence to : Dr. A. Chakravarty, 59, Beadon Street,Calcutta - 700 006, India.E-mail : [email protected]

VIEWS AND REVIEWS

Material and Methods

During the period of study, a total of 19 patients wereadmitted with diagnosis of eclampsia fulfilling thecriteria mentioned earlier. Total obstetric admissionsin the hospital during the same period had been20,273 and total confinements were 15,411. Of these,eight cases were referred to the neurological services,principally because of recurrent seizures, prolongedalteration of sensorium, severe headache and visualloss in varying combinations. The patients wereevaluated clinically several times till full recovery andwere later followed up in OPD. All but one had initialCT scan of brain and three patients (including the onewho did not have CT) had MR brain imaging at theinitial stage. During follow-up, imaging studies wererepeated between three to six months of discharge.

Results

General : The age range of the subjects varied from 24to 30 years. Six were primigravida and two secondgravida. None had prior history of hypertension, renaldisease, diabetes or seizure disorder. All patients hadbeen attending the antenatal clinic of the hospital andnone except one showed any clinical evidence of pre-eclampsia upto the time of last clinic visit (3 to 4weeks prior to admission). All were subsequentlyadmitted with history of having had either a seizure oraltered sensorium. Blood pressure on admission wasover 140 mm Hg systolic and 100 mm Hg diastolic inall, with pedal edema and proteinuria. One patient hadspontaneous expulsion of a dead fetus and sevenunderwent emergency cesarean section with onlythree live births.

Neurologic evaluation : All patients had generalizedtonic clonic recurrent seizures (3 or more over 24hours). The seizures started prepartum in 5 andpostpartum in 3 cases. At initial neurologic evaluation,all were at varying stages of altered sensorium (GCS8-10) without any localizing sign but withhyperreflexia and bilateral extensor plantars. Sixpatients complained of severe holocranial headache atsome stage of their illness and five complained ofblurred vision either prior to losing consciousness orafter improvement in level of consciousness. Thevisual problem in all appeared to be cortical in nature.Fundus examination revealed retinal arterial spasm inall eight patients. Four patients had diffuse retinaledema but no hemorrhages. None had any meningealsign. Improvement in sensorium started 36-48 hoursafter seizure control and all were fully conscious after72 hours. Blurred vision persisted for 5-7 days afteradmission in 5 patients who had this symptom.

Neurologic management : All patients were prescribedmethyldopa by their obstetricians for control ofhypertension and one needed intravenous infusion ofglyceryl trinitrate. Obstetricians also put all patientson diazepam infusion (20-30 mg over 12 hrs.) butseizures persisted inspite of this. No patient was givenmagnesium sulphate. Seizure control in 8 patientsreferred to the neurologists was achieved withintravenous phenytoin, using a similar protocol aspracticed in status epilepticus but at a slower rate.Phenytoin 15 mg/kg was given by infusion pump over60 minutes and was followed by bolus injections of100 mg intravenous every 6 hours for 48 hours andthereafter oral therapy was instituted. No patient hadbreakthrough seizures. In addition, intravenousinfusion of mannitol was given intermittently in thefirst 48 hours. At the time of discharge (10-14 daysafter admission), no patient had any residualneurologic sign or symptom. Oral phenytoin wascontinued for 3 months after discharge.

Neuroradiological evaluation : CT scan of brain wasdone within 48 hours after admission in sevenpatients. All showed bilateral symmetrical occipitalhypodense lesions involving more of white matterthan the grey. In five patients, lesions extended to theparieto-temporal areas of both sides (Fig. 1) but neverextended anteriorly beyond the sylvian fissure. Nolesions could be detected in the brain stem or in thebasal ganglionic regions. Areas of hyperdensity withinthe hypodense areas (suggesting hemorrhages) wereseen in 3 patients. MR study could be done early in 3cases only, including one case where CT was notdone. The lesions corroborated well with the CTfindings. Hypointense lesions on T1WI andhyperintense lesions on T2WI and proton/flaresequences were seen symmetrically in both occipitalregions with some extension in the parietotemporalregions (Fig. 2). The lesion involved more of whitethan grey matter. In one case, small hyperintenselesions were seen on T2WI and proton density imagesin posterior limb of internal capsule, both thalami andsubcortical white matter of right frontal lobe. Thepons also revealed hyperintense lesion on T2WI(Fig. 3) and proton density images, with the largerlesion in right paramedian aspect. The latter lesionmost likely represented an area of hemorrhage. MRangiographic studies were not done in any patient.

Follow up neuroradiological evaluation : Sevenpatients had follow up contrast CT scan of brain, 3-4months after discharge. Neurologically, all werenormal with normal blood pressure, without anymedication. The repeat scan did not show anyevidence of the lesions detected earlier (Fig. 4). This

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Neurology of Eclampsia

Neurology India, 50, June 2002

suggested that the earlier hypodense lesions weremost likely areas of edema rather than infarction. Thehemorrhagic areas also resolved completely. Thesingle case with pontine lesion had a repeat MR scan6 months later. While all the cerebral lesions

completely resolved, a tiny area of hypointensity onT1WI (Fig. 5) and hyperintensity in T2WI persisted inthe pons, suggesting presence of either a small infarctor a posthemorrhagic gliotic area. She was clinicallyasymptomatic and had no residual neurologic signs.

Discussion

Pathogenesis and cerebral pathology : Pre-eclampsia/eclampsia is now considered to beprimarily a placental disorder. Both poor placentationas well as hyper-placentosis (e.g. twins/molarpregnancies) are associated with this condition.3 It isbelieved that either an unknown factor (factor X, assome call it) or villous debris from the malformedplacenta manage to reach the maternal circulation,eliciting an immunological response from themothers system.4 Other variables like dietary factors,namely protein and caloric deficiency, lack ofessential fatty acids, deficiency of magnesium,calcium, zinc and an excess of sodium as well asgenetic factors like abnormal alleles for the genes ofTNF-, angiotensinogen, factor V and nitric oxidesynthase (NOS) predispose to this event.5-8 Thematernal response is primarily immunological withincreased activation and functional abnormalities ofmaternal neutrophils, high circulating levels of thecell-adhesion molecule VCAM-1 (which helps tomediate neutrophil activity) and occurrence ofimmune-complexes in the placenta, maternal serum

130Neurology India, 50, June 2002

Chakravarty and Chakrabarti

Fig.1 : CT scan showing symmetrical hypodense lesions inthe parieto-occipital regions in an eclamptic patient.

Fig 2 : MR Imaging (T2WI) showing symmetrical occipitalhyperintense lesions (Patient SS).

Fig. 3 : MRI (T2WI) showing pontine lesion in patient SS.

and various organs.9,10 The effect of this maternalresponse is widespread cellular dysfunction withmulti-system involvement.11 There is endothelialdamage with increased capillary permeability, raisedfibronectin levels and electron microscopic evidenceof damaged endothelium.12,13 Coagulationabnormalities occur, caused by increased activationand consumption of platelets, low antithrombin IIIlevels, abnormal prostaglandin metabolism and in afew cases, florid DIC.13,14 Endocrine anomaliesinclude activation of the renin-angiotensin-aldosterone axis, abnormal catecholamines andabnormalities in progesterone metabolism.13 Thesepathophysiological changes lead to hypertension,edema, proteinuria, bleeding tendencies, renaldysfunction, liver damage and the neurologicalabnormalities.

Neurological effects of pre-eclampsia/eclampsia canbe antepartum or post-partum, the latter being morecommon.15 These are due to irregularities in theautoregulation of cerebral circulation.16 Disruption ofthe blood-brain barrier occurs due to both thehypertension-induced capillary damage and theimmune-mediated endothelial dysfunction. This leadsto extravasation of red cells and plasma proteins intoperivascular space causing cerebral edema.17 Cerebralvasospasm, produced by a combination of reaction tohypertension, prostaglandin deficiency, defects in thee-NOS gene (coding for nitric oxide systhase) andendothelial damage, play an important role, producingischemia and infarction in the brain tissue.18-19 Theimpaired blood coagulation system and the

abnormalities and deficiency of platelets predispose tointra-cranial bleeds.20 Thus, a varied picture ofcerebral pathology, showing evidences of cerebraledema, micro-infarcts, cortical petechiae andpericapillary hemorrhages is observed in the brains ofpatients with pre-eclampsia or eclampsia, whichclinically manifest as headache, visual disturbances,confusion and seizures.

Neurologic features : The hallmark of eclampsia isonset of seizures, which may be focal motor orgeneralised tonic clonic. As indicated earlier, theymay appear before, during or after childbirth butusually within first 24 hours postpartum. Delayedonset of seizures has also been reported.21 In thepresent series, however, seizure onset was moreprepartum (5 cases) than postpartum (3 cases). Thisneed not necessarily represent the general pattern asonly selected cases referred to neurologists wereincluded. All had generalised tonic clonic seizures.None of the patients had any focal neurologic deficitthough all had bilateral symmetrical pyramidal signs.Vision related symptoms are well recognised ineclampsia.22 Retinal arterial dilatation, papilledema,angiospasm, occlusion of central artery, hemorrhages,exudates and edema - all have been described. Whileall 8 cases in the present series had angiospam and 4had retinal edema, none had papilledema,hemorrhages or exudates on fundoscopy. The blurredvision complained by 5 subjects was thought to be ofcentral origin and was corroborated with imagingfeatures of bilateral occipital involvement. Affectionof the posterior part of visual pathway has been wellrecognized.22-26 The visual cortex was affected by

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Fig 5 : Follow up MR (T1WI) showing tiny residual pontinelesion in patient SS.Fig. 4 : Resolution of CT lesions in follow up scan (patient

AD).

132

edema, micro-infarctions and microhemorrhages in allpatients in the present series. Visual symptoms, ofcourse, normalised in all in a few days time.

Neuroimaging in severe pre-eclampsia/eclampsia :The pathological features described earlier werereflected in the neuroimaging features seen in thepresent series. CT scan in eclampsia patients revealeda wide spectrum of findings ranging from normal tofocal occipital or more widespread lesions which werehypodense and non-enhancing and were ascribed tolocalised edema.27 Repeat CT has shown partial orcomplete resolution within 2 weeks. Cerebralhemorrhage including subarachnoid hemorrhage hasalso been described.28 A number of MR studiesconfirm the presence of hyperintense lesions on T2WIin eclampsia.29-31 Commonly, these have been foundin the posterior circulation territory with involvementof cortical and subcortical white matter in occipitaland posterior parietal lobes. These lesions arebilaterally symmetrical and follow the gyri in aserpentine manner. Lesions have been described in thedeep white matter and basal ganglionic areas, whichare hyperintense in long TR images but occasionallyalso in T1WI, suggesting microhemorrhages. Almostall such lesions were transient, suggesting thedevelopment of edema due to failure of autoregulatorymechanism or transient vasospasm. Reversiblecerebral vasospasm by MR angiography has recentlybeen described in pre-eclampsia.32 On the other hand,cerebral blood flow measured by SPECT in onepatient during an attack of visual disturbance showedincreased blood flow in the occipital cortex.33 Thecombination of vasodilatation and vasospams in thepathogenesis of ecalmpsia has already beencommented upon in the section on pathogenesis.

CT and MRI findings in the present seriescorroborated with those described earlier. On CTscanning, the lesions never extended anteriorly, butfrontal white matter lesions could be detected on MRI.Similarly, central grey matter lesions were moreapparent on MRI than on CT scan. The observation ofpontine lesion on MRI in one subject, though shenever developed any classical pontine clinicalsyndrome, was interesting. Such brain stem lesionshave not been highlighted in earlier studies. This wasalso the only case in the present series where a tinyresidual abnormality presisted on repeat scanningafter 6 monhts. MRI, indeed, gives more accurateassessment of the degree of CNS involvement ineclampsia.

Seizure control in eclampsia : All eight patients in the

present series had been treated with intravenousphenytoin (PHT) with initial loading dosage, followedby intermittent intravenous bolus doses over next 48hours. No doubt, some eyebrows would be raised inthis regard especially among obstetric colleagues.Although five of the eight patients in this series hadantepartum onset of seizure, by the time they wereseen by the neurologists, one already had spontaneousexpulsion of the fetus and the rest 7 had emergencycesarean section done. Attempt at initial seizurecontrol was made by the obstetricians withintravenous diazepam and no patients receivedmagnesium sulfate (MgSO4). PHT was resorted tolater after neurologic referral, either for control ofongoing seizure or prevention of further seizure. PHTproved to be successful in this regard and no maternalcomplications in the postpartum period could beattributed to PHT therapy. There is a lot of controversyin the literature and in medical practice about thechoice of anticonvulsants in eclampsia. An idealanticonvulsant should have good seizure control,should not affect uterine function, should loweroverall maternal morbidity and mortality and shouldnot affect fetal morbidity or mortality, if usedantepartum. It is also important to consider whetherthe drug has been used during the stage of pre-eclamspia to prevent onset of seizures or duringeclamptic phase to control seizures. These issues needto be carefully judged and remembered whileexamining the results of several trials done in recenttimes. Rapid control of a single seizure episode cancertainly be achieved with a bolus dose of diazepam.The efficacy of intravenous infusion in preventingseizure recurrence is doubtful and repeated bolusinjections not usually practiced in pregnancy for itspossible adverse effects on the fetus e.g. hypotonia,hypothermia, apnea etc.34 The need, therefore, is for alonger acting drug and MgSO4 and PHT seem to bethe main contenders.

Most obstetricians all over the world probably still useMgSO4 both in pre-eclampsia to prevent seizures andin eclampsia to control and prevent recurrence ofseizures. Mechanism of action is not clearly known.This may involve blockade of NMDA receptorsinvolved in seizure genesis35 or calcium channelblocking, preventing cerebral vasospasm.36 MgSO4,in experimental seizure models, does not appear tohave a very significant anticonvulsant action37,38 andcertainly is not a standard anticonvulsant for treatmentof epileptic seizures. A closer look at available recentliterature would however suggest, that more emphasishas been given to prevention of seizures in pre-



eclampsia, with MgSO4, than actual rapid seizurecontrol and preventation of recurrent seizures. Thereare also problems associated with MgSO4 includinglocal irritant effect, loss of patellar reflex (a commonsign used by many obstericians in this country tocheck for toxicity), lethargy and depression in motherand newborn and recurrence/refractoriness of seizuresin many.39,40 From neurologists stand point, rapidcontrol of seizures and preventing its recurrence needsto be achieved with a time tested properanticonvulsant e.g. phenytoin. This view is graduallybeing shared by obstetricians as well. The efficacy ofPHT in controlling eclamptic seizure was probablyfirst reported by Slater et al in 198741 andsubsequently several reports were published in thefirst half of 1990s.42 Some early reports on break-through seizures were probably related to lowtherapeutic level achieved. The dosage schedule issimilar to that used in status epilepticus, but given at aslower rate, preferably with checking of serum levelsfrom time to time (difficult to perform in our settingand not done in any case in the present series). Otherdosage regimes have also been suggested. A singlehigh dose intravenous PHT (900 mg) had been usedwith success in patients with eclampsia, given onadmission, with no untoward effects in the mother andthe neonate.43 A study in a premier obstetric hospitalin U.K. compared different loading doses of PHT andpreferred a dosage of 15 mg/kg and stressed the needto follow it up with boosting doses to maintaintherapeutic plasma level.44 Occasionally, however,seizures recurred even with serum PHT level wellwithin the therapeutic range.

Quite a few controlled trials in recent times have triedto establish the efficacy MgSO4 over PHT. Lucas etal45 randomised over 1000 patients with pregnancyinduced hypertension and pre-eclampsia to receiveeither drug and concluded that MgSO4 is superior toPHT in preventing eclampsia (the two groups beingcomparable regarding the risk). Naidu et al46 usedtranscranial doppler (TCD) to assess degree ofcerebral vasospasm in eclamptic patients receivingeither MgSO4 or PHT. MgSO4 significantly reducedthe pulsatality index and mean flow velocitycompared to PHT in the middle cerebral artery andthus appeared to be a better drug to reverse cerebralvasospasm, a major factor implicated in thepathogenesis of eclampsia. Chien et al47 tried toestablish the efficacy of MgSO4 from retrospectiveanalysis of randomised trials through online search ofMedline database between 1966-1995. 1743 patients

with pre-eclampsia included in nine randomised trialswere assessed for seizure activity and maternal death.On both the scores, MgSO4 was favoured as comparedto PHT and the authors concluded MgSO4 to be asuperior drug compared to PHT in preventing seizuresin eclampsia and seizure prophylaxis in pre-eclampsia. A recent Indian study48 randomlyallocated 50 pregnant women with eclampsia toreceive either MgSO4 or PHT. Women treated withPHT had a higher incidence of recurrent seizures butperinatal mortality and morbidity and maternalmortality were comparable in both groups. The mostrecent data is available from the Cochrane databasesystem review.49 Four well controlled trialsencompassing 823 women were included. MgSO4 (ascompared with PHT) was associated with a substantialreduction of recurrence of seizures, a favourable trendin maternal mortality, reduction in risk of pneumonia,ventilation and admission in ICU of mother andadmission of babies in special care units and reductionin perinatal mortality. All these favoured use ofMgSO4 compared to PHT.

A close look at the forementioned trials would bringforth a few important points. In the eye of aneurologist, PHT is a proper well-tested anti-convulsant and not MgSO4. But the latter appears tohave some disease modifying effect in the setting oftoxemia of pregnancy. Hence, in a patient admittedwith seizures, ideal treatment would be control of theseizures first using a loading dose of properanticonvulsant like PHT and supplementary therapywith MgSO4 may provide added benefit in preventingrecurrence of seizures and inproving maternal andperinatal mortality or morbidity. On the other hand, inpatients admitted with severe pregnancy inducedhypertension and pre-eclampsia, MgSO4 wouldundoubtedly be the drug of choice for preventingonset of seizures and reducing morbidity andmortality. In the present series, PHT was used in allpatients, as all presented with recurrent seizures andrapid seizure control deemed mandatory.Furthermore, as neurologists, we were moreaccustomed to use PHT than MgSO4. No clearguideline is given anywhere for the duration ofanticonvulsant therapy in eclampsia. In the presentseries, oral anticonvulsants were continued for 3months postpartum, based only on the observationthat the radiological resolution of the CNS lesions(discussed earlier) occured in about 3 months. It is feltthat management of eclampsia and severe pre-eclampsia must be made through close liaisonbetween the obstetricians and the neurologists.

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Accepted for publication : 13th September, 2000.

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