In one line
Two questions decide management: is this new neurology a pre-eclampsia complication or a primary CNS event?, and how do I keep a woman with epilepsy seizure-free on the least teratogenic regimen? Everything else (stroke, headache, myasthenia, IIH) is pattern recognition layered on those two reflexes.
This chapter assumes the groundwork in hypertension and pre-eclampsia basics; it covers the discrimination between mimics, the subtype-specific regimens and how they differ, the primary-literature appraisal, and the judgement calls.
Assessment
The seizure / new-deficit triage. Any first seizure, focal deficit or thunderclap headache after 20 weeks is eclampsia until proven otherwise — check BP, proteinuria and platelets before reaching for a CT. But eclampsia does not explain a lateralising deficit, a depressed conscious level that does not recover post-ictally, focal signs, or seizures before 20 weeks; those mandate neuroimaging. Do not let "it must be eclampsia" anchor you past a cerebral venous sinus thrombosis (CVST) or intracerebral haemorrhage — maternal stroke is now a leading direct cause of maternal death in high-income audits and is repeatedly missed as "atypical pre-eclampsia."
Five conditions sit on the same eclampsia look-alike spectrum, each with a different mechanism and a different treatment. The difficulty is not recognising textbook eclampsia; it is parsing the woman who almost fits.
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Eclampsia / PRES (posterior reversible encephalopathy syndrome). Mechanism: failure of cerebral autoregulation under acute hypertension → hyperperfusion, blood–brain-barrier breakdown and vasogenic oedema, classically parieto-occipital. The clinical consequence is cortical blindness, seizures and headache that recover as BP is controlled and the placenta is removed. PRES on MRI (bilateral posterior white-matter oedema, restricted-diffusion-negative) is the radiological signature of pre-eclampsia with severe features and resolves — if it does not resolve, question the diagnosis.
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Reversible cerebral vasoconstriction syndrome (RCVS) / postpartum angiopathy. This is the mimic that most often catches the clinician who reflexively gives magnesium. Mechanism: transient dysregulation of cerebral arterial tone → segmental, multifocal vasoconstriction ("string-of-beads" on angiography), typically in the first days to two weeks postpartum, often after an uncomplicated delivery. The distinguishing feature is recurrent thunderclap headache (maximal in under a minute) rather than the building headache of pre-eclampsia, and crucially the angiogenic-factor imbalance of eclampsia is not present. It can co-exist with PRES and can cause both ischaemic infarction and convexity subarachnoid haemorrhage. Vasoconstriction is the lesion, so calcium-channel blockade (nimodipine) is the directed treatment and serotonergic/vasoconstrictor drugs (ergometrine, triptans, SSRIs, sympathomimetics) must be avoided — the opposite reflex to "she's postpartum, give ergometrine."
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CVST. Mechanism: pregnancy/puerperium is a hypercoagulable, stasis-prone state (the puerperium especially) → dural-sinus thrombosis → venous hypertension → headache (often positional, worse lying flat), seizures, focal deficits and venous (often haemorrhagic) infarction that does not respect arterial territories. Because the problem is venous occlusion, the treatment is anticoagulation even in the presence of haemorrhagic venous infarction — counter-intuitive, and the most common error is withholding heparin because "there's blood on the scan."
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Arterial ischaemic / haemorrhagic stroke. Mechanism varies (paradoxical embolism, cardio-embolism, dissection, and in the pre-eclamptic the haemorrhagic stroke of uncontrolled severe hypertension). A lateralising deficit or a focal seizure is arterial/structural until imaged, and reperfusion is time-critical.
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Eclampsia in a woman who also has primary epilepsy. Do not assume a known epileptic's late-pregnancy seizure is "just her epilepsy" — superimposed pre-eclampsia is common, so check BP, platelets and urate in every peripartum seizure regardless of the past history.
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Imaging is not contraindicated. Non-contrast CT delivers a negligible fetal dose; MRI/MRV is first-line for suspected CVST and posterior circulation events; CT venography or contrast is justified when it changes management. Withholding imaging to "protect the fetus" is the classic medicolegal trap.
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Headache red flags: thunderclap onset, postural component (worse lying down suggests raised ICP/CVST; worse upright after a dural puncture suggests post-dural-puncture headache), new aura, fever/neck stiffness, papilloedema, any focal sign, or seizure. A migraine diagnosis in pregnancy is one of exclusion — first-ever "migraine with aura" in the third trimester is a deficit until imaged. The differential of the peripartum thunderclap headache is RCVS, CVST, subarachnoid haemorrhage and pituitary apoplexy (Sheehan's in the haemorrhaged postpartum pituitary) — not migraine.
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Epilepsy booking review: seizure type and frequency, current antiseizure medication (ASM) and dose, last seizure, adherence, contraception/folate history, and whether the woman of childbearing potential is on valproate — which should already have been switched preconception, not in the booking clinic.
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Investigations: platelets, urate, LFTs and urine PCR to stage pre-eclampsia; ASM levels matter most for lamotrigine (clearance rises ≥65% by the first trimester and up to ~3-fold by late pregnancy → breakthrough seizures); lumbar puncture (opening pressure) for suspected idiopathic intracranial hypertension (IIH) or to exclude SAH/meningitis once mass effect is excluded.
Severity stratification and the judgement calls. Stratification turns less on a score than on three trajectory questions: (1) Is the conscious level recovering? A Glasgow Coma Scale that does not climb back after a post-ictal period is a structural lesion until proven otherwise. (2) Is the deficit focal or global? Global cerebral irritability fits eclampsia; a hemiparesis, a homonymous field defect or a III-nerve palsy does not. (3) Is the headache positional or thunderclap? — because that single discriminator separates CVST and RCVS from the pre-eclamptic headache. In epilepsy the stratification is different again: the woman whose seizures cluster, who has had a generalised tonic-clonic seizure in this pregnancy, or whose lamotrigine level has fallen below her preconception therapeutic level is the one at risk of status and SUDEP, and is the one to admit and re-titrate.
This builds on hypertension and pre-eclampsia basics; the discipline is not defaulting to that diagnosis.
Management
Immediate — the acute seizure / acute stroke.
| Scenario | First action |
|---|---|
| Seizure + features of pre-eclampsia | Treat as eclampsia: magnesium sulphate (SA NDoH loading 4 g IV over 10–20 min + 1 g/h IV, or Pritchard IM regimen where no pump), control BP, deliver |
| Status epilepticus in known epilepsy | IV benzodiazepine (lorazepam/diazepam) → IV levetiracetam or phenytoin; protect airway, left lateral, treat hypoglycaemia |
| Acute ischaemic stroke | Time-critical neurology referral; pregnancy is not an absolute contraindication to thrombolysis or thrombectomy — decide by risk/benefit, not gestation |
| Suspected CVST | Therapeutic-dose LMWH, even in the presence of venous haemorrhagic infarction; neurosurgery only for impending herniation |
The named magnesium regimens and exactly how they differ. Magnesium is the proven agent both for eclampsia treatment and pre-eclampsia seizure prophylaxis; there are three regimens, each making a different trade-off.
