Author Information
Parihar AS*, Warke HS**, Mayadeo NM***
(* First Year Resident, ** Associate Professor, *** Professor, Department of Obstetrics and Gynecology, Seth G.S. Medical College and K.E.M. Hospital, Mumbai, India.)
Abstract
Migraine is a primary headache disorder. It affects mainly women of the reproductive age group. Migraine is believed to be a neurovascular disorder. Mechanism of migraine starts within the brain and then tends to involve the blood vessels. Pre-eclampsia is a hypertensive disorder of pregnancy. It occurs due to general endothelial dysfunction. Migraine and pre-eclampsia share common pathophysiological characteristics. We present a case of pre-eclampsia in a patient of hemiplegic migraine.
Introduction
Migraine is a recurrent headache disorder. They are more common amongst women, lifetime prevalence estimates around 16-32% with a peak in prevalence in the third and fourth decades of life.[1,2] Preeclampsia, a vascular disorder of pregnancy characterized by hypertension and proteinuria, complicates up to 8% of all pregnancies, and it is a leading cause of maternal morbidity worldwide, particularly in developing countries.[3] Endothelial dysfunction, hypercoagulation and inflammation is common to both pre-eclampsia and migraine.
Migraine has no apparent adverse effects on the outcome of pregnancy in otherwise healthy women.[4] Migraine changes little in the first trimester of pregnancy.[5] During the second and third trimesters, up to 80 per cent of women with migraine will experience fewer attacks compared with the pre-pregnancy state.[6] In the week immediately post partum, headache is common, affecting around 30 to 40 per cent of women.[7] The treatment of migraine should be safe as migraine poses no threat to pregnancy. Paracetamol is the drug of choice for mild to moderate pain in pregnancy and lactation. Aspirin and NSAIDs are safe for first and second trimesters of pregnancy but should be avoided near term and dihydroergotamine is contraindicated during pregnancy and lactation.
Case Report
A 33 year old primigravida 37 weeks and 6 days of gestation came with complaints of pain in abdomen. She was a known case of hemiplegic migraine with recurrent transient ischemic attacks. In 1994, she had a road traffic accident following which she was unconscious for less than 5 minutes. Contused lacerated wound was sutured in the frontal region. Three years later, she had history of persistent severe headache followed by left sided hemiparesis (right handed) and tingling and numbness over the left hand for few minutes. She had no history of diplopia, dysphagia or deviation of the face. MR angiography was done which was suggestive of hypoplastic A1 segment of right anterior cerebral artery. A 2D Echo was done. It was within normal limits. ANA, anti- dsDNA and thrombophilia profile was negative. She was started on tablet Aspirin 75 mg once a day. She took the above medications for 3 years and then stopped voluntarily. Since then she had intermittent complaints of headache with 4 episodes of hemiplegia which were managed conservatively. Last episode occurred in May 2016.
She was registered in our tertiary care center in the 10th week of gestation. She had regular ANC visits and received calcium, hematinics and 2 doses of injection tetanus toxoid. No episodes of migraine occurred during ANC period. She was diagnosed to be hypothyroid in the fourth month of gestation and was started on oral levothyroxine 25 mcg once a day.
She came with complaints of pain in abdomen at 37 weeks and 6 days of gestation. On examination her general condition was fair, pulse was 90 beats/ minute. Blood pressure (BP) was 130/80 mm of Hg and there was no pedal edema. On per abdominal examination `uterus was 32-34 weeks, cephalic presentation, FHS were 140 beats per minute and uterine activity was 1/10/10. On per vaginal examination she was 1 cm dilated, poorly effaced, station -2 and pelvis was adequate. Urine albumin was trace and knee jerks were normal. There were no premonitory symptoms. During the antenatal visits BP was always normal. Ultrasound (USG) obstetric Doppler was suggestive of single live intrauterine gestation of 33 weeks with fetoplacental insufficiency. Intrapartum monitoring was reassuring. PIH profile was normal. Hb was 11.7 gm %, WBC 4800 cells/ mcl, platelet count of 2.02 lakhs/ cmm. INR was 0.93. SGOT was 25 U/L, SGPT was 11 U/L, Alkaline Phosphatase was 191 U/L, BUN was 11 mg %, creatinine was 1gm%, total protein was 6.1 gm%, and albumin was 3.6 gm%. Neuromedicine opinion was taken. Their advice was to avoid ergots, prostaglandins to be used only if lifesaving with high risk consent whereas oxytocin could be used safely. She complained of leaking per vaginum next day and her BP was 150/90 mm of Hg, urine albumin was +2, and knee jerks were normal. She had no premonitory symptoms. She had uterine activity of 2/10/10 and on per vaginal examination she was 2-2.5 cm dilated, 40% effaced, membranes absent, liquor was not demonstrable. After half an hour, BP rose to 180/110 mm of Hg, urine albumin was +4, knee jerks became brisk but there were no premonitory symptoms. Capsule nifidepine 10 mg was given immediately and then 6 hourly. Injection MgSO4 therapy was started by Pritchart’s regimen. PIH profile and fundus examination was normal. After one hour, BP was 160/100 mm of Hg. She progressed well and delivered a male child of 1.824 Kg, who cried immediately after birth (Apgar 9/10). There was hind water meconium. Post delivery BP was 160/90 mm of Hg, and uterus was well contracted. There was no active vaginal bleeding, knee jerks were brisk, urine albumin was +2. She developed headache two hours post delivery and BP was 160/100 mm of Hg. Tablet Labetalol 100 mg was added; twice daily. Capsule nifidepine 10 mg four times a day was continued. Headache resolved 7 hours after delivery. Knee jerks became normal 6 hours after delivery. PIH profile post delivery was within normal limits. BP monitoring was done and MgSO4 therapy was discontinued 24 hours post delivery. On day 4 postpartum nifidepine was stopped and she was started on nifidepine retard 20 mg twice daily. She was discharged on day 6 with BP of 130/90 mm of Hg.
Discussion
Preeclampsia is a disorder in pregnancy characterized by onset of high blood pressure and often a significant amount of protein in the urine. The condition begins after 20 weeks of gestation. Pre-eclampsia is thought to result due to abnormal placentation. Abnormal development of placenta leads to poor placental perfusion. This results in oxidative stress, hypoxia and the release of factors that promote endothelial dysfunction and inflammation.
Hemiplegic migraine is a rare type of migraine headache, which is associated with temporary paralysis on one side of the body. Three genes are known to be associated with hemiplegic migraine-CACNA1A,[8] ATP1A2,[9] SCN1A.[10] Atleast two attacks of migraine with aura, weakness, and vision/ speech/ language symptoms are required for the diagnosis of hemiplegic migraine. These symptoms should not persist after headache improves.
Recent studies have shown that pre-eclampsia is common in women with history of migraine headache as both are vascular phenomenon.[11,12,13]
Since migraine poses no threat to pregnancy, it is particularly important to ensure that drugs used for treatment of this condition are safe. Prostaglandins and diethylergotamine are to be avoided during pregnancy and delivery. Prostaglandins can lead to intracranial headache and precipitate migraine and thus should be avoided. Oxytocin can be used for augmentation of labor.
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Citation
Parihar AS, Warke HS, Mayadeo NM. Preeclampsia In A Patient Of Hemiplegic Migraine. JPGO 2017. Volume 4 No.9. Available from: http://www.jpgo.org/2017/09/preeclampsia-in-patient-of-hemiplegic.html