Author Information
Shah A*, Chauhan AR**.
(* Second Year Resident, ** Professor, Department of Obstetrics and Gynecology, Seth G.S. Medical College and K.E.M. Hospital, Mumbai, India.)
Abstract
Hemiparesis is unilateral paresis i.e. weakness of the entire right or left side of the body. Ischemic strokes are rare in pregnancy and may present in a setting of common causes like smoking or hypertension, or rarer causes such as postpartum cardiomyopathy, coagulopathies or vasculopathy. A 1955 study in Minnesota USA reported an incidence of 3.5 ischemic strokes per 100000 population.[1] We present a case of sudden onset hemiparesis without any previous medical illness in a pregnant patient, where other causes of hemiparesis were ruled out.
Case Report
26 years, married since 6 years, G3P2L2, 32 weeks of gestation, presented to the emergency room of our tertiary care center with sudden onset right-sided weakness and headache. She had no history of vomiting, altered sensorium, convulsions or loss of consciousness. Past medical and surgical history was not contributory. Her previous obstetric history was not significant; she had previous two uneventful pregnancies with full term normal deliveries.
On examination, the patient was conscious and oriented. Her pulse was 98 beats per minute and blood pressure was126/ 86 mm of Hg. Obstetric evaluation was unremarkable. Eye movements were normal and there was no evident facial asymmetry. Fundus examination was also normal; there was no evidence of papilledema. There were no signs and symptoms suggestive of arthritis, skin changes (malar rash) or renal involvement. Thorough neurological examination revealed:
On examination, the patient was conscious and oriented. Her pulse was 98 beats per minute and blood pressure was126/ 86 mm of Hg. Obstetric evaluation was unremarkable. Eye movements were normal and there was no evident facial asymmetry. Fundus examination was also normal; there was no evidence of papilledema. There were no signs and symptoms suggestive of arthritis, skin changes (malar rash) or renal involvement. Thorough neurological examination revealed:
Right
|
Left
|
|
Power Upper Limb
|
3
|
5
|
Power Lower Limb
|
3
|
5
|
Tone
|
||
Plantar Reflex
|
Increased
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Decreased
|
Patient was admitted and investigated. Carotid artery Doppler examination revealed normal findings. However magnetic resonance imaging (MRI) of the brain was suggestive of acute non-hemorrhagic infarct in the left posterior communicating artery territory (PCA). MR angiography revealed occlusion of the left PCA along with an aberrant right subclavian artery. Left PCA was not visualized beyond the P2 segment.
To rule out possible causes of stroke in young adults like autoimmune factors, atherosclerosis, hematological and cardiac disorders, the patient was fully investigated. Lipid profile, anti nuclear antibody (ANA), anti double stranded DNA (dsDNA), anti cardiolipin antibody (ACLA), anti phospholipid antibody (APLA), β2 glycoprotein and homocysteine levels were advised; all were negative except ANA which was weakly positive (1:80) +4, fine speckled + cytoplasmic. Complement studies (C3, C4) were also normal. Neurology and rheumatology opinions were sought; they advised medical line of management with no neurological intervention; patient was started on tab aspirin 150 mg and tab atorvastatin 40 mg daily along with daily physiotherapy. Though lipid profile was normal, atorvastatin was initiated empirically as a plaque stabilizer. Thorough cardiac evaluation was also done including 2D- echocardiography which was normal with an ejection fraction of 60 %. Routine antenatal investigations and USG were normal. During the course of her admission, fetal heart sounds were regularly auscultated and there was no adverse pregnancy event.
The patient recovered spontaneously over the course of two weeks and was discharged with power of 5/5. She followed up regularly in the antenatal clinic and had no complaints. She presented at 38 weeks’ of gestation in active labor, and had an uneventful full term normal delivery. Postnatal neurological examination revealed no abnormality. Mother and baby were discharged on the fourth postnatal day.
To rule out possible causes of stroke in young adults like autoimmune factors, atherosclerosis, hematological and cardiac disorders, the patient was fully investigated. Lipid profile, anti nuclear antibody (ANA), anti double stranded DNA (dsDNA), anti cardiolipin antibody (ACLA), anti phospholipid antibody (APLA), β2 glycoprotein and homocysteine levels were advised; all were negative except ANA which was weakly positive (1:80) +4, fine speckled + cytoplasmic. Complement studies (C3, C4) were also normal. Neurology and rheumatology opinions were sought; they advised medical line of management with no neurological intervention; patient was started on tab aspirin 150 mg and tab atorvastatin 40 mg daily along with daily physiotherapy. Though lipid profile was normal, atorvastatin was initiated empirically as a plaque stabilizer. Thorough cardiac evaluation was also done including 2D- echocardiography which was normal with an ejection fraction of 60 %. Routine antenatal investigations and USG were normal. During the course of her admission, fetal heart sounds were regularly auscultated and there was no adverse pregnancy event.
The patient recovered spontaneously over the course of two weeks and was discharged with power of 5/5. She followed up regularly in the antenatal clinic and had no complaints. She presented at 38 weeks’ of gestation in active labor, and had an uneventful full term normal delivery. Postnatal neurological examination revealed no abnormality. Mother and baby were discharged on the fourth postnatal day.
Discussion
Stroke associated with pregnancy is a recognized entity, wherein pregnancy itself may be responsible for the increased incidence. Stroke related to pregnancy is associated with significant morbidity and mortality. The incidence during pregnancy was reported to be 5 infarctions per 100,000 pregnancies in Glasgow, Scotland.[2] Although the risk of pregnancy-related stroke is reported to be higher among women aged 35 years and older, ischemic subtype has been associated with a younger maternal age.[3] Pregnancy specific causes of ischemic stroke include preeclampsia, eclampsia, amniotic fluid embolism, peripartum cardiomyopathy, postpartum cerebral angiopathy and choriocarcinoma.[4] A study by Bremme concluded that most arterial strokes present in the third trimester and puerperium.[5] The physiological adaptations in the cardiovascular and coagulation systems in pregnancy, which are more significant around delivery and in the peurperium, are likely to contribute to the increased risk of an ischemic stroke.[4] Due to the hypercoagulable state in pregnancy, the risk of venous stasis and consequently of thromboembolic events increases. Modifications of hemostatic factors during pregnancy are: a) an increase in procoagulant factors like Fibrinogen (Factor I), von Willebrand factor, Factors V, VII, VIII, IX, X, XII, XIII, fibrinolytic factors like plasminogen activator inhibitor 1 and 2 (PAI-1, PAI-2); b) decrease in coagulation inhibitors like protein S; c) increase in other factors like prothrombin fragment 1+2, thrombin-antithrombin complex and D-dimer.[6]
In the case presented above the patient spontaneously developed hemiparesis. As per the investigations no significant cause could be found. ANA 1:80 titer is not significant enough to cause cerebral infarction; all other reports were within normal limits. Thus in the above case we can consider pregnancy itself to be an independent principal factor and the primary cause of ischemic stroke.[6]
In the case presented above the patient spontaneously developed hemiparesis. As per the investigations no significant cause could be found. ANA 1:80 titer is not significant enough to cause cerebral infarction; all other reports were within normal limits. Thus in the above case we can consider pregnancy itself to be an independent principal factor and the primary cause of ischemic stroke.[6]
References
- Wiebers DO, Whisnant JP. The incidence of stroke among pregnant women in Rochester, Minn, 1955 through 1979. JAMA. 1985; 254(21): 3055–3057.
- Cross JN, Castro PO, Jennett WB. Cerebral strokes associated with pregnancy and the puerperium. BMJ. 1968; 3: 214–218.
- Kittner SJ, Stern BJ, Feeser BR, Hebel R, Nagey DA, Buchholz DW, et al. Pregnancy and the risk of stroke. N Engl J Med. 1996; 335(11): 768–774.
- Bremme KA. Haemostatic changes in pregnancy. Best Pract Res Clin Haematol. 2003; 16(2): 153–16.
- Jaigobin C, Silver FL. Stroke and Pregnancy. Stroke. 2000; 31(12): 2948–2951.
- Martin PJ, Enevoldson TP, Humphrey PR. Causes of ischemic stroke in the young. Postgrad Med J.1997; 73(885): 8–16.
Shah A, Chauhan AR. Pregnancy The Primary Cause Of Ischemic Stroke. JPGO 2017. Volume 4 No. 1. Available from: http://www.jpgo.org/2017/01/pregnancy-primary-cause-of-ischemic.html