Novel Insights from Clinical Practice Fetal Diagn Ther DOI: 10.1159/000500023 Received: January 8, 2019 Accepted after revision: March 27, 2019 Published online: July 26, 2019 Sonographic Detection of Seizure-Like Activity in Fetuses with Congenital Infection: Report of Three Cases and Review of the Literature Jose Hector Ochoa a Alberto Sosa-Olavarria b Hector Quiroga c Waldo Sepulveda d a DIAGNUS, Prenatal Diagnosis Center, Cordoba, Argentina; b Universidad de Carabobo, Valencia, Venezuela; c Centro Profesional Rosancar, Barquisimeto, Venezuela; d FETALMED, Maternal-Fetal Diagnostic Center, Fetal Imaging Unit, Santiago, Chile Established Facts • Fetal seizure-like activity is a very rare prenatal finding that can be detected by prenatal ultrasound. However, its episodic occurrence prevents it from being recognized on a relatively short-time ultrasound examination. • Any abnormality or insult severe enough impacting on the fetal central nervous system (CNS), such as hypoxic-ischemic encephalopathy, congenital anomalies, and metabolic or genetic disorders, can cause seizure-like activity. • The association between fetal seizures and congenital infections has not been reported. Novel Insights • This report documents the prenatal sonographic detection of seizures in fetuses with proven congenital infection. • The presence of seizure-like activity in fetuses with congenital infection is an additional poor prognostic sign that suggests a severe dysfunction of the CNS. Abstract Fetal seizure is a very rare prenatal finding and associated with an almost invariably poor outcome, the most common causes being hypoxic-ischemic encephalopathy, congenital anomalies of either the central nervous system (CNS) or mus- © 2019 S. Karger AG, Basel E-Mail karger@karger.com www.karger.com/fdt culoskeletal system, and metabolic disorders. The prenatal detection of seizure-like activity in fetuses with congenital infection has not been previously reported. In this report, we describe 3 cases of seizures in fetuses with congenital infection including Zika virus (n = 2) and toxoplasmosis (n = 1). All 3 fetuses had associated CNS abnormalities and the perinatal outcome was uniformly poor. This report suggests that for fetuses with proven congenital infections an extended and targeted sonographic examination may be helpful in ­detecting associated fetal seizures that may even worsen the neonatal outcome. © 2019 S. Karger AG, Basel Jose Hector Ochoa, MD, PhD DIAGNUS, Prenatal Diagnosis Center 9 de julio 726 Córdoba, X5000EMP, Province of Córdoba (Argentina) E-Mail josehochoa.cba @ gmail.com Downloaded by: Göteborgs Universitet 130.241.16.16 - 8/4/2019 3:35:26 PM Keywords Fetal seizures · Seizure-like activity · Zika virus · Toxoplasmosis · Fetal cerebral lesions · Abnormal fetal movements · Prenatal ultrasound Fig. 1. Case 1. Transventricular axial view at 27 weeks shows mild ventriculomegaly and cortico-subcortical hyperechogenicity. Fig. 3. Case 2. Photograph of the newborn infant presenting with severe microcephaly. Fig. 4. Case 2. Three-dimensional computed tomography recon- struction of the bony structures reveals microcephaly and subcortical calcifications. forehead and microcephaly. Case Reports Case 1 A 21-year-old primigravida was referred for further evaluation at 27 weeks of gestation after the detection of several abnormal findings on prenatal sonography. Her obstetric history was remarkable for Zika virus (ZKV) infection at 8 weeks of gestation. The 11–13-week scan showed shrinkage of the choroid plexus with abnormal choroid plexus area/lateral ventricle area ratio. At referral, polyhydramnios, microcephaly, signs of cortical atrophy with 2 Fetal Diagn Ther DOI: 10.1159/000500023 ventriculomegaly and calcifications, megacisterna magna, dysmorphic ears, and hypoplastic thymus were observed (Fig. 1). During sonographic evaluation, abnormal repetitive rhythmic motion of the fetal body with simultaneous atypical movement of the head, left hand, and mouth, consistent with seizure-like activity, were evident (online suppl. Video 1; for all online suppl. material, see www.karger.com/doi/10.1159/000500023). At 32 weeks of ges­ tation, the patient was admitted in advanced labor and a 1,200-g male newborn was delivered vaginally. Five hours after delivery the newborn presented generalized tonic-clonic and subtle localized seizures that were ameliorated with the administration of phenobarbital. Specific IgM in the cerebrospinal fluid was positive for ZKV and postnatal cerebral magnetic resonance imaging (MRI) confirmed the presence of severe brain lesions. The infant developed status epilepticus with severe psychomotor delay and died at 6 months of age (Fig. 2). Ochoa/Sosa-Olavarria/Quiroga/Sepulveda Downloaded by: Göteborgs Universitet 130.241.16.16 - 8/4/2019 3:35:26 PM Fig. 2. Case 1. Postnatal photograph depicting downward sloping Case 2 A 17-year-old primigravida was referred at 30 weeks of gestation for evaluation of “an abnormal fetal head biometry.” The patient had a history of ZKV infection at 10 weeks of gestation. At that time, simultaneously with a ZKV infection burst in the community, she presented mild fever for 3 days, cutaneous rash, and mild joint pain with complete and uneventful recovery. At referral, sonographic examination revealed fetal long bones and abdominal biometry consistent with dates; however, fetal head biometry and transverse cerebellar diameter were below the 3rd percentile. An isolated fetal brain calcification and mild ventriculomegaly of 10.5 mm were noted as additional findings. During fetal evaluation the fetus suddenly started having abnormal, forceful, jerky, and repetitive fetal movement of the head and also repeated movements of the lips including sucking and chewing. Some of the movements lasted for more than 30 s (online suppl. Video 2). Fetal seizures were suspected and confirmed postnatally by physical examination and electroencephalogram. The patient delivered vaginally at 38 weeks and physical examination of the neonate confirmed severe microcephaly (Fig. 3). Computed tomography scan after delivery also showed cerebral calcifications (Fig. 4). Postnatal neurodevelopment has been poor with severe handicap and frequent convulsive events. Case 3 A 32-year-old woman, gravida 2, para 1, was referred for a second opinion at 28 weeks of gestation with the diagnosis of fetal hydrocephaly. She had no relevant personal or family history. First-trimester serological analyses were within normal reference ranges, including a toxoplasmosis indirect immunofluorescence test reported as negative. Sonographic examination confirmed severe hydrocephaly with ventricular atrial diameter measuring 21 mm. The cerebral parenchyma exhibited increased periventricular echogenicity creating a striking contrast with the hypoechoic basal ganglia where a thalamic echogenic nodule was detected (Fig. 5). Middle cerebral artery Doppler study showed high end-diastolic velocities and a low pulsatility index of 1.05 suggestive of cerebral vasodilation. Ocular abnormalities consistent with chorioretinitis (Fig. 6) and hepato-splenomegaly were also present. Amniotic fluid volume was normal. Although the fetal activity was significantly diminished, abnormal tonic-clonic movements in the extremities lasting for few minutes and repeated after a short pause consistent with seizure-like activity were documented during the scan (online suppl. Video 3). Fetal MRI depicted severe cerebral injury (Fig. 7). Repeated serological IgG and IgM tests were positive for toxoplasmosis. Treatment with spiramycin was started. Cesarean section was performed at 32 weeks of gestation. The newborn was severely depressed and died at 3 h of life. After birth maternal IgG was positive at 1:16.384 dilution. Fig. 5. Case 3. Axial view of the fetal head shows severe ventric­ ulomegaly, periventricular hyperechogenicity, and hyperechoic nodule in basal ganglia (arrow). Fig. 6. Case 3. Axial view at the level of the orbits depicting a retrolental echogenic mass in one eye, corresponding to chorioretinopathy. Discussion Fetal Seizures Fig. 7. Case 3. T2-weighed fetal MRI in parasagittal view depicting severe ventriculomegaly and generalized cerebral lesions. Also, a hyperintense nodule in optic thalami is seen (arrow). Fetal Diagn Ther DOI: 10.1159/000500023 3 Downloaded by: Göteborgs Universitet 130.241.16.16 - 8/4/2019 3:35:26 PM The development of fetal movement in the first and second half of pregnancy has been extensively studied and well documented by conventional real-time sonography [1–6]. The similarity between prenatal and postnatal movements is so striking that the same names used previ- Table 1. Fetal seizures. Review of the literature First author Cases, n Detection/remarks GA Abnormalities Underlying cause/remarks Postnatal seizures Outcome Badr El-Din [Cit in 8], 1960 3 siblings (AR familial clustering totalizing 8) #1 Reported by mother* – Not described Unknown + PMD, status epilepticus; died at 10 months #2 Reported by mother* – Not described Unknown + Status epilepticus; died at 3 months #3 Reported by mother/index case 5 months Not described Unknown + PMD, status epilepticus; died at 16 months #1 Reported by mother* 5 months Not described; PN: ventriculomegaly Pyridoxine dependent + BW 3,400 g; died at 7 weeks #2 Reported by mother* 5 months Not described Pyridoxine dependent + BW 3,300 g; died at 2 days #3 Reported by mother/index case 7 months Not described Pyridoxine dependent + BW 3,850 g; mild PMD 3 siblings Ford [Cit in 8], 1976 2 Reported by mother – Not described Asphyxia Conover [Cit in 8], 1986 2 #1 US (mother inform similar episodes from 25 weeks)/ polyhydramnios 36 weeks Narrow palpebral fissures, hypertelorism, clinodactyly, bilateral transverse palmar creases, hypospadias, and micropenis Not clear/no autopsy/ PN KTP: 46XY #2 US (mother inform abnormal rapid movements –2 weeks)/ polyhydramnios 30 weeks Hydranencephaly CNS lesion No data + Born at 36 weeks; BW 2,080 g; died at 3 days TOP Maouris [Cit in 8], 1987 1 Abnormal FHR tracing; moderate PE Term PN: right cerebral infarction Asphyxia + Born at term; BW 3,100 g; left flacid hemiparesis at 2 months Landy [Cit in 8], 1989 1 US 35 weeks (mother noticed it 1 week before) IUGR; KTP: 46XX 35 weeks Soft palate cleft, poorly ossified clavicles Unknown + Born at 35 weeks; BW 2,060 g; PMD at 10 months; microcephaly, motor and hearing impairment Shimizu [Cit in 8], 1991 1 US 39 weeks None Unknown + PMD du Plessis [13], 1993 1 Reported by mother; confirmed by US 3rd trimester Flat nasal bridge, high arched palate, micrognathia, pectus excavatum; flexion contractures of elbows and knees; PN CT: asymmetric ventriculomegaly, nodular periventricular calcifications, thin corpus callosum, and pachygyria Cerebral cortical dysgenesis/ lissencephaly + Born at 35 weeks; BW 2,400 g; abnormal EEG; died at 10 days 4 Fetal Diagn Ther DOI: 10.1159/000500023 Ochoa/Sosa-Olavarria/Quiroga/Sepulveda Downloaded by: Göteborgs Universitet 130.241.16.16 - 8/4/2019 3:35:26 PM Bejsovec [Cit in 8], 1967 Table 1 (continued) First author Cases, n Detection/remarks GA Abnormalities Underlying cause/remarks Postnatal seizures Outcome Abrams [Cit in 8], 1996 1 US: bilateral choroid plexus cyst at 19 weeks, KTP: 46 XX, polyhydramnios at 24 weeks 35 weeks PrN: abnormal limb and head position; PN CT: retarded cerebral development and cerebellar atrophy, enlarged fourth ventricle Unknown + Born at 37 weeks; BW 2,725 g; severe neurological impairement; died at 3 months Skupsky [Cit in 8], 1996 3 #1 US/ polyhydramnios 35 weeks Microcephaly, micrognathia, joint contractures, rocker bottom feet, small phallus, enlarged fourth ventricle, and others Pena-Shokeir phenotype Stillborn at term; pulmonary hypoplasia #2 US/ polyhydramnios; KTP: 46XX 20 weeks Flexion-extension postural abnormalities Congenital muscular dystrophy TOP #3 US/ polyhydramnios; KTP: 46XX 21 weeks Flexion-extension deformities, edema, small thorax Primary myopathy TOP; lung hypoplasia US (also felt by mother the night before) 37 weeks None; PN CT: subarachnoid hemorrhage and cerebral edema Asphyxia + Born at 37 weeks; BW 3,090 g; low activity EEG; died at 4 days #1 Mother reported abnormal jerking movements 38 weeks None; PN CT: cerebral atrophy Asphyxia + Born at 40 weeks; BW 3,010 g; died at 26 days #2 US (mother referred unusual jerking fetal activity) 39 weeks None Asphyxia + Born at 39 weeks; BW 3,700 g; brain death; died at 2 days + Normal EEG at 5 years; hypotonia; motor and developmental delay 1 Ingemarsson 2 [Cit in 8], 1998 Gospe [Cit in 8], 1998 1 of 2 cases Felt by mother in third trimester Term None Pyridoxine dependent Westgate [Cit in 8], 1999 1 US and felt by the mother simultaneously; oligohydramnios 41 weeks None Asphyxia Mitra [Cit in 8], 1999 2 siblings (1 previous normal pregnancy) #1 US (also detected by the mother)/ polyhydramnios 30 weeks PN CT: marked hypoplasia of the cerebellum, pons and medulla along with cerebral atrophy and mild dilatation of the fourth, third and lateral ventricles Olivopontocerebellar hypoplasia Exaggerated Born at 34 weeks; startle BW 2,350 g; died at reflex 4 days #2 US/ polyhydramnios 28 weeks PrN US: markedly hypoplastic cerebellum, mild dilatation of the fourth ventricle and then 3rd ventricle; PN MRI: marked hypoplasia of the cerebellum and brain stem, cerebral atrophy, mild ventriculomegaly and marked hypoplasia of the upper spinal cord Olivopontocerebellar hypoplasia Exaggerated Born at 37 weeks; startle BW 2,950 g; died at reflex 14 days Fetal Seizures Fetal Diagn Ther DOI: 10.1159/000500023 BW 5,220 g; died at birth 5 Downloaded by: Göteborgs Universitet 130.241.16.16 - 8/4/2019 3:35:26 PM Osiovich [Cit in 8], 1996 First author Cases, n Detection/remarks GA Abnormalities Underlying cause/remarks Postnatal seizures Outcome Keogh [14], 2000 8 cases of abnormal episodes of excessive fetal “fits” that had sought medical advice #1 Felt by mother; baby’s sibling had intrauterine seizures 27–37 weeks None Benign familial seizures + Born at 41 weeks; recurrent clonic seizures at 18 h #2 Felt by mother at 30 weeks PN: thalamic and basal ganglia infarct, cerebral atrophy, encephalomalacia Not clear + Born at 40 weeks; recurrent tonic seizures at 8 h; quadriplegia, microcephaly, epilepsy; died in infancy #3 Felt by mother at 30 weeks following antepartum haemorrhage; PE PN US: generalized cerebral edema HIE + Born at 40 weeks; recurrent clonic seizures at 4 h; abnormal EEG #4 Felt by mother daily from 27 weeks PN: right parietal infarction HIE + Born at 39 weeks; repeated clonic seizures left arm and leg at 12 h; EEG repeated seizures #5 Felt by mother; PE PN: left parietal infarction; renal anomalies HIE + Born at 38 weeks; clonic seizures all limbs at 30 h (3 episodes); abnormal EEG* #6 Felt by mother in 3rd trimester; PE Cystic hygroma HIE + Born at 38 weeks; multiple focal clonic seizures at day 6; US and CT scan normal; abnormal EEG #7 Felt by mother in 3rd trimester; family history of cerebral palsy and epilepsy; maternal seizure in second trimester; PE PN: Left parietal infarction HIE + Born at 40 weeks; focal clonic seizures at 11 h; triple anticonvulsants; abnormal EEG #8 Felt by mother in last 2 months; maternal history of febrile seizures; PE PN: right parietal infarction HIE + Born at 40 weeks; recurrent clonic seizures starting in labor ward; hemiplegia; EEG; multifocal seizures PN MRI: diffuse polymicropachygyria and lissencephaly CNS migrational disorder + Generalized tonic– clonic seizure at 20 min; died at 6 months Patane [Cit in 8], 2001 6 1 Mother referred two episodes of sudden, unusually strong fits of fetal movements 1 months preceding delivery at 42 weeks Fetal Diagn Ther DOI: 10.1159/000500023 38 weeks Ochoa/Sosa-Olavarria/Quiroga/Sepulveda Downloaded by: Göteborgs Universitet 130.241.16.16 - 8/4/2019 3:35:26 PM Table 1 (continued) Table 1 (continued) Cases, n Detection/remarks GA Abnormalities Underlying cause/remarks Postnatal seizures Outcome Hobson [15], 1 out of 2 2005 Mother experienced unusual fetal movements* 3rd trimester PN imaging: cranial US images, brain MRI and EEG findings were thought to be strongly suggestive of severe HIE Isolated sulphite oxidase deficiency + Born at 38 weeks; NICU on day 2 because of poor feeding, irritability, seizures and abnormal posturing; died on day 20 Patel [16], 2006 #1 Mother noted rhythmic fetal movements at midsecond trimester 2nd trimester PN CT: cerebral and cerebellar hypoplasia Olivopontocerebellar hypoplasia + Born at 38 weeks; seizures on day 1; died on day 3 #2 US at 25 weeks; mother noted seizure-like movements around 18 weeks; KTP: 46XX 18 weeks Cerebellar hypoplasia at 25 weeks; microcephaly, mild micrognathia, and camptodactyly Olivopontocerebellar hypoplasia TOP at 27 weeks #3 US; seizure-like myoclonic movements around 18 weeks; KTP: 46XX 18 weeks Micrencephaly, cerebellar hypoplasia Olivopontocerebellar hypoplasia TOP at 20 weeks #1 US: repetitive tonic-clonic bursts of movements; sonographic features of AMC from 17 weeks 14 weeks Bilateral clubfeet, contractures of arms and legs, and polyhydramnios AMC #2 US: abnormal movements 13 weeks Bilateral clubfeet and extended legs AMC TOP at 17 weeks TOP; BW 1,300 g Sheizaf [17], 2007 3 affected siblings 2 affected siblings – Born at 35 weeks; died 1 h after birth Usta [8], 2007 1 US; polyhydramnios; KTP: normal 31 weeks Small stomach, ventriculomegaly, absent CSP, ACC, facial and hand deformities Lissencephaly Jung [18], 2008 1 US (mother felt abnormal movements 2 weeks before) 30 weeks Right hydronephrosis, single umbilical artery; PN CT and MRI: normal Unknown + Born at 36 weeks; BW 4,295 g; PMD at 5 months Ruiz [19], 2008 1 Felt by the mother at 31 weeks 33 weeks PN: brain imaging performed at 3, 25 and 35 days showed progressive hypomyelination and global atrophy Pyridoxamine 5-phosphate oxidase deficiency + Born at 33 weeks; BW 2,355 g; orobuccal rhythmic movements accompanied by myoclonus from birth; died at 48 h Darin [20], 2016 3 out of 7 cases #1 Abnormal IU movements NA None Vitamin-B6dependent epilepsy + Born at 40 weeks; seizures <24 h; PMD; microcephaly #2 Abnormal IU movements NA None Vitamin-B6dependent epilepsy + Born at 36 weeks; seizures <24 h; PMD; microcephaly #3 Abnormal IU movements NA None; brain underdevelopment, white matter edema, petechial hemorrhages at 2 months Vitamin-B6dependent epilepsy + Born at 36 weeks; seizures <24 h; PMD; microcephaly Fetal Seizures Fetal Diagn Ther DOI: 10.1159/000500023 7 Downloaded by: Göteborgs Universitet 130.241.16.16 - 8/4/2019 3:35:26 PM First author Table 1 (continued) First author Cases, n Detection/remarks GA Abnormalities Underlying cause/remarks Postnatal seizures Outcome McNally [21], 1 2016 Reported by mother; confirmed by US at 35 weeks 26 weeks Fetal macrosomia; diffuse skin thickening; abnormal posturing of extremities and movements De novo heterozygous mutation in SCN8A + Born at 38 weeks; arthrogryposis; abnormal EEG; abnormal MRI-DWI This study #1 US at 27 weeks; polyhydramnios 27 weeks Microcephaly, ventriculomegaly, megacisterna magna; PN MRI: cerebral atrophy, abnormal sulcation, ventriculomegaly Congenital ZKV syndrome + Born at 32 weeks; microcephaly; severe handicap and PMD; died at 6 months #2 US at 30 weeks 30 weeks Microcephaly, ventriculomegaly, calcification Congenital ZKV syndrome + Born at 38 weeks; abnormal EEG; microcephaly #3 US at 28 weeks 28 weeks US and fetal MRI: hydrocephaly, severely affected brain, echogenic nodules; chorioretinitis; hepatoesplenomegaly Congenital toxoplasmosis – Born at 32 weeks; died at 3 h 3 * Retrospectively reported. ACC, agenesis of corpus callosum; AMC, arthrogryposis multiplex congenita; AR, autosomal recessive; BW, birth weight; CSP, cavum septi pellucidi; CT, computed tomography; DWI, diffusion-weighted imaging; EEG, electroencephalogram; FHR, fetal heart rate; GA, gestational age; HIE, hypoxic-ischemic encephalopathy; IU, intrauterine; IUGR, intrauterine growth restriction; KTP, karyotype; MRI, magnetic resonance imaging; NA, not available; NICU, neonatal intensive care unit; PE, preeclampsia; PMD, psychomotor delay; PN, postnatal; PrN, prenatal; TOP, termination of pregnancy; US, ultrasound; ZKV, Zika virus. 8 Fetal Diagn Ther DOI: 10.1159/000500023 can be felt by the mother and may lead to search for medical advice. Usta et al. [8] reviewed 22 cases of fetal seizure-like activity. Including this series we found a total of 50 cases reported (Table 1) [8–10, 13–21]. In 25 cases, the abnormal fetal activity was perceived only by the mother; in 11 cases, it was noted by the mother and confirmed by realtime ultrasound; in 13 cases, the fetal scan was the only evidence of the seizure-like activity; and in 1 case, the authors retrospectively attributed the abnormal fetal heart rate monitoring to fetal seizures. The underlying etiology of all documented antenatal cases, including ours, is shown in Table 2. Hypoxic-ischemic encephalopathy was the leading cause of fetal seizures accounting for 14 cases (28%) and all of them had severe brain injuries detected on postnatal studies. Fetal cerebral anomalies were also frequent, totalizing 10 cases (20%). Although pyridoxinedependent seizures are a very rare entity, its prevalence in cases of fetal seizures is relevant (9 cases, 18%); therefore, it should be considered in all fetuses with seizures in the absence of congenital malformation. The prognosis in cases of fetal seizure-like activity was invariably poor; indeed, only one case with benign familOchoa/Sosa-Olavarria/Quiroga/Sepulveda Downloaded by: Göteborgs Universitet 130.241.16.16 - 8/4/2019 3:35:26 PM ously for the postnatal movement patterns are given to the fetal movements [6]. They occur in a specific and recognizable pattern that makes them candidates for diagnostic purposes in the compromised fetus [3, 5]. In fact, a recent study on fetal motor behavior using cine MRI shows that combined structural and functional imaging may improve the characterization of early neurologic integrity and could be potentially informative on the outcome [7]. Fetal seizures are described as abnormal movements because of their forcefulness, jerkiness, periodicity, involvement of the whole fetal body, and occurrence on repeated occasions distinct from other fetal movements [8]. Clonic convulsions are described as very intense movements at a rate of about 2 per second [8, 9], while lightening convulsions are very regular and intense movements of the fetus characterized by single twitches occurring several times per minute [9]. They can be differentiated from hiccup or agonal gasping that involve just the diaphragm and chest wall [10]. The absence of general movements may, on its own, be a sign of disturbed integrity of the CNS and the combination of reduced activity with abrupt movements may reinforce the probability of fetal seizures [11, 12]. These different patterns of movement Table 2. Causes of fetal seizures (n = 50 cases) Underlying cause Specific disease reported n Subtotal, n (%) Asphyxia or encephalopathy Hypoxic-ischemic encephalopathy 14 14 (28) Neuro-metabolic disorders Pyridoxine-dependent seizures Sulphite oxidase deficiency Pyridoxamine 5-phosphate oxidase deficiency 7 1 1 9 (18) SNC lesion or malformation Olivopontocerebellar hypoplasia Lissencephaly/migration disorder Hydranencephaly Cerebellar anomaly 5 3 1 1 10 (20) Fetal akinesia deformation sequence Pena-Shokeir phenotype Congenital muscular dystrophy Primary myopathy Arthrogryposis multiplex congenita 1 1 1 2 5 (10) Fetal infections* Congenital ZKV syndrome Congenital toxoplasmosis 2 1 3 (6) Genetic De novo heterozygous mutation in SCN8A 1 1 (2) Unknown/not confirmed Family history of seizure Some fetal abnormalities No family history, no abnormalities 4 3 1 8 (16) * Described in this report. ZKV, Zika virus. Fetal Seizures we want to emphasize the need of being aware about this condition whenever the mother tells about the perception of different or strange fetal movements. We also advise about the necessity of an extended real-time sonographic examination in these cases, with attention to the extremities and the face, in order to pick up these abnormal movements, especially in those fetuses with the suspicion or diagnosis of CNS involvement. Acknowledgement W.S. was supported by an unrestricted research grant from the Sociedad Profesional de Medicina Fetal “Fetalmed” Ltda., Chile. Statement of Ethics The authors have no ethical conflicts to disclose. Disclosure Statement The authors have no conflicts of interest to disclose. Fetal Diagn Ther DOI: 10.1159/000500023 9 Downloaded by: Göteborgs Universitet 130.241.16.16 - 8/4/2019 3:35:26 PM iar seizures had an apparently normal outcome. Twentytwo fetuses/neonates died, 7 women terminated the pregnancy because of associated fetal anomalies, and 17 had congenital cerebral lesions or an impact on mental or psychomotor development. In total, there were 9 cases of ­microcephaly. In 3 cases, there were no consistent data on follow-up. In this report, we present 3 cases of fetal seizures due to congenital infection that were documented by realtime sonography. To the best of our knowledge, ours is the first one describing the prenatal diagnosis of seizures secondary to fetal congenital infection. In the first case, there was repetitive rhythmic motion of the fetal body, atypical movement of the head, left hand, and mouth. Similarly, in the second case, the abnormal jerky movement compromised the head and mouth with repetitive sucking and chewing movements for more than 30 s. The third case had a tonic-clonic pattern of movement of the extremities in a setting of a generalized persistent hypokinesia. 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