ANTENATAL BRAINSTEM CORD - keywords
antenatal brainstem cord
references to antenatal damage to brainstem and cord
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Haldeman S, Fowler GW, Ashwal S, Schneider S. Acute flaccid neonatal paraplegia: a case report. Neurology 1983;33(1):93-95.
Hellström B, Sallmander U (1968) Prevention of spinal cord injury in hyperextension of the fetal head. Journal of the American Medical Association 20: 101-. Herrera DA, Ruge NO, Florez MM, Vargas SA, Ochoa-Escudero M, Castillo M. Neuroimaging Findings in Moebius Sequence. AJNR Am J Neuroradiol. 2019 May;40(5):862-865.
Kim N, Kim JH, Kim JS, Hwang JM. Möbius syndrome: clinico-radiologic correlation. Graefes Arch Clin Exp Ophthalmol. 2018 Nov;256(11):2219-2223.
Kobayashi S, Kanda K, Yokochi K, Ohki S (2006) A case of spinal cord injury that occurred in utero. Pediatr Neurol 35:367-369.
Koyanagi T, Horimoto N, Maeda H, Kukita J, Minami T, Ueda K, Nakano H. Abnormal behavioral patterns in the human fetus at term: correlation with lesion sites in the central nervous system after birth. J Child Neurol 1993;8:19-26.
Leck E, Pickett GE. Two Curious Cases of Complete Cerebellar Agenesis. Can J Neurol Sci. 2022 Sep;49(5):719-721.
Leong S, Ashwell KW (1997) Is there a zone of vascular vulnerability in the fetal brain stem ? Neurotoxic Teratol 19:265-275.
Maekawa K, Masaki T, Kokubun Y. Fetal spinal-cord injury secondary to hyperextension of the neck: no effect of caesarean section. Dev Med Child Neurol 1976;18:228-32.
Malinger G, Zahalka N, Kidron D, Ben-Sira L, Lev D, Lerman-Sagie T. Fatal outcome following foetal cerebellar haemorrhage associated with placental thrombosis. Eur J Paediatr Neurol 2006;10(2):93-6.
Mamelak AN, Cogen PH, Barkovich AJ. The ‘filum intermedium’ sign: focal in utero spinal cord infarct and extraspinal thecal sac. J Neurosurg 1994;81(6):941-946.
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Menshawi K, Mohr JP, Gutierrez J (2015) A Functional Perspective on the Embryology and Anatomy of the Cerebral Blood Supply). Journal of Stroke 2015;17(2):144-158.
Milunsky A. Hypoxic spinal cord injury and/or abnormality in utero. Pediatr Neurol 2007;37:76.
Natzume J, Watanabe K, Kuno K, Hayakawa F, Hashizume Y (1995) Clinical, neurophysiologic, and neuropathological features of an infant with brain damage of total asphyxia type. Pediatr Neurol 13:61-64.
Norman MC, Wedderburn LC (1973) Fetal spinal cord injury with cephalic delivery. Obstet Gynecol 42:355-8.
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Norman MG (1974) Unilateral encephalomalacia in cranial nerve nuclei in neonates: report of two cases. Neurology 24:424-427.
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Pollack MA, Llena JL, Fleischman A, Fish B (1983) Neonatal brainstem infarction. Arch Neurol 40:52-53.
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Prats JM, Monzon MJ, Zuazo E, Garaizar C (1993) Congenital nuclear syndrome of oculomotor nerve. Pediatr Neurol 9:476-478.
Qajia H, Choumad S, El Bakari F, Eddahoumi Y, Allali N, Chat L, El Haddad S. Unilateral agenesis of the right cerebellar hemisphere in a child: When one hemisphere is missing, the brain adapts. Radiol Case Rep. 2026 May 7;21(8):3032-3034.
Ranzini AC, Shen-Schwarz S, Guzman ER, Fisher AJ, White M, Vintzileos AM. Prenatal sonographic appearance of hemorrhagic cerebellar infarction. J Ultrasound Med 1998;17(11):725-7.
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Robins JB(1), Mason GC, Sener RN. Cerebellar agenesis versus vanishing cerebellum in Chiari II malformation. Comput Med Imaging Graph 1995;19(6):491–4.
Robinson RO, Trounce JQ, Janota I, Cox T (1993) Late fetal pontine destruction. Pediatr Neurol 9:213-215.
Roessmann U, Parks PJ. Hydranencephaly in vertebral-basilar territory. Acta Neuropathologica 1978;44:141–143.
Roche-Herrero MC, Miranda-Cid C, Royo-Orejas A, Escudero-Lou RM (2004) Atrophy of the cervical spinal cord as a consequence of a prenatal ischemic infarct. Rev Neurol 39(10):932-934.
Rousseau S, Metral S, Lacroix C, Cahusac C, Nocton F, Landrieu P. Anterior spinal artery syndrome mimicking infantile spinal muscular atrophy. Am J Perinatol 1993;10:316-318.
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Sarnat HB (2004) Watershed infarcts in the fetal and neonatal brainstem. An aetiology of central hypoventilation, dysphagia, Moebius syndrome and micrognathia. Eur J Paediatr Neurol 8(2):71-87.
Sarnat HB, Benjamin DR, Siebert JR, Kletter GB, Cheyette SR. Agenesis of the mesencephalon and metencephalon with cerebellar hypoplasia: putative mutation in the EN2 gene-report of 2 cases in early infancy. Pediatr Dev Pathol 2002;5(1):54-68.
Schmahmann JD, Sherman JC. The cerebellar cognitive affective syndrome. Brain 1998;121(Pt 4): 561–79.
Simanovsky N, Stepensky P, Hiller N (2004) The use of ultrasound for the diagnosis of spinal hemorrhage in a newborn. Pediatr Neurol 31:295-7.
Strong OS. A case of unilateral cerebellar agenesis. J Comp Neurol 1915;25:361–91.
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Wilson ER, Mirra SS, Schwartz JF (1982) Congenital diencephalic and brain stem damage : neuropathological study of three cases. Acta Neuropathologica (Berl) 57:70-74.
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Young RS, Towfighi J, Marks KH (1983) Focal necrosis of the spinal cord in utero. Arch Neurol 40:654-5.
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CHARGE association
Moebius sequence
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Specific cerebral antenatal injury leads to entities like porencephaly, hydranencephaly, multicystic encephalopathy, germinolysis, striatal arteriopathy and others. Cerebelloclastic fetal injury is also well described for antepartum haemorrhage or stroke. Unilateral cerebellar hypoplasia is a typical result.
Injury to brainstem and cord can also occur in utero. In some genetic disorders injury is everywhere, including in brainstem (Meuwissen et al. 2016). Angimatous tumors of brainstem and cord have also been reported in the perinatal period. Symmetrical brainstem damage is present with the Leigh phenotype of neonatal presentation of severe mitochondrial dysfunction.
Moebius sequence is a condition typically presenting with neonatal facial palsy. Some Moebius sequences are vascular in origin. Some infants with CHARGE association also have cranial nerve palsies, of a somewhat different type and not due to infarction.
Congenital brainstem disconnection is diagnosed when a lage part of the pons is symmetrically absent (Robinson et al. 1993, Sarnat et al. 2002), most often not due to infarction. Similar reports have referred to this clastic mode of genesis with the term ‘isolated vertebro-basilar hydranencephaly’, possibly due to haemorrhagic infarction with cerebellar destruction (Roesmann and Parks 1978).
Isolated focal infarcts (asymmetrical or not) have been rarely reported. A very recognizable and repeatedly reported spinal cord infarction is associated with extension in breech presentation.
focal brainstem infarction
midbrain disconnection
unilateral cerebellar hypoplasia
anterior spinal artery stroke
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focal spinal cord infarction
tegmental necrosis in asphyxia
Moebius sequence
antenatal damage to brainstem and spinal cord
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brainstem disconnection
antenatal damage to brainstem and cord: summary
Focal ischaemia can cause apparent congenital brainstem destruction in vascular territories. Usually the infarct is then asymmetrical or partial, leaving parts of the brainstem intact (see references below: basilar artery thrombosis and infarction of one oculomotor nucleus; wedge-shaped infarction of the left cerebral peduncle and left cerebral hemiatrophy presenting as neonatal ptosis and ophthalmoplegia, later with right hemiparesis; significant thinning to almost absence of the medulla at olivary level, with convoluted abnormal vessels around a defect at endoscopy, with on a vertebral angiogram normal basilar and vertebral arteries and branches. The brainstem midline may be a vulnerable area in the young fetus, when it is avascular for protracted periods and thus a watershed area, perhaps becoming one of the causes of Moebius sequence.
Norman MG (1974) Unilateral encephalomalacia in cranial nerve nuclei in neonates: report of two cases. Neurology 24:424-427. [preterm with basilar artery thrombosis and infarction of one oculomotor nucleus]
Pollack MA, Llena JL, Fleischman A, Fish B (1983) Neonatal brainstem infarction. Arch Neurol 40:52-53. [cystic necrosis in pons and right cerebellar hemisphere following coarctectomy on day 17, together with right arm gangrene due to brachial artery catheter-related thrombosis; also extensive cerebral grey and white matter infarction]
Prats JM, Monzon MJ, Zuazo E, Garaizar C (1993) Congenital nuclear syndrome of oculomotor nerve. Pediatr Neurol 9:476-478. [wedge-shaped infarct of the left cerebral peduncle and left cerebral hemiatrophy presenting as neonatal ptosis and ophtalmoplegia with left ventricle dilatation, later with right hemiparesis]
Bode H, Bubl R, Tutishauser M, Nars PW (1994) Congenital tetraplegia, respiratory insufficiency, and hypoplasia of medulla oblongata. Pediatr Neurol 10:161-163. [significant thinning to almost absence of the medulla at olivary level, with convoluted abnormal vessels around the defect at endoscopy, whereas the vertebral angiogram had shown normal basilar and vertebral arteries and branches]
Leong S, Ashwell KW (1997) Is there a zone of vascular vulnerability in the fetal brain stem ? Neurotoxic Teratol 19:265-275. [study of rat brainstem vascular development, focusing on pontine and medullary tegmentum in a search for a hypothesis behind the vulnerability to focal ischaemia in Moebius syndrome]
antenatal brainstem stroke
Unilateral hemispheric cerebellar hypoplasia can
be asymptomatic, present with Moebius syndrome
or be part of PHACES syndrome. Vermis is involved
in about half. The ipsilateral cerebellar peduncles
and the contralateral inferior olivary nucleus are
secondarily atrophied (Strong 1915, Quajia et al. 2026).
A strong case has been made for the possibility that
focal cerebellar disruption with clefts in the parenchyma,
connected or not to the fourth ventricle, is the result of prenatal infarction or bleeding (Poretti et al. 2016). Cerebellar haemorrhage is not rare in fetal ultrasound between 18 and 24 w PMA. Postnatal MR with SWI can (not always) detect the haemorrhagic mechanism.
Minor asymmetry of the cerebellar hemispheres is often an incidental finding, whereas marked unilateral hypoplasia may present with signs in infancy or early childhood: truncal and limb ataxia, hypotonia, squint, and head nodding, headache. Cognitive outcome is variable, cerebellar vermis aplasia/atrophy apparently bing a good predictor of poor cognition: difficulties in memory and executive functions, graphomotor and arithmetical skills, social perception. Dysarthria and lack of expressive language are common in children with unilateral cerebellar hypoplasia. Attention deficit hyperactivity disorder, depressive mood, anxiety, and catatonia with obsessive-compulsive disorder may also occur in some minor variation of the same in older children and adults with unilateral cerebellar destruction (Shmahmann and Sherman 1998).
With bilateral absence of the hemispheres there is a high likelihood of a genetic condition. Postnatal unilateral cerebellar atrophy is seen following extensive cerebellar infarction or bleeding, often in preterm infants. Such events, if occurring in utero, will present with uni- or bilateral cerebellar hemisphere destruction.
after Quaija et al. 2026
unilateral cerebellar hypoplasia/destruction
Cardinal neonatal clinical features in CHARGE association are: coloboma, conotruncal heart defect, choanal atresia, genital anomalies, ear anomalies (hearing deficit). Cranial nerve involvement in CHARGE-association differs from Moebius syndrome in that it rarely combines with ophthalmoplegia and tongue paralysis; brainstem dysplasia is probably due to early embryonic neural crest pathology and can clinically resemble Joubert syndrome (Byerli and Pauli 1993). Reported anomalies in CHARGE include arhinencephaly, holoprosencephaly, septal agenesis, abnormal gyration and hindbrain defects. Brain anomalies correlate with choanal atresia. High quality postnatal MR imaging demonstrates olfactory anomalies, including either absence or hypoplasia of the olfactory bulbs and olfactory sulci (Blustajn et al. 20028). Diagnosis of CHARGE association is a challenge during pregnancy. If the diagnosis is raised careful examination is needed to identify external ear anomalies (Biard et al. 2021), choanal atresia, absence of olfactory sulci or microphthalmia (Busa et al. 2016). Fetal brain MRI can be helpful, but a normal result does not exclude the diagnosis. When CHARGE syndrome is suspected, CHD7 molecular analysis may confirm the diagnosis.
CHARGE association
CHARGE association with cranial pareses: a slender brainstem with a rounded, mildly enlarged, somewhat square fourth ventricle
Midline hyperechoic change in brainstem on sagittal ultrasound scan in a term infant with Moebius syndrome, corresponding with medullopontine calcification on axial CT scan (Govaert et al. 1989).
Subclavian artery supply disruption is one of the proposed mechanisms of fetal brainstem ischaemia (Bavinck and Weaver 1986, Zaidi et al. 2023). A border zone exists in the brainstem tegmentum, between the terminal perfusion of the paramedian and long circumferential arteries, paired segmental branches from the basilar artery (Sarnat 2004). The vertebrobasilar circulation achieves this configuration and caudorostral flow by 9 weeks gestation. Reduced basilar artery perfusion in the fetus, either early or later in gestation, may result in symmetrical longitudinal columns of infarction in the tegmentum of the mesencephalon, pons and medulla oblongata. Within this zone are cranial nerve nuclei III-XII, the nucleus and tractus solitarius or central pneumotaxic center, as well as the nucleus ambiguus and other somatic motor nuclei that subserve muscles of swallowing, mastication and tongue movement. Watershed infarcts in the human fetal and neonatal brainstem are clinically expressed as multiple cranial neuropathies, failure of central respiratory drive and apnoea, dysphagia and aspiration, Moebius syndrome and Pierre Robin sequence. A persistent primitive trigeminal artery may lead to brainstem dysfunction similar of Moebius sequence (Okanishi et al. 2007).
Neonatal facial palsy from birth can accompany the Chiari malformation and facial diplegia is a feature of established anoxic-ischaemic fetal brain damage and of some extensive spinal muscular atrophy instances. Facial palsy of brainstem origin is also seen with 22q11 deletions. In arthrogrypoid syndromes due to muscular or spinobulbar pathology, normal brain imaging is expected. Facial palsy has to be differentiated from Cayler cardiofacial syndrome (with unilateral aplasia of the depressor anguli oris muscle) and from diplegic faces of children with congenital muscle disorders like myotonic dystrophy and myotubular myopathy. Other causes may be birth trauma, luetic meningitis and focal brainstem arterial ischaemic stroke.
The combination of static congenital facial paralysis and external ophthalmoplegia is called the Moebius sequence for an entity with late embryonic or early fetal infarction of the tegmentum of the hindbrain, probably due to occlusion of a branch of the primitive trigeminal artery in the second month after conception (Möbius 1888)(as in de Groot-van der Mooren et al. 2026 where misoprostol for induction of abortion may have been the cause). The histopathological findings include calcification, neuronal loss, gliosis and/or focal hypervascularity. Several familial descriptions suggest the existence of genetic variants as well (Bell et al. 2019, Palma-Martinez et al. 2020). Another variant presents with absent facial and abducens nerves (Kim et al. 2018). Several disorders with congenital facial paresis may cause or mimic the sequence. Rarely, hemicerebellar atrophy is associated with congenital cranial paralyses, as can total absence of the pons and severe atrophy of the medulla oblongata and the inferior surface of the pons with global cerebellar atrophy. Known other associations of Moebius syndrome are Poland anomaly, limb reduction defects and talipes. Moebius sequence with severe limb reductions is referred to as oromandibular limb dysgenesis. Although it has yet to be shown that the brainstem lesion of Moebius syndrome can be identified with MRI, one can diagnose the condition in vivo with CT by recognition of calcifications in front of the fourth ventricle (Govaert et al. 1989). We and others have also been able to show this zone of infarction as hyperechoic dots or short strands (Yoon et al. 1997). Especially on a sagittal section, a region of hyperechogenicity without acoustic shadow is noticeable in the floor of the fourth ventricle. Axial sections can confirm this focus. Tectal beaking and flattening of the dorsal pons have been reported (absence of the colliculus facialis) (Herrera et al. 2019, Ngyen et al. 2023). One of the supratentorial associated lesions is fusion of the thalami (Herrera et al. 2019).
An infant (see images) with absence of pons and basilar artery, presented with immediate stridor at birth, absence of facial mimicry, absent sucking and swallowing, congenital tetraplegia with clonus, normal breathing but with erratic apnoea, absent vestibular/Moro/corneal/ gag/ATNR reflexes. Pupillary responses were normal.On MRI the pons gap was filled by a generally hypoplastic and anteverted cerebellum, disconnected from the brainstem.
Absence of inferior olives and straightening of the dentate nuclei has been reported in a similar instance, suggesting possible basilar artery stroke in mid-third trimester, certainly later than the formation of an atrophied but present pyramidal tract at medullary level.
brainstem disconnection
Bednarek et al. 2005 reviewed four instances where the brainstem at lower mesencephalic and higher pontine level was absent. Clinical presentation was with micrognathia, slow but regular breathing, severe hypotonia, absent sucking and temperature instability. In one case an anomalous fixation of the corticospinal tract to the clivus suggested that a genetic disturbance of rhombomere 1 development might also explain this type of brainstem disconnection.
antenatal spinal cord stroke
T
There have been several descriptions of spinal cord infarction before birth, associated with neck hyperextension in utero and subsequent spinal ischaemia (anterior spinal artery territory) in the lower cervical to higher thoracic cord (Hellström and Sallmander 1968, Norman and Wedderburn 1973, Bresnan and Abroms 1974, Maekawa et al. 1976, Chapman et al. 1978, Darwish et al. 1981, Young et al. 1983, Haldeman et al. 1983, Koyanagi et al. 1993, Rousseau et al. 1993, Mamelak et al. 1994, de Leon et al. 1995, Berck et al. 1998, Rugieri et al. 1999, Carrascosa-Romero et al. 2002, Ebinger et al. 2002, Roche-Herrero et al. 2004, Blount et al. 2004, Kobayashi et al. 2006, Milunsky 2007, Govaert 2009).
Most children were quadriplegic from birth, often delivered with caesarean section. Some had paraplegia or paralysis of the arms. The use of an abdominal binder to maintain fetal position after external version has been implicated as a mechanism. Focal absence of the cord at T9 to T12, graphically named ‘filum intermedium’, following late fist trimester destruction, can present at birth with paraplegia and a neurogenic bladder.
Similar injury has been documented in newborn infants following umbilical artery catheterization (Adamkievicz artery) or in preterms without clear mechanism and within the anterior spinal artery area.
A girl was delivered by caesarean section at 35 weeks due to breech presentation and loss of fetal movement (Felter et al. 2019). She was born apneic without response to tactile stimulation. Her brain MRI was normal, spine MRIs were consistent with injury from the cervicomedullary junction to T2 with sparing at C3-C5. Functional progress was observed at at 3 years of age following activity-based therapies (ABT), with improvement in milestone achievement including
fine and gross motor skills and social/cognitive development.
The sonographic contribution to detection of spinal cord injury in the newborn is well established (de Vries et al. 1995, Simanovsky et al. 2004).
Berck DJ, Mussalli GM, Manning FA (1998) Atraumatic fetal cervical spinal cord injury and cruciate paralysis. Obstet Gynecol 91(5 Pt 2):833-834.
Blount J, Doughty K, Tubbs RS, Wellons JC, Reddy A, Law C, Karle V, Oakes WJ (2004) In utero spontaneous cervical thoracic epidural hematoma imitating spinal cord birth injury. Pediatr Neurosurg 40:23-27. [term elective caesarean for breech presentation; C5 to mid-thoracic epidural mass on late neonatal MR compatible with haematoma of subacute (antenatal) origin; no recovery despite surgical removal of old clot and fibrous mass; authors discuss need for urgent decompression in postnatal spinal epidural hematoma]
Bresnan MJ, Abroms IF (1974) Neonatal spinal cord transection secondary to intrauterine hyperextension of the neck in breech presentation. J Pediatr 84:734-7.
Carrascosa-Romero MC, Ruiz-Cano R, Abad-Ortiz L, Calatayud-Perez V, Martinez-Gutierrez A, Tebar-Gil R (2002) Intrauterine spinal cord injury resulting from a transverse lie. Magnetic resonance imaging. Rev Neurol 35:398-9.
de Leon GA, Radkowski MA, Crawford SE, Swisher CN, Uzoaru I, de Leon W (1995) Persistent respiratory failure due to low cervical cord infarction in newborn babies. J Child Neurol 10(3):200-204. [autopsy-confirmed spinal cord infarctions in two premature babies who survived for several months; bilateral, multisegmental infarction at the lower cervicothoracic arterial zone (inferior cervical sector), predominantly within the territory of the anterior spinal artery; both infants had acute respiratory failure, diaphragmatic respiration, intercostal paralysis, bell-shaped deformity of the thorax, and bilateral arm paresis; at the level of the infarction, multiple, scattered scars were found at postmortem in central, perimedullary, and intramedullary arteries, but occlusions were not found not in their large parent arteries]
Chapman GP et al. (1978) Spinal cord transection in utero. Br Med J 2:398. [unsuccessful podalic version at 36w, elective caesarean for breech presentation at term; normal facial mimicry in contrast with immobile upper limbs and absence of respiratory movements at birth; hyperreflexia in lower limbs; lower cervical and upper thoracic cord softening at postmortem, with presence of a normal anterior spinal artery and selective anterior root atrophy in contrast with conservation of posterior spinal roots]
Darwish H, Sarnat H, Archer C, Brownell K, Kotagal S (1981) Congenital cervical spinal atrophy. Muscle & Nerve 4:106-110. [breech, elective caesarean at term and bilateral muscular upper limb atrophy at birth in case 1, precipitate cephalic vaginal delivery in case 2 with atrophy of hand muscles at birth, uneventful delivery and floppiness in case 3; no respiratory problems and long survival follow-up, without MR demonstration of the levels of injury]
de Vries E, Robben SG, van den Anker JN (1995) Radiologic imaging of severe cervical spinal cord birth trauma. Eur J Pediatr 154:230-2.
Ebinger F, Boor R, Brühl K, Reitter B (2002) Cervical spinal cord atrophy in the atraumatically born neonate: one form of prenatal or perinatal ischaemic insult ? Neuropediatrics 34:45-51. [review of literature up to 2002; two instances of prenatal, one of perinatal origin added; levels C4-T5, C4-T2 and C1-C4; all atrophied cord parts demonstrated on postnatal MRI; all with non-progressive limb paralysis from birth and apparently non-traumatic delivery at term, in this small cohort without immediate neonatal respiratory distress]
Haldeman S, Fowler GW, Ashwal S, Schneider S (1983) Acute flaccid neonatal paraplegia: a case report. Neurology 33(1):93-95.
Hellström B, Sallmander U (1968) Prevention of spinal cord injury in hyperextension of the fetal head. Journal of the American Medical Association 20: 101-.
Kobayashi S, Kanda K, Yokochi K, Ohki S (2006) A case of spinal cord injury that occurred in utero. Pediatr Neurol 35:367-369. [stargazing breech at 30w, decreased fetal movements several weeks prior to caesarean section at term for cord prolapse; apparent cord rupture at C7-T1 on MRI at 8 months]
Koyanagi T, Horimoto N, Maeda H, Kukita J, Minami T, Ueda K, Nakano H (1993) Abnormal behavioral patterns in the human fetus at term: correlation with lesion sites in the central nervous system after birth. J Child Neurol 8:19-26. [one term infant with focal C5-C6 infarction of antenatal onset with heterogeneous aspect on MRI; presence of diaphragmatic motion in contrast with absence of fetal limb movement on antenatal ultrasound scanning]
Maekawa K, Masaki T, Kokubun Y (1976) Fetal spinal-cord injury secondary to hyperextension of the neck: no effect of caesarean section. Dev Med Child Neurol 18:228-32. [hyperextended breech and weak fetal movements; elective caesarean near term; mild respiratory distress; flaccid upper limbs in contrast with hypertonic lower limbs; bell shaped thorax and abdominal breathing]
Mamelak AN, Cogen PH, Barkovich AJ (1994) The ‘filum intermedium’ sign: focal in utero spinal cord infarct and extraspinal thecal sac. J Neurosurg 81(6):941-946.
Milunsky A (2007) Hypoxic spinal cord injury and/or abnormality in utero. Pediatr Neurol 37:76. [podalic version and abdominal binder one week prior to vacuum delivery at term; severe cord atrophy at T1-7 on MRI at 9 months: ? von Haller radiculomedullary artery stroke]
Norman MC and Wedderburn LC (1973) Fetal spinal cord injury with cephalic delivery. Obstet Gynecol 42:355-8.
Roche-Herrero MC, Miranda-Cid C, Royo-Orejas A, Escudero-Lou RM (2004) Atrophy of the cervical spinal cord as a consequence of a prenatal ischemic infarct. Rev Neurol 39(10):932-934. [severe cord atrophy around C4-C6 on follow-up MRI, compatible with ischaemia in ASA territory]
Ruggieri M, Smarason AK, Pike M (1999) Spinal cord insults in the prenatal, perinatal, and neonatal periods. Dev Med Child Neurol 41:311-7.
Rousseau S, Metral S, Lacroix C, Cahusac C, Nocton F, Landrieu P (1993) Anterior spinal artery syndrome mimicking infantile spinal muscular atrophy. Am J Perinatol 10:316-318. [postmortem confirmation of spinal cord ischaemic destruction mid thoracic and below, best compatible with Adamkiewicz artery occlusion and not ASA occlusion as suggested in the abstract; the ASA was normal at postmortem; this fetus had polyhydramnios and reduced fetal movements weeks before delivery at 36w by caesarean section for fetal distress]
Simanovsky N, Stepensky P, Hiller N (2004) The use of ultrasound for the diagnosis of spinal hemorrhage in a newborn. Pediatr Neurol 31:295-7.
Young RS, Towfighi J, Marks KH (1983) Focal necrosis of the spinal cord in utero. Arch Neurol 40:654-5. [hyperextended breech presentation but elective caesarean and immediate finger contractures plus reduced fetal movements for two weeks; almost certain antenatal lesion at postmortem with discolouration and softening at C1-C2 with complete destruction of grey and white matter at cervical level]
arteries of brainstem and spinal cord
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