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CORD STROKE AND LACERATION - keywords
cord stroke and laceration references to spinal cord stroke and laceration r e f e r e n c e s n a v i g a t o r < Abroms IF et al. (1973) Cervical cord injuries secondary to hyperextension of the head in breech presentations. Obstet Gynecol 41:369-78. Adams C et al. (1988) Spinal cord birth injury: value of computed tomographic myelography. Pediatr Neurol 4:105-9.  Allen JP et al. (1969) Laceration of the spinal cord related to breech delivery. JAMA 208:1019-22. Amine AR (1976) Spinal cord injury in a fetus. Surg Neurol 6:369-70. Aziz EM, Robertson AF (1973) Paraplegia: a complication of umbilical artery catheterization. J Pediatr 82:1051-1052. Babyn PS et al. (1988) Sonographic evaluation of spinal cord birth trauma with pathologic correlation. AJR Am J Roentgenol 151:763-6. Baehr M, Frotscher M (2012) Duus’ Topical Diagnosis in Neurology: Anatomy, Physiology, Signs, Symptoms. 5th edition. 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Yamano T et al. (1992) Cervical cord birth injury and subsequent development of syringomyelia: a case report. Neuropediatrics 23:327-8.Yoon K, Yoo SJ, Suh DC, Lee YA, Kim KS, Choe G (1997) Möbius syndrome with brain stem calcification: prenatal and neonatal sonographic findings. Pediatr Radiol 27(2):150-2. Young RS, Towfighi J, Marks KH (1983) Focal necrosis of the spinal cord in utero. Arch Neurol 40:654-5.  Zaidi SMH, Syed IN, Tahir U, Noor T, Choudhry MS. Moebius Syndrome: What We Know So Far. Cureus. 2023 Feb 19;15(2):e35187.  > adult cord stroke neonatal cord stroke perinatal spinal cord stroke and laceration neonatal cord laceration neonatal medulla contusion In the perinatal period, with acute presentation shortly after birth, the rare occurrence of spinal cord infarction and laceration has been documented with immediate imaging. Although the spinal cord types of infarction in adults are not reported in detail in the newborn, their presentation must be similar, because neonatal spinal cord arteries are identical to the mature ones.  Both stroke and cord laceration may be related to mechanical forces developed during delivery. Cord laceration is therefore discussed here together with cord stroke. These lesions are rare, but catastrophic.  Manipulation of the aorta by surgery or catheterisation is a rare cause of radiculomedullary artery embolism and cord stroke leading to paraplegia. This event can occur any time during the neonatal period.  s u m m a r y antenatal cord stroke perinatal spinal cord stroke and laceration: summary 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 The spinal cord is supplied by multiple radiculomedullary arteries (RMAs), which feed the anterior spinal (ASA) and two posterior spinal arteries (PSA)(Sarnat 2004, Balestreros et al. 2013, Gailloud 2013, Netter 2013, Colman et al. 2015, Weidauer et al. 2015). These radicular arteries stem from spinal segmental branches of the large cervical and thoracoabdominal arteries (vertebral, costovertebral, subclavian, aorta …). From the spinal arteries, traversing the intervertebral foramina, many radicular arteries pass medially to supply the anterior and posterior nerve roots. Paired segmental arteries form a muscular and a spinal branch; spinal branches are provided along the cord in 12 unpaired vessels to form a rich posterior spinal collateral network. Although any radiculomedullary artery may split in an anterior and posterior radicular artery, often only one branch runs along the ventral or dorsal nerve root to the spinal cord.  Only some of the larger arteries reach the dura mater, where they give off small meningeal branches and then divide into ascending and descending branches to contribute to the spinal arteries. The anterior RMA’s are usually larger than the posterior ones, because they provide perfusion to about 2/3 of the cord substance.  In the lumbar region, pelvic and lateral sacral vessels arising from the internal iliac artery feed the thoracolumbar cord and conus medullaris. The anterior spinal artery (ASA), most often branching off bilaterally from the intracranial segment of the vertebral artery distal to the origin of PICA, lies within the midline pia along the entire length of the cord. At the craniocervical level, the confluence of two intradural branches originating from the vertebral artery generates the apical anterior spinal artery. Besides missed fusion of the two vertebral branches resulting in two anterior spinal arteries, segmental duplication for a short distance is frequent. In these cases, each one of the dual anterior spinal artery supplies one inner half of the cord. Therefore, sulcocentral spinal artery syndrome may be a likely consequence of unilateral occlusion in anterior spinal artery duplication. This arterial anatomy explains the occurrence, in adults mainly, of several types of arterial ischaemic cord injury. Six to ten anterior RMAs contribute to the ASA. Blood from the ASA is distributed to the anterior two thirds of the substance of the spinal cord via central (or sulcocommissural) branches and paramedian penetrating branches. The cervical and first two thoracic segments of the cord are supplied by RMAs arteries from the subclavian artery. Variability is common, and the branches may arise from either the right or the left (often alternately) to join the ASA at an angle. Not uncommonly, one anterior RMA branch arises from the vertebral artery and accompanies the C3 nerve root, one branch arises from one of the branches of the costocervical trunk (often the deep cervical artery) and accompanies the C6 root, and one branch arises from the superior intercostal artery and accompanies the C8 root. The midthoracic region of the spinal cord (T3 to T7) usually receives only one RMA, which accompanies the T4 or T5 nerve root, and this artery can be referred to as von Haller’s artery (Colman et al. 2015). Between 8 and 9/10 have at least 1 ASA contributor between T3 and T7; if no some may have one at an immediately adjacent level (T2 or T8).  The most frequent origin of upper thoracic anterior RMAs is left T5, only left T9 and left T8 are more common. A significant upper thoracic anterior RMA distinct from the artery of Adamkiewicz appears to be a constant anatomic feature, which undermines the classic concept of an arterial watershed zone in the thoracic region (Gailloud 2013). The thoracolumbosacral part of the spinal cord (T8 to the conus medullaris) derives its main arterial supply from the almost constant (9/10) left intercostal or lumbar artery of Adamkiewicz (most between T9 and L2). In the 15% of cases in which the Adamkiewicz artery reaches the cord between T5 and T8, the lower cord is supplemented by a RMA of the conus medullaris. The artery of Adamkiewicz has a large anterior and a smaller posterior branch. On reaching the anterior aspect of the spinal cord, the anterior branch ascends a short distance and then makes a hairpin turn to give off a small ascending branch and a larger descending branch to the level of the conus medullaris, where it forms an anastomotic circle with the terminal branches of the two posterior spinal arteries.  At the anterior commissure of the cord the sulcocommissural branches of the ASA turn alternately right and left to supply the corresponding halves of the cord, except in the lumbar enlargement, where the left and right branches arise from a common trunk. Their perfusion is thus from central to peripheral and highest vascular density is in grey matter.  The terminal branches ascend and descend within the cord, supplying overlapping territories. Branches from each central artery overlap with those from adjacent arteries. The central arteries supply the anterior commissure and adjacent white matter of the anterior columns, anterior horns, bases of the posterior horns, Clarke’s columns, corticospinal tracts, spinothalamic tracts, anterior parts of the gracile and cuneate fasciculi, and the region around the central canal.  The paired posterior spinal arteries (PSA) course on the posterolateral aspects of the entire length of the spinal cord, although they may become discontinuous at times. They originate from the intracranial corresponding vertebral artery, and receive 10 to 23 posterior RMAs arteries. The PSAs distribute blood to the posterior third of their respective sides of the cord. In the cervicothoracic region, the PSA receives one, and sometimes two, tributaries at each segment. Between the T4 and T8 levels, there are usually two or three posterior radiculomedullary branches, while in the thoracolumbar region, there are several feeders, one of which may be the posterior radicular branch of the artery of Adamkiewicz. The PSA branches perfuse the posterior cord from peripheral to central.  Pial Arterial Plexus. Small pial branches arise from the spinal arteries and ramify and interconnect on the surface of the cord to form a pial plexus. Penetrating branches of the plexus are radially oriented to supply the outer part of the substance of the cord; they follow the posterior median sulcus and the posterior intermedian sulcus to reach the anterior and posterior horns. The peripheral pial branches supply outer portions of the posterior horns, most of the posterior columns, and the outer portion of the white matter of the periphery of the spinal cord. There is some degree of overlap in the distribution of the peripheral and central arteries at the capillary level, but they do not anastomose at the arterial level, and hence both types are end arteries.  spinal cord stroke in neonates There have been several descriptions of the rare event of acute paraplegia (lower limb paralysis) in neonates with normally moving legs prior to an insult. The high position (above T9) of an umbilical artery catheter in the aorta has been associated with cord infarction (Aziz et al. 1973, Dulac and Aicardi 1975, Haldeman et al. 1983, Brown and Phibbs 1988). In the discussion of relevant arterial anatomy the authors have diagnosed this event as likely an embolic occlusion of the large low thoracic radiculomedullary artery of Adamkiewicz.  In early days of neonatal care this was already rare, but the event has almost disappeared after choosing for low (lumbar) arterial catheter positions, adding low doses of heparin in the infusion and avoiding its use for total parenteral nutrition. But as any other body part an embolic infarct into that vessel is possible, even in the absence of prior aortic cannulation. The event has been reported in utero as well (see antenatal spinal cord infarction). A similar event of acute paraplegia has been reported following thoracic surgery, e.g. for correction of aortic coarctation or transposition of the great vessels (Brewer et al. 1972, Amitay et al. 1993, Lemke et al. 1996). But it is exceedingly rare (Ungerleider et al. 2013). spinal cord stroke in adults In adult clinical practice the following types of infarction are possible (Baehr 2025):• Segmental large artery stroke can be observed with recognisable phenotypes: stroke within the large (70 % on the left) anterior segmental art. from the aorta at T9 to L2 level (high or low position) called the Adamkiewicz artery; this vessel is vulnerable to hypoperfusion of the aorta (coarctation, aortic surgery) or to aortic catheter-induced emboli or vasospastic agents (UAC in high position, above T9-L2); a similar left frequent anterior radiculomedullary artery exists around T5 and is referred to as von Haller’s artery. • Hypoperfusion within the anterior spinal artery may cause necrosis on both sides (central cord syndrome) or on one side (partial Brown-Séquard syndrome), all depending on the presence of anastomoses between anterior and posterior spinal circulation. Muscular characteristics of the lower anterior spinal artery indicate it has capacity to control aspects of spinal cord blood flow. Neck hyperextension may lead to occlusion/spasm in this vessel at low cervical level. The cardinal clinical features are: flaccid para- or quadriplegia, evolving into spasticity (lesions of cortico- and rubrospinal tract); loss of pain and temperature sensitivity below the upper level of the infarct with preserved touch and vibration sensitivity; bowel and bladder paralysis. Initially the clinical presentation may simulate spinal muscular atrophy. Congenital upper limb flaccid paralysis by cord infarction has been referred to as cruciate paralysis (Berck et al. 1998). • Centromedullar syndrome (anterior spinal artery syndrome): flaccid paresis at the level and (spastic) para- or tetraparesis below the level of infarction, positive Babinski sign (lesions of cortico- and rubrospinal tract), dissociated sensation deficits (loss of pain and temperature sense), bladder and bowel dysfunction, possibly vegetative dysfunctions and Horner’s syndrome. Atypical proximal infarction (depending on anatomic variation of arteries) may present as “man in the barrel syndrome” (isolated upper limb paralysis with normal cranial nerve function). • Sulco-commissural spinal artery syndrome: ipsilateral flaccid paresis at and spastic (hemi-)paresis below the level of infarction, contralateral dissociated sensation deficits. • Posterior spinal artery syndrome: disturbance of proprioception (light touch and vibration sense), ataxic gait disturbance.Patients with posterior spinal artery syndrome have back pain and leg paresthesias together with loss of touch, vibration sensitivity and position sense below the lesion; due to partial damage to the lateral corticospinal tract a milder degree of flaccid paralysis may be associated. • Syndrome of the artery of Adamkiewicz: (in-)complete transverse spinal cord syndrome: flaccid paresis at the level and (spastic) paraparesis below the level of infarction, positive Babinski sign, (in-)complete loss of sensation, bladder and bowel dysfunction. • Interarterial watershed injury will cause centro-spinal infarction syndrome (pencil-shaped on sagittal MRI, en crayon); this may be seen above and below a genuine anterior spinal infarct. perinatal traumatic cord laceration Crothers and Putnam 1927 laceration contusion A recent literature review is by Volpe in 2008.(references from there completed by cross-referencing, added to the reference list) There can exist predisposition to mechanical cord trauma during birth by the presence of fetal hypotonia (e.g. by anaesthesia, muscle disease, asphyxia), which may be relevant in a medicolegal context. Bony abnormalities (malalignment of the cervical vertebrae) may also predispose to cord injury, e.g. during delivery or intubation (Fenger-Gron et al. 2008; Meinecke FW 1978). The obstetric context is often one of rotation by forceps (not all forceps instruments offer this possibility) of the head during cephalic vaginal delivery, or of traction/elongation of the neck during vaginal breech delivery. But several other circumstances have been reported: vaginal cephalic delivery with fundal pressure, shoulder dystocia following vaginal cephalic delivery, forceps extraction at caesarean section, caesarean section following the Zavanelli manoeuvre (repositioning of the head into the pelvis after failed vaginal cephalic delivery)(Hankins 1998), difficult vaginal delivery from transverse presentation, caesarean section from breech presentation with neck hyperextension and even apparently uneventful vaginal cephalic delivery. Even direct transabdominal cord trauma by stabbing has been reported (Amine et al. 1976). There are two types of cord trauma during birth that stand out, most common is at high cervical level (above C4): - C1-4: associated with rotation by forceps, bony lesions common but may be absent, must be carefully sought at postmortem; when the mechanical manoeuvre is detailed, rotation of the neck by forcep blades for more than 90° is singled out as the likely mechanism (Menticoglou et al. 1995); - C4-T4: traction-elongation and flexion during breech delivery; especially if in utero hyperextension and than sudden flexion during delivery (both in breech and transverse presentation); hyperextension narrows the spinal canal most around C8. 5 % Of breech infants are in hyperextension (star gazing) and they are at a 25 % risk of cord injury during breech delivery. Similar events may affect the flying fetus, in transverse lie with neck hyperextension.  In both situations primary caesarean section is recommended, but even than cord injury remains possible. Early pathological changes are: haemorrhage (central and dorsal most common), contusion, cord laceration (may be with intact dural sac), infarction (at vertebral level or in lower segments due to arterial compromise). Late changes include: atrophy, syringomyelia, transsynaptic dying back below and above lesion. Cord lesions can occur in the absence of permanent bone displacement or of tearing of ligaments. The lesions can be visualised with high frequency linear ultrasound, although the haemorrhagic component in the cord or around it, testimony of trauma in most cases, can only be depicted with MRI. In many infants an early scan documents the lesion, a later scan better delineates the extent and excludes other diagnoses as appropriate (tumor, vascular anomaly, epidural bleeding with cord compression, primary arterial ischaemic stroke …). Traumatic cord injury by traction or rotation (transection) is recognized by excluding other causes and by depicting both oedematous and haemorrhagic changes in the cord itself. CT myelography is no longer needed when MRI can be used. Clinical presentation is with: so-called “asphyxia"; a dural snap heard and felt at delivery of aftercoming head; respiratory failure [above C4 total insufficiency; below C4 paradoxical (diaphragmatic) breathing (phrenic nerve in motor roots C3-5, mainly C4)]; normal facial mimicry, brainstem reflexes and cranial nerves; soft, bulging abdomen; apparent limb movements may be vigorous withdrawal reflexes; presence of a sensory level below which sensation is absent (may be asymmetrical) (pinprick and watch facial mimicry, not just withdrawal); neurogenic (spastic) bladder and patulous anus. Above T1 lesions may cause Horner’s syndrome. Temperature swings are common in young infants. The motor problem consists of flaccid limb paralysis with absent tendon reflexes: below T1 lower limbs, above C5 lower and upper limbs. One can observe hypertonic Thorburn posture due to C5-6 lesion, a C7-T1 lesion will cause hypotonic arm paralysis. Apparent ascension of a level due to oedema is possible in the first days. Affected limbs may remain flaccid (if nerves and/or anterior horn cells involved) or develop spastic paralysis after weeks to months (recovery from spinal shock). At the end of the first month the evolution or not to spinal spasticity should be clear. Respiratory recuperation, if not present 48 h after birth, is unlikely later on. Cervical spinal cord birth trauma includes: (1) nerve plexus lesions and/or (2) cord lesions and/or (3) lesions to bone and ligaments and/or (4) direct vascular injury. The cord is less elastic than dura and bony columns, this permits stretching of the column to a greater extent than the cord, which is fixed at the brainstem and the cauda equina. Other possible foci of injury in a context of injury to the cervical cord are thoracolumbar cord injury (breech delivery) and occipital osteodiastasis (breech or forceps delivery with contusion of the inferior cerebellar surface). In conditions that bear resemblance to the ones that lead to cord transection, damage to the lower brainstem has also been described. The classical reference from Crothers and Putnam in 1927 concludes with a timeless quality, based on the previous literature (first description by Parrot in 1870) and on extensive personal experience of 28 cases, like this: “The spinal column of the infant consists of a series of elastic rings joined by relatively brittle discs and ligaments. Inside of the vertebral canal lies the tube of dura mater, attached by many strong fibrous bands in the cervical and lumbar regions, but very loosely attached to the surrounding canal in the thoracic region. The cord itself is anchored firmly by the brachial plexus above and by the cauda equina below with but little support in the thoracic region. On the whole, it is relatively inelastic and friable. Obviously excessive elongation of the spinal column may put intolerable strain upon the cord or upon the meninges or upon both, between the two relatively stable anchorages. Also it is evident upon study of cadavers that lateral traction upon the head against a fixed shoulder, through tension upon the plexus, draws the cord to one side of the canal and fixes it there. Under these circumstances an increased pull, particularly if abrupt, may result in avulsion of the plexus from the cord. In addition to traction, hyperextension and torsion are forces to be considered. There is abundant evidence that fracture dislocations in the cervical region are common. Clearly such injuries may or may not involve the central nervous system. Since most of these injuries are high enough to prevent the initiation of breathing if the cord is injured they are of relatively little importance in relation to the clinical disturbances to be considered. On the whole a study of the literature and a review of our own cases adds to the definite conclusion that most of the cases reported are due to the imposition of the unphysiological force of traction. Obviously in occasional cases the evidence is lacking, but there is no valid reason for concluding that asphyxia or generalized pressure are responsible in the atypical cases. Since traction upon a part of the foetus already delivered against the resistance of the part still within the birth canal is an entirely unphysiological procedure, it is evidently wise to determine the resistance of the tissues upon which it is exerted. The evidence upon this point seems to us quite clear. The most fragile and least elastic structures are the spinal cord, the membranes protecting it and the nerves issuing from it. As the force imposed is entirely under the control of the operator, it is incumbent upon him to realize that he is exerting it upon the nervous system and the membranes covering it as well as upon the strong and elastic tissues about it. It is, of course, quite inadmissible for those who do not deliver babies, to lay down principles for those who deal with the emergencies of childbirth. On the other hand, owing to the concentration of babies injured at birth in our clinic, we are in a position to emphasize the fact that traction is an important source of disability.  The contrast between the almost complete silence of obstetrical textbooks upon the danger and upon the non physiological nature of traction, and the evidence which has accumulated is striking. We feel that, until writers of obstetrical textbooks take up the control of stress upon the nervous system of the foetus as an important factor in successful delivery, accidents will occur in unnecessary numbers. We believe that the present serious situation can be corrected by careful revision of obstetrical teaching with increased emphasis upon the methods of avoiding injury and decreased attention to asphyxia.” Cothers and Putnam 1927 A medullary haemorrhage/contusion was seen on axial sections of the brainstem above and behind the ear, as an hyperechoic portion of brainstem below the pons. Focal medial striate and ipsilateral left posterior truncal MCA stroke were associated. MR angiography did not reveal basilar artery occlusion in the second week of life. Mechanical distortion and spasm of the basilar artery, is a plausible hypothesis, but multiple emboli from unknown source (e.g. carotid artery) or multiple arterial traction/distortion lesions are alternative hypotheses perinatal brainstem contusion In conditions similar to those that lead to cord transection, damage to the lower brainstem has been reported. A personal observation following a Zavanelli manoeuvre is presented here.  Term delivery with caesarean section following failed instrumental traction. The head had to be pushed up into the uterine cavity to make caesarean section possible (Zavanelli manoeuvre). This boy remained quadriplegic and apnoeic from birth untill death at the end of the first month following withdrawal of ventilation. He was alert and had normal facial mimicry and eye movements.  Mac OS X  2ÖATTRÜ,Ücom.apple.TextEncodingë com.apple.provenanceöcom.apple.quarantineutf-8;134217984Â.Im0ÖWq/0081;00000000;;