OUTER HOUSE, COURT OF SESSION
 CSOH 63
OPINION OF LORD HODGE
in the cause
Pursuer: Dunlop, Q.C.. Gianni; Morisons
Defenders: Stacey, Q.C., Stuart; R F Macdonald
McKenzie is a twelve-year-old boy who suffers from cerebral palsy which was
caused by events when his mother was in labour before his birth. He was born at 2344 hours on
Admission of Liability
 The defenders lodged a Minute of Admission of Liability in the following terms:
"That for the purposes of this action only, and without prejudice to their rights and pleas in relation to causation and quantum of damages, the defenders hereby admit liability to make reparation to the pursuer, as guardian for Kyle McKenzie, for any loss, injury and damage sustained by Kyle McKenzie as a result of his not being born by 2140 hours on 25 February 1994".
pursuer's contention on liability was that the defenders were negligent in
failing to deliver Kyle either two hours and thirty minutes or in any event two
hours before he was born. Shortly after
2000 hours on
The parties' contentions on causation
 The pursuer's contention was that if Kyle had been delivered two hours before he was, he would not have suffered the cerebral palsy from which he has suffered since birth. The defenders' contention was that the damage to Kyle's brain was caused by an undetected event several hours before his birth and, in particular, before 2000 hours; thus the admitted negligence of the defenders' employee did not cause him to suffer the injury that has caused his cerebral palsy.
The nature of Kyle's condition
condition is not in dispute; Dr Christopher Steer, a Consultant Paediatrician
 The parts of Kyle's brain that suffered the most severe damage were the basal ganglia. These are particularly susceptible to asphyxial damage because of their high metabolic activity. They are involved with the regulation of voluntary movements at a subconscious level and when damaged can cause involuntary movements of the face and limbs. He also has suffered epilepsy and some learning difficulties which indicate that he suffered some damage to the cerebral cortex. There appears to be hippocampal damage, in the temporal lobe, which could explain Kyle's cognitive impairment and epilepsy. Kyle's intellectual function has been relatively preserved but he has difficulty in communicating. Kyle also suffered short-term mild to moderate damage to his kidneys which manifested itself in blood in his urine and elevated levels of urea and creatinine in the days immediately after his birth.
 There is no dispute as to the cause of a dyskinetic form of cerebral palsy: it is caused predominantly by an acute profound asphyxia. That form of asphyxia involves a relatively sudden shutting off of a foetus's oxygen supply before its body can adapt to the problem. This causes damage principally to the parts of the brain such as the basal ganglia with high metabolic activity while sparing parts of the brain with less metabolic requirement. Dr Brian Kendall, a Consultant Neuroradiologist at the Royal Free Hospital and honorary Consultant Neuroradiologist at the Hospital for Sick Children and the National Hospital for Neuroradiology and Neurosurgery, London, gave expert evidence on the damage to Kyle's brain that was revealed by the neuro-imaging of a cranial CT scan which had been performed in April 1997. That neuro-imaging revealed damage to the lentiform nuclei which form part of the basal ganglia, to the pre and post central gyri in the cerebral cortex and in the superior vermis of the cerebellum. These three regions are centres of high metabolism in a mature foetus and therefore vulnerable to an acute and generalised drop of the circulation of oxygenated blood to the brain.
 The cerebral palsy was caused by an injury to his brain in the intrapartum period; that is during the course of labour. While in their written pleadings the defenders averred that the damage occurred at least twelve hours before delivery, the one expert witness whom they led at proof accepted that it was likely that Kyle sustained the injury during labour. There was no expert evidence led before me to suggest otherwise. Therefore the issue in this case is: when during labour did that acute event occur? To determine that I have first to summarise the facts of the pursuer's pregnancy and labour which were established and most of which were never in dispute.
The pursuer's pregnancy and labour
 The pursuer had an uneventful pregnancy. She had no major risk factors except that she was a moderate smoker. But Kyle demonstrated none of the complications associated with smoking. Foetal growth was assessed as appropriate at all stages. There was no evidence of reduced liquor volume. There was no evidence of an inadequate placenta giving rise to growth retardation. In short, there were no obvious antenatal complications. His birth weight was 3.26 kg, which was within the normal weight range at birth. There was no evidence of any early intrauterine brain damage or of any malformation of the brain. Thus in prospect and with hindsight there was nothing which pointed to any antenatal compromise.
 The pursuer was admitted to
 The pursuer's membranes ruptured spontaneously at 1200 hours. The rupture revealed liquor stained with meconium (the contents of the foetal bowel). Initially the defenders appeared to suggest that the meconium indicated that Kyle might have suffered the insult to his brain which caused his cerebral palsy at a time before he came into hospital. But Mrs Stacey (reflecting the evidence of her expert witness) presented her closing submissions on the basis that it was more likely that Kyle suffered the relevant insult during the afternoon or early evening when the CTG was recording his heart rate. She did not invite me to treat the meconium staining at 1200 hours as significant. This was consistent with the evidence of Professor Greer, the Professor of Obstetrics and Gynaecology at Glasgow University and Honorary Consultant in Obstetrics and Gynaecology at Glasgow Royal Infirmary and Princess Royal Maternity Hospital, and Dr David Lloyd, Consultant in Perinatal Medicine in Grampian University Hospitals NHS Trust, who opined that the presence of meconium on the rupture of the membranes was not unusual with babies who were delivered after their forty-week term. In support of this view I was referred to research articles by Steer and Others (1989) and by Meis and Others (1978).
 The CTG was temporarily discontinued for ten minutes between 1610 hours and 1620 hours when an epidural anaesthetic was being set up. Otherwise the CTG monitored the foetal heart rate continuously from 1245 hours and revealed that, although there were occasional variable decelerations, it was within the normal range. This was consistent with the wellbeing of the foetus. At 1930 hours the CTG showed a baseline tachycardia (an increase of the heart rate above the normal) but the heart rate had normal variability. This did not indicate foetal distress. But after 2000 hrs the CTG trace revealed an erratic foetal heart rate with late decelerations. Late decelerations are thought to be associated with foetal hypoxia. Professor Greer explained that the CTG trace showed a serious tachycardia at 2012 hours, that the foetus's baseline variability was flat and that late decelerations occurred at 2015 hours and 2026 hours. The tachycardia remained at 2100 hours, when the pursuer was reviewed; late and variable decelerations and reduced variability were observed. Professor Greer described the CTG trace as showing multiple serious abnormalities consistent with foetal distress and opined that the syntocinon infuson should have been stopped and steps taken to deliver Kyle by Caesarean section by 2140 hours. Thereafter the CTG trace revealed baseline tachycardia, and late decelerations following uterine contractions with reduced baseline variability. By 2300 hours the pursuer's cervix was fully dilated and the pursuer was encouraged to push actively in the second stage of labour. At around 2316 hours the CTG revealed a baseline bradycardia (a slowing of the heart rate below the normal), a heart rate of about 100 beats per minute ("bpm") with reduced baseline variability and late decelerations which continued until delivery at 2344 hours. Professor Greer described the foetal heart rate recorded on the CTG as having been pathological for three hours and forty-five minutes, in other words since 2000 hours.
Kyle's condition at and after his birth
 As much of the dispute between the parties turned on the interpretation of the symptoms that Kyle showed shortly after birth, it is necessary for me to record the findings of those who treated him in some detail. There has been no criticism of the way in which Kyle was resuscitated and thereafter cared for. I therefore do not record his treatment except where it is relevant as the context in which findings were made. The medical notes described Kyle on delivery as flat, cyanosed and pale with no spontaneous movement. There were no respiratory movements. Meconium was noted in his mouth and pharynx. At one minute after birth his heart rate was 50 bpm. Doctors applied a bag and mask to get oxygen into him and that rapidly increased his heart rate to over 120 bpm. As a result his colour improved. But at five minutes of age he remained flat and he was still making no respiratory movements. His Apgar scores were recorded as two at one minute after birth, three at five minutes and five at ten minutes. A registrar arrived and intubated Kyle, noting that he was flat, but pink centrally. Irregular respiratory efforts started at seven minutes of age. Kyle was transferred to the Special Care Baby Unit at 0010 hours on 26 February. On arrival in that Unit he was noted to be tense on handling at 0010 hours (twenty-six minutes of age). Arterial blood gases were taken at 0020 hours and sent to laboratory for analysis. That analysis revealed that Kyle had a profound metabolic acidosis: his blood had a pH of 6.95 and a Base Excess of 22. A metabolic acidosis arises where the foetus is deprived of oxygen and in metabolising glucose creates acid and is consistent with a significant hypoxic ischaemic event.
 Kyle commenced spontaneous movements at forty-five minutes of age and became agitated and tense on handling. He was recorded as making fisting and cycling movements at ninety minutes of age and the note also recorded that no seizures were seen. Witnesses expressed differing views as to whether the cycling movements were subtle seizures or were release phenomena - see paragraphs ,  and  below. He passed urine containing blood. Kyle was given plasma protein and sodium bicarbonate and as a result his blood pH improved and was almost normal by 0400 hours on 26 February (four and a quarter hours after birth). At 0430 hours (at four hours and forty-six minutes of age) it was noted that he had been extremely agitated over the past two hours. He displayed extensor thrusting, arched his back, clenched his hands and he was boxing with his arms. These findings were consistent with severe cerebral irritation. At 1010 hours he was extubated. He was noted to be very hypertonic (stiff) and he cried when disturbed. He was noted to be almost opisthotonic and he had stridor. Opisthotonus is extreme arching of the back and stridor is a crowing noise made during inspiration; the former was a very worrying sign indicating involvement of the brain stem; the latter may have been the result of intubation.
 On 27 February Kyle had two epileptic seizures in the morning
and was given anticonvulsant medication.
He remained in a very arched position.
There was evidence that his kidneys were not functioning; his urinary
output was minimal and contained blood and protein; he had elevated urea and
creatinine. He was diagnosed as
suffering from acute tubular necrosis, which was a sign that the kidneys had
received a recent insult. He was
hypertonic in all four limbs; his arms were flexed and his legs were
extended. He remained hypertonic on 28
February and still did not pass significant amounts of urine. His urine had large amounts of blood and
protein in it. On
 Kyle was admitted to hospital on
 There was no significant disagreement between experts on the categorisation of Kyle's condition at birth. I was referred to research by Sarnat and Sarnat (1976) which was discussed in Stevenson and Sunshine's "Fetal and Neonatal Brain Injury" (2nd ed.1997) (chapter 18). Within the Sarnat classification, the experts agreed that Kyle was most appropriately classified as having Stage 2 (moderate) hypoxic ischemic encephalopathy.
The cause of Kyle's dyskinetic cerebral palsy
(i) The parties' cases
 The pursuer's case was that there was clear evidence from the
CTG trace of an acute ischaemic hypoxic insult in the final stages of labour
which was of a nature that could cause the dyskinetic cerebral palsy from which
Kyle suffers. The acute event occurred after 2140 hours
 The defenders' case that the acute event which caused Kyle's dyskinetic cerebral palsy occurred during labour but before 2000 hours on 25 February 1994 rested on the expert evidence of Dr Robert McWilliam, a Consultant Paediatric Neurologist at the Royal Hospital for Sick Children in Glasgow. He opined that it was likely that the acute ischaemic brain insult which caused Kyle's cerebral palsy occurred not less than six hours before his birth. He noted that both the brain and the kidneys were compromised. While he recognized that there was uncertainty as to the timing of perinatal insults, from observation in medical practice he had noted that after an infant had suffered a generalised brain insult which caused permanent neurological damage there was always a period of almost complete inactivity of its central nervous system for between six and twelve hours. In his oral evidence Dr McWilliam qualified this statement by saying that the period of inactivity was usually not less than six hours and was always greater than four hours. He considered that what he had observed with infants could be applied to a foetus at the final stages of a pregnancy. Clinically the inactivity manifested itself as hypotonia (a state of reduced tension in muscles) and lack of responsiveness. This pattern was evident in infants who had strokes. He noted that Kyle was described as "tense" at twenty-six minutes of age and that he showed extreme irritability and extensor thrusting at four and a quarter hours of age. He associated the fisting and cycling movements that Kyle made at ninety minutes of age with release phenomena - movements caused by the brain stem which was not being effectively controlled by higher centres in the brain. He suggested that the speed with which Kyle manifested active neurological symptoms and also recovered normal respiratory control after his birth pointed strongly to the occurrence of a hypoxic ischaemic brain insult many hours earlier. He opined that the hypoxic ischaemic insult which Kyle suffered in the thirty minutes immediately before his birth, which he described as "a potentially damaging circumstance", did not add significantly to brain damage which was already present.
 In support of his view he pointed out that asphyxia at birth of
the degree that Kyle suffered occurred quite frequently (in about one in every
hundred births) without the development of a neonatal encephalopathy or
cerebral palsy. While there had been a
considerable reduction in the incidence of asphyxia in recent years, there had
been no corresponding decline in the incidence of dyskinetic cerebral palsy
which remained at one in one thousand births.
He suggested that this allowed one to infer that birth asphyxia was not
an important cause of dyskinetic cerebral palsy. Secondly, he supported his view by the
observation that the temporary damage to Kyle's renal function was an unusual
consequence of a single acute hypoxic insult.
He suggested that Kyle's renal damage was a manifestation of an earlier
insult in which his body had undergone physiological changes to protect the
brain at the expense of other organs. He
also suggested that the difficulties that Kyle encountered after 2000 hours on
 In deciding between the parties' contentions it is in my opinion important to start by considering the nature of Kyle's condition and the process that caused that condition. As I have said, parties agreed on these matters. See paragraphs  to  above. Dyskinetic cerebral palsy is a relatively unusual form of cerebral palsy when a child is delivered at term. I was referred in this regard by both parties to a paper by Lewis Rosenbloom (1994) about a study of the connection between birth asphyxia and dyskinetic cerebral palsy from data collected in Merseyside. Dyskinetic cerebral palsy is caused by damage to the basal ganglia which in turn is caused by brief near-total asphyxia, an acute event which does not allow the foetus to adapt to the insult and which damages the structures of the brain which have high energy requirements. Animal studies by Myers (1972) have given rise to a paradigm discussed by Pasternak (1993) of the acute hypoxia allowing full recovery if the insult lasts less than ten minutes, but inflicting increasingly severe neuronal damage when the insult lasts between ten and twenty-five minutes, and causing irreversible vascular collapse and death after twenty-five minutes. The acute total asphyxia created in the laboratory rarely if ever occurs in human infants; it is more common for an acute near-total asphyxial event to be preceded by partial asphyxia caused by the impairment of the exchange of gases between the mother and the foetus. Animal studies have shown that preceding partial asphyxia can cause the foetus to deteriorate more rapidly when exposed to acute asphyxia thereafter.
 When did the acute near-total asphyxial event occur? In recent years medical literature has warned against an uncritical attribution of the cause of neonatal encephalopathy to pre-birth asphyxia in the later stages of labour. Among others, Stanley, Blair and Alberman (2000) have suggested that in the past researchers and clinicians have overestimated the significance of birth asphyxia in the aetiology of cerebral palsies and that an antenatal insult or condition was the cause of most cerebral palsies. As is stated in the template to which I refer in the next paragraph, epidemiological studies have suggested that in about ninety per cent of cases intrapartum hypoxia could not have been the cause of cerebral palsy and that in the remaining ten per cent intrapartum signs compatible with damaging hypoxia might have had antenatal or intrapartum origins. Nonetheless, as Dr Zuberi pointed out, Aicardi and Bax (1992) suggest that the incidence of perinatal factors is higher in cases of dyskinetic cerebral palsy than in other forms of cerebral palsy.
 Fortunately, in this case it is not necessary to consider the
likelihood of an acute near-total asphyxial event before the onset of
labour. The pursuer's expert witnesses
all suggested that the acute event which caused Kyle's cerebral palsy occurred intrapartum (during labour). Dr McWilliam, on cross-examination, agreed
but placed the event at some time before 2000 hours on
 What we do know however is that the CTG trace of Kyle's heart
rate after 2300 hours on
 Mrs Stacey in her closing submission suggested that the issue in this case was simply a question for consultant paediatric neurologists such as Dr McWilliam and Dr Zuberi and implied that experts from other disciplines had little to offer in helping the court to decide on the balance of probabilities when Kyle suffered the damage which caused his cerebral palsy. I am satisfied that that submission is incorrect. In my opinion it is appropriate that I should look not only at the evidence of the neurologists as to the timing of the emergence of active symptoms after Kyle's birth but also at the whole circumstances including the views of experts of other medical disciplines on what may properly be inferred from the circumstances both before and after Kyle's birth.
 In particular, it is significant that from 1245 hours on
 Significantly, Professor Greer also opined that the borderline tachycardia that Kyle exhibited at about 1930 hours (and for some time thereafter) was inconsistent with his having suffered major hypoxic damage before then: he would not have expected a severely damaged baby to exhibit normal responses on a CTG to the stresses of labour. Dr Kendall also expressed the view that it was improbable that Kyle suffered an acute hypoxic event which was not picked up on the CTG. There was no evidence of a period of bradycardia before 2000 hours and such bradycardia was needed to inflict the damage that Kyle suffered. He did not believe that Kyle's heart rate would have reverted to normal after an episode of bradycardia that caused the damage that he suffered. Dr Pearse expressed the view that it was very unlikely that Kyle suffered an acute and damaging asphyxia, made a spontaneous recovery and then showed a normal trace on his CTG, in which his heart rate reacted appropriately to stimuli during labour. Dr Lloyd also relied on the absence of evidence in the CTG trace that Kyle suffered any damage during labour before 2000 hours to support his view that such early damage did not occur.
 I consider this uncontradicted evidence of distinguished medical experts from disciplines other than paediatric neurology to be highly relevant to the question of causation. Unless there were persuasive and properly vouched evidence from neurologists that the timing of the emergence of symptoms after birth meant that the acute event must have occurred earlier during labour than the CTG suggested, I would consider this evidence sufficient to satisfy me that the acute event that caused the damage to Kyle's brain occurred within the final forty minutes of labour, preceded by a period of partial asphyxia after 2000 hours. Was there such contrary evidence?
 In my opinion there was not. Dr McWilliam's view, that there was invariably a period of at least four hours after a generalised brain insult which caused permanent neurological damage before active abnormal neurological behaviour emerged, was based on his own observation of infants. It was not supported by the medical literature.
 The template referred to in paragraph  above did not identify the timing of the emergence of such behaviour as an indicator of a causal relationship between an intrapartum event and cerebral palsy. There was considerable debate in evidence over the meaning of a passage in Volpe (chapter 9, p.333) in which he discussed the clinical aspects of hypoxic-ischaemic encephalopathy. Among the clinical features of severe hypoxic-ischaemic encephalopathy in the first twelve hours after birth Volpe lists (in table 9.4) the occurrence of hypotonia with minimal movement more than hypertonia. It was suggested in evidence that Volpe's classification of the severely affected infant was broadly equivalent to Sarnat and Sarnat Stage III classification, and that appears to be correct. Volpe goes on to state:
"The large majority of infants at this stage are markedly and diffusely hypotonic with minimal spontaneous or elicited movement. Less-affected infants have preserved tone or occasionally some increase in tone. The latter is particularly likely with prominent involvement of the basal ganglia."
In the period from twelve to twenty hours after birth, Volpe states that infants with involvement of the basal ganglia may exhibit an increase in their hypertonia, especially in response to handling. Dr McWilliam suggested that Volpe was less specific in his views than he was but that nothing Volpe said contradicted his opinion as to timing. Nonetheless, what Volpe says does not unequivocally support Dr McWilliam's view. In particular, if, as was suggested by Dr Lloyd and Dr Zuberi, Volpe's reference to less- affected infants with basal ganglia damage in the passage quoted above was broadly equivalent to Kyle's classification (i.e. Sarnat and Sarnat Stage II), an increase in tone in the first twelve hours after birth was to be expected.
 Studies by Constantinou and Others (1989) and by Ahn and Others (1998) suggest that the interval between an asphyxial event and the ensuing encephalopathy may vary considerably and that there is no reliable time relationship between perinatal asphyxial insults and the onset of seizures. See the chapter by Dear and Newell on cerebral palsy and intrapartum events (chapter 14) in Clements' "Risk Management and Litigation in Obstetrics and Gynaecology" (2001). The study by Ahn and Others (1998) suggests that the onset of seizures after birth does not of itself appear to be a reliable indicator of the timing of foetal brain injury. While it was pointed out that in that study the authors used evidence of abnormal foetal heart rates detected by monitoring as the likely time of the hypoxic ischaemic events (and therefore the results were not inconsistent with Dr McWilliam's thesis in cases where an abnormal foetal heart rate was a symptom of an earlier damaging event), the study provides no support for Dr McWilliam's position.
 Dr McWilliam's view on timing was also not shared by Dr Zuberi, the only other paediatric neurologist who gave evidence. Dr Zuberi expressed the view that there was no clear pattern of timing of the onset of abnormal active cerebral activity and spoke of having seen hypertonia and seizures within the first hour after a global ischaemic injury. He opined that one could not reach conclusions with any confidence as to the timing of an otherwise silent global ischaemic insult from the time at which such symptoms emerged. He based his views on his own clinical experience and his review of the literature. In his evidence he referred to Volpe (above) and to a paper by Pasternak and Gorey (1998) which, in a study of eleven infants born at term after an acute, near-total uterine asphyxia at the end of labour, suggested that there was a wide range in the timing of the onset of seizures following such an insult. I accept that it is not possible on the published information to compare with any accuracy the severity of the insult to each of the infants in that study to that which Kyle suffered. Nonetheless, the paper does not suggest that the time of onset of seizures is a reliable guide to the timing of the causative insult. Dr Zuberi also referred to an illustrative case in Pasternak's 1993 paper (referred to in paragraph  above) in which a woman suffered a uterine rupture and had her baby delivered within twenty minutes of presentation at hospital and her baby suffered seizures at forty-five minutes of age. I accept, as Mrs Stacey submitted, that one cannot take very much from the case because the reader of the paper does not know the timing of the uterine rupture before the mother arrived in hospital and because the baby had more severe acidosis than Kyle. Nevertheless it does not appear to support Dr McWilliam's general thesis. While Dr Zuberi had practised in his specialty for considerably fewer years than Dr McWilliam, he was, like Dr McWilliam, a distinguished medical practitioner and I saw no reason to discount his evidence and to prefer Dr McWilliam's on the ground of seniority. In my opinion Dr Zuberi's view, that the timing of onset of hypertonia and seizures is a poor indicator of the timing of the asphyxial event, is supported by the medical literature to which I was referred. In addition he was supported by the evidence of neonatologists: both Dr Lloyd and Dr Pearse thought that the early emergence of Kyle's hypertonia was consistent with very recent damage to his basal ganglia.
 For the sake of completeness, I should make clear that I am not persuaded that it makes any difference if active symptoms such as fisting and cycling were subtle epileptic seizures or brainstem release phenomena. Whichever they were, I am not satisfied that their early emergence after birth is a reliable indicator that the acute insult occurred four or more hours beforehand. On this matter I accept the evidence of Dr Zuberi.
 I can deal briefly with the other points that Dr McWilliam made in support of his theory, which I summarised in paragraph  above. I am not persuaded that the decline in birth asphyxia and the absence of a corresponding decline in dyskinetic cerebral palsy would allow me to infer that birth asphyxia is not an important cause of that type of cerebral palsy. As only a small proportion of cerebral palsies is caused by birth asphyxia, and as dyskinetic cerebral palsy is a relatively unusual form of cerebral palsy, I would not necessarily expect an overall decline in birth asphyxia to give rise to a detectable decline in the incidence of dyskinetic cerebral palsy. Secondly, the temporary renal damage that Kyle suffered, an acute tubular necrosis that resolved within about six days, does not appear to be inconsistent with an acute event. I note that in Pasternak and Gorey's study (1998) three of the eleven infants who suffered acute near-total intrauterine asphyxia had oliguria (unusually low urine output) lasting more than thirty-six hours and two others had an elevated creatinine. Dr Pearse described Kyle's renal damage as "mild to moderate" and this categorisation was consistent with Pasternak and Gorey's observation that in the context of an acute insult, injury to non-brain organs, when present, is usually mild. Thirdly, although it is possible that problems revealed by a CTG trace may be a manifestation of damage caused by an earlier insult, in Kyle's case the absence of any evidence of a sustained bradycardia in the afternoon of 25 February 1994 persuades me that, on the balance of probabilities, Kyle did not suffer an acute hypoxic insult at the time that Dr McWilliam suggested that it was likely that he did.
 I accept that there is much to learn about the effect of a
hypoxic insult on a foetus and that it is therefore necessary to be cautious
before one concludes that there is a causal link between intrapartum events that manifest themselves as a non-reassuring
foetal heart trace on a CTG and the emergence of neonatal encephalopathy. Nonetheless,
I am satisfied on the balance of probabilities that in Kyle's case the hypoxic
insult which caused his dyskinetic cerebral palsy was an acute event that
occurred at the end of labour after 2300 hours on
 Accordingly, if the obstetric registrar, who was the defenders' employee, had acted with reasonable care by stopping the syntocinon infusion and arranging the prompt delivery of Kyle by 2140 hours on that date, I consider that Kyle would not have suffered the brain damage which has given rise to this action. I conclude therefore that the admitted negligence of that employee caused that damage.
 I therefore sustain the pursuer's first plea-in-law, repel the defenders' second and third pleas-in-law and allow a proof before answer on the quantification of loss.
Ahn MA, Korst LM, Phelan JP, Martin GI. Clinical Pediatrics 1998. Vol 37. 673.
Aicardi J and Bax M. Diseases of the Nervous System in Childhood. Clinics in Developmental Medicine No 115/118 (1992). 330.
Constantinou, JE, Gillis, J, Ouvrier, RA, Rahilly PM. Archives of Disease in Childhood 1989. Vol 64. 703
Dear PRF and Newell SJ in Clements RV "Risk Management and Litigation in Obstetrics and Gynaecology" (2001) ch 14.
Maclennan A and Others. British Medical Journal 1999. Vol 319. 1054.
Meis PJ, Marshall Hall III, Marshall JR, Hobel CJ. American Journal of Obstetrics and Gynaecology 1978. Vol 131. 509
Myers RE. American Journal of Obstetrics and Gynaecology 1972. Vol 112. 246.
Pediatric Clinics of
Pasternak JF and Gorey
Rosenbloom L. Developmental Medicine and Child Neurology. 1994. Vol 36. 285
Sarnat HB and Sarnat MS Archives of Neurology 1976. Vol 33. 696
Steer PJ, Eigbe F, Lissauer TJ and Beard RW. Obstetrics and Gynaecology 1989. Vol 74. 715
Stevenson DK and Sunshine P. Fetal & Neonatal Brain Injury. (2nd ed) (1997) ch 36 by Robertson CMT.
Volpe JJ. "Neurology of the Unborn" (4th ed) (2001) chs 5 & 9.