S v Road Accident Fund (17386/2014) [2016] ZAGPPHC 491; [2016] 3 All SA 637 (GP) (24 June 2016)

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[2016] ZAGPPHC 491
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S v Road Accident Fund (17386/2014) [2016] ZAGPPHC 491; [2016] 3 All SA 637 (GP) (24 June 2016)

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IN THE HIGH COURT OF
SOUTH AFRICA
(GAUTENG DIVISION,
PRETORIA)
Case Number: 17386/2014
DATE:  24/6/2016
Reportable
Of interest to other
judges
Revised.
In the matter between:
S
S                                                                                                                 1
ST
PLAINTIFF
S S OBO
C                                                                                                    2
ND
PLAINTIFF
And
ROAD ACCIDENT
FUND

DEFENDANT
JUDGMENT
Fabricius J,
1.
On 10 December 2012, the
First Plaintiff, being pregnant with a child subsequently born on 28
February 2013, was involved in a head-on
collision. The mother, S,
did not sustain serious injuries and the child C, was born with
cerebral palsy some seven weeks after
this collision. Her parents
sustained severe injuries. The occupants of the other vehicle were
killed. The only question in this
tragic case that I need to decide
is whether or not the condition of cerebral palsy was caused by the
high-velocity impact, or
whether it is a congenital defect. Brief
evidence was led by the mother as to what had occurred and during the
trial it became
common cause that the said collision could be
described as a “high-velocity impact”. The other vehicle
that crashed
into the vehicle in which the Plaintiffs were passengers
was almost totally destroyed as is evident from the photographs
presented
to me. In my view, even a layman can see that a collision
at high speed had occurred. The agreed upon high-velocity impact is
in
my view a relevant consideration as will become apparent when I
deal with the medical evidence presented during this trial. Viewed

differently, as Defendant does, can it be reasonably said that C’s
condition was not at all related thereto?
2.
The mother can be glad,
to put it mildly, that she escaped this horrendous accident with
relatively minor injuries. According to
the Particulars of Claim she
sustained soft tissue injury to the hand and neck, blunt chest
contusion, abrasions on the left shoulder,
and multiple scarring. The
Particulars of Claim further allege that the birth of C was normal
but, subsequent development milestones
confirmed that she was brain
damaged. The clinical presentation was that of cerebral palsy and
quadriplegia. It was pleaded that
these injuries were caused by the
collision and that the “accelerated deceleration” during
the point of impact “caused
bleeding” in C’s brain.
Damages were claimed in respect of both Plaintiffs, but the quantum
issue is not before me.
3.
Defendant denied that the
said condition was caused by the collision and in the alternative
pleaded that the injuries were the result
of pre-existing condition.
Alternatively, it was averred that the injuries referred to, resulted
post-accident.
4.
The mother’s
evidence can be summarised as follows:
She was 28 weeks pregnant
with C at the time and on 10 December 2012, was a passenger in a
Toyota Hilux Bakkie. A BMW drove into
this vehicle at high speed
which she estimated to have been 180km per hour. She also testified
that the Hilux, after the impact,
tipped over onto its side. I will
refer to this evidence again when I deal with the medical opinions,
because as innocuous as this
may seem at this stage, it becomes an
important consideration. Her parents were critically injured in the
accident and the occupants
of the BMW were killed. The mother also
testified that at the time she felt as if her whole body “wanted
to climb through
the windscreen”.
5.
Mrs S was taken to
hospital and she informed the paramedics that she was 28 weeks
pregnant. She was examined for lacerations and
an x-ray was done to
determine whether there were any other orthopaedic injuries. A few
hours after the accident, she was transferred
to the maternity ward
where a sonar scan was performed. She was told that she had gone into
early labour which needed to be arrested.
The bedside sonar scan that
was done showed that the foetus was “fine”. She was
discharged from the Welkom Medi-Clinic
on 11 December 2012. On the
next day, she again experienced pre-term contractions and again
consulted Dr Myburgh at the hospital.
Another sonar scan was done and
medication was prescribed to stop the contractions. Mrs S also
testified that during the rest of
her pregnancy with C she
experienced less foetal movement and again consulted with her general
practitioner and also requested
a further sonar scan.
6.
Dr Coleman was Mrs S’s
gynaecologist/obstetrician. She consulted him three or four times
during the pregnancy. The first of
these consultations was on 8
August 2012, during which the routine blood-tests were performed. No
abnormalities with the foetus
were detected. The last visit to Dr
Coleman prior to the accident was in early December 2012, during
which she was told that the
foetus’ development was normal,
that its growth patterns were normal and that the foetus was
positioned correctly in utero.
7.
Post-accident, Mrs S
attended further consultations with Dr Coleman. A further sonar scan
was done and the test on the umbilical
cord, i. e. to test whether
the oxygen levels were within acceptable parameters, showed no
abnormalities. Dr Coleman’s clinical
notes do not show that she
reported reduced foetal movement. This is not of a particular concern
inasmuch as the later medical
evidence made it clear that foetal
movement varied from time to time, and from person to person. C was
born on 28 February 2013
and no abnormalities with the birth were
experienced. After the birth, the mother noted that C was
particularly restless, did not
sleep as expected, had dietary
problems and would become spastic for certain periods. As a result,
she consulted a paediatrician,
Dr Kriel, who after about four months
advised her of the possibilities of neurological problems. She then
consulted Dr De Witt,
a specialist paediatrician of Arwyp Clinic in
Kempton Park. He admitted C to hospital and following an examination,
noted that
her legs had a tendency to “scissor”. He
advised the mother that C needed occupational therapy. C remained in
this
hospital for three days during which several tests were
performed on her, including:
7.1 A MRI-scan on 3 July
2013;
7.2 A barium-swallowing
test;
7.3 A test for the
presence of bowel-obstruction;
7.4 Tests for allergies.
After these tests, Dr De
Witt informed C’s parents that she had “static brain
damage”. The mother was told that
C would have to see a
neurologist, Dr Wilson at the Sunninghill Hospital. C’s formal
diagnosis is called “mixed cerebral
palsy with spastic dystopia
and limp upper body”. The mother testified that C cannot sit,
stand, walk, feed herself or hold
her head upright without
difficulty. Mrs S also testified that there was no history of
cerebral palsy in her family. During cross-examination,
the question
arose whether or not Mrs S had sustained cracked or broken ribs, but
I do not believe that this is a significant factor
in these
proceedings. It is clear that she assumed that ribs were broken on
her right side due to the pain she felt there. She
also testified
that at the time of the accident, the safety belt was not resting
over her abdomen, but rather across her pelvis.
There was also a
debate about the absence of foetal distress and it is clear from the
relevant clinical notes that no such distress
was noted. First
Plaintiff was re-called by myself on 13 May 2016 and I will deal with
that evidence and why I deemed it proper
to re-call her. C
accompanied her and I noted certain observations pertaining to
asymmetry of her face.
8.
Dr Coleman:
He treated Mrs S both
before and after the accident and all the routine tests that were
done by him resulted in a finding of no
abnormality. He saw First
Plaintiff on 10 January 2013, about a month after the accident and at
that stage the mother did not raise
any concerns. Routine sonars also
showed no abnormalities. He also mentioned that he delivered C on 28
February 2013 after a normal
and uncomplicated birth.
9.
Dr Myburgh:
She treated Mrs S on the
day of the accident and did sonar scans which resulted in her finding
no abnormality and no bleeding. Nothing
of any particular
significance, apart from what I have said, emanated from her
evidence.
10.
Dr Pistorius:
I will deal with his
evidence in some detail as major parts thereof were challenged by
Defendant’s expert witness Dr Okoli,
a neurosurgeon. He has an
impressive
Curriculum Vitae
. It is necessary that I refer to
this in some detail as well. He is the holder of a PhD degree in
foetal brain imaging from the
University of Utrecht in the
Netherlands. He is also the holder of a diploma in foetal medicine
from the Foetal Medicine Foundation
in London. The PhD was obtained
in 2008, and this diploma in 2000. His initial MBChB degree was
obtained
Cum Laude
in 1986 from the University of Pretoria and
the MMed degree from the Stellenbosch University in 1993. He has
authored and co-authored
more than 50 scientific publications. At
present, and since July 2013, he is a maternal and foetal medicine
specialist at the Tygerberg
Hospital and the University of
Stellenbosch. From 2004 to 2013, he was a gynaecologist, maternal and
foetal medicine Fellow and
later maternal and foetal medicine
specialist at the University Medical Centre Utrecht.
His medico-legal report
on the child C dated 7 June 2015 said the following:
“
Available
information:
Mrs
S’s first pregnancy was uncomplicated under the care of dr
Johan Coleman. Routine blood tests, screening tests for
Down-syndrome and neural tube defects as well as routine ultrasound
examinations were uneventful.
Mrs
S was involved in a head-on collision on 10 December 2012 (at a
gestational age of 30 weeks) in the Free State and sustained
minor
injuries to the upper body. Other occupants of the same vehicle were
transferred to hospital by helicopter. Ultrasound
examinations on
the day of the accident showed no foetal abnormality.
Subsequent
antenatal care did not demonstrate any abnormalities.
A
normal vaginal delivery resulted in a female infant with good Apgar
scores at a gestational age of 39 weeks 6 days.
MRI
scan (performed on 5 July 2013) shows substantial brain pathology
probably caused by previous injury and bleeding.
Discussion:
There are no other known
antenatal, intra-partum or postnatal factors present which would
conceivably cause the brain injuries as
described by Prof Lotz in his
report. The pattern of brain damage would correspond to ante natal
injury (see, for example,
Prameela Karimi, Ronald Ramus, Jill
Urban and Jeffrey M. Perlman: Extensive Brain Injury in a Premature
Infant Following a Relatively
Minor Maternal Motor Vehicle Accident
with Airbag Deployment. Journal of Perinatology (2004) 24, 453 –
457
). As such, the most likely cause of the brain damage is
the motor vehicle accident occurring at 30 weeks of gestational age.
Signed at Parow on
Sunday, 7 June 2015”.
It is common cause that
the reference to “30 weeks” is an error and that it
should read “28 weeks”.
11.
Dr Pistorius said that he
was a maternal and foetal specialist, which was a sub-speciality of
obstetrics and gynaecology. He has
specialised in this particular
field for the last eight years. It involves the detection of foetal
problems and ultrasound scans
are often performed to determine
whether these problems or abnormalities exist. His daily practice
involves primarily diagnostic
work with occasional surgical
procedures. He also regards himself as a specialist at foetal brain
imaging. He testified that he
considered the following when
formulating his opinion:
11.1 Photocopies of the
clinical notes emanating from the Welkom Medi-Clinic;
11.2 The clinical records
of Dr Coleman and his delivery report;
11.3 The MRI scans of C’s
brain and Prof Lotz’s report thereon. (Prof Lotz was the next
witness).
12.
It will serve no useful
purpose if I simply repeat all the evidence of Dr. Pistorius. The
essential parts of his evidence will however
be referred to and
analysed in the light of the later evidence of Prof Lotz and
Defendant’s expert witness Dr Okoli, who
is a neurosurgeon.
13.
Dr Pistorius testified
that C’s injury most likely occurred during the second part of
the pregnancy and not before 20 weeks
gestation and not after her
birth. The reason for this was the pattern of damage to C’s
corpus callosum, as observed on the
MRI images of C’s brain.
The corpus callosum consists of nerve fibres connecting the
structures of the left hemisphere of
the brain with the right. C’s
corpus callosum was fully formed which occurs after the 20 weeks
gestation. Nevertheless, whilst
fully formed, it was thinned. If this
condition had occurred prior to 20 weeks gestation, the corpus
callosum would be partially
or even totally absent and certainly not
fully formed. As a result, this condition could not have occurred
prior to 20 weeks gestation.
In addition, this condition was unlikely
to have occurred after C’s birth. This was so because C’s
brain damage had
affected her right basal ganglia whereas an “insult”
to the brain following directly after delivery of a baby usually

affects more superficial areas of the brain. The condition of the
corpus callosum, which is thinner, is a
secondary result
of
the damage to the right side of her basis ganglia. The basal ganglia
are a set of nuclei controlling muscle movement and muscular

development. There are left and right counterparts. The damage to the
right basal ganglia therefore resulted in reduced communication

between the brain hemispheres, and the corpus callosum therefore
thinned as a result thereof.  Accordingly, Dr Pistorius was
of
the view that because of the focalised destruction of the various
structures of C’s basal ganglia, the condition resulted
from
reduced blood supply (ischemia) to that region of the brain.
14.
Dr Pistorius was also
referred to the expert summary report of Prof Lotz. He testified that
no other known factors could have led
to the pattern of damage in
question. He testified, also again in the context of Dr Lotz’s
report that “severe spasm
was the most likely pathology”.
Any “placental insufficiency” would have presented a more
global presentation
in the brain. ‘Cord’ damage, would
have led to blood shunting to the cerebellum and brainstem and would
then also have
exhibited a more global presentation. “Direct
injury to the carotid vessels” would most likely also have
exhibited
a more global presentation and in addition thereto there
was no clinical evidence of any bleeding to support this pathology.
He
said that when a foetus is involved in a high velocity impact the
foetus experiences rapid deceleration. Different body parts of
the
foetus decelerate at different rates and the foetus’ head, as a
relatively smaller object, decelerates more rapidly than
the foetus’
body. This rapid deceleration also resulted in sudden flexion of the
foetus’ neck. A lateral flexion would
most likely have been
involved since foetuses typically lie with their spines to the side
at 28 weeks gestation. It must in this
context also not be forgotten
that Mrs S testified that her vehicle flipped over after the impact.
Blood vessels near the skull
then experience stretching and or
twisting i. e. flexion/ torsion forces. As a result, arteries become
stretched across the skull
base. When this happens they go into
spasm. There was no need for an extremely strong contraction. This
resulted, in the present
case, in the localised reduction of blood
flow to the right basal ganglia. This led to destruction of brain
tissue in C’s
right basil ganglia which as a result was
deprived of oxygen and waste products build up in the tissues. When
cells are deprived
in this way, they usually die after about five
minutes. The cysts that are present in C’s brain and are
observed on the MRI
images are build-ups of cerebral-spinal fluid,
resulting from dead cells having been removed and replaced. The
cerebral-spinal
fluid is therefore present where the basal ganglia
would have been in C’s brain, but for the trauma. Dr Pistorius
testified
that this is a well-documented pathology in medical
literature. The corpus callosum of C
subsequently
thinned as a
result of the damage to the basal ganglia.
15.
Dr Pistorius also
mentioned the following other important aspects:
15.1 There was no
specified threshold of severity of an accident required to cause
trauma to a foetus. There was however a positive
correlation between
the severity of an accident and the likelihood of foetal trauma;
15.2 Part of his training
involved research into the causative links between maternal trauma
and foetal neurological trauma;
15.3 The high-velocity
impact was definitely of sufficient degree to have caused the
relevant trauma;
15.4 There was no direct
link between reduced foetal movement and foetal abnormalities;
15.5 Ultrasound tests,
both prior to - and post - accident would not likely have revealed
brain damage;
15.6 Dr Okoli, the
neurosurgeon, to be called by Defendant was not suitably qualified or
experienced to testify about what the clinical
effect of what was
found on the MRI image ought to be, and he had no expert knowledge of
embryology;
15.7 In the context of
the clinical notes of Drs Coleman and Myburgh, he confirmed that
there was no evidence of placental problems
in utero, nor of any
umbilical cord problems or of blood on the brain;
15.8 Any blood products
would not likely to have remained in the time span between the
accident (10 December 2012) and the date
of the first MRI scan (3
July 2013);
15.9 The corpus callosum
was fully formed in length by gestational week 20;
15.10 As far as the
interpretation of MRI images was concerned, the opinion of an
experienced neuro-radiologist like Prof Lotz should
be deferred to;
15.11 Dr Okoli lacked
experience in foetal development and he therefore incorrectly applied
his experience in adult brains to the
field of embryology. His own
expertise in pre-natal persons was more refined and focused than that
of a neurosurgeon. His own daily
practice involved the development of
the foetus in uterus, and the medical literature supported his view;
15.12 The corpus callosum
of a foetus is more susceptible to thinning as a result of right
basal ganglia damage than of an adult,
because the foetus has yet to
develop myelin, a sheath of fatty tissue surrounding the nerve
fibres. This phenomenon was well-documented
in scientific literature;
15.13 C’s clinical
presentation, i. e. whole-body spasticity was reconcilable with the
MRI evidence that only her right basal
ganglia were compromised;
15.14 If the defect was
congenital then both sides of the brain would have been affected.
Here the MRI showed that the basal ganglia
were partially absent on
one side. Dr Okoli’s scenario was therefore improbable. On his
version the relevant vessels would
have had enough blood supply for a
certain period of time, and would then have stopped functioning
without an accident, which was
improbable.
16.
Prof Lotz:
Prof J. Lotz has the
following related qualifications:
MBChB in 1972. He
obtained the MMed, Master of Medicine, in diagnostic Radiology (
Cum
Laude
) in 1980. He is a Fellow of the College of Radiology of
South Africa and London. In 1993 he obtained the MSc (Med) in
Anatomy.
(Unfortunately I did not ask him why he also obtained a
Masters degree in History in 1997). He has vast professional
experience
and since 2005 has been Professor of Radiology (Academic)
at the University of Stellenbosch. His medico-legal practice has been

similarly impressive and I quote from his CV:
“
2007 – 2014
· Specializing in
medico legal assessment of MRI features of hypoxic ischemic injury in
pre-term and term infants.
· On-going
international correspondence with leading experts in the field of
hypoxic ischemic injury in infants.
· Compilation of a
database of more than (500) cases of hypoxic ischemic injury in
infants in a chronic stage of evolution.
Comparative figures not
available, but assumed to be one of the largest in the world.
· On-going
academic evaluation of database and development of didactic teaching
material in the field of hypoxic ischemic
injury in children.
· Support of
research in the field of hypoxic ischemic injury by affording
prospective PhD candidates access to the unique
database.
· Active in
addressing the unique issues and problems of hypoxic ischemic injury
in children in the South African context.
· Active in
propagating an ethical, scientific and financially sustainable
national plan to address a major cause of significant
mortality and
morbidity in the neonatal population.
· Expert opinion
on concluded and on-going civil actions relating to hypoxic ischemic
injury in the neonate in an estimated
250 cases.”
17.
Prof Lotz studied the
relevant MRI images and observed the following:
17.1 The child had
focalised brain damage in her right basal ganglia;
17.2 Three of the nuclei
of the right basal ganglia were either damaged or destroyed. These
were the caudate nucleus which was damaged,
the lentiform nucleus –
which is destroyed, and the thalamus, a portion of which was
destroyed. This indicated that this
condition could only have been a
vascular problem which occurred at the same time. He could not think
of a condition that would
do this gradually at all angles over days.
There was no embryological basis for the absence of these nuclei, and
text books supported
his view (Slide 3);
17.3 The corpus callosum
was thinner than normal, and
17.4 There was evidence
of border-zone infarction in C’s brain;
17.5 If this was a
congenital condition, it had to be asked why only three nuclei were
destroyed, and all at the same time? He could
not think of any
condition that would do this gradually.
18.
The commonality between
the three nuclei was that they shared a common blood supply. The
portion of the thalamus which remained
alive was however supplied by
a different vascular system than the other nuclei. As a result, the
only objective and logical explanation
for the pattern of damage in
C’s brain was that a vascular problem had affected the vessels.
An intra-uterine traumatic event
was the likely cause of this
pathology. He emphasized that his findings were based exclusively on
his consideration and interpretation
of the MRI images, in which he
was a specialist.
19.
When he compiled his
medico-legal report, he was aware of the occurrence of the accident.
In the report he stated that there was
no evidence of genetic or
congenital anomalies. The “discussion” part of his report
dated 18 March 2015 and based on
the MRI scan of 11 March 2015, read
as follows:
- “The pathology is
centred in the anterior vascular territory in middle and anterior
cerebral arterial distribution area,
more so on the right. Bilateral
border zone infarction and basal ganglia involvement is consistent
with a profound hypoxic ischemic
event, most likely the result of
hypotension;
- The pattern of
destruction is not that of periventricular leukomalacia of
prematurity or of hypoxic injury of the term infant;
- Anterior distribution
territory suggests that the carotid arteries were involved. The scan
fails to identify a definitive cause,
but placental insufficiency,
cord damage (both with posterior circulation redistribution), direct
injury to the carotid vessels
or severe spasm are reasonable and
logical considerations;
- It is my considered
opinion that on a balance of probabilities, an intra-uterine
traumatic event to have been the most likely
cause for this extensive
brain injury, now in a chronic stage of evolution”.
20.
It is clear from the
third unnumbered paragraph of this discussion that he referred to
four “reasonable and logical considerations”
as to how
the particular damage was caused. He testified that he mentioned
these only for the purpose of a differential diagnosis.
In the
present instance, the clinical evidence ruled out three of these, and
the only mechanism that he found to be the most probable
cause was
“severe spasm”. Because a specific area of the brain was
affected only, the event had to be vascular, and
there was no other
logical explanation. There was no embryological basis for the
condition seen on slide 7 of the brain, i. e.
the absence of certain
nuclei. One could not find such a congenital condition in the text
books.
21.
Prof Lotz further
testified that it was highly improbable that the three nuclei in C’s
brain were damaged at three separate
times. Damage caused on three
separate occasions would then most likely be the result of an embolic
disease, but this would have
meant that three separate embolisms
would have had to travel the same vascular pathway to the right basal
ganglia, which was, to
him, highly improbable.
22.
Explaining the reason for
his conclusion as to the cause of C’s damaged brain, he
testified that one needed to consider the
auto-regulatory system of
the brain in this context. This was a system whereby adequate blood
supply to various parts of the brain
is ensured. Blood vessels had
the ability to contract and dilate and influence blood flow to the
brain. When a blood vessel was
subjected to stretching and/or
twisting forces, it had a tendency to go into spasm. Such spasms
could last for short periods, or
a few hours up to some four days
even. In C’s case the spasm must have lasted for at least half
an hour, but more likely
even several hours.
23.
In C’s case, the
corpus callosum was fully formed at 20 weeks gestation. It had
assumed its final shape, but lacked in thickness.
Her brain must
therefore have been injured between 26 and 34 weeks gestation, given
this presentation. The condition of her corpus
callosum could not
have been caused by a congenital defect given that it is fully
formed, but thin. This thinning was the consequence
of damage to her
right basal ganglia. He had never seen a pattern caused by a
congenital defect where the nuclei on one side only
were destroyed.
24.
Prof Lotz also referred
to heterotopia. He defined this as a condition where cells did not
migrate to their normal position in the
brain, and concluded that he
did not find any congenital, genetic or inflammatory pathology and no
evidence of heterotopia.
25.
He also testified that C
suffered border-zone infarction. This meant that there had been a
transient drop in blood pressure in her
brain. The damage to this
border-zone was less severe than the damage to the nuclei in her
basal ganglia. This border-zone infarction
was of relevance in that
it provided a larger picture of what had occurred in her brain. Where
there had been a blockage of blood
vessels that supply the basal
ganglia, this resulted in a drop of pressure in the brain and
affected the right border-zone. The
pattern of injury which I have
described and which he saw on the MRI images was not consistent with
the presence of a congenital
defect. He testified that there were
over 120 000 congenital defects, and he saw no evidence for any
of them. As far as the
mechanism of an injury was concerned, he
testified that indirect forces could cause injury to blood vessels,
and added that a sudden
deceleration of the foetus inside the womb
led to it experiencing a multitude of indirect forces. He added that
the two classical
works on neonatal neurology (by
Wolpe and
Markowitz
) did not contain reference to a single defect that
could cause such an unknown or unnamed congenital defect. The crux
was that
C’s corpus callosum had been fully formed, although it
was thin.
I must add at this stage
that Defendant tendered the following formal admissions during the
trial and before Dr Okoli gave evidence:
25.1 At 28 weeks
gestation, cerebral arteries are capable of constricting and causing
spasm;
25.2 The corpus callosum
can further develop in thickness after 24 weeks gestation;
25.3 C’s MRI images
showed a border-zone infarction. It was initially put to Prof Lotz
that there was no border-line infarction.
Prof Lotz replied that Dr
Okoli needed to explain the presence of white material on one MRI
slide (Slide 6).
26.
The experience and
expertise of Dr Okoli was put to him for comment. He testified that
he had never heard of a neurosurgeon being
involved in an ante-natal
case. Neurosurgeons were better suited to comment on post-natal brain
conditions. As far as his own expertise
and experience were
concerned, he repeated that a radiologist had to undergo five years
of training to qualify and that neo-natal
radiology was an even
further specialization. He added that even neurosurgeons specializing
in paediatric cases generally defer
to the opinion of a radiologist
regarding brain imaging. Dr Okoli was not trained to interpret an
image of a natal brain. He noted
from Dr Okoli’s CV a paucity
of paediatric and neo-natal experience as well as radiological
experience and their fields of
expertise were widely apart. He
obviously did not intend to negatively comment on Dr Okoli’s
experience or expertise as a
neurosurgeon. It was put to him on
behalf of Defendant that Dr Okoli would agree that in C’s case
a disruption of the cerebral
artery had occurred. It was also put to
Prof Lotz that Dr Okoli would not agree with his conclusion that
“severe spasm”
was a probable cause of C’s brain
condition, but he maintained that he saw no other reason for the
pattern of the damage.
He added that Dr Okoli could not form an
independent opinion in a field that was highly specialised. A
neurosurgeon would have
no knowledge of ante natal damage and he
should not have given evidence on this topic.
27.
Dr B. Okoli
:
Dr Okoli is the holder of
a Bachelors of Medical Science degree (Human Anatomy), which he
obtained in 1986 at the University of
Port Harcourt in Nigeria. He
also obtained a Bachelor of Medicine degree at that University in
1989 and it is a “Bachelor
of Surgery”. In 2000, he
obtained the degree Master in Medicine (Neurosurgery) from the
Medical University of South Africa.
He has practiced as a specialist
neurosurgeon since 2001.
28.
His medico-legal report
is dated 15 March 2016. He examined C, and stated the following: She
is obviously neuro-physically and mentally
retarded. She has
dysmorphic facial feature. She has poor neck control, poor trunk
control and poor limb control. She has spastic
limbs. He stated that
C’s milestones have been delayed, and it is obvious that she
suffers from cerebral palsy. Under the
heading “The
implications of the MRI reports are as follows”, he mentioned
the following:
- “There was no
haemorrhage in the brain of C either intra-uterine or extra-uterine.
- There are radiological
features that are suggestive of ischaemic phenomena.
- Almost all the
ischaemic features are within the territory of blood supply of the
anterior cerebral artery.
- The pathological
findings in the brain have not involved the back part of the brain
called the cerebellum, so it is not all of
the brain that is involved
in this pathology.
- There is evidence that
not all the MRI findings can be explained on the bases of global
ischaemic phenomena at 28 weeks of gestation.
- There is disorder of
neuronal migration with grey matter heterotopia that has failed to
reach their final destination from their
place of birth which usually
occurs between 6 to 16 weeks of gestation.
- The part of the corpus
callosum that is particularly affected is the body of the corpus
callosum.
- Embryologically the
corpus callosum is fully formed and has assumed its final shape by 18
to 20 weeks of gestation.
- If only the body of the
corpus callosum is hypoplastic, it cannot be explained on the bases
of a global ischemia that occurred
at 28 weeks when it is expected to
have been fully formed.”
29.
It is also important to
refer to his “Deductions” in that report, which were the
following:
- “The history of
the motor vehicle accident does not suggest a direct blow to the
abdominal wall.
- There were no abdominal
bruises.
- The probable pathway of
involvement of the abdomen is the tightening or traction of the
seatbelt against the abdominal wall.
- This caused an
excitatory irritation to the abdominal/uterine muscle with a
resulting contraction.
- The degree of uterine
contraction does not seem to have been severe and could not have
caused hypo-perfusion injury through the
placenta.
- A hypo-perfusion injury
through the placenta should affect the foetus and is expected to
elicit foetal distress.
- This was absent
throughout her period of observation and care.
- The ultrasound
examination after the MVA did not reveal placental injury or
disruption.
- The ultrasound
evaluations after the MVA also did not reveal a blood clot in the
brain.
- C has
neurodevelopmental abnormality in the MRI images of the brain that
could only have resulted from an arrest prior to the
motor vehicle
accident in question and this specifically refers to the neuronal
heterotopia and hypoplasia of the body of the corpus
callosum.
- The region of blood
supply from the left and right anterior cerebral arteries bear the
brunt of the brain damage.
- It is highly improbable
that this trauma has selectively damaged these arterial vessels with
the exclusion of other arterial vessels
in the brain.
- It is also all the more
improbable that a global hyper-perfusion injury will selectively
affect the left and right anterior cerebral
artery.
- Most likely, there is a
malformation involving the anterior cerebral arteries which are
unrelated to the motor vehicle accident
under considerations.
- Conclusion: I am unable
to associate the radiological pathology in the brain to the motor
vehicle accident of 10 December 2012
when C was intra-uterine aged 28
weeks”.
30.
Dr Okoli testified that
he dealt with neo-natal cases with congenital malformations at least
once every two weeks or so. From time-to-time
referrals are made to
him where the patient has a surgically correctable brain legion. It
is common cause that C has cerebral palsy.
Dr Okoli however testified
that in his opinion a radiologist cannot diagnose cerebral palsy
since it was a clinical diagnosis which
emanated from an examination
of the particular patient. He did however confirm that a MRI scan
could provide a reason for such
palsy. He was also capable of
interpreting MRI images which he sees in practice every day. He did
not agree with Plaintiff’s
case on the basis that C experienced
trauma in utero. He gave evidence about the make-up of the basal
ganglia, which are a collection
of neurons primarily responsible for
“supple movements”. He also referred to the slides
provided by Prof Lotz when
he gave evidence, and testified what he
saw on these images. He said that the tissues of the basal ganglia on
the left side of
C’s brain were fully developed, but not the
right side. The under-developed nuclei of the right basal ganglia
were simply
smaller than those on the left, and there was in his view
no MRI evidence that the nuclei on the right were ever damaged. The
lacunae
in the brain on the right basal ganglia region, where they
should have been fully developed nuclei, are instead filled with
cerebral
spinal fluid and no gliosis is present. (Dr Pistorius
testified that gliosis is a proliferation of microglia, which are
“scavenger”
cells in the brain that remove damaged or
dead cells. Dr Okoli did not agree with that part of Dr Pistorius’
evidence in
that brain tissue which is dead does not “disappear”
in the brain, but instead gliosis remains present. This phenomenon

could be seen, and was so seen by him, regularly in stroke victims,
and he observed MRI evidence of gliosis every second day. He
referred
to a well-known text book read by every neurosurgeon, namely
Neurological Surgery, 5
th
Edition by H. R. Winn
. This assessment was based
entirely on his interpretation of the MRI images of C’s brain.
He added that this pattern of damage
was indicative of a congenital
anomaly that resulted in the under-development of the nuclei of the
right basal ganglia, and not
that of ischemia. He also admitted that
there was evidence of border-zone infarction in C’s brain,
which Prof Lotz had described
in some detail. He also agreed with
Prof Lotz that the corpus callosum in C’s brain was fully
formed in length, but not in
thickness. I asked Dr Okoli what, in his
view, had caused the thinness of the corpus callosum and he stated
that it was “under-formed”.
Defendant’s Counsel,
prior to Dr Okoli’s evidence, had conceded that at 28 weeks
gestation, cerebral arteries were
capable of constricting and causing
spasm. During his evidence he qualified this concession by stating
that blood vessels acquire
“optimum ability” at a
gestational age of 34 weeks, and that he did not think that a foetus’
blood vessels could
contract optimally at 28 weeks gestation. It is
not clear whether the reference to “optimally” was
intended to detract
from the previous concession made. Regarding the
mechanism of the injury, he, as was common cause, referred to the
high velocity
head-on collision. In this context he said that the
foetus experienced linear forces. A direct force on the foetus would
be applied
by an object such as the dashboard or safety belt. In the
case of indirect forces, the foetus’ head would hit the wall of

the mother’s womb and for a brain injury to follow from this,
the brain would be “rattled” in the foetus’
skull.
In both cases, he said, the result would have been brain bleeding and
brain swelling. This would be evident on an ultrasound.
No such
evidence existed of this in C’s case. I must add at this stage
that Dr Okoli was not aware of the fact that Mrs S
had testified that
her vehicle had flipped onto its side after the collision. In the
context of the “linear forces”
that he referred to, he
stated that a sudden deceleration force could not cause injury to the
blood vessels in the brain without
there being an avulsion from the
brain of those vessels, i. e. that the vessels would have “pulled
off” from the surrounding
brain tissue. He further said that if
the internal carotid artery experienced stretching or twisting, this
would invariably result
either in brain bleeding or an injury to the
inner-lining of the blood vessels causing an embolism. There was no
evidence of such
an embolism.
31.
While he was giving
evidence, Dr Okoli produced a copy of a passport photo of C and said
that her eyes were asymmetric and that
her forehead was irregular. In
his report under the heading of “Examination”, he had
stated that C had “dysmorphic
facial feature”. Neither
Counsel delved into this observation at the time, and as a result of
Dr Okoli’s production
of the passport photo, I deemed it in the
interests of justice and of the child, not to leave this topic
hanging in the air as
it were, but to re-call First Plaintiff and
also Dr Pistorius. It is clear from the provisions of s. 6 of the
Children’s Act 28 of 2005
that all proceedings in
a matter concerning a child must respect, protect, promote and fulfil
the child’s rights set out
in the
Bill of Rights
.
The relevant section in the
Constitution of the Republic of
South Africa
is s. 28 which states in s. 28 (2) that a
child’s best interests are of paramount importance in every
matter concerning the
child. It seemed to me that the Defendant’s
Counsel regarded my decision in this context as “unusual”,
but it
must be remembered that a Court has a discretion to re-call a
witness for further examination or cross-examination, also in civil

trials.
See:
Herbstein &
Van Winsen, The Civil Practice Of The High Courts South Africa, 5
th
Edition, Vol 1, at 899
.
Quite apart from that, it
is my view that where the interests of children are at hand, a Court
should take the best interests of
the children into account and, as
in the present context, re-call a witness and ask pertinent questions
to ensure that topics that
may appear to be particularly relevant are
not left hanging in the air, because of Counsel’s oversight,
inexperience or lack
of appreciation of the importance of the
particular topic. For the same reason, I also deemed it in the
interests of justice, and
in the interests of the child, to re-call
Dr Pistorius. I will deal with this evidence hereunder. At this stage
Dr Okoli added
that C’s dysmorphic face, as he described it,
could not be explained on the basis of trauma. It could only be
explained on
the basis of a congenital defect. Had this been
otherwise, there would have been fractures to C’s skull which
there were
not. He also said that congenital malformation of the
occipital bone could have caused the asymmetry of the eyes. The
foetus’
face was fully developed at 28 weeks gestation and as a
result the facial malformation could only have been caused either by
a
fracture or a congenital defect.
32.
Dr Okoli also was of the
view that C’s physical symptoms, namely spasticity on both
sides of her body, did not accord with
the condition of her right
basal ganglia in that he would have expected her to have spasticity
in only the left side of her body,
given that only her right basal
ganglia are abnormal. He was therefore of the view that C presents
with symptoms that accord with
global generalised brain problem
indicative of a congenital defect. Furthermore, having regard to the
clinical notes of Drs Coleman
and Myburgh, he testified, as they did,
that there was no evidence of foetal distress and as a result he said
the foetus could
not have experienced trauma.
33.
Cross-examination
of Dr Okoli:
Dr Okoli conceded that a
maternal and foetal specialist was more qualified to comment on
issues concerning foetal development than
himself. He argued however
that the issue at hand was more about the brain structure. It is
common cause that Dr Okoli does not
have a degree in radiology. He
said however that radiology was part of the neurosurgical training
and that he had looked at “uncountable”
number of scans.
He conceded at the same time that a radiologist who specialises in
neonatal brain-imaging was more qualified than
himself to provide an
interpretation of MRI images of a neonatal brain. In the present
context this concession was correctly made
and it is of importance,
in regard to the qualifications and experience of Prof Lotz. He was
asked about his practice in the context
of diagnosis of congenital
defects and he testified that obstetricians and paediatricians often
approach him after they had made
a diagnosis involving congenital
defects and where a surgical correction was an option. In some of
these cases however he was also
involved in diagnosis.
34.
He considered the MRI
images of C’s brain during the process of compiling his
mentioned medico-legal report. As far as C’s
corpus callosum
was concerned, he conceded that it was fully developed in terms of
its structure, but that it was thin. This, in
his view, was an
inherent condition that C was born with. The reason for the thin
corpus callosum was exclusively a congenital
defect which she would
have had prior to 20 weeks, while in utero. The reason for this firm
conclusion was that there was no evidence
of intra-uterine trauma and
no evidence of dead tissue on C’s MRI images. He was then asked
whether he considered that the
thin corpus callosum could have been a
secondary effect, and answered in the negative. However, he added at
the same time that
this thinning could not have been caused by a loss
of blood supply. Counsel for Plaintiff put to him the Plaintiff’s
actual
explanation for C’s thin corpus callosum, namely that it
was a
consequence
of the damage to her right basal ganglia,
and the subsequent loss of communication between her right and left
basal ganglia. Dr
Okoli was of the view that the thinning did not
follow from basal ganglia destruction. He had often observed stroke
victims who
had suffered brain damage to one brain hemisphere without
subsequent corpus callosum thinning. In essence, he remained of the
view
that the thinning was the result of a congenital defect, because
he did not find gliosis on the MRI images and because he deemed
the
loss of blood supply to the corpus callosum highly improbable. His
conclusion therefore was that C’s corpus callosum
had fully
developed in its proper proportions and had then
subsequently
thinned and that he attributed this to a congenital defect. Prof Lotz
had testified in this context that he did not know of any
congenital
defect that would have caused this particular result. Dr Okoli
however was of the view that the defect was “hypoplasia”

and that he had seen such frequently. According to him, hypoplasia
was an under-formation. Examples of congenital defects that
caused
corpus callosum hypoplasia could be found in medical literature and
he had experienced this as well. Dr Okoli referred to
an article in
the ‘Neurology’ magazine of the American Academy of
Neurology of 2011, headed “Distinguishing 3
classes of corpus
callosal abnormalities in consanguineous families”. He did not
know of the authors and could say nothing
about their expertise. This
article had also not been put to the Plaintiff’s expert
witnesses for comment. The topic discussed
therein is contextually
also totally different. Dr Okoli should have been referred to the
Journal of Perinatology (2004)
, mentioned by Dr
Pistorius for comment, but was not.
35.
In his report, Dr Okoli
referred to an abnormality in the MRI images of the brain “that
could only have resulted from an arrest
prior to the motor vehicle
accident in question”. During cross-examination he elaborated
on that by stating that he made
this observation because of the
mentioned under-development of the corpus callosum which by the
gestational age of 20 weeks would
have been fully formed. The
“arrest” must have occurred prior to 20 weeks gestation.
It was then put by Plaintiff’s
Counsel that his report and his
evidence were inconsistent in this respect inasmuch as in his report
he made mention of an “arrest”
that must have occurred
prior to 20 weeks gestation, whilst in his testimony he attributed
the thinness to an inherent congenital
defect. He denied that this
was an inconsistency and suggested to Counsel that the whole picture
be considered inasmuch as the
particular malformation could not be
explained on the basis of global ischemia. He was of the view that
when a foetus experienced
brain damage at 28 weeks, gliosis would be
apparent on MRI images. He then further testified that he had
observed heterotopia on
the MRI images. This was a neural migration
problem and was related to malformation. This would not have been
apparent on a routine
sonar scan. He regarded his observation of
heterotopia on the MRI images as very important regarding his
conclusion that C had
a congenital defect, since it was indicative of
the fact that not everything had developed. He however later on
testified that
the presence of heterotopia was only one factor that
he considered in concluding that C had a congenital defect. I may
mention
at this stage that both Dr Pistorius and Prof Lotz had seen
no evidence of heterotopia. He also excluded the possibility of a
vascular
injury, because in such an instance the pattern of brain
damage would have been more generalised and less focal than it was.
Prof
Lotz’s explanation of the pattern was put to him, namely
that the single unifying commonality that the damaged or destroyed

nuclei in the basal ganglia share, is that they are all supported by
the same vascular system. Dr Okoli however persisted in his
view that
the pattern of brain damage could not have been induced by trauma.
36.
Prof Lotz had testified
in some detail about the presence of a border-zone infarction on the
MRI images, and Dr Okoli conceded that
there was evidence of such.
Prof Lotz said in this context that the presence of a border-zone
infarction provided a bigger picture
of what had happened in C’s
brain, more particularly that there had been a transient loss of
blood pressure. Dr Okoli’s
view in turn was that the particular
infarction could not be explained on the basis of a right middle side
artery involvement.
37.
As far as the mechanism
of the injury was concerned, he conceded that blood vessels could
react to indirect forces. Dr Pistorius’
opinion in this context
was put to him, but Dr Okoli disagreed therewith for the following
reasons:
37.1 The foetus would not
have experienced any complex vertical or twisting forces;
37.2 The force exerted on
the foetus would most probably have been linear in a head-on
collision, which would have impacted directly
on the wall of the
womb.
I have already mentioned
the undisputed evidence of Mrs S that her Toyota had flipped onto its
side after the high impact collision.
Dr Okoli was, and had been,
unaware of this evidence, but did not offer an opinion whether this
fact would change his view relating
to linear forces. Prof Lotz had
testified that no-one could describe the mechanics after the impact
exactly. He favoured a scenario
including tortion after an indirect
force which would not all have been on the same plane.
38.
As far as spasm in blood
vessels was concerned, he had conceded that at 28 weeks gestation
these vessels had the ability to contract.
He also conceded that Dr
Pistorius’ evidence that smooth muscle developed in the vessels
in the foetus’ brain by 22
weeks gestation was correct. He
agreed that most babies born prematurely from 20 weeks gestation
onward survived. He stated that
this was so, because their organs
were sufficiently developed. He stated that he was not sure that this
capability to survive must
also be due to sufficient smooth muscle
development in the brain’s blood vessels, and because they had
a functional auto-regulatory
system. I have already mentioned that it
was put to him that smooth muscle at 28 weeks gestational age could
contract sufficiently
to prevent blood flow. His view was that
vessels at this stage could not “maximally” contract. He
then proceeded to
qualify this concession by stating that there was a
degree of development and that smooth muscle development was
maximally optimal
at approximately 34 weeks gestation. Prof Lotz’s
opinion was put to him, namely that a vessel spasm could cause injury
to
the inner-lining of the vessel which could result in an embolism
which would subsequently block smaller vessels in the brain.
According
to Dr Okoli this was unlikely, because any embolism would
flow upward.
39.
It was also put to him
that the presence of a congenital defect in C was never mentioned in
his medico-legal report. He conceded
this, but said that the word
“malformation” indicated his consideration of a
congenital defect. This congenital defect
“may” involve
malformation of the anterior cerebral artery. Dr Pistorius’
evidence was put to him, namely that
a congenitally malformed artery
would cause on-going brain damage whilst the pattern of C’s
brain damage was indicative of
a transient event. It was therefore
highly improbable that such a congenital condition would cause
transient vascular problems.
Dr Okoli testified on this topic that
the condition was one of under-development of the brain structures
and that supply of blood
was sub-optimal at the outset of C’s
development. He drew this inference on the basis that there was no
evidence of basal
ganglia damage. He conceded that he could not name
the particular congenital defect, but stated there were in excess of
a 120 000
possibilities in this context. He did not comment on
Dr Pistorius’ evidence that signs of foetal distress do not
necessarily
accompany foetal injury.
40.
C’s
“dysmorphic” facial feature (facial deformation):
Reference to this
dysmorphic facial feature appeared in Dr Okoli’s report, but it
was scarcely dealt with, either in examination,
or cross-examination,
until Dr Okoli produced C’s passport photo which he had
obtained from his secretary as a matter of
routine. He testified that
the facial asymmetry of C’s eyes was a result of a generalised
muscle imbalance. A bone fracture,
if there had been one, could have
healed in deformity, as he put it. He conceded that only a mild
deformity was present. Dr Pistorius,
who was re-called by me, gave a
different opinion. He said that C’s eye-asymmetry was merely a
squint of the left eye because
of the muscular imbalances in her
entire body, including her face. When Mrs S was re-called by myself,
she testified that she had
not observed any such facial deformity at
the time of C’s birth and I need to note that neither Dr
Coleman, nor Dr Myburgh
made any reference thereto. At the time of
this evidence C was sitting on Mrs S’s lap and I made my own
observations. I did
note a squint in the left eye and I also noticed
that when C smiled at me repeatedly, such smile was not uniform. I
could not see
any irregularity in C’s forehead and when this
was put to Dr Okoli he stated that there was only a slight or mild
deformity
in this context, something that I could not see. Dr
Pistorius’ view was that C’s “lazy” eye and
the boney
facial asymmetry was a particular feature of cerebral palsy
and that there was no evidence that there had been any boney
malformation
in her face or skull which could have healed in
deformity as Dr Okoli had said.
41.
Plaintiff’s
argument:
41.1
In summary, it was
contended that it stood to reason that Dr Pistorius’ and Prof
Lotz’s reasoning should be preferred
to that of Dr Okoli. The
former considered two parts of the brain in their commonality,
whereas the latter only considered two
“obstacles” that
were not relevant to Plaintiff’s explanation of C’s thin
corpus callosum.
41.2
Dr Okoli’s
submission that the thinning of C’s corpus callosum was the
result of a congenital defect should be rejected.
When Prof Lotz said
that there was no known congenital defect that would produce this
result, Dr Okoli contended that the defect
was “hypoplasia”.
This however, is not a defect, but a symptom. Dr Okoli himself
defined it as “under-formation
or sub-optimal formation which
results in something being incompletely formed”. Essentially
therefore, what Dr Okoli stated,
was that the congenital defect that
caused C’s corpus callosum to thin, was “thinning”.
When this was pointed
out to him during cross-examination, so it was
contended, he could not name a single congenital defect that causes
part of the
corpus callosum to develop fully, and another part to
under-develop. Even when it was put to him that Dr Pistorius and Prof
Lotz
had testified that they had never heard of such a congenital
defect, he was unable to provide a single name to describe such a
defect, even as a mere possibility. In this context, it was therefore
contended, that his answers were vague, evasive and non-committal.
41.3
Prior to Dr Okoli’s
testimony, Defendant conceded that muscles were sufficiently
developed at 28 weeks gestation to cause
the arteries to go into
spasm. This was a contradiction to what was put to Dr Pistorius
during cross-examination and was indicative
of the fact that Dr Okoli
changed his opinion in this regard during the cause of the trial.
Despite this concession, Dr Okoli further
testified that he did not
believe that muscle spasm could have caused loss of blood supply in
C’s case, because at 28 weeks
gestation, the vessels could not
have “maximally” contracted. Dr Okoli held this view
despite having conceded the following
points emanating from Dr
Pistorius’ testimony that:
41.3.1   Smooth
muscle develops in the vessels in the foetus’ brain by 22 weeks
gestation;
41.3.2  Dr Pistorius
regularly measures the blood flow in foetuses using ultrasound scans,
from which he can infer that smooth
muscles in the blood vessels are
developed;
41.3.3  Most babies
born prematurely from 26 weeks gestation onward survive.
41.4
Despite making the above
concessions, Dr Okoli resisted the ineluctable conclusion that at 28
weeks gestation, it was indeed possible
for a foetus’ blood
vessels to go into spasm and arrest blood supply. It was contended
that this was indicative of both bias
and paucity of experience and
knowledge in the field of brain development.
41.5
Dr Pistorius and Prof
Lotz also testified that a rupture of the blood vessels in the
foetus, as well as the damage to the tissue
inside the blood vessels,
will only occur automatically in case of direct force applied to the
vessels. They also explained that
vessels reacted differently to
indirect forces. These were the basic principles of medicine taught
at the third and fourth year
of medical school.
41.6
Prof Lotz testified that
in C’s case, the spasm probably lasted for several hours, given
the extent of her brain damage. There
was no collateral/factual
evidence that contradicted this view if one takes into account the
time when the accident occurred and
the time when the first
ultrasound was done in hospital, some hours after the accident.
41.7
It was therefore
submitted that the logical medical explanation was that spasm in the
mid-cerebral artery caused the loss of blood
supply to C’s
right basal ganglia.
41.8
Dr Pistorius and Prof
Lotz provided two reasonable and logical explanations on how the
mechanics of the spasm injury or “intra-uterine
traumatic
event”, would have operated following the foetus’ sudden
deceleration caused by the high-velocity impact.
Prof Lotz testified
that the exact specifics of an indirect force can be countless, and
that there was a multitude of possible
indirect forces that could
influence the reconstruction of the mechanics of injury. Dr Okoli
considered only a forward movement
as the most probable indirect
force, but seemed to change his opinion after he was informed that
the motor vehicle had turned to
its side after the impact. He however
had no firm view about this and did not deal with it. Dr Pistorius
also said that head and
body react differently to deceleration,
because of their different weight.
41.9
It was therefore
contended that the evidence of Dr Pistorius and Prof Lotz on the
probable mechanics of the injury, took cognisance
of the multitude of
ways in which indirect forces could have operated. There was no
reason why their explanation could not be regarded
as logical and
probable. From a medical perspective, these indirect forces could
indeed have caused vascular spasm, and that spasm
could indeed have
caused constriction of blood supply to C’s right basal ganglia.
41.10
The evidence of Drs
Coleman and Myburgh did not change the conclusion of Dr Pistorius
that the brain damage, as seen on the MRI
scan, was in all
probability caused by the accident that occurred at 28 weeks
gestation.
41.11
As far as the alleged
congenital defect relied upon by Dr Okoli was concerned, it was
submitted that he could not name any particular
defect in this
context, but merely referred to a congenital defect that caused
malformation of an artery which caused loss of blood
supply and
border-zone infarction. He also mentioned a congenital defect that
caused partial under-development of the corpus callosum,
whilst
denying it to fully develop in form. He also said that it could be a
defect that only affected basal ganglia on one side
of the brain, and
further mentioned a congenital defect that caused facial dysmorphia.
It was put to him that the characteristics
of such congenital defects
were unknown to Dr Pistorius and Prof Lotz, and were excluded by the
two “Bibles” of neo-natal
neurology. Nevertheless, Dr
Okoli could not identify a single congenital defect from a text book
even as a possibility. This was
so even after it was put to him that
his evidence implied that there could be more than one type of
congenital defect that affected
C. It was therefore submitted by
Plaintiff’s Counsel that one would reasonably have expected Dr
Okoli, if he was an expert
on this topic, to at least have identified
one probable congenital defect. The result was that Dr Okoli’s
assertion in this
context should be rejected on the basis that it was
vague, impossible and at best forms part of a variety of any one out
of 120 000
possibilities.
41.12
As far as facial
deformity is concerned, it was submitted that Dr Okoli greatly
exaggerated the extent of this deformity. During
his
evidence-in-chief, he created the impression that the deformity was
substantial and that, other than a congenital defect, a
bone fracture
would have been required to cause such deformity. When C was seen in
Court, during Mrs S’s re-call, it became
apparent that C’s
forehead was not irregular. These observations were made, both by
myself and Dr Pistorius, and were a far
cry from the “dysmorphic
facial features” that Dr Okoli had referred to. It was also
contended that once C had been
seen by myself in his presence, and in
the presence of Dr Pistorius, and C’s mother, he contradicted
his evidence-in-chief.
During that evidence, he had said that “a
congenital defect of the occipital bone” was the likely cause
of the asymmetry
of C’s eyes. During cross-examination he said
that generalised muscle imbalance and not the boney problem might be
the cause
of the alleged deformity. He also stated that a bone
fracture could have “healed in deformity”. This
contradicted his
evidence-in-chief in which he testified that the
accident could not have caused the alleged deformity, because there
was no evidence
of a bone fracture. During cross-examination he also
conceded that the milder the deformity, the more other explanations
for the
alleged deformity may exist. Dr Pistorius’ opinion that
C’s “lazy” eye and expressive facial asymmetry,

both of which were attributable to muscular problems, was a feature
of her cerebral palsy, and that this was a far more likely

explanation for any asymmetry in C’s face, since there was
clearly no evidence at all that there had been any boney
malformations
in her face or skull.
41.13
Dr Okoli’s
explanation that the clinical diagnosis of whole body spasticity does
not match the findings on the MRI scan was
illogical. The argument
implied that there must be something further than what one sees on
the MRI scan that caused this whole
body spasticity. Dr Okoli then
resorted to the congenital defect as being an explanation, without
explaining how that would operate
in the body of C in order to cause
spasm on both sides. In this context it was contended that Dr
Pistorius’ evidence was
more logical. He testified that the
damage to the side of the basal ganglia would cause spasticity to the
left side of the body,
but that this spasticity would cross over to
the other side of the body and would cause less severe spasticity to
the right side.
It was submitted that this is by far the more
probable and logical explanation that reconciles C’s clinical
diagnosis with
the damage one saw on the MRI scan.
42.
In summary it was
therefore contended that Dr Okoli’s evidence, that C’s
face was deformed, was entirely exaggerated,
illogical and
improbable. The discrepancies between his evidence-in-chief and his
responses during cross-examination, led ineluctably
to the impression
that he sought further reasons to justify his opinion that C had a
congenital defect. He therefore assumed the
role of advocate and was
intent to convince the Court that his theory on congenital defect was
correct. Once independent observations
of C’s facial features
were recorded, he was forced to change his opinion and make certain
concessions. This brought his
objectivity into question.
43.
As I have said herein
above, my own observations in Court of C’s face, in the
presence of Dr Okoli and Dr Pistorius, do not
show a clear asymmetry.
I could also notice no malformation of the skull or forehead.
44.
Defendant’s
argument:
The crux of Defendant’s
argument is that C’s whole body spasticity and paraplegia are
neurologically not compatible
with a one sided basal ganglia injury
and a limited injury to the corpus callosum. It was contended that
Plaintiff’s case
advanced no relevant explanation in respect
thereof and in fact, ignored it. It was also contended that in asking
whether Plaintiff
discharged the onus resting on it on a balance of
probabilities, it failed to present an objective and acceptable
description of
the probable manner in which C might have been injured
in the motor vehicle collision. Plaintiff’s experts were also
criticized
for failing to place an objective consideration of all
relevant facts before me. It was said that Plaintiff’s experts
had
prepared only limited expert summaries, had deviated from them
extensively and had only given selective evidence regarding the topic

of arterial spasms. No probable mechanism of the brain injury was
allegedly put forward and it was contended that a number of probable

explanations were tendered by them.
45.
Defendant’s Counsel
presented a very detailed written Heads of Argument for which I am
grateful, as I am for Plaintiff’s
written Argument, and the
following material submissions were made:
45.1
C’s actual
condition, as I have said, namely that of whole bodied spasticity,
paraplegia and mental retardation, does not
fit in with the one-sided
basal ganglia injury. Dr Okoli had said that the basal ganglia
controls opposing sides of limb movement.
Whole body spasticity can
only fit in with a more generalised brain injury than that described
by Plaintiff’s experts;
45.2
Dr Pistorius, according
to Defendant’s Counsel, expressed an immediate bias towards Dr
Okoli, especially relating to the question
whether he was capable of
making a diagnosis of the cause of C’s cerebral palsy. Prof
Lotz in turn, so it was contended,
expressed himself outside the
field of his own expertise on numerous occasions. (It must however be
remembered that Dr Okoli himself
had conceded during
cross-examination that Prof Lotz was more qualified than him to
consider radiological examinations and investigations.);
45.3
Despite this concession,
Dr Okoli was experienced enough to have relied on his own
interpretation of the relevant MRI imaging, and
his conclusion was
that the structural problem identified on such images could not be
explained simply by reference to “trauma”;
45.4
Dr Okoli had also
conceded that in respect of neo-natal development, Dr Pistorius was
better qualified than himself, but nevertheless,
because of his
practical experience, he was qualified to come to the conclusions
that he did;
45.5
Exhibit “J”
contained various images of C’s brain and also depicted normal
brain sketches. The crux of Dr Okoli’s
opinion in this context
was that there was no scarring present in the brain which indicated
that the relevant parts never developed.
In the absence of gliosis
(scarring), the relevant nuclei were under-developed;
45.6
The under-developed
middle section of C’s corpus callosum related to hypoplasia due
to a congenital defect. Dr Okoli said
in this context that he saw
hypoplasia probably twice a year only. The crux really was, as I have
already said, that because there
was no gliosis present, malformation
was indicated. If, according to Plaintiff’s thesis, a reduction
in blood flow due to
a spasm that had been present, more areas of the
corpus callosum would have thinned out;
45.7
The probability of an
arterial spasm having occurred could not explain the very focal brain
injury, the whole body spasticity, paraplegia
as well as mental
retardation;
45.8
Dr Okoli had also
conceded in cross-examination that in respect of foetal development,
Dr Pistorius was better qualified than he
was;
45.9
Despite these concessions
it was contended that Prof Lotz lacked sufficient expertise in the
field of neurosurgery and neurology,
and that he had refused to
objectively assist the Court. I must say at this stage that I find
this a rather strange submission
and I will deal with it when I
analyse the argument;
45.10
As I have said, Dr Okoli
was of the view that a decelerating effect would most probably have
caused a generalised injury and not
a focal injury as C presents. It
must be remembered in this context that Dr Okoli had not been aware
of the fact that the Toyota
in which Plaintiff was a passenger had
flipped over after the high-velocity impact, and also had not
considered that C’s
head had been shown to have turned
downwards at the last gynaecological examination;
45.11
The fact that I re-called
Dr Pistorius, thereby interrupting the cross-examination of Dr Okoli,
was according to Defendant’s
Counsel “a somewhat strange
development in the course of the trial”. I will deal with this
topic hereunder, but I must
state at this stage that Dr Pistorius is
based in Stellenbosch and obviously arrangements had to be made for
him to return to this
Court. I deem this not only in the interest of
justice in general, but also in the interest of the child, that the
topic of dysmorphia
that Dr Okoli had introduced himself by producing
C’s ID-document, not be left hanging in the air as it appeared
to me that
it could be an important factor to be considered in
general;
45.12
Defendant’s Counsel
did not wish me to make any credibility finding although he did
criticise First Plaintiff’s evidence
relating to the presence
of foetal distress, which was not supported by clinical observations
at the time. This however is not
a relevant topic and I will not deal
with it, nor with First Plaintiff’s evidence relating to less
numerous foetal movements.
Prof Lotz was however criticised because
his evidence went beyond the contents of paragraph 3 of his expert
summary, which referred
to a number of “reasonable and logical
considerations”, relating to the cause of C’s condition.
He had also not
examined C, had never consulted medical text books in
that context, and did not consider congenital defects, so it was
contended.
It will be convenient to add at this stage that during
cross-examination Prof Lotz was asked how a congenital defect would
present
itself on MRI imaging. On the one hand Prof Lotz said that
the MRI did not show any congenital defect, but also added that he
could
not answer the question, because he did not know which
congenital defect was being referred to, because there were thousands
upon
thousands;
45.13
Upon analysis of
Defendant’s Heads of Argument, it appears that the major part
of the criticism levelled against Prof Lotz,
is that he did not
consider other probable causes apart from his arterial spasm theory.
In that context he failed in his duty as
a supposedly objective
witness, so it was said.
45.14
Dr Pistorius gave
detailed evidence, but this was rather inappropriately described by
Defendant’s Counsel as being a “miraculous
theory”.
In essence his opinion had been that the destruction of the basal
ganglia by a loss of blood supply for an undetermined
period was the
cause of the thinning of the corpus callosum. If there had been any
other cause for this injury to the corpus callosum,
a more global
destruction of the brain would have been expected. It must be
remembered at this stage that Dr Okoli agreed that
at some stage poor
blood supply to the cerebral arteries must have been present, because
both the basal ganglia and the corpus
callosum were involved. The
cause of the reduced blood supply in this context is the essential
difference of opinion between that
of Dr Pistorius and Dr Okoli. It
was submitted that Dr Pistorius’ evidence was “an
incredulous explanation”.
This was his submission in the
context of his evidence as to how the sudden deceleration would have
caused a flexion in C’s
neck. It would in fact have been most
likely a lateral flexion, which would be supported by Mrs S’s
evidence that the vehicle
had flipped onto its side after the impact.
It is true that Prof Lotz had said that no one knew exactly what
happened to C’s
body at the time of the impact and immediately
thereafter. Defendant’s Counsel however, criticised Dr
Pistorius who presented
his theory without even testifying as to the
position of C in the womb. Dr Coleman however had said that C had
already turned in
the womb;
45.15
Plaintiff’s
witnesses were furthermore criticised on the basis that neither Dr
Pistorius, nor Prof Lotz, could say with any
certainty as to how long
the blood supply had been interrupted. Counsel’s conclusion in
the context of the expert evidence
was that not even Plaintiff’s
experts could agree as to what had happened to C. According to him
the blind led the blind,
which is a rather inappropriate observation
in this sad case having regard to the experience and expertise of the
medici. Lastly,
Defendant’s Counsel made a surprising
submission for which there was no evidence whatsoever, and which had
never been put
to any witness at all, namely that C’s face did
not present the asymmetry initially testified to by Dr Okoli, because
she
had received “botox treatment”. The less I say about
this contention, the better, but it is totally without foundation.
46.
Recalling of
witnesses and observations in Court:
It is not that unusual in
civil trial proceedings that the Court recalls a witness who has
already given evidence for further examination
or cross-examination.
A Court does have this discretion, and, in the interests of justice,
it may be necessary where a glaring
uncertainty has not received the
necessary attention. By this I mean that such uncertainty, when it
appears, ought at least to
be of a material nature. Contextually,
see:
Oosthuizen v Stanley
1938 AD 322
at 333
.
It is obviously not
a Court’s duty to recall a witness to promote or defeat a
party’s claim where Counsel intentionally
or inadvertently
failed to adequately address a particular issue. Prejudice to the
opposing party must be considered, and it should
be made clear on
which topic the additional evidence will be focussed on, and limited
to.
See:
The South
African Law of Evidence, 2
ND
Edition, D. Zeffert and A. Paizes, Lexis Nexis, at 927
,
and
Hladhla v President
Insurance Company Ltd 1965 (1) 614 AD
.
Apart from these
considerations, I considered it in the best interests of the child
that Dr Pistorius be recalled after Dr Okoli
had deemed it fit to
produce C’s identification document from his records. No one
had seen this before and the topic of asymmetry
of her face had
received only scant attention. A child’s interest remains of
paramount importance in every matter concerning
a child. Section 28
(2) of the
Constitution
is abundantly clear as are the
provisions of s. 6 of the
Children’s Act 28 of 2005
.
The question of what she looked like to a specialist physician and
why, was a material consideration when I made this decision.
Dr Okoli
was still being cross-examined at the time, and Dr Pistorius‘
evidence on this topic was interposed so that the
former could also
put his observations on record, and I my own. I have said what these
were. Obviously I cannot say what the cause
of C’s “squint”
in the left eye was and the way her smile differed each time, but it
seemed to me that Dr Okoli
had over-stated his observation in this
regard, and that the factual observation of Dr Pistorius accorded
more with my own observation,
which I was entitled to make and note
it on the record. I did not see an obvious deformity in C’s
face, such as initially
referred to by Dr Okoli. I saw what Dr
Pistorius saw.
See:
The South
African Law of Evidence, supra at 859.
47.
How does a Court
evaluate conflicting medical expert evidence?
This topic has been dealt
with in a number of foreign jurisdictions and also in South Africa,
including dicta by the Appellate division
and the Supreme Court of
Appeal. I do not intend repeating the well-known dicta relating to
the principles that need to be applied
in great detail, but certain
basic observations in this regard are apposite. Before dealing with
conflicting evidence and attempting
to arrive at the most probable
finding in this particular context, it is necessary to refer to the
classic English judgment in
National Justice Compania Naviera
SA v Prudential Assurance Company Ltd (“The Ikarian Reefer”)
[1993] 2 Lloyds Rep 68
at 81
, where the duties of an expert
witness were set out, and these duties have been confirmed by various
judgments of the South African
Courts since then. In the present
context, the most important duty of an expert witness is that he
should provide independent assistance
to a Court by way of an
objective, unbiased opinion in relation to matters within his
expertise. In the same vein, an expert witness
should make it clear
when a particular question or issue falls outside his expertise. The
crux really is in any given case that
an expert comes to Court to
give the Court the benefit of his or her expertise. An expert does
not assume the role of an Advocate,
nor gives evidence which goes
beyond the logic which is dictated by the scientific knowledge which
that expert claims to possess.
A further important consideration is
the following: an expert’s bold statement of his opinion is not
of any real assistance
to a Court. Proper evaluation of the opinion
can only be undertaken if the process of reasoning which led to the
conclusion, including
the premises from which reasoning proceeds, is
disclosed by the expert.
See:
Coopers SA Ltd
v Deutsche Gesellschaft Für Schädlingsbekämpfung MBH
1976 (3) SA 352
(A) at 371 F – G
.
In
South African
Law of Evidence supra at 328
, the learned authors say, and
this also appears from a number of important reported decisions, that
ultimately the determination
by the Court depends on the examination
of the opinions and the analysis of the reasoning behind them.
48.
An expert witness is also
expected to state the facts or assumptions upon which his opinion is
based. He should not omit to consider
material facts which could
detract from his concluded opinion. Stubborn dogmatism is of course
of no benefit to the Court. In this
context it is important to
remember that in civil cases, in finding facts and making inferences,
the Court may decide upon a mere
preponderance of probability, even
although its so-doing does not exclude every reasonable doubt.
See:
Govan v
Skidmore
1952 (1) SA 732
N at 734 A
.
This dictum was approved
by the Appellate Division in
AA Onderlinge Assuransie Bpk v De
Beer
1982 (2) SA 603
at 614 H – 615 B
. The Appellate
Division also approved the
Govan
dictum at 734 C, where
it was said that “It seems to me that one may, as Whigmore
conveys in his work on
Evidence (3
RD
Edition, par. 32)
, by balancing probabilities select a
conclusion which seems to me the more natural, or plausible,
conclusion from amongst several
conceivable ones, even though that
conclusion may not be the only reasonable one.”
The same passage was
referred to with approval by Holmes JA in
Ocean Accident and
Guarantee Corporation Ltd v Koch
1963 (4) SA 147
(A) at 159 C to D
,
where the following was said in respect of the word “plausible”:
“I need hardly add that “plausible”
is not here
used in its bad sense of “specious” but in the
connotation which is covered by words such as acceptable,
credible,
suitable…”
49.
In
Michael and
Another v Linksfield Park Clinic (Pty) Ltd and Another
2001 (3) SA
1188
SCA at 1201
, two important dicta appear: the one is that
when dealing with expert opinion, a Court must be satisfied that such
opinion has
a logical basis. I may also add my humble opinion to this
admonition, namely that the importance of logical thought in any
given
context is not new, and it is undisputed that Greek
philosophers laid the basis for logical thinking and deductions more
than 2400
years ago. Aristotle (384 322 BC) was the leading
thinker on this topic.
See:
Think, Simon
Blackburn, Oxford University Press 1999, Chapter 6.
The most important dictum
of the Supreme Court of Appeal in the
Linksfield
case
supra, is, for present purposes the following (at par. 40): “Finally,
it must be borne in mind that expert scientific
witnesses do tend to
assess likelihood in terms of scientific certainty. Some of the
witnesses in this case had to be diverted
from doing so, and were
invited to express the prospects of an event’s occurrence, as
far as they possibly could, in terms
of more practical assistance to
the forensic assessment of probability, for example, as a greater or
lesser than 50% chance and
so on. The essential difference between
the scientific and the judicial measure of proof was aptly
highlighted by the House of
Lords in the Scottish case of
Dingley
v The Chief Constable, Strathclyde Police 2000 SC (HL) 77
,
and the warning given at 89 D to E, that “one cannot entirely
discount the risk that by immersing himself in every detail
and by
looking deeply into the minds of the experts, a Judge may be seduced
into a position where he applies to the expert evidence
the standards
which the expert himself will apply to the question whether a
particular thesis has proved or disproved – instead
of
assessing, as a Judge must do, where the balance of probability lies
on a review of the whole of the evidence”.”
I certainly do not intend
to be seduced in that manner and I will apply the judicial measure of
proof to the evidence that I have
referred to.
50.
In
Louwrens v
Oldwage
2006 (2) SA 161
SCA at 174 H
, with reference to the
Linksfield Park
decision supra, the following was said:
“What was required of the trial Judge was to determine to what
extent the opinions
advanced by the experts were founded on logical
reasoning and how the competing sets of evidence stood in relation to
one another,
viewed in the light of probabilities.” Logical
reasoning can lead one to the probabilities and to the judicial
standard of
proof that I have mentioned. I have some philosophical
reservations whether, on the other hand, it can be said that one can
arrive
at a probable answer on the basis that it is logic. Either a
process of thought is logic or it is not logic. Can one say that
something
is probably logic?
See:
Mutual and
Federal Insurance v SMD Telecommunications
[2011] 2 All SA 34
SCA at
45 par. 27
.
In “Evaluation of
Divergent Expert Opinions” by L. Meintjies-Van der Walt in
The
South African Journal of Criminal Justice 2011 at 213
, she
referred to a passage in an article which pointed out the limitations
of logic: “Logic, or any other formalism, will
not determine
what is and what is not true. Logic determines the consequences of
believing certain things to be true; logic is
concerned with
arguments, not truth. It provides an analysis of arguments that are
in some formal sense justifiable, e.g. valid
arguments which are
sound with respect to the formal semantics. But it does not tell you
what things you should believe to be true
in the first place”.
The author of that article also advises that a number of other
factors should be kept in mind which
may not always show specific
features of logical reasoning, for instance the question whether the
experts’ methods and reasoning
enjoy general acceptance in the
relevant scientific community?
In
Buthelezi v
Ndaba
2013 (5) SA 437
SCA at 442 G
, with reference to
opposing views of expert witnesses, the Court said that its
determination must depend on the analysis of the
cogency of the
underlying reasoning which led the experts to their conflicting
opinions. The relevant dictum in the
AA Onderling Assuransie
decision supra was also recently approved by the Supreme
Court of Appeal in
Golias v MEC for Health 2015 (2) 1997 at 107
par. 19
, where the following was said: “… it is
important to bear in mind that in a civil case it is not necessary
for a Plaintiff
to prove that the inference that she asked the Court
to draw is the only reasonable inference; it suffices for her to
convince
the Court that the inference that she advocates is the most
readily apparent and acceptable inference from a number of possible

inferences.”
The mentioned dicta in
the
Govan v Skidmore
case supra, the
AA
Onderlinge Assuransie
supra and
Ocean Accident v
Guarantee Corporation Ltd
supra, were again referred to with
approval by the Supreme Court of Appeal in
Cooper and Another
N.O v Merchant Trade Finance Ltd
2000 (3) SA 1009
at 1028 A to D
.
The approach to the
evaluation of medical evidence as stated in the
Linksfield
decision supra, was also recently endorsed by the
Constitutional Court in
Oppelt v Department of Health 2016 (1)
SA at 339 par. 36
. The crux really is that a Court must not
assess the cogency of scientific evidence by scientific standards,
but by the legal standard
of the balance of probabilities (par. 38).
51.
I therefore intend
deciding this action on the basis that I must accept the inference
that is the most readily apparent and acceptable
inference from the
other possible inferences that emerged from the evidence and that in
doing so I must apply the judicial standard
of proof and not the
scientific standard. Logical thinking in this process will assist in
arriving at the final result, but philosophically
speaking, it cannot
determine it.
52.
An interesting article on
the topic of the evaluation of scientific evidence appears in the
South African Law Journal, Vol 120, 2003 at 352
, by the
mentioned L. Meintjies-Van der Walt, titled “
Expert
Odyssey: Thoughts on the Presentation and Evaluation of Scientific
Evidence”
. In the present context, having regard to the
qualifications and expertise of the three main witnesses, namely Drs
Pistorius, Lotz
and Okoli, I deem the reference to
Menday v
Protea Assurance Company (Pty) Ltd
1976 (1) SA 565
(ECD)
, of
particular importance: “However eminent an expert may be in a
general field, he does not constitute an expert in a particular

sphere unless by special study or expertise he is qualified to
express an opinion on that topic. The danger of holding otherwise
–
of being overhauled by a recycle of degrees and diplomas – is
obvious; the Court then has no way of being satisfied
that it is not
being blinded by pure “theory” untested by knowledge or
practice. The expert must either himself have
knowledge or experience
in the special field on which he testifies (whatever general
knowledge he may also have in pure theory)
or he must rely on the
knowledge or experience of others who themselves are shown to be
acceptable experts in that field.”
On the topic of logic,
the learned author said that the theory on which the expert bases his
or her evidence must exhibit internal
consistency and logic. The
premises of the theory, along with the observations and data, must
lead to conclusions through logically
valid reasoning. I agree with
that approach.
53.
Analysis of the
crux of the evidence and findings
:
At the time of the
high-velocity impact and sudden deceleration, C’s corpus
callosum was fully formed. There is no dispute
about that. Dr
Pistorius is a highly qualified and experienced specialist in the
field of foetal medicine and foetal brain imaging.
Prof Lotz has vast
relevant experience in radiology and imaging. Both agree that C’s
right basal ganglia were damaged, and
that this caused the thinning
of the corpus callosum. This could not have occurred prior to 20
weeks gestation and not after her
birth. There was thus focalised
destruction and an intra-uterine traumatic event was the likely
cause. No other known factors could
have caused this.
Dr Okoli is an
experienced neurosurgeon. He does not remotely have the
qualifications and experience of the other specialists in
ante-natal
radiology, imaging and diagnosis. I agree with Prof Lotz’s
comment that it is obvious that their fields of expertise
were wide
apart, and that there is merit in his suggestion that Dr Okoli should
not have accepted this instruction or brief to
express an opinion and
to give evidence. This comment was not intended to reflect on his
knowledge or expertise as a neurosurgeon.
It was also admitted by
Defendant that at 28 weeks gestation, cerebral arteries are capable
of constricting and causing spasms.
The corpus callosum can further
develop in thickness after 24 weeks gestation. C’s MRI image
showed a border-zone infarction.
These facts are supportive of
Plaintiff’s experts’ view that severe arterial spasms
resulting from likely flexion of
the foetus’ neck would have
caused a localised reduction of blood flow to the right basal
ganglia. This then caused the thinning
of the corpus callosum and C’s
present condition. Dr Pistorius and Dr Lotz saw a positive
correlation between the severity
of the accident and the likelihood
of trauma. Dr Okoli saw none. He fought valiantly to overcome
superior forces of expertise,
supported by medical literature, but
valiance, and some Judges would have called this stubborn dogmatism,
cannot withstand the
process of logical reasoning based on particular
expertise. The dictum in
Menday v Protea
supra, is
particularly apposite. Dr Pistorius was also of the view that if C’s
condition was congenital, both sides of the
brain would have been
affected, and damage would not have been so localised. The fact that
only a specific area of the brain was
affected, pointed to a
traumatic vascular event. There was no other logical explanation.
Prof Lotz was of the same opinion. Added
to this was the fact that Dr
Okoli had agreed that there had been a border-zone infarction (but
after initially denying it). The
vastly experienced Prof Lotz, and I
refer particularly to his expertise in ante-natal imagery/radiology,
had seen no evidence of
any congenital, genetic or inflammatory
pathology and also no evidence of heterotopia. The congenital defect
relied upon by Dr
Okoli did not exist, it could not be found in any
literature, and Dr Okoli himself was unable to identify it. I asked
Dr Okoli
specifically what had caused the thinness of the corpus
callosum and he replied that it was “under-formed”. He
gave
no specifics as to why, when and how. At no stage did Dr Okoli
testify that at 28 weeks gestation the particular foetal arteries

could not go into spasm and therefore arrest the blood supply. At
best, according to him, they could only do so “optimally”

at 34 weeks gestation. There was no reason indicated by him why an
“optimal” spasm was required in the present case.
Dr
Okoli was very firm in his view that C’s whole body spasticity
did not support the opinion of Dr Pistorius and Prof Lotz
of
focalized brain damage. He had however agreed that at some stage poor
blood supply to the cerebral arteries must have been present
because
both the basal ganglia and the corpus callosum were involved. No
details of this “stage” were given or its
cause. The
cause of this reduced blood supply is the essential difference of
opinion between that of Drs Pistorius and Okoli. Dr
Pistorius’
view in this context was that the damage to the side of the basal
ganglia would have caused spasticity to the
left side of the body,
but that this spasticity would cross over to the other side of the
body and would cause less severe spasticity
to the right side. Dr
Pistorius was not challenged on this particular point at all during
cross-examination, which I deem important
in the over-all mosaic of
this challenging case.
I have already dealt in
some detail with the topic of C’s “dysmorphic facial
features”. Dr Okoli’s evidence
in this regard is not
consistent, and also does not accord with my own observations in
Court, nor those of Dr Pistorius.
54.
Applying therefore the
judicial measure of proof that I have referred to, keeping in mind
also the particular experience and expertise
of the experts, and
considering where the balance of probability lies on a review of the
whole of the evidence, I have no hesitation
in finding that the most
natural and plausible conclusion is that the relevant accident on 10
December 2012, was the cause of C’s
present condition, as well
as the injuries sustained by the First Plaintiff.
The following order is
therefore made:
It is declared that
Defendant is liable to compensate Plaintiffs for the injuries
sustained by them as the result of the collision
on 10 December
2012;
Defendant is ordered to
pay the costs of the action;
The parties are given
leave to present to me, within 14 days from date hereof, a more
specific draft order relating to costs,
should they deem it fit to
do so.
_____________________________
JUDGE H.J FABRICIUS
JUDGE OF THE GAUTENG HIGH
COURT, PRETORIA DIVISION
Case number: 17386/2014
Counsel for the
Plaintiff:

Mr Uys Jordaan
of Uys Jordaan Attorney
Attorney for the
Plaintiff
Counsel for the
Defendant:

Adv M. Hugo
Instructed by: Maponya
Inc
Date of
Hearing:

28 April; 3, 4, 5, 9, 10, 13 & 17 May 2016
Date of
Judgment:

24 June 2016 at 10:00