A Comprehensive Report On Brain Damage Caused by DPT Vaccination C 1960 1970 and Its Possible Connections To Autism Spectrum Disorder

Updated 6 March 2017
A Comprehensive Report on Brain Damage caused by DPT Vaccination c1950-1970

and its possible connections to autism spectrum disorder
Alan Challoner MA (Phil.) MChS 9 April 2003
This report has arisen from a claim in law that eventually went to Judicial Review. 1 The course of
action was terminated when Daniel Brennan QC gave an adverse opinion to the Prime Minister, Tony
Blair. On the basis of that opinion the Legal Aid Area Office withdrew the Legal Aid Certificate in
1998. It was reinstated later following my appeal. The substance of this appeal was that Daniel
Brennan had not considered up-to-date scientific evidence on the manner in which the brain can be
damaged by pertussis vaccination. It was that knowledge that ought to have been used to contradict
the then experts views given in Loveday v Renton.2,3 The appeal was not upheld. (See also
Appendix Two)
GENERAL COMMENTS
The Advice to the Legal Services Commission by Lord Daniel Brennan QC, dated 5th
September 2001
I have concern about the way in which the matter of consideration of new information, including
current and recent past research, has been undertaken. I deal with the papers referred to by Lord
Brennan below, as well as some that do not appear in his list.
Further than that I am also at a loss to understand why the analysis of material associated with
vaccine damage has not been assessed by a neuro-pharmacologist and/or a neuro-psychologist. Unless
I have misunderstood the papers that have been given to me, Lord Brennan seems to have been his
own expert in these matters. These cases have been ongoing now for many years. The future of the
claimants is very much dependent upon the outcome of their individual case. The need to show cause
is partly based upon a lack of scientific evidence produced for consideration so far. It is of the utmost
importance that, before any Legal Aid Certificates are rescinded, there is a very large degree of
certainty that all relevant material has been assessed by (an) expert(s).
Comment must also be made about the dichotomy that exists between government departments on
the matter of vaccine damage. Whilst the Legal Aid Commission is arguing that there is not enough
evidence to substantiate the continuance of all cases, the Vaccine Damage Payments Unit (and its
predecessor) has paid an award for such damage to most, if not all, of those who are plaintiffs in this
litigation. A good summary of the Vaccine Damage Payments Scheme can be seen here. 4 Letters
from the Vaccine Damage Tribunal, showed that medical opinion confirms that the claimant is
disabled as a result of vaccination ... the extent of the disability arising from vaccination ... amounts
to severe disablement. Details of the vaccine damage awards paid from 2000 to 2012 can be seen
here.5 [See also Addendum on page 30]
In addition letters from the Department of Health and Social Security states that, ... a payment is due
(under the Scheme) for severe damage by vaccination.
1
Judgment of Mr Justice Simon Brown in R v. Legal Aid Area No. 8 (Northern) Appeal Committee
Ex Parte, Parkinson, Garside, Angell, Kelly, Skates, Challoner & Cavanagh . [Referred to in the text as,
claimants]
2 Loveday v Renton and Wellcome Foundation Ltd: 1990. 1 Med LR 117, [1990] 1 MLR 1. Coram:
Stuart-Smith LJ.
3 Loveday v Renton (No 2): 1992. 3 All ER 184. Coram: Hobhouse J.
4 http://pubmedcentralcanada.ca/pmcc/articles/PMC1627257/pdf/archdisch00766-0005.pdf (p579-580)
5 https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/551864/foi_3426_2012.pdf.
1
A further statement, in claimants Deed of Trust, from The Secretary of State reads, ... the Secretary
of State is satisfied that (the claimant) is severely disabled as a result of vaccination... This statement
was repeated in 2001, in a later Trust Deed that accompanied a further payment under the Vaccine
Damage Payments Act 1979.
There were no qualifications on these statements, and it is difficult to understand why the Legal Aid
Commission sees fit to ignore them.
History of Suspected Neurological Events in Association with Pertussis Vaccines
The possibility that pertussis immunisation might cause adverse neurologic events resulting in
permanent brain injury was first raised following a report of two cases by Madsen (1933) and case
reports published in the 1940s (e.g., Byers and Moll, 1948; Globus and Kohn, 1949; Toomey, 1949
[see Appendix One]. Subsequent descriptions of encephalopathies of various types occurring at
differing time periods after pertussis immunisation followed (e.g., Berg, 1958; Cockburn, 1958;
Globus and Kohn, 1949; Malmgren et al., 1960; Sutherland, 1953). On the basis of these reports,
Strom (1960) questioned whether the risk of adverse neurologic effects following immunisation might
be more of a concern than the risk of pertussis itself, a view reiterated in reports by Chevrie and
Aicardi (1975), Cavanagh et al. (1981), Ehrengut (1980), Kulenkampff et al. (1974), and Stewart
(1977, 1979).
[This is a restricted list of publications pre-1990] Fuller details can be located in Howson et al. 6
Of these, the reports by Globus and Kohn (1949) and Berg (1958) are particularly significant. Globus
& Kohn documented the reactions of two male infants who experienced convulsions and
unresponsiveness subsequent to pertussis vaccination. One infant (9 months old) continued to
experience convulsive episodes at follow-up; the second infant, experienced convulsions, became
comatose, and subsequently died; autopsy revealed evidence of degenerative processes in the brain.
The authors concluded that an allergic form of encephalopathy was caused by an antigen-antibody
reaction. 7 Berg in his Summary remarks wrote: The value of pertussis immunization is emphasized,
as is the grave danger of further inoculations when a previous one has produced any
suggestion of a neurological reaction. 8 (My emphasis)
From the many papers and books written on the subject over the last 70 years, it is obvious that
many of the descriptions of events and terminology are not consistent or rationalised. It is not always
possible to determine the exact nature of the events from the terms and descriptions used.
Also in some cases, because there is a probability that even where the eventual outcome was severe,
the triggering event was restricted to a comparatively short period of time, and there then seemed to
be a recovery to normality. The reason for this is that the damage caused was to areas of the brain
that were in the course of development, and which were not fully functional at the age of
vaccination. This would explain why the sequelae were only obvious at a later time.
The National Childhood Encephalopathy Study 1976
In response to the controversy surrounding whole-cell pertussis vaccination, in the United Kingdom,
The National Childhood Encephalopathy Study (NCES) was established in 1976 to determine if
whole-cell pertussis vaccine does cause brain damage in children and, if it does, to establish how often
such damage occurs. This was a prospective case controlled study and the results of the first one
6
Howson, Christopher P.; Howe, Cynthia J. and Harvey V. Fineberg, (Editors). Adverse Effects of
Pertussis and Rubella Vaccines. A Report of the Committee to Review the Adverse Consequences of
Pertussis and Rubella Vaccines. Division of Health Promotion and Disease Prevention. Institute of
Medicine. National Academy Press, Washington, D.C. 1991. Can be read online at:
http://books.nap.edu/books/0309044995/html/R1.html
7 Globus JH, Kohn JL. 1949. Encephalopathy following pertussis vaccine prophylaxis. Journal of the
American Medical Association 141:507-509.
8 Berg JM. (1958) Neurological complications of pertussis immunization. British Medical Journal 2:24-
27.
2
thousand cases for the three years ending June 30, 1979, was reported. A case was defined as acute
neurological illness in a 2- to a 36-month-old child that required hospitalisation. Permanent brain
damage was defined as a case with residual effects after one year.
This study will of course have missed the many children who had serious reactions and who
were not admitted to hospital.
Lord Brennan dismisses the 1976 NCES as being unhelpful in supporting this litigation. However the
Opinion of Simeon Maskrey QC, in July 2000, had this to say:
At Page 11, para. 13; It is one thing to say that Loveday is not an impediment to
further litigation. It is another to say that the further litigation will be successful. As I
understand Dr Kinsbourne, he considers that the NCES study is crucial in proving a causal
link. He emphasises that the NCES study does not of itself establish a causal link. What it does
is to exclude coincidence as an explanation for damage occurring in close temporal proximity
with the administration of vaccine. However the exclusion of coincidence, together with
proof that there is no scientific reason to deny possibility of a causal link between the vaccine
and damage, is sufficient (in the absence of any other identified cause for the damage) to
establish that the causal link is probable.
Also at Page 15, para 18.1; Given that it is proved that the vaccine does cause
permanent damage in some cases, it seems to me to be arguable that if a given claimant
meets the criteria established and used by the NCES, and if the chance of coincidence is then
proved to be (say) one in four or one in five, he will have proved that on balance of
probabilities, his injury was caused by the vaccine.
For previously normal children, the estimated risk of permanent neurological illness attributed to
immunisation with DTP vaccine was one in 310,000 immunisations. In addition to this rare rate of
major brain damage there is the very real possibility that the highly neurotoxic whole-cell pertussis
vaccine may cause minor brain damage in a much higher percentage of vaccine recipients. This
damage might manifest itself in loss of intelligence quotient, (I.Q.) points, reading problems, language
difficulties and autism. Since these types of brain damage show up years after vaccination, we
may never know who was truly damaged by whole-cell pertussis vaccination.
In 1985 The Institute of Medicine, (IOM), of the U.S. National Academy of Sciences after an extensive
review of the problem of adverse reactions to pertussis vaccine gave the highest possible priority to
switching from whole-cell pertussis vaccine to acellular vaccine to prevent monetary loss and personal
suffering. In 1990, after extensive hearings another IOM committee concluded that the evidence was
sufficient for them to conclude that whole-cell pertussis vaccine caused acute encephalopathy.
They were unable to conclude satisfactorily whether whole-cell pertussis vaccine caused permanent
brain damage. (See Causation, Page 4) They never said what level of proof they required to come to
their conclusion. This was important because scientists generally require 95 percent or better certainty
for such a conclusion, but U.S. Courts only require a more likely than not standard. In 1993 a ten-year
follow-up of the NCES was published, to help address this legitimate criticism. This study again
concluded that whole-cell pertussis vaccine most likely caused permanent brain damage, in
otherwise apparently normal children, if they developed significant neurological symptoms within
seven days of the pertussis vaccination.
Infantile Spasms & Epilepsy
Most, if not all, claimants had neither symptoms of epilepsy nor incidents of infantile spasms prior to
vaccination. Following the DPT vaccinations most, if not all, claimants had neither symptoms of
epilepsy or incidents of infantile spasms nor any similar events. Some were examined by use of
electroencephalograph on several occasions, from childhood to adulthood, and in those cases there
have been no diagnoses of epilepsy. Thus the convulsions and associated reactions which occurred
very shortly after each vaccination are the only such episodes that have occurred in their life. No
contrary evidence to vaccine-induced brain damage has been put forward by any medical examiners
who have assessed at least one of the claimants.
Advent of adverse reactions following vaccination

3
DPT Vaccine Dosage The Green Book published by HMSO is a reference text about
vaccinations. In Chapter 24.2.1 and 24.2.2 it advises that each dose should be 0.5ml. On some
occasions, claimants, medical records show that they received a 1cc dose.
Loveday v Renton The claim for damages in Loveday v Renton and The Wellcome
Foundation, heard in the High Court of Justice in London, from early October 1987 until late
February 1988, dealt with the general issue of whether, on the balance of probabilities, pertussis
vaccine could cause permanent brain damage.
The cornerstone of the claim that pertussis vaccine can cause permanent brain damage has always
been the apparent clustering of onset of neurological disorders within the first 2448 h after
vaccination. One of the main finds of the National Childhood Encephalopathy Study9 however,
which was not divulged in any published report but emerged in the course of the hearing, was that
permanent brain damage did not occur within 48 h of DTP vaccination in any child in England,
Scotland and Wales from mid-1976 to mid-1979 when 2 million doses of vaccine were used. 10
Many of the research papers, that have been used in attempting to define causation in cases of
possible brain damage following vaccination with DPT, have involved subjects whose initial reaction
was beyond 48-hours after the vaccination. However, in others, adverse reactions occurred on the
same day as the vaccinations.
The Green Book at Chapter 24.6.1b, it states, Immunisation should not be carried out in
children who have a history of a general reaction to a preceding dose. (My emphasis) It
seems that this advice was not followed in some cases brought by claimants. This was not seen as
possible negligence.
Bedford & Ellman state that, There are few reasons for refraining from vaccinating a child. Contraindications are
uncommon and most children in whom there is a true permanent contraindication will be under the care of a
paediatrician. 11 This of course would not be the case if the child did not have any previous medical conditions
that had required a paediatrician. In my experience, it was unusual for a child who had an adverse reaction to
the DPT vaccination to be referred to a paediatrician in the immediate aftermath of the encephalopathy.
However, Robinson has written that, The Dudgeon and Meade reports strongly suggest that the
contraindications have a sound medical basis. Forty-nine per cent of the cases of serious neurological disorder
which the Meade panel regarded as likely to be caused by pertussis immunisation had at least one
contraindication to this immunisation, and in the smaller number of cases examined by the Dudgeon panel there
was also a significant number in whom the relevant immunisation had been contraindicated. From the purely
medical, as well as the medico-legal, point of view it is of the utmost importance to observe the
contraindications strictly. 12
CAUSATION.
That vaccinations are helpful to society is without question; however, that
some individuals suffer permanent and damaging sequelae to vaccinations is
also well documented. The purpose of this section is to offer a mechanism by
which vaccination-induced neuronal damage in some individuals can be
understood.
9 Miller, DL & Ross, EM. National Childhood Encephalopathy Study: an interim report. Br Med J. 1978
Oct 7; 2(6143): 992993.
10 Griffith, A. H. Permanent brain damage and pertussis vaccination: is the end of the saga in sight?
Vaccine; Volume 7, Issue 3; June 1989, Pages 199-210.
11 Bedford, H & Elliman, D. Education and debate: Concerns about immunisation. BMJ 2000;320:240-
243 ( 22 January )
12 Robinson, RJ. Current topics: The whooping-cough immunisation controversy. Archives of Disease in
Childhood, 1981, 56, 577-580
4
Lord Brennan on page three of his report, Opinion & Advice to the Legal Services Commission,
wrote, The question is not whether the vaccine can cause seizures, or febrile reactions, but
permanent brain damage. What is meant by permanent brain damage?
The brain consists of about 100 billion interconnected neurones (nerve cells). There is a huge
variation in the number of neurones that different people have. Each neurone has a cell body out of
which axons extend. Axons are like wires along which electronic information flows. At the end of
each axon, chemicals are released that excite or inhibit the next neurone. In this way, all the neurones
are interconnected.
The two main chemicals released are glutamate, which excites neurones, and GABA, which inhibits
them. A substantial amount of inhibition is required, otherwise the brain would be a mass of
excitation all the time. Seizures are like an electrical storm, with a lot of neurones firing and releasing
substantial amounts of glutamate.
In 1957 it was shown that at high enough concentrations, glutamate is toxic to neurones. Glutamate is
the major excitatory neurotransmitter of the mammalian central nervous system. Excessive exposure
to glutamate can kill central neurons (Lucas and Newhouse 13 ; Olney 14) and such neurotoxicity, or
excitotoxicity, likely contributes to the neuronal loss associated with several neurological diseases.
There is evidence that prolonged seizures in convulsive status epilepticus may lead to damage of
nerve cells. Blood pressure drops during a seizure. If the seizure is prolonged and blood pressure
remains low for longer, insufficient blood will reach the brain. Blood transports oxygen and also
glucose, which is the food for cells. If seizures are prolonged, the brain will eventually be deprived of
oxygen and the nerve cells start dying. In addition, a convulsion uses up glucose, therefore if
insufficient blood reaches the brain to provide enough glucose, this too can cause damage to nerve
cells.
When a nerve cell dies it cannot be resuscitated. In the long-term other neurones may take over some
or all of the work of the dead neurones, but that will not guarantee that the loss of the damaged
neurones will be mitigated. The realisation that prolonged seizures can damage the brain is not new.
It was noted as far back as 1825 that long seizures seemed to cause damage to the hippocampus15, the
part of the brain important for the formation of memory.
The fever-induced convulsions that some young children suffer, appear to have no long-term impact
on their brain functioning. However, there is a risk of developmental problems when infants suffer
the seizures. Recent research shows that children with a history of fever-induced seizures actually
outperformed others in tests of memory and learning capacity. The exception was for children who
suffered febrile convulsions before the age of 1 year. These children were at increased risk for deficits
in mental abilities. However, it also reinforces the concern that during infancy, these seizures may
injure certain brain cells and lead to more profound dysfunction. 16, 17
Serious reactions that might imply the existence of brain damage from the vaccine, were tabulated by
Greco et al and quantified as indirect evidence that pertussis vaccines may result in a post-vaccine
encephalopathy. 18
The US federal government maintained that, on rare occasions, permanent brain damage does occur.
The report of a single case-control study in support of this position prompted the establishment of a
special committee under the sponsorship of the United States Public Health Service, the Institute of
Medicine, and the National Research Council to determine the validity of the report. The special
committee concurred that pertussis vaccine does produce permanent brain damage in rare instances.
13 D. R. Lucas & J. P. Newhouse. The toxic effect of sodium l-glutamate on the inner layers of the
retina. Archives of Ophthalmol, vol. 58, no. 2, pp. 193201, 1957.
14 Olney, J. W. Brain lesion, obesity and other disturbances in mice treated with monosodium
glutamate. Science 164:7 19-72 1; 1969.
15 Bouchet, C., Cazauvieilh, C. De lepilepsie consideree dans ses rapports avec la lalienation mentale.
Arch. Gen. Med. 1825; 9, 510542.
16 Baram, T Z. & Shinnar, S. Do febrile seizures improve memory? Neurology 2001 57: 7-8
17 Chang, Y. C.; Guo, N. W.; Wang, S. T; Huang, C.C.; & Tsai J.J. Working memory of school-aged
children with a history of febrile convulsions: A population study. Neurology 2001 57: 37-42.
18 Greco D, Salmaso S, Mastrantonio P, et al. A controlled trial of two acellular vaccines and one
whole-cell vaccine against pertussis. N Engl J Med. 1996;334:341-348.
5
Physicians in the USA are required to warn all responsible parties of vaccine recipients that pertussis
vaccine may cause "lasting brain damage." This requirement has been authorised by Congress and the
National Childhood Injury Act of 1986. 19
Another patient study indicates that seizure activity originating in a specific location of the brain
(hippocampus) causes the region to become irreversibly damaged. 20
Earlier reports had presupposed that infantile convulsions following DPT vaccinations were only
triggered and not caused by the vaccine. This was one of the pillars of the Loveday v Renton case.
Cherry et al, have refuted this.
Pertussis immunisation is a precipitating factor of the first febrile convulsion in children
prone to have febrile convulsions... [People should not generalise by concluding that only
children who are 'genetically predisposed' have vaccination-induced febrile seizures (FS).]
In a similar study, with more focused data, only 6 of 60 and 15 of 60 children with severe
DPT reactions had personal or familial history of prior seizures, indicating that the majority of
children with severe reactions had no prior personal or familial FS as indicators of 'genetic
predisposition'. 21
Cytokines and vaccine-induced brain damage

Following vaccination, cytokines22 are released in response to:
(i) as part of the processes by which vaccinations induce antibody formation, and
(ii) as indicated by the occurrence of fever and, in many children, lethargic behaviour.
The cytokines so released are causally associated with two other processes:
(i) oedema within the central nervous system, and
(ii) clonal expansions of T-cell and B-cell subsets already activated by specific antigens from
recent processes within the central nervous system.
Of significance to autism, is that some T-cells and B-cells in peripheral circulation may be encoded
with neuron-derived epitopes (NdE) 23 subsequent to various infections and/or various treatments
with antibiotics.
In children having such NdE-encoded T-cells, B-cells, and antibodies, vaccination-induced clonal
expansions of those T-cells and B-cells may, in some cases, initiate further neuronal damage. In other
words, brain regions whose pre-vaccination neuronal damage had been relatively insignificant may,
via vaccination-induced clonal expansions, suffer additional damage.
The sequence is as follows: individuals primed with NdE-encoded immunological cells may, given
cytokines-release induced by one or more vaccinations, experience clonal expansions of those T-cells
and B-cells, which can re-cross the blood brain barrier into the brain and then induce additional
damage, i.e., resulting in vaccination-enhanced neuropathy presenting clinically as autism.
19 Sepkowitz S. Perverse reactions to pertussis vaccine by government medical agencies. J Okla State Med
Assoc. 1996 Apr; 89(4):135-8 (ISSN: 0030-1876)
20 Theodore, W. H.; Bhatia, S.; Hatta, J.; Fazilat, S.; DeCarli, C.; Bookheimer, S. Y. & Gaillard,
W. D. Hippocampal atrophy, epilepsy duration, and febrile seizures in patients with partial seizures.
Neurology 1999 52: 132.
21 Cherry JD, Holtzman AE, Shields WD, et al. Pertussis immunization and characteristics related to
first seizures in infants and children. Journal of Pediatrics 1993;122:900-903.
22 "Cytokine" is a word that comes from cyto- a combining form meaning "cell" - and -kinin - a combining
form used in naming hormones, especially peptide hormones (e.g., bradykinin). Nomenclature has
always been a problem because these factors were originally named for the activity that they described.
This resulted in a large number of three or four or occasionally five letter acronyms. The idea that the
"interleukin" - between leukocytes - designation would simplify nomenclature has not proved to be the
case. A review in 1979 by Byron Waksman listed almost 100 apparently distinct activities. At the time
no one knew whether these represented distinct cytokines or a few cytokines with multiple activities.
The answer is: some of both.
23 Epitopes: A part of an antigen to which an antibody binds.
6
In his book, Harris Coulter makes an important observation: in many children, post-vaccination traits
appear to be similar to those described as sequelae to various central nervous system infections.24
Coulters hypothesis presents molecular mechanisms that may account for the similarities in sequelae
to various central nervous system infections and, in some children, to vaccinations. 25
Based upon the facts,
(i) that fever is a vaccination reaction experienced by many individuals 26, and
(ii) that fever and oedema are stimulated by similar cytokines 27, 28, 29.
A subset of vaccinated children as a direct result of vaccination-induced cytokines release may be
likely to experience both encephalitis and subsequent encephalopathy. 30
For instance, research findings are instructive regarding autistic children for whom as neonates,
infants or toddlers medical records show a history of infections, antibiotic treatments, vaccinations,
and temporally associated onset of autistic traits (e.g., Baker et al (idem), & Coulter (idem).
As suggested by Coulter (idem), a range of mild but significant post-vaccination neuropathies may
occur.
Fever is strongly associated with interleukin-1, interleukin-6, and tumour necrosis factor alpha (IL-
1, IL-2, TNF-alpha; (Luheshi et al, idem)).
Brain inflammation is strongly associated with those same cytokines .
31, 32
IL-1 and IL-6 are among primary components in inflammatory expansions of B-cells and T-cells,
which can migrate to tissues from which, for instance, the anti-neural epitopes are derived.
Furthermore, because the very mechanism of vaccination-induced immunity derives from clonal
expansions of B-cells 33, cytokines needed for B-cell clonal expansions are induced and present as
a causally related response to vaccination.
If, prior to or immediately subsequent to vaccination, any neuronal damage, however slight, has
occurred in response to the child's infections and/or antibiotic treatments, then the child probably has
some activated microglia 34 and some anti-neuronal antibodies, as well as activated T-cells and B-cells
whose epitopic focus is derived from neurons that were injured either,
(i) during the prior infections and treatment, or
24 Coulter, H.L. (1990), Vaccination, social violence, and criminality: The medical assault on the
American brain. Berkeley, North Atlantic Books; Washington, Center for Empirical Medicine.
25 Allen, A.J., Leonard, H.L., & Swedo, S.E. (1995), Case study: a new infection-triggered, autoimmune
subtype of pediatric OCD and Tourette's syndrome. Journal of the American Academy of Child and
Adolescent Psychiatry, 34, 307-311.
26 Bellanti, J.A., Fishman, H.D., & Wientzen, R.L. (1987). Adverse reactions to vaccines. Immunology
and Allergy Clinics of North America, 7, 3, 423-445.
27 Luheshi, G., & Rothwell, N. (1996), Cytokines and fever. International Archives of Allergy and
Immunology, 109, 301-307 [listing IL-1, IL-6, and TNF-alpha as the primary cytokine pyrogens].
28 Quagliarello, V.J., Wispelwey, B., Long, Jr., W.J., & Scheld W.M. (1991), Recombinant human
interleukin-1 induces meningitis and blood-brain barrier injury in the rat: characterization and
comparison with tumor necrosis factor. Journal of Clinical Investigation, 87, 1360-1366.
29 Yamasaki, Y., Matsuura, N., Shozuhara, H., Onodera, H., Itoyama, Y., & Kogure, K. (1995),
Interleukin-1 as a pathogenetic mediator of ischemic brain damage in rats. Stroke, 26, 676-81.
30 Baker, S.M., & Pangborn, J. (1996), Clinical assessment options for children with autism and related
disorders: a concensus report of the Defeat Autism Now! (DAN!) Conference, Dallas, Texas, January
1995. San Diego, Autism Research Institute.
31 Banks, W.A., Kastin, A.J., & Gutierrez, E.G. (1993), Interleukin-1-alpha in blood has direct access to
cortical brain cells. Neuroscience Letters, 163, 41-44.
32 Ceriani, G., Macaluso, A., Catania, A., & Lipton, J.M. (1994), Central neurogenic anti-
inflammatory action of alpha-MSH: modulation of peripheral inflammation induced by cytokines and
other mediators of inflammation. Neuroendocrinology, 59, 138-143.
33 Ada, G.L. (1993), Vaccines. In: Fundamental Immunology, 3rd edition, Paul, E.P., editor, New York:
Raven Press, Ltd.
34 Microglia are the smallest of the glial cells. Some act as phagocytes cleaning up CNS debris. Most serve
as representatives of the immune system in the brain. Microglia protect the brain from invading micro-
organisms and are thought to be similar in nature to microphages in the blood system.
7
(ii) as a result of vaccination-induced oedema 35

.
Not only do inflammatory cytokines modulate blood-brain barrier permeability 36, but perivascular
microglial cells of the blood brain barrier can become antigen-presenting cells encoded with epitopes
from the injured tissue within the brain, and these perivascular cells allow activated T-cells to pass
from peripheral circulation, across the blood brain barrier, into cerebro spinal fluid wherein
additional autoimmune-like damage can ensue. A similar crossing of the blood brain barrier occurs
with activated B-cells.
If, from the child's prior infection(s) and/or from vaccination-induced oedema, activated T-cells and
B-cells exist with neuronally derived epitopes, at least in some individuals during their response to
vaccination, the following sequence may ensue:
(i) clonal expansions of existing T-cells and B-cells having neuronally derived epitopes,
(ii) further activation of microglia in brain regions already damaged,
(iii) increases in blood brain barrier permeability, thereby allowing activated T-cells, etc., to
enter the brain.
(iv) furthermore, as the clonally expanding T-cells, etc., travel toward brain cells having
sequences similar to the neuronally derived epitopes, encephalitis would be one result of
these events and, more importantly, additional sequelae would include increased
autoimmune-like damage to neurons that, prior to the vaccination, had been only mildly,
perhaps even unnoticeably damaged by the prior infections.
In extreme cases of individuals having vaccination-induced clonal expansions of immunological cells
with neuron-based epitopes, autism might be a result.
Nearly any vaccine may have the potential for inducing neuronal damage in persons with neuronally
derived epitopes. In other words, any vaccination that induces strong antibody responses,
(i) would appear to be capable of inducing fever-generating cytokines and, therefore at least
hypothetically,
(ii) could simultaneously induce clonal expansions of pre-existing T- and B-cells encoded with
neuronally derived epitopes, thereby leading to increased neuronal damage in varying
degrees across individuals.
Three additional concepts are helpful for understanding inflammation-related pathologies of the
central nervous system:
(i) molecular mimicry whereby epitope sequences are virtually identical between an
immunogenic pathogen and a naturally occurring molecular sequence 37
(ii) cross-reactivity e.g., when a lipo-polysaccharide amidst a cellular bilipid layer induces a
wider range of immunological responses involving self-membrane sequences 38, and
(iii) epitope-spreading or "determinant spreading", i.e., a process that also describes
spontaneously occurring widening ranges of immunogenicity.
Each of these three processes illustrates ways that autoimmune neuronal damage may be induced and
the range of neuronal targets expanded in response to fever-related levels of cytokines release that
occur in response to vaccinations. These processes would be more likely in some children if, due to
infections and/or antibiotics, the child has T- and/or B-cell subsets encoded with neuronally derived
epitopes.
35 Fukuyama, Y., Seki, T., Ohtsuka, C., Miura, H., & Hara, M. (1996), Practical guidelines for
physicians in the management of febrile seizures. Brain & Development, 18, 479-84.
36 Banks, W.A., & Kastin, A, J. (1991), Blood to brain transport of interleukin links the immune and
central nervous systems. Life Sciences, 48, PL117-PL121.
37 Baum H, Davies H, & Peakman M. (1996), Molecular mimicry in the MHC: hidden clues
to autoimmunity? Immunology Today, 17, 64-70.
38 van Rooijen, N. (1989), Are bacterial endotoxins involved in autoimmunity by CD5+ (Ly-1+) B cells?
Immunology Today, 10, 334-336.
8
In extreme cases, sufficient interleukin-2 levels in damaged areas of the central nervous system could
mobilise lymphokine-activated killer cells), which then might induce a more general damage, thereby
yielding increasingly severe neurological deficits.
Additional factors may augment the mechanisms of neuronal damage outlined above:
Targeting the cerebellum and temporal lobe: Swartz 39 mentions that the temporal lobe and
cerebellum are likely targets for oedema-induced neuronal damage. Furthermore, certain
hippocampal regions as well as Purkinje cells of the cerebellum have a relative deficit of
apoptosis-related protein Bcl-2, thereby inclining cells in those regions toward apoptosis 40 if and
as oedema-induced injury occurs 41.
Cerebellum: Discrete lesions of the cerebellum are associated with mania, depression, bipolar
disorders, and OCD; and more than thirty bacterial, fungal, and viral infectious agents are known
to be able to affect the cerebellum 42.
Other inflammatories: In addition to IL-1, IL-6, and TNF-alpha, the following are additional
factors influencing brain inflammation: Platelet-activating factor, prostaglandins E2 and I2,
leukotriene B4, and polymorpho-nuclear neutrophil leukocytes 43.
As stated in guidelines for physicians, vaccination-induced inflammation ought to be treated
aggressively (Fukuyama et al, idem), and better understanding of pathogenic processes, of risk factors,
and of preventive or corrective measures are worthwhile goals.
The Association between Autism and Developmental Disability
There may sometimes be confusion in diagnosis where both of these conditions are thought to co-
exist in a subject. Developmental disability is attributed to those with an IQ of less than 70. Some of
these subjects will also have social impairments; this is especially so in those with an IQ of less than
50. Even in those who are diagnosed with the full, typical picture of autism, over 90% will have IQs
of between 20 and 69. Whether one adopts a broad or narrow perspective on this issue, one needs
to consider the source and significance of the association between developmental disability and
autism-like impairments in interpersonal relatedness. 44
It is important in such cases for there to be cognisance of the possibility that brain damage, having
caused developmental abnormalities to a degree that is accepted as developmental disability, may
also mimic autism-like impairment. It also needs to be understood that by the sporadic nature of
brain damage caused by the toxins in vaccinations, there can be parts of the brain damaged that are
those which are involved in classical autism. 45, 46
39 Swartz, M.N. (1984), Bacterial meningitis: more than just the meninges. New England Journal of
Medicine, 311, 912-913.
40 There are 3 different mechanisms by which a cell commits suicide by apoptosis. (1) one generated by
signals arising within the cell, (2) another triggered by death activators binding to receptors at the cell
surface. [TNF-a; Lymphotoxin; and Fas ligand (FasL)]; (3) a third that may be triggered by dangerous
reactive oxygen species.
41 Hara, A., Hirose, Y., Wang, A., Yoshimi, N., Tanaka, T., & Mori, H. (1996), Localization of Bax
and Bcl-2 proteins, regulators of programmed cell death, in the human central nervous system.
Virchows Archives. 429, 249-53.
42 Cohen, B.A., & Lipton, H.L. (1990). The cerebellum and CNS infections. In: Infections of the central
nervous system. D Schlossberg, editor; New York: Springer-Verlag.
43 Saez-Llorens, X., Ramilo, O., Mustafa, M.M., Mertsola, J., & McCracken, G.H. (1990),
Molecular pathophysiology of bacterial meningitis: Current concepts and therapeutic implications. The
Journal of Pediatrics, 116, 671-684.
44
Hobson, R Peter. Autism and the Development of Mind. Psychology Press 1997. (pp. 9)
45
Kates, WR et al Neuroanatomical and neurocognitive differences in a pair of monozygous twins
discordant for strictly defined autism. Annals of Neurology; Vol. 43, Issue 6, June 1998; Pages 78279.
46 Challoner, A. Brain Damage caused by Vaccination. https://www.scribd.com/doc/19408267/Brain-
Damage-Caused-by-Vaccination.
9
Social Behaviour and the Amygdala Dr. David Amaral, 47 of the University of California, Davis
Department of Psychiatry, Center for Neuroscience, California Regional Primate Center, and MIND
Institute has presented animal data on the neuroanatomy of the amygdala and its connections with
the orbitofrontal and temporal cortices. This was done with a view toward developing a larger
picture of how the amygdala affects social behaviour through which one could investigate how
disruptions of amygdaloid connections might affect social impairments of functioning such as autism.
He suggested that early works by Brothers48 and Rosvald and colleagues49, 50 were important in
understanding these connections. Rhesus dominance hierarchies were disrupted when a subject had
progressive amygdaloid lesions and was then reintroduced to a troupe. This permitted the inference
that the amygdala was related to the emitting of socially appropriate behaviours, and that its lesions
disrupted that functioning. Connections of the amygdala with the neocortex, basal forebrain,
hippocampus, thalamus, and hypothalamus supported this.
Amygdala and Vaccine-induced Autism For more than a decade, the amygdala has been
identified as a substrate whose dysregulation is likely to contribute to some aspects of autism. Via
artificially induced status epilepticus (SE), Tuunanen et al, 51 identified a number of amygdaloid
regions experiencing SE-induced neuronal damage, most sensitive to damage were neurons within the
accessory basal, lateral, basal, medial, and anterior cortical nuclei. Based upon neuro-anatomical
studies of the amygdala in higher primates including humans, the sub-areas identified by Tuunanen et
al are linked with certain traits in autism.
The specific amygdaloid areas identified by Tuunanen et al include:
(i) within deep nuclei: accessory basal, lateral, and basal nuclei;
(ii) within superficial nuclei: anterior cortical, medial, and posterior cortical nuclei, as well as lesions in
the lateral olfactory tract, the bed nucleus of the accessory olfactory tract, and the peri-amygdaloid
cortex; and
(iii) within additional nuclei such as anterior amygdaloid area, central nucleus, amygdalo-
hippocampal area, as well as the intercalated, lateral, and basal nuclei.
This paper presents an indication of how the Tuunanen et al article may be important for
understanding aetiology and patho-physiology in a large subgroup of those affected by autism and
other individuals along the pervasive development disorder spectrum.
Tuunanen et al (idem) suggest that their findings about SE-induced neuronal damage also may apply
to effects induced by febrile seizures, which is reinforced by the febrile seizures / status epilepticus
relationships cited above. In some individuals, if by these processes certain amygdala neurons die,
then numerous autonomic, emotional, motivational, behavioural, and social processes will become
atypical. For these reasons, the Tuunanen et al findings may,
(i) delineate the neuropathological substrate and

(ii) provide the "acceptable animal model" that Golden and O'Donohoe did not feel existed in 1990
and 1994.52, 53
The additive-effects principle may account for some cases of inter-individual variation, even among
siblings including twins. Consider the subset of children whose autism may have come via the " febrile
seizures (FS) to status epilepticus (SE) to amygdaloid-damage" route. The medical history of each
47 Amaral D. Amygdala, social behavior and autism. Program and abstracts of the American Academy of
Child and Adolescent Psychiatry 49th Annual Meeting; October 22-27, 2002; San Francisco, California.
Institute IIIB.
48 Brothers L. The social brain: a project for integrating primate behavior and neurophysiology in a new
domain. Concepts Neurosci. 1990;1:27-51.
49 Rosvald HE, Mirsky AF, Sarason I. Amygdalectomy and social behavior. J Comp Physiol Psychol.
1954;11:10-93.
50 Rosvald HE, Mirsky AF, Sarason I, Bransome ED, Beck LM. A continuous performance test of
brain damage. J Consult Psychol. 1956;90:343-350.
51 Tuunanen J, Halonen T, Pitkanen A. Status epilepticus causes selective regional damage and loss of
GABAergic neurons in the rat amygdaloid complex. Eur J Neurosci 1996;8:2711-2725.
52 Golden GS. Pertussis vaccine and injury to the brain. J Pediatr, 1990:116;854-861.
53 O'Donohoe NV. Epilepsies of Childhood. 3rd ed. Oxford: Butterworth- Heinemann Ltd, 1994.
10
sibling, while very similar in regard to vaccination timings, nonetheless may have been different with
regard to one or more early, severe infections. As a result, when a subsequent fever and related
cytokines-release occurred (Luheshi et al, idem), the sibling with one or more extra FS in his or her
medical history would, in contrast with other siblings, have been more inclined to have had a FS- and
SE-induced neuropathy within the amygdala 54. Another source of inter-individual variations is
presented in Tuunanen et al (idem), wherein status epilepticus stimulation led to variations in degrees
of damage within primary and secondary amygdaloid locales having neuronal death.
The possibility remains that, in some individuals, reactions to a single infection or a
vaccination may be sufficient for inducing the sequence from febrile seizures to status
epilepticus to amygdaloid-damage. 55 (My emphasis)
Thimerosal 56
UPDATE Mercury is an extremely poisonous metal, a powerful neurotoxin which has

long given doctors and environmentalists cause for concern. It is present in the
environment, in foods including fish, household products, medications, make-up and
vaccines where, in the form of thimerosal, it is used as a preservative for its anti-fungal and
anti-bacterial properties.
The decision to take the mercury out of the vaccines given to British babies was made in
2004 and this was welcomed for it removed one way in which the poison enters the body.
By 2003, the manufacturer of the DPT vaccine (Glaxo) had not responded to questions on the level of
Thimerosal in the batch used in the claimants vaccinations. The Green Book published by HMSO is a
reference text about vaccinations. It suggests that Thimerosal is added at a concentration of 0.01%. The
National Network for Immunisation Information (see below) suggests that in some instances the
concentration may be as high as 3 micrograms for each 1cc dose
Pichichero et al tell us that, concentrations of mercury in infants exposed to Thimerosal following
vaccination were very variable, and assessment depended upon the time lapse between vaccination
and testing. Although mercury concentrations were uniformly low, the highest levels were recorded
soon after vaccination.57 Most of the toxic effects of organic mercury compounds take place in the
central nervous system, although the kidneys and immune system can also be affected. Organic
mercury readily crosses the blood-brain barrier, and foetuses are more sensitive to mercury exposure
than are children or adults. The researchers estimated that the half-life of mercury in blood after
vaccination to be seven days.
The US Food & Drug Administration has produced a safety review58 of the use of mercury in plasma-
derived products. This refers to the version dated 29th January 2003. The committee involved with
the review reports that it, ... believed that the effort to remove thimerosal from vaccines was a
prudent measure in support of the public health goal to reduce mercury exposure of infants and
children as much as possible. Furthermore, in this regard, the Committee urged that, full
consideration be given to removing thimerosal from any biological product to which infants,
children, and pregnant women are exposed.
54 Verity CM, Ross EM, Golding J. Infantile febrile status epilepticus: risk factors and outcome. Brit Med
J 1993:307;225-228.
55 Binstock, T. Febrile Seizures and the Amygdala in autism-spectrum disorders. Researcher in
Developmental and Behavioral Neuroanatomy, University of Colorado Health Sciences Center, Denver.
{Direct communication, 31 Jan 1997 }
56 Thimerosal in Vaccines
https://www.fda.gov/BiologicsBloodVaccines/SafetyAvailability/VaccineSafety/UCM096228
57 Pichichero ME, Cernichiari E, Lopreiato J, Treanor J. Mercury Concentrations and Metabolism in
Infants Receiving Vaccines Containing Thimerosal: A Descriptive Study. Source: The Lancet, November
30, 2002, Vol. 360:1737-1741.
58 Thimerosal in Vaccines. http://www.fda.gov/cber/vaccine/thimerosal.htm.
11
Ball et al 59 have reported that, delayed-type hypersensitivity reactions from thimerosal exposure are
well recognised. They have identified acute toxicity from inadvertent high-dose exposure to
thimerosal including neurotoxicity and nephrotoxicity. Chronic, low-dose methylmercury exposure
may cause subtle neurologic abnormalities. Depending on the immunisation schedule, vaccine
formulation, and infant weight, cumulative exposure of infants to mercury from thimerosal during the
first 6 months of life may exceed EPA guidelines. Their review revealed that some infants might be
exposed to cumulative levels of mercury during the first 6 months of life that exceed EPA
recommendations.
The National Network for Immunisation Information (http://www.immunizationinfo.org/) suggests
that the safe levels of Thimerosal for a six-month-old child have been calculated as 0.8 micrograms.
Some vaccines have at least 3 micrograms for each 1cc dose.
Another valuable reference on this subject is the Immunisation Safety Review: Thimerosal -
Containing Vaccines and Neurodevelopmental Disorders (2001) Institute of Medicine (IOM). It can
be read online at: http://books.nap.edu/books/0309076366/html/R1.html
Strangely and despite the above the NHS Choices website:
http://www.nhs.uk/Conditions/vaccinations/Pages/vaccine-ingredients.aspx
Still maintains that: Although there have been concerns in the past that vaccines that contain
thimerosal can cause autism, there is no scientific evidence that this is the case. The World Health
Organization (WHO) has stated there is no risk from thimerosal in vaccines.
The Injection Site60

Most vaccines should be given via the intramuscular route into the deltoid (upper arm) or the
anterolateral aspect of the thigh. This optimises the immunogenicity of the vaccine and minimises
adverse reactions at the injection site. Scientific studies have highlighted the importance of
administering vaccines correctly. 61
In the case of vaccines in which the antigen is adsorbed to an aluminium salt adjuvant such as
diphtheria, tetanus, and pertussis vaccines, the intramuscular route is strongly preferred because
superficial administration leads to an increased incidence of local reactions such as irritation,
inflammation, granuloma formation, and necrosis.
The injection technique and needle size both determine how deep a substance is injected. Injection
technique involves stretching the skin flat before inserting the needle or pinching a fold of skin before
injection, which may necessitate the use of longer needles. To make sure the needle reaches the muscle
and that vaccine does not seep into subcutaneous tissue the decision on the size of the needle and
injection site should be made individually for each person. It should also be based on the person's age,
the volume of material to be administered, and the size of the muscle.
Consideration should be given to needle gauge. A wider bore needle ensures that the vaccine is
dissipated over a wider area, thus reducing the risk of localised redness and swelling. A standard size
of needle will not guarantee successful intramuscular injection in all people.
It is therefore relevant to consider that incorrect procedure may contribute to an adverse reaction.
This ought to give rise to a view that although individual factors may not of themselves contribute
entirely to an adverse response, a series of militating factors might do so.
59 Ball, Leslie K.; Ball, Robert; and Pratt, R. Douglas. An Assessment of Thimerosal Use in Childhood
Vaccines. Pediatrics Vol. 107 No. 5 May 2001, pp. 1147-1154.
60 BMJ 2000; 321:1237-1238 ( 18 November 2000 ) Editorials
61 The importance of injecting vaccines into muscle
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1118997/
12
Non-specific effects of vaccines 62-63

This report shows that the increase in mortality from the DPT and polio vaccines is worrying, but
they are preliminary findings. There is a clear message from this study: in areas of high mortality,
vaccines may have substantial effects on mortality from all causes through non-specific effects on
deaths from diseases other than those targeted by the vaccines.
The Guinea-Bissau investigators speculate that DPT vaccine may have adverse non-specific effects
because the aluminium adjuvant stimulates Th2 immunity. (See section on cytokines page 6) It has
been suggested that reduced exposure to BCG and other microbes combined with increased exposure
to aluminium, DPT vaccine, and other Th2 adjuvants may have contributed to the apparent increase
in allergic disease in developed countries
Some will argue that the Guinea-Bissau data should not have been published, because publication
might damage immunisation programmes. However, it would be inappropriate to suppress this
evidence just as it would be inappropriate to withhold DPT vaccine on the basis of these preliminary
results.
Certiva
In 1998, North American Vaccine, Inc., manufacturers of Certiva (Diphtheria and Tetanus Toxoids
and Acellular Pertussis Vaccine Adsorbed), has stated:
Routine vaccination with whole-cell DTP vaccine has significantly reduced pertussis-
related morbidity and mortality. However, concerns regarding reactogenicity of
whole-cell DTP vaccine have spurred development of safer pertussis vaccines. The role
of different components produced by B. pertussis in either the pathogenesis of, or the
immunity to, pertussis is not well understood.
This admission seems not to have been seen by Lord Brennan. With reference to page 11, para. 28 in
his September 2001 Advice to the Legal Services Commission, it should be noted that whilst it may
not be negligent to use the whole cell vaccine, despite its reactogenicity (Certiva), the precautions
brought forward by Berg (1958) [See pages 1, 2, 13, 19 & 26] and Feldman (2002) [See pages 20 &
26], need to be emphasised. Lord Brennan does not pay attention here to the possibility that batches
of vaccine vary and that a particular specimen may have been faulty by dint of time lapse rather than
manufacture, or that the vaccination procedure and the quantity of vaccine used may vary in
individual cases.
Tripedia
The manufacturers leaflet from Avensis for Tripedia includes the following under Contraindications.
Encephalopathy not due to an identifiable cause, occurring within 7 days of a prior

whole-cell pertussis DTP or DTaP immunization and consisting of major alterations of
consciousness, unresponsiveness, generalized or focal seizures that persist for more than
a few hours and failure to recover within 24 hours should be considered a
contraindication to further use; this includes severe alterations in consciousness
with generalized or focal neurologic signs. Even though causation cannot be
established, no subsequent doses of pertussis vaccine should be given and
immunization with DT should be continued to complete the series. 64 (My emphasis)
_______
62
BMJ 2000;321:1423-1424 ( 9 December ) pp 1435 Editorials
63 UPDATE Shann, F. The Nonspecific Effects of Vaccines and the Expanded Program on
Immunization. J Infect Dis (2011) 204 (2): 182-184. https://doi.org/10.1093/infdis/jir244 Published: 15
July 2011.
64
http://www.vaccineshoppe.com/US_PDF/298-10_4043_4058.pdf

13
Comments on the scientific evidence quoted in Counsels Advice

Menkes, J.H and Kinsbourne, M., Neuropediatrics 21 (1990) 171-176, Workshop on Neurologic
Complications of Pertussis and Pertussis Vaccination.
At the Workshop on Neurologic Complications of Pertussis and Pertussis Vaccination, held from
September 29 to October 1, 1989 at Airlie House, Warrenton, Virginia, the matter considered was the
neurologic complications of pertussis vaccine. The report by Professor J. H. Menkes and Dr M.
Kinsbourne. Drew attention to:
In evaluating side-reactions to the vaccine, the following must be kept in mind:
1. Vaccines are not standardised between manufacturers.
2. For a given manufacturer, vaccines are not standard from one batch to the next.
3. Unless the vaccine is properly prepared and refrigerated, its potency and reactivity
varies with shelf life.
In fact, the whole question of vaccine detoxification has never been systematically
investigated.
Lord Brennans difficulties with this paper can be understood. Cases probably cannot be fully
comparable if similar vaccines can have variable characteristics. The manufacturers of Certiva (see
above) also accept this difficulty. However if the lack of standardisation, or the lack of a possibility of
standardisation, causes scientists to be unable to anticipate what the side effects of any particular
batch of vaccine might be, then there is a safety issue which is not being administratively
acknowledged by the NHS and other health departments. If some children have been vaccinated with
vaccines that may have been unsafe or, worse, that the vaccinating doctors have not flowed the
numerous guidelines that were available (see above) then that surely must go some way to indicating
negligence.
Lord Brennan wrote in his September 2001 Advice to the Legal Services Commission, when referring
to the 1989 Workshop, that he did not gain any idea from the outcome of the Workshop that there
were any convincing scientific conclusions when it reported, that damage is associated with this type
of vaccine. (His emphasis) I do not share his apparent troubled doubtfulness with the semantics of
the report from which he quotes. If brain damage is, associated with this type of vaccine, then that
indicates that if following vaccination, brain damage ensues, then it can be associated with the
vaccine used. The common sense proviso is that there is not any other more likely cause. From there,
each case must stand on its merits. The questions which then need to be asked are:
1. Was there any evidence of encephalopathy prior to vaccination?
2. Once the period of illness had abated, (and in the absence of any other vaccination) were there
any further instances of encephalopathy during a reasonable period (or at all) afterwards?
If the answers to both these questions are no, then it is more than probable that the vaccine caused
the illness. This must be considered now that the mechanism of vaccine-induced brain
damage is known. (My emphasis)
Epidemiologically, vaccination is usually seen, by those given responsibility for the
work, as a job to be done at all costs. If, in order to achieve herd immunity, corners
are being cut in terms of safety, then it is not acceptable for technical manoeuvring to
outwit the legal system.
Other issues at the workshop: The incidence of post-vaccine encephalopathy is difficult to

ascertain. The most carefully conducted retrospective case-control study reported that the relative risk
of a previously normal infant for the onset of an illness leading to encephalopathy with permanent
subsequent disability was 4.2 times greater during the first 72 hours following DPT vaccination than
in controls. From this study, the risk for permanent brain damage following DPT has been calculated
as 1:310,000 doses.
(MY NOTE 1:310,000 doses translates to an actual risk of 1:62,000 this figure is from the
National Childhood Encephalopathy Study which excluded any child whose seizure lasted for less
than 30 minutes and who was not hospitalised as a result of their seizure. The Green Book published
14
by HMSO is a reference text about vaccinations. At Chapter 8.1.8 it states, During 1995 ... there
were 152 reports that included reactions classified as serious. To put this in perspective, over 14
million doses of these vaccines were distributed in the UK in 1995. Thus, serious suspected reactions
were reported at a rate of approximately one per 100,000 distributed doses of vaccine. Clearly such
statistics are uncertain indicators of risk.)
It was the consensus of the workshop, and in particular of the participating neurologists, that
although the vaccine may possibly accelerate neurologic signs or symptoms in some children, and a
small proportion of apparent complications may be coincidental, there was no inherent difficulty in
assigning cause and effect to the vaccine and subsequent permanent neurologic residua.
In implicating pertussis vaccination in the evolution of subsequent neurologic residua, a careful
consideration of the mechanism for vaccine-induced brain damage plays an important supporting
role. Pertussis toxin (Ptx) has been shown to alter cellular signalling. It also affects the
catecholaminergic and GABAergic systems in the brain. (See also page 5) Although normally a protein
the size of Ptx would not allow it to cross the blood-brain barrier. Factors known to disrupt the
blood-brain barrier include brief hypertensive episodes such as might occur during a coughing
paroxysm, hypoxia and prolonged seizures, whether or not they are accompanied by hypoxia. In
addition, a direct endotoxin-mediated attack on the endothelial cells could create a local defect of the
blood-brain barrier. In addition, in at least one of the claimants, there was clear evidence that the
screaming that accompanied the acute phase of the encephalitic response was so intense that it caused
whole body petechia. Such force could possible extend the time when the blood-brain barrier was
vulnerable to the passage of toxins.
I believe that Lord Brennan has cast aspersions on this workshop outcome that are an attempt to
reduce its relevance. There are several issues of importance in the paper, and to suggest that it would
be too expensive to study them further is a slight to those who have been damaged by vaccination. I
was not aware that justice in this country was so limited.
In summary, it was the consensus of the workshop that there was sufficient experimental data to
implicate both endotoxin and Ptx in adverse neurologic reactions to pertussis vaccine.65 Later
research has further identified issues around causation see page 5.
Miller D, et al (1985). Pertussis vaccine and whooping cough as risk factors in acute neurological
illness and death in young children. Dev Biol Stand. 1985; 61:389-94. PMID: 3879684; UI:
86221304.
The National Childhood Encephalopathy Study received reports on 1182 cases of serious acute
neurological illnesses in children admitted to hospital in Britain. The frequency of risk factors in cases
was compared with matched controls. A personal or family history of convulsions was found
significantly more often in cases than in controls, but no such excess was found for a history of
allergy. Case children were significantly more likely to have received diphtheria, tetanus and pertussis
(DTP) vaccine within seven days before onset and to have a history of whooping cough during the
month of onset. The risk of serious acute brain conditions after the disease was more than six times
that of three doses of DTP. In addition, there is evidence that deaths attributed to whooping cough
may seriously underestimate the number associated with pertussis infection. PMID: 3879684, UI:
86221304. 66
In connection with his comments on Miller (page 8, para, 17), and in his search for certainty, Lord
Brennan wrote in his September 2001 Advice to the Legal Services Commission, Some cases (of
severe acute neurological illnesses) may occur by chance or have other causes. He does not develop
this idea, nor does he tell us by what means this chance may occur, or what the other causes might
be. He goes on to emphasise that, The rle of pertussis vaccine as a prime or concomitant factor in
the aetiology of these illnesses cannot be determined in any individual case. He does not show how
he has come to hold this view. In the very nature of adverse vaccination events, it is more than
probable that because the percentage of such events, when set against the total number of
65 http://www.whale.to/a/encephalopathy.html
66
http://www.whale.to/a/encephalopathy.html
15
vaccinations given, is comparatively small, that there will be particular circumstances in individual
cases which might determine the outcome.
He goes on to say (page 9, para. 18c), Evidence of consistency is not probative of an actual causative
effect. Possibly not, but it does go a long way to set the scene for potential probability. Add to the
consistency the other ingredient, a lack of an alternative aetiology, and we might be much nearer to
that probability than Lord Brennan is prepared to admit.
Geier
Lord Brennan does not show the references for the two papers on which he comments, except to
indicate some idea of date.
A Geier paper in the journal Toxicology Mechanisms and Methods, issue of January to March, seems
not to be the one to which Lord Brennan refers. However it is worthy of note:
Geier, David A.; Geier, Mark R. An Analysis of the Occurrence of Convulsions and Death after
Childhood Vaccination. Toxicology Mechanisms and Methods, 2002; Volume: 12 Number: 1 (Jan-
Mar) Page: 71-78 DOI: 10.1080/10517230252875912.
Abstract
The association between the whole-cell diphtheria, tetanus, and pertussis (DTP) vaccine and the
occurrence of convulsions and death has long been debated by the medical and scientific
communities. A certified copy of the Vaccine Adverse Events Reporting System database was obtained
from the Centers for Disease Control, and the data were analysed using the Microsoft Access
program.
The results of this analysis reveal a statistically (p < .01) higher rate of occurrence of convulsions and
death after whole-cell DTP vaccination than after acellular DTP and DT vaccination, showing, as do
the previous findings of many other scientists, that acellular DTP vaccine is much less reactogenic than
is whole cell DTP vaccine.
This study helps to validate the decision by American vaccine manufactures and the Food and Drug
Administration to use only acellular DTP for the American childhood vaccination schedule. However,
acellular DTP vaccine is still more reactogenic than is DT vaccine, probably because the pertussis
component of most currently available acellular DPT vaccines contains toxoided Ptx that has a
significant rate of reversion to active toxin. This suggests the need to use the newer acellular
pertussis vaccines, which are of higher purity and in which the reversion of the Ptx is prevented.
(My emphasis)
The Geiers have published a paper on the Internet on The Story of Whole-Cell DPT. In it they write:
The first modern whole-cell pertussis vaccine was put in its currently known form by
Kendrick in 1942, combining its whole-cell pertussis component with that of toxoided
diphtheria and tetanus, thus forming DTP or DPT vaccine. This vaccine was produced
by growing the bacteria either on solid or liquid media for at least one day, between
the temperatures of thirty-four degrees Celsius and thirty-seven degrees Celsius. The
bacteria were then harvested by the use of a centrifugation step.
Depending on the company that manufactured the vaccine, the concentration of
supernate and cells used to make the vaccine varied. Whatever the concentration of
either component, it has been well established that the mixture contains filamentous
hemagglutinin, (FHA), and lymphocytosis-promoting factor (LPF). The vaccine then
underwent deactivation by exposure to mild heat and was stored in a cold
environment either with Thimerosal or formalin. The product pertussis vaccine could
be used by itself, or as is more commonly done it could be mixed with diphtheria and
tetanus toxoids, forming the DTP vaccine.
Drs. Geier, Merril, and Petricciani, while working with bacteria phage lambda at the National
Institutes of Health, doing some of the earliest genetic engineering work, began to screen various
biological substances in the laboratory for phage contaminants and found that vaccines were full of
bacteria phage. The result was a symposium held at the NIH, with the vaccine manufactures to
determine if indeed vaccines were contaminated with bacterial phage, which if true would be a
16
violation of governmental regulations requiring that vaccines contain a single strain specific virus.
Additionally, after this work Geier and colleagues continued their work with vaccines and
demonstrated that whole-cell pertussis vaccine contained enough endotoxin that it could be diluted
100,000 to one and still be detected by the Limulus endotoxin assay.
Geier and colleagues also stated that endotoxin is not necessary for immunity in pertussis vaccination.
Additionally, endotoxin is one of the most feared poisons in medicine. Doctors and scientists ensure
the absence of endotoxin from most medicines, IV tubing, syringes, etc. before using them. With the
high levels of endotoxins in whole-cell DTP vaccines it is not surprising that virtually all children who
get the vaccine get a fever. It is also not surprising that a smaller percentage of children get more
severe reactions which may include seizures, shock, collapse, and even death.
Virtually every year from 1933 to the early 1980s an article was published describing the adverse
effects from whole-cell pertussis vaccine. The scientific communitys awareness of the dangers
associated with whole-cell pertussis vaccine led to many different techniques and procedures to
produce a less harmful vaccine. The very first was developed by Parke Davis and Company, in the
1920s, which produced and sold a pertussis vaccine made from just the bacterial cell and was virtually
free from all toxins. Despite being a highly impure form of acellular vaccine, it was associated with
markedly fewer adverse reactions than whole-cell pertussis vaccine, because it was free of the toxic
components of pertussis bacterial cultures. Acellular vaccine was more available from 1937 but, due
to its comparable cost with whole-cell vaccine, it was not well taken up until the mid-1980s.
In 1937, Lederle Laboratories patented an acellular pertussis vaccine which used soluble Ptx. The cells
were removed and the Ptx was toxoided with formaldehyde. This vaccine was widely successfully
used in the United States in the 1940s. This pertussis vaccine was made from one of the two same
antigens used today by the Japanese in their acellular vaccine. This is the acellular pertussis vaccine
currently in widespread use in the United States today. The 1937 Lederle acellular vaccine was shown
to be 94 percent protective in children with definite exposures to pertussis bacteria. This protection
surpasses the protection offered by a whole-cell vaccine administration and roughly equates to the
protections found in the currently used Japanese acellular vaccine. Lederle Laboratories from 1944 to
1948 actively marketed its 1937 acellular vaccine. Lederle ceased to market this acellular pertussis
vaccine in 1948 when it switched to production of Tri-Immunol DTP using a whole-cell pertussis
vaccine.
The results of this growing concern, caused individuals to study exactly how reactogenic whole-cell
pertussis vaccine was in vaccine recipients. Clinical studies of the more common adverse reactions
were compiled by Barkin and Pichero in 1979, Hopkins in 1979, Cody and colleagues in 1981 [see
Appendix One], and on the possible relationship to vaccine-associated encephalopathy by Alderslade
and colleagues in 1981 67. In the prospective study reported by Cody and colleagues in 1981, reaction
rates were recorded following the injection of DTP and DT vaccines, so as to determine what
influence whole-cell pertussis vaccine had on adverse reaction rates.
The reaction DTP/DT rates were as follows,
A local redness, 37.4/7.6 percent;
Local swelling, 40.7/7.6 percent;
Pain, 50.9/9.9 percent;
Fever, 31.5/14.9 percent;
Drowsiness, 31.5/14.9 percent;
Fretfulness, 53.4/22.6 percent;
Vomiting,6.2/2.6 percent;
Anorexia, 20.9/7.0 percent
Persistent crying, 3.1/0.7 percent.
67
Alderslade R, Bellman MH, Rawson NSB, Ross EM, Miller DL. 1981. The National Childhood
Encephalopathy Study: a report on 1000 cases of serious neurological disorders in infants and young
children from the NCES research team. In: Whooping Cough: Reports from the Committee on the
Safety of Medicines and the Joint Committee on Vaccination and Immunisation. Department of Health
and Social Security. London: Her Majesty's Stationery Office.
17
Nine of 15,752 DTP immunisations resulted in convulsions, and nine other children had hypo-tonic
hypo-responsive episodes (HHE).
HHE is a term used to describe a somewhat heterogeneous group of clinical disorders that have been reported
primarily in association with whole-cell pertussis vaccination. In a Report of a US public health service workshop,
HHE after pertussis immunisation, it was stated that,
Probably the most important question about HHE is whether it has any permanent sequelae.
The workshop assessed the possible contribution Vaccine Adverse Event Reporting System68
(VAERS)-based studies could make to answering this question and found substantial
methodologic problems; however, ongoing studies in Sweden and The Netherlands have the
potential to provide useful information on this question.
The most useful contribution of VAERS data would be in a descriptive study of HHE, with a
possible case-control study of factors that may affect the risk of HHE after vaccination, rather
than a study of possible permanent sequelae.
The workshop participants felt that a detailed descriptive study of approximately 100 HHE
events reported during a 1- to 2-year period could provide a more in-depth description of HHE
cases in greater numbers than has been published previously, but the study would not address
the issue of long-term sequelae of HHE.
Better descriptive data may lead to new hypotheses concerning risk factors, aetiology, and
patho-physiology of HHE that might be evaluated further by studying subsequent cases and
controls from VAERS or from other sources, depending on the hypothesis.
In 1976 two babies in Japan died as a result of their DPT vaccinations. The Japanese Government, fed
up with the continued use of the reactive whole-cell pertussis vaccine given to them by the U.S. after
World War II, sent one of their scientists, Dr. Sato, to the National Institutes of Health in the United
States to study purification of the product. After less than one year of investigation and using
American technology developed in the 1950s and 1960s Dr. Sato developed an acellular pertussis
product. The procedure the Japanese used to produce their acellular vaccine involves the growth of
pertussis vaccine in a static culture. The supernant, which contains FHA and Ptx, is removed after
centrifugation, subjected to ammonium sulfate differential precipitation cuts, and is subjected to
sucrose gradient centrifugation. After the centrifugation, the heavy layers containing endotoxin are
discarded, and the lighter fractions containing FHA and Ptx, and some other proteins are pooled.
Toxicity, due to Ptx is deactivated with formalin. The potency is determined with a modified mouse
potency test, and then the pertussis is combined with tetanus and diphtheria. The production lots of
Japanese acellular pertussis vaccine contain less than one-twentieth of the endotoxin of a comparable
whole-cell vaccine and less than 4 percent of the amount of active Ptx.
Drs. Mark Geier and David Geier, taking up the banner of this research have conducted extensive
research into this area. They have found that the total number of adverse reactions reported to
VAERS from 1991 through 1998 following DPT vaccination has substantially decreased.
Additionally, they have analysed the number of cases brought for damage by DPT vaccine. They
again have found a substantial decrease. There can only be one true explanation for these significant
drops in the number of adverse reactions and cases and that is the whole-cell DPT vaccine is far more
reactogenic than the acellular vaccine. Furthermore, the data strongly argues the majority of
major adverse reactions reported following with whole-cell DPT vaccine are caused by the
vaccine rather than being coincidentally associated in time with the vaccine. (My emphasis)
Kulenkampff, M, Schwartzman, JS, Wilson, J; Neurological Complications of Pertussis
Inoculation; Archives of Disease in Childhood; 1974, 49, 46.
The importance of this paper is that it shows results from a clustering of complications following DPT
vaccination which occurred in the first 24 hours after inoculation. The authors believe that this
suggests a causal rather than a coincidental relation.
Licensed Vaccines (1999?) I am unable to find any reference to this book which is mentioned by
Lord Brennan on page 11, in his Opinion and Advice to the Legal Services Commission. He questions
the concept of pertussis vaccine encephalopathy. There seems substantial evidence that such a
68 https://vaers.hhs.gov/index
18
response to this vaccine has occurred, some of this from the manufacturers. (However I have put
forward an explanation of the causation beginning on page 5)
__________
Comments on the Appendix of Lord Brennans September 2001 Advice

to the Legal Services Commission.
PAGE 1, PARA.1 One area of potential negligence is where the advice of Berg (1958) was not
followed. In 1958, Berg summarised the findings of 25 case reports or case series of adverse effects of
pertussis vaccine, and one personally observed case. His review, encompassing 107 cases of
neurological sequelae of pertussis immunisation, characterised: patient medical history; dosage and
type of pertussis vaccine; clinical features of reaction (time interval, presence of convulsion, paralysis);
and outcome (recovery, developmental disability, and death). Berg's report highlighted early onset of
neurological symptoms, convulsions, and changes of consciousness. An overall recovery rate of 50%,
a persistent morbidity rate of 30%, and a mortality rate of 15% are cited. 69
PAGE 1, PARA.2 An analysis using Medline as a search engine for papers and other
publications is not exhaustive. Rosenthal et al have pursued reputed serious reactions from a much
larger database, that of the United States, the largest denominator in the industrialised world. Others
are noted here.70
PAGE 2, PARA 3F Lord Brennan seems to pick and choose how he wants to attribute
acceptability to Professor Behans work. Here he seems to use it to support his ideas, whilst on the
preceding page (para. 3c) he castigates it.
PAGE 4, PARA. 13 Lord Brennan draws attention to the new level of vaccine damage payment
which is now 100,000. (2003) I wonder what he feels is an appropriate level of compensation for
those so affected, and considering that the payments he mentions are just awards and not
compensations. As a guide, he may like to consider that the annual cost for staff alone in 2003 to
cover complainants care needs can be over 50,000.
Page 4, Para. 14 Lord Brennan asks for the medical literature which currently suggests that
pertussis vaccine can lead to serious neurological consequences. I have given many examples in this
document, including those from the manufacturers. He also asks for substantiation of proof of cause.
This proof has been shown through animal studies, but obviously it is not possible to put in place
experimental studies using infants as guinea pigs.
SCIENTIFIC EVIDENCE NOT INCLUDED IN COUNSELS ADVICE
Contraindications for DPT Vaccine Medscape Pediatrics 4(1), 2002. 2002

Medscape Portals, Inc. http://www.medscape.com/viewarticle/420703
Sandor Feldman, MD, Professor, Department of Pediatrics, and Chief, Pediatric Infectious Diseases,
University of Mississippi Medical Center, Jackson, Mississippi. 22/1/2002.
There are 2 absolute contraindications to DTP and DTaP: an immediate anaphylactic reaction, and
encephalopathy within 7 days. [1,2] The latter is defined as a severe, acute central nervous system
disorder unexplained by another cause, which may be manifested by major alterations of
consciousness or by generalized or focal seizures that persist for more than a few hours without
recovery within 24 hours.
69 Berg JM. 1958. Neurological complications of pertussis immunization. British Medical Journal 2:24-27.
70 http://www.vaers.org/bibliographies/vaersbib_pub_1990_2002.pdf
19
Precautions for immunisation are adverse events that were formally contraindications but now
require careful consideration before administration of additional doses. [1,2] These reactions have not
proven to cause permanent sequelae. They are:
1. Seizure with or without fever, occurring within 3 days of immunisation with DTP or DTaP;
2. Persistent, severe, inconsolable screaming or crying within 3 days for 3 or more hours
within 48 hours;
3. Collapse or shock-like state (hypotonic-hyporesponsive episode) within 48 hours;
4. Temperature >/= 40.5C (104F), unexplained by another cause, within 48 hours.
The reader is referred to the Red Book (Report of the Committee on Infectious Diseases by the
American Academy of Pediatrics) for a detailed discussion on DTP and children with underlying
neurologic disorders and children with a family history of seizures. [1,3]
References
1. Pickering L, ed. Report of the Committee on Infections Diseases. 25th ed. Elk Grove, Ill:
American Academy of Pediatrics; 2000:435-448.
2. Atkinson W, Wolfe C, Humiston S, Nelson R, eds. Centers for Disease Control. Epidemiology
and Prevention of Vaccine Preventable Diseases. 6th ed. Atlanta, Ga: Centers for Disease
Control; 2000:67-83.
3. Pickering L, ed. Report of the Committee on Infections Diseases. 25th ed. Elk Grove, Ill:
American Academy of Pediatrics; 2000: 68.
Lenard HG, Fest U, Scholz W. [Complications of pertussis immunisation (author transl)]
Monatsschr Kinderheilkd. 1977 Jun; 125(6): 660-7. German. PMID: 18670 [PubMed - indexed for
MEDLINE]
Abstract:
16 cases of neurological disease and/or death shortly after pertussis immunisation are
reported. Eight patients had convulsions, six with ensuing permanent defects. Severe
polymyositis71 was observed in one case. Five infants died 12 h to 4 days after vaccination:
two after acute encephalopathy and three in the form of a sudden unexpected death (SID).
In two fatal cases the morphological changes in the brain corresponded to those of pertussis
encephalopathy: neuronal degeneration in various parts of the cortex, especially in the region
of the ammons horn (the hippocampus proper), and in the cerebellum. There were no signs
of inflammation. Three cases underwent forensic autopsy and death was attributed to
bronchopulmonary infection. Complete neuropathological work-up was only done in one
case, in which the brain was normal. The critique of episodical reports and the demand for
prospective studies is appreciated. Knowledge of all possible forms of complications,
however, is indispensable for future investigations. Polymyositis and SID have so far not been
listed as abnormal reactions to immunisation. The majority of our cases became known
accidentally from hospital sheets or from discussions with colleagues. For a detection of all
possible cases a greater awareness of doctors for the problem of pertussis immunisation
appears necessary. Only another 23 cases have been reported to the health authorities of the
state of Lower Saxony during the last 6 to 7 years. Of those, nine were either harmless
reactions or diseases probably unrelated to vaccination. Two were cases of SID, 12 and 72 h
after vaccination. It is concluded that only a minor proportion of possible complications is
presently reported to the health authorities.
Redhead K, et al. The activity of purified Bordetella pertussis components in murine

encephalopathy. J Biol Stand. 1987 Oct; 15(4): 341-51. PMID: 3680302; UI: 88059141.
Abstract:
A murine encephalopathic syndrome can be induced by the administration of BSA
and whole-cell pertussis vaccine. The present paper reports studies of the capacity of
purified individual pertussis components to induce this effect. Ptx and endotoxin
71
Polymyositis is a type of chronic inflammation of the muscles (inflammatory myopathy).
20
together with a highly immunogenic sensitizer protein were required to induce the
effect. The strength of the antibody response to the sensitizer appeared to be more
important than the H-2 type of the recipient in determining the susceptibility of
different mouse strains. 72
Wiedmeier SE, et al. Murine responses to immunisation with Ptx and bovine serum albumin: I.
Mortality observed after bovine albumin challenge is due to an anaphylactic reaction. Pediatr Res.
1987 Sep; 22(3): 262-7. PMID: 3309858; UI: 88015343.
Abstract:
It has been suggested that Ptx is involved in the pathogenesis of the adverse neurologic
reactions that can occur in infants and children after pertussis immunisation. One group
of investigators has recently reported that a clinical syndrome with pathological
features very similar to post-pertussis vaccination encephalopathy can be induced in
specific strains of mice after their immunisation with bovine serum albumin (BSA) and
Ptx. The aim of this investigation was to further characterize the immunologic
mechanisms operative in this murine model. Studies were undertaken to determine
whether the role played by Ptx in this condition required the A-protomer of the toxin
to enter a cell and ADP-ribosylate a nucleotide binding protein (a Class I activity) or
was dependent upon the binding of the B-oligomer of the toxin to the surface of target
cells (a Class II activity). The results of our experiments have established that the disease
induced by co-immunizing mice with Ptx and BSA is due to an immediate type
hypersensitivity reaction rather than an encephalopathy and that the mechanism of
action of Ptx in this system seems to be dependent upon a Class II activity of the toxin
and independent of its ADP-ribosyl transferase activity. 73
Munoz JJ, et al. Anaphylaxis or so-called encephalopathy in mice sensitized to an antigen with the
aid of pertussigen (pertussis toxin). Infect Immun. 1987 Apr; 55(4): 1004-8. PMID: 3557617; UI:
87164489.
Abstract:
Sensitization of mice with 1 mg of bovine serum albumin (BSA) or chicken egg albumin
(EA) given intraperitoneally and 300 to 400 ng of pertussigen (pertussis toxin [Ptx])
given intravenously (iv.) induced a high degree of anaphylactic sensitivity when the
mice were challenged i.v. with 1 mg of antigen 14 days later. Regardless of H-2
haplotype, all of the strains tested (CFW, BALB/cJ, DBA/2J, and C3H.SW/SnJ) were
susceptible to anaphylaxis.
Sensitization of mice by a multiple-dose procedure that has been reported to induce
fatal encephalopathy in mice (L. Steinman, A. Weiss, N. Adelman, M. Lim, R. Zuniga,
J. Oehlert, E. Hewlett, and S. Falkow, Proc. Natl. Acad. Sci. USA 82, 8733-8736, 1982)
1 mg of BSA on day -1, 100 to 400 ng of Ptx on day zero 1 mg of BSA on day +1, 100
to 400 ng of Ptx on day +2, and 1 mg of BSA on day +6) induced shock in BALB/cJ,
DBA/2J, and C3H.SW/SnJ mice, but not in CFW mice. When EA was used instead of
BSA, CFW, BALB/cJ, and C3H.SW/SnJ mice did not develop fatal shock, whereas
DBA/2J mice did.
When dose 3 of antigen (BSA or EA) was postponed to day +21, all mouse strains
sensitized by the multiple-dose procedure were found to be susceptible to shock. The
fatal shock induced by this procedure, as well as that induced by giving a single
sensitizing dose of antigen and Ptx, could be prevented by one to three 1-ml doses of
saline given i.v. at the time signs of severe shock appeared. Although only one dose of
saline was often sufficient to save the mice, two or three doses were usually needed.
72
73 http://www.whale.to/a/encephalopathy.html
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Microscopic changes were not found in mid-sagittal sections of the brains of mice
sensitized by either procedure. This was true of mice that died from shock or were
saved from shock by injections of saline. From these results, we concluded that the
proposed model for encephalopathy induced in mice by Ptx and BSA demonstrates
only the well-known anaphylactogenic effect of Ptx or pertussis vaccine. 74
Steinman L, et al. Pertussis toxin is required for pertussis vaccine encephalopathy. Proc Natl Acad Sci
U S A. 1985 Dec; 82(24): 8733-6. PMID: 2867545; UI: 86094299.
Abstract:
A mouse model for encephalopathy induced by pertussis immunisation has been

described; it has features that closely resemble some of the severe reactions, including
seizures and a shock-like state leading to death, occasionally seen after administration
of Bordetella pertussis (whooping cough) vaccine.
Susceptibility to encephalopathy maps to genes of the major histocompatibility
complex and correlates as well with the genetic regulation of the level of antibody
response to bovine serum albumin. In this study we have investigated which bacterial
determinant is responsible for the encephalopathy.
Two lines of evidence implicate pertussis toxin as the active bacterial component.
Single-site mutants of B. pertussis with single affected virulence factors were tested. A
mutant that produces a defective pertussis toxin had greatly diminished capacity to
induce encephalopathy, whereas a hemolysin- and adenylate-cyclase-deficient
avirulent mutant had the same activity in the mouse model as a virulent strain. Purified
pertussis toxin plus bovine serum albumin was tested and found to induce the lethal
encephalopathy, demonstrating that the toxin was the critical constituent of B.
pertussis responsible for encephalopathy. 75
Steinman L, et al. Murine model for pertussis vaccine encephalopathy: role of the major
histocompatibility complex; antibody to albumin and to Bordetella pertussis and pertussis toxin. Dev
Biol Stand. 1985; 61:439-46. PMID: 2872126; UI: 86221311.
Abstract:
A mouse model for pertussis immunisation encephalopathy has been described with
features that closely resemble the severe adverse reactions occasionally seen after
pertussis vaccine administration, including seizures and a shock-like state leading to
death. These reactions are produced with nearly one hundred percent efficiency
provided that the mice immunized with Bordetella pertussis have:
1) the appropriate major histocompatibility (H-2) genotype,
2) have been sensitized to bovine serum albumin (BSA), and
3) that the injected B. pertussis contained sufficient amounts of pertussis toxin.
Antibody titres were measured in mice with haplotypes H-2d.s.k. that are highly
susceptible to encephalopathy as well as in H-2b mice that are totally resistant. Mice
with H-2d.s.k. haplotypes were high responders to BSA, while H-2b (B10) mice were
non-responders to BSA. Both H-2d and H-2b mice responded well to B. pertussis.
Encephalopathy was induced in resistant H-2b mice with B. pertussis and passively
administered anti-BSA antiserum, but not with B. pertussis and anti- (T,G)-AL
antibody.
This indicated that B. pertussis and anti-BSA were absolutely required for development
of encephalopathy. Encephalopathy could be induced in mice decomplemented with
74
75 http://www.whale.to/vaccines/animal3.html
22
cobra venom factor and given BSA and B. pertussis. Several single-site mutants of B.
pertussis affecting single virulence factors were induced with transposon Tn5. One of
these mutants, BP357, deficient in pertussis toxin production, had a greatly reduced
encephalopathic potential in the mouse model compared to the virulent strain BP 338,
or to BP348, an adenylate cyclase and hemolysin double mutant, or to BP 349, a
hemolysin mutant.
Ehrengut W, Bias in evaluating central nervous system (CNS) complications following pertussis
immunisation. Acta Paediatr Jpn, 1991 Aug; 33(4): 421-427.
Ehrengut W at Institute of Vaccinology and Virology, Hamburg, Germany states, "Bias

in the evaluation of CNS complications following pertussis immunisation are the
following:
1) Notifications of post-immunisation adverse events,

2) Publications by vaccine producers on the frequency of adverse reactions,
3) Comparison of permanent brain damage after DPT and DT immunisation,
4) Pro-immunisation,
5) Immunisation associated viral encephalitis,
6) Accuracy of statistics,
7) Personal. A review of these points indicates an underestimation of CNS
complications after pertussis immunisation."
Cherry, J.D (1988), Brunell, P.A., Golden, G.S., Karzon, D.T., (1988), Report of the task force on
pertussis and pertussis immunisation, Pediatrics 81:6 Part 11 (June 1988) Supplement pp 936-984.
Extract:
For more than 25 years, it has been known that pertussis vaccine is a reliable adjuvant
for the production of experimental allergic encephalitis. This experimental allergic
encephalomyelitis is mediated by sensitized lymphocytes rather than serum antibody
mechanisms. 76
Hewlett, EL; Roberts, CO; Wolff, J; Manclark, CR; Biphasic Effect of Pertussis Vaccine on Serum
Insulin in Mice; Infection and Immunity; July 1983; p 137-144
Abstract:
Administration of pertussis vaccine, consisting of whole-killed Bordetella pertussis

organisms, causes hyperinsulinemia and enhanced secretion of insulin in response to a
variety of secretagogues in rats and mice. In examining the time course and properties
of this phenomenon, we discovered two distinct and separate effects of the bacteria
on glucose and insulin levels in mice. First, a heat-stable (80C for 30 min) component
causes a brief hyperinsulinemia which is measurable by 1 h. maximal at 8 h. and ends
in less than 48 h.
This effect appears to be due to B. pertussis endotoxin and is associated with a
transient, mild hypoglycaemia. Second, there is a heat-labile component of the B.
pertussis organism which induces a sustained (>14 days), dose-dependent
hyperinsulinemia which reaches a maximum at 5 to 7 days and has no associated
hypoglycaemia.
The two effects are further distinguishable in the early, endotoxin-induced
hyperinsulinemia exhibits the normal suppressibility by exogenous epinephrine,
whereas epinephrine markedly enhances the hyperinsulinemia occurring at 7 days.
76
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These two effects of B. pertussis appear to me mediated by different mechanisms and

may be important in the well-recognised reactogenicity of pertussis vaccine in humans.
Levine, S & Sowinski, R; Hyperacute Allergic Encephalomyelitis: A localised form produced by passive
transfer and pertussis vaccine; American Journal of Pathology; 73:247-260, 1973
Abstract:
A hyperacute form of experimental allergic encephalomyelitis (EAE) has been

produced previously by administering pertussis vaccine to rats actively immunised with
neural antigen or given passive transfer of lymphoid cells from donors with EAE.
Now, a localised form of hyperacute EAE has been produced within 1 day of passive
transfer. The speed with which pertussis acts tends to exclude antibody production as
the mechanism for conversion of EAE to the hyperacute form. With this rapid system,
it has been found that pertussis, or its histamine-sensitising factor, inhibited the host
mononuclear cell component of the pervascular lesions.
When the immune injury was sufficiently severe (high doses of donor EAE cells), the
decrease in the number of mononuclear cells was accompanied by an increase in the
amount of fibrin and the number of neutrophils in the lesions. This inverse relationship
may be explained by the loss of the protective effect of mononuclear cells on vessels,
a concept for which there is increasing evidence.
Murphy, J.V., Sarff, L.D., Marquardt, K.M. Recurrent Seizures after Diphtheria, Tetanus, and
Pertussis Vaccine Immunization; AJDC, Vol 138, Oct 1984; 908-911.
Twenty-two patients with recurrent seizures that started less than 24 hours after
immunisation with diphtheria, tetanus and pertussis (DTP) vaccine were
retrospectively studied.
The initial seizure generally occurred after one of the first three DTP vaccine
immunisations, and followed that immunisation by less than 12 hours. Two of the 22
patients were siblings. Eight patients had additional immunisations with DTP vaccine
and four had immediate worsening of their seizures. Of the 22 patients, only one was
seizure free and stopped taking anti-convulsants. Three patients exhibited normal
development and 11 had severe developmental delays.
Based on these observations, we reviewed current contraindications for immunisation
with pertussis vaccine.
________
From the Merck Manual
Encephalitis: An acute inflammatory disease of the brain due to direct viral invasion or to
hypersensitivity initiated by a virus or other foreign protein.
Secondary encephalitis, usually a complication of viral infection, is considered to have an
immunologic mechanism. Examples are encephalitides secondary to measles, chickenpox, rubella,
smallpox vaccination, vaccinia, and many other less well defined viral infections. 77
Acute disseminated encephalomyelitis (post-infectious encephalomyelitis see also Acute Viral
Encephalitis and Aseptic Meningitis in Ch. 176) is characterized by perivascular CNS demyelination,
77
Merck Manual http://www.merck.com/pubs/mmanual/section14/chapter176/176c.htm
24
which can occur spontaneously but usually follows a viral infection or viral vaccination (or, very
rarely, bacterial vaccination), suggesting an immunologic cause.
Acute inflammatory peripheral neuropathies that follow a viral vaccination or the Guillain-Barr
syndrome (see Ch. 183) are similar demyelinating disorders with the same presumed immune-
pathogenesis, but they affect only peripheral structures. 78
Adverse Effects of Pertussis and Rubella Vaccines (1991)

Christopher P. Howson, Cynthia J. Howe, and Harvey V. Fineberg, Editors; Committee to Review
the Adverse Consequences of Pertussis and Rubella Vaccines, Institute of Medicine 382 pages, 6 x 9,
1991.
See complete book at: http://books.nap.edu/books/0309044995/html/index.html
This is a substantial treatise on the subject, and it reminds us that although many of the serious
neurological illnesses which follow DPT vaccination may or may not cause permanent brain damage,
those that dont, may contribute to developmental abnormalities which permanently impair the
mental capabilities of those affected.
It also draws attention to, Zellweger H. (1959. Pertussis encephalopathy. Archives of Pediatrics
76:381-386.) He reviewed 148 cases of whooping cough encephalopathy. He noted two clinical
presentations:
(1) the sudden onset of convulsions followed by coma and

(2) a more insidious onset with somnolence progressing to coma over a period of days.
Cases of both types were more common in children under age 10 years and were more common in
females. Onset was usually during the second to fourth weeks of illness. Laboratory findings indicated
elevations of blood lymphocytes and normal Colony Stimulating Factor (CSF). The duration of the
encephalopathy varied from several days to several weeks.
One-third of the children died, one-third recovered completely, and one-third were left with varying
degrees of neurologic disability, including developmental disability of varying severity, paralyses and
palsies, focal or generalised convulsions, ataxias, amauroses (blindness, especially that occurring
without apparent lesion of the eye, such as from disease of the optic nerve, spine, or brain), and
changes of personality or behaviour.
This would support the view that there is a possibility that vaccination with whole cell pertussis,
might lead to neurological disability. There is also a very important injunction that needs to apply to
past scientific papers. Some contain truths, which still apply, and some (including the former) contain
statements that no longer apply due to later research proving them to be erroneous. An example is
from the Zellweger (1959) paper, which includes the statement, There is no evidence that any of the
toxins associated with pertussis vaccine have produced specific pathologic effects in either animals or
children. It will be seen from this document that in several references between pages seven to 13,
that such evidence is now available which shows pathological effects.
For other papers worthy of consideration see Appendix One
Conflicts of Interest
There have been reports of conflicts of interest on scientists who have given evidence in defence of
vaccine manufacturers. 79
____________
78 Merck Manual http://www.merck.com/pubs/mmanual/section14/chapter180/180a.htm

79
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SUMMARY
So what have we got which shows that the Further Advice from Lord Brennan is insufficient for the
purposes of determining withdrawal of the Legal Aid Certificates?
On the matter of scientific papers which he did consider, he seems to have been heavily dependent
upon aspects of each presentation which predicated the less confident approach to causation, rather
than weigh them with the more robust ones. There were also many scientific papers that are very
pertinent to the questions being asked about brain damage from the DPT vaccination, that Lord
Brennan did not seem to access or consider.
He did not give much attention to the historical documents that have existed almost from the time the
DPT vaccines came into use. He failed to respond to the research, which shows that children, who had
an adverse response within 48 hours of the vaccination, were prone to severe and permanent brain
damage.
In attending to the NCES study he failed to comment upon the fact that all the children involved were
those whose reactions occurred seven days or more after vaccination and who were subsequently
hospitalised. This took out of the research many children who should have been included. The study
was therefore not an adequate portrayal of events as they happened to all children who were
vaccinated at that time.
Likewise he paid no attention to the age of the vaccine at the time of its use; nor did he pay enough
attention to the implications of organic mercury as a constituent of the vaccines. He did not consider
implications such as the vaccine site and vaccination procedure as well as other non-specific effects of
vaccines.
He has shown no understanding of the causes of autism, and that some of those who suffer from the
autism spectrum of disorders, have been so affected by post-natal brain damage. Further that science
has so far not attributed such damage to any other cause than the vaccination process, for those with
a temporal association.
His understanding of causation such a vital element of any discussion on vaccine damage, is flawed.
This has come about partly through a possible lack of understanding of brain science, but also because
he has not paid attention to recent scientific papers, some of which are referred to above.
He gave no credence at all to the paradigms of such as Sandor Feldman (see page 20) that there are
two absolute contraindications to DTP and DTaP: an immediate anaphylactic reaction, and
encephalopathy within 7 days. This has heavy portents for claims of negligence against those who
ignored them. It is not as if this information is new, Berg stated almost the same in 1958.
Since Lord Brennans Advice has been published, further scientific papers have been received. These
include papers on the adverse reactions to other vaccines, including those of brain damage.
Additionally, one has to ask whether Lord Brennan is sufficiently independent from government to
have been involved in providing the Further Advice. In all but name he seems to have been a
government servant, having been asked by a government department to take on the rle of arbiter.
Not only that, but he seems not to have sought any independent adviser to help him sift through all
the available evidence. He has, in practice, been his own expert. Apart from himself there were others
who may have had conflicts of interest, and on whom he may have relied for his Advice.
I believe that the matters covered above strongly indicate that further funding should be
granted to pursue unresolved issues in these cases.

26
REFERENCES (Noted in the text)
Berg JM. (1958) Neurological complications of pertussis immunization. British

Medical Journal 2:24-27
Byers RK, Moll RC. (1948) Encephalopathies following prophylactic pertussis
vaccine. Pediatrics 1:437457.
Cavanagh NPC, Brett EM, Marshall WC, Wilson J. (1981) The possible adjuvant
role of Bordetella pertussis and pertussis vaccine in causing severe encephalopathic
illness: a presentation of three case histories. Neuropediatrics 12:374-381.
Chevrie, J.-J. & Aicardi, J. (1975) Duration and Lateralization of Febrile
Convulsions. Etiological Factors. Epilepsia, 16: 781789. doi:10.1111/j.1528-
1157.1975.tb04765.x
Cockburn W. (1959) Hazards of Pertussis Vaccination: Proceedings of a Symposium
on Immunization in Childhood. London: E & S Livingston Ltd.
Ehrengut W. (1980) Lsst Sich die Reserve gegenber der Pertussis-Schutzimpfung
begrnden? [Is the reserve in respect of protection against pertussis by immunization
well-founded?] Paediatrische Praxis 23:3-13.
Globus JH, Kohn JL. (1949) Encephalopathy following pertussis vaccine
prophylaxis. Journal of the American Medical Association 141:507-509.
Kulenkampff M, Schwartzman JS, Wilson J. (1974) Neurological complications
of pertussis inoculation. Archives of Disease in Childhood 49:46-49.
Madsen T. (1933) Vaccination against whooping cough. JAMA 101:187188.
Malmgren B, Vahlquist B, Zetterstrom R. (1960) Complications of
immunisation. British Medical Journal 2:1800-1801.
Strom J. (1960) Is universal vaccination against pertussis always justified? British
Medical Journal 2:1184-1186.
Stewart GT. (1977) Vaccination against whooping-cough: efficacy versus
risks. Lancet 1:234-237.
Stewart GT. (1979) Toxicity of pertussis vaccine: frequency and probability of
reactions. Journal of Epidemiology and Community Health 33:150-156.
Sutherland JA. (1953) Encephalopathy following diphtheria-pertussis
inoculation. Archives of Disease in Childhood 28:149-150.
_______

27
APPENDIX ONE
Other papers worthy of consideration
Bolukbasi O, et al. Acute disseminated encephalomyelitis associated with tetanus vaccination. Eur
Neurol. 1999; 41(4): 231-2. No abstract available. PMID: 10343155; UI: 99276501.
Cody C. (1981) Nature and Rates of Adverse Reactions Associated with DTP and DT Immunisation in
Infants and Children, Pediatrics 68(5): 650-660
Diphtheria and Tetanus Toxoids and Acellular Pertussis Vaccine Adsorbed Package Insert,
Certiva, North American Vaccine. http://www.nava.com/insert.html
Feldman, S. Contraindications for DPT Vaccine. http://www.medscape.com/viewarticle/420703
Grant, C C; McKay, E J; Simpson, A & Buckley, D. Pertussis encephalopathy with high
cerebrospinal fluid antibody titers to pertussis toxin and filamentous hemagglutinin. Paediatrics 1998
Gross T., et al. (1989) Bulging Fontanelle after Immunisation with DTP Vaccine and DT Vaccine, J
Pediatr 114(3): 423-425
Jacob J., et al. (1979) Increased Intracranial Pressure after Diphtheria, Tetanus And Pertussis
Immunisation, Am J Dis Child 133:217- 218
Mancini J, et al. Relapsing acute encephalopathy: a complication of diphtheria-tetanus-poliomyelitis
immunisation in a young boy. Eur J Pediatr. 1996 Feb; 155(2): 136-8. PMID: 8775230; UI:
96371395.
Menkes J. (1990) Neurologic Complications of Pertussis Vaccination, Ann Neurology 28:428
Miller D., et al. (1993) Pertussis Immunisation And Serious Acute Neurological Illnesses In Children,
Br Med J 307:1171-1176
Olin P., Rasmussen F., Gustafsson L. Hallander H. and Heijbel H. (1997) Randomized
Controlled Trial Of Two, Three, and Five-Component Acellular Pertussis Vaccines Compared With
Whole-Cell Pertussis Vaccine, The Lancet 350:1569-1577
Peroutka S., Kitamura K., Lim M. (1987) Treatment of Lethal Pertussis Vaccine Reaction with
Histamine H1 Antagonists, Neurology 37:1068-1072
Sepkowitz S. (1996) Reputed Brain Damage and Serious Reactions from DTP Vaccines, Arch Pediatr
Adolesc Med 150(5): 457-465
Shorvon, S & Berg, A. Pertussis vaccination and epilepsyan erratic history, new research and the
mismatch between science and social policy. Epilepsia, 49(2):219225, 2008 doi: 10.1111/j.1528-
1167.2007.01478.x
Stetler H., et al. (1985) History Of Convulsions And Use Of Pertussis Vaccine, J Pediatr 107:175-179
Terpstra G. (1979) Comparison of Vaccination of Mice and Rats with Hemophilus Influenzae and
Bordetella Pertussis as Models, Clin Exp Pharmac Physiol, 6(2): 139-149
Toomey J. (1949) Reactions To Pertussis Vaccine, JAMA 139(7): 448-450
Torch W. (1986) Characteristics of DPT Post-vaccinal Deaths and DPT-caused SIDS, Neurology 36(1)
U.S. Vaccine Manufacturers Statement on Thimerosal. Press Release (1999)
http://www.phrma.org/press/newsreleases//1999-07-08.75.phtml
Vaccine Safety Forum (1997) Summary of Two Workshops, Institute of Medicine
http://www.nap.edu/readingroom/books/vaccine/
Walker A., et al. (1988) Neurologic Events Following Diphtheria-Tetanus-Pertussis Immunisation,
Pediatrics 81:345-349

28
Walker AM. "Neurologic events following diphtheria- tetanus-pertussis immunisation," Pediatrics

1988 Mar; 81 (3): 345-349.
Wilkins J. (1988). DTP Reactions (Letter to the Editor), Pediatrics 81(6)
Wilson G. (1998) Vaccination & Behaviour Disorders (1-78)
Other Information:
Post-vaccinal Encephalitis http://www.whale.to/vaccines/encephalitis.htm
A Report of the Committee to Review the Adverse Consequences of Pertussis and Rubella
Vaccines. Washington (DC): National Academies Press (US); 1991. 4, Evidence Concerning Pertussis
Vaccines and Central Nervous System Disorders, Including Infantile Spasms, Hypsarrhythmia, Aseptic
Meningitis, and Encephalopathy. Available from: https://www.ncbi.nlm.nih.gov/books/NBK234367/
APPENDIX TWO
In the Queen's Bench Division Loveday v Renton and another
before Mr Justice Stuart-Smith March 29 and 30 1988.
In an action claiming damages for brain damage alleged to have been caused by
whooping cough (pertussis) vaccination the plaintiffs failed on a preliminary issue to
show on the balance of probabilities that the vaccine was capable of causing brain
damage.
THE FACTS
The plaintiff, Susan Jacqueline Loveday, now aged 17 (1988), claimed damages
against Dr George Renton for permanent brain damage after the administering of
whooping cough vaccine in 1970 and 1971. The judge heard a preliminary issue as
to whether pertussis vaccine could cause permanent brain damage in young children.
Depending on the outcome of the present case there were 200 other cases waiting
to come to trial.
THE DECISION
Mr Justice Stuart-Smith said that the burden of proof rested on the plaintiff to show on a
balance of probability that it was more likely than not that the vaccine could cause permanent
brain damage.
Medical and expert opinion was deeply divided on the issue. The question had to be
determined on all the evidence in the case, which was primarily the oral evidence of witnesses,
tested in cross-examination. But the question was not answered by showing that there was a
respectable and responsible body of medical opinion that the vaccine, albeit rarely, caused
permanent brain damage, or that that view might be more likely than the contrary.
The opinion of others not called to give evidence was not admissible to prove the truth of the
opinion. The works of learned and qualified authors formed part of the general corpus of
medical and scientific learning on the subject and could be relied on and adopted by suitably
qualified expert witnesses who might have their opinions tested in the light of that literature.
Similarly the contra-indications against the vaccine published from time to time in this country
by the DHSS and similar bodies in other countries could not be relied upon as though it was
evidence of qualified experts not called as witnesses, that the vaccine in fact caused brain
damage.

29
Reports of cases in the case series, or by clinicians of encephalopathy (inflammation of the

brain), resulting in some cases in brain damage or death (where the onset of the illness occurred
shortly after vaccination) raised the hypothesis that the vaccination might cause brain damage
or death. It did not prove the hypothesis nor raise a prima facie case.
What it did establish was that encephalopathy resulting occasionally in permanent brain
damage or death did sometimes occur in close temporal proximity to pertussis vaccination.
The hypothesis appeared to be that the vaccine might cause that condition where the conset
of symptoms occurred within about 72 hours, more usually 24 hours. That was the
overwhelming effect of the evidence called on both sides.
There were potential areas where evidence could be sought that might establish a causal link
between permanent brain damage and pertussis vaccine. There was no evidence of an
identifiable clinical syndrome which was specific to pertussis vaccine nor a specific pathology
which was peculiar to cases of death following the vaccine. Nor was there animal
experimentation showing that encephalopathy leading to permanent brain damage occurred
within 72 hours of injection of pertussis vaccine.
The plaintiff's case was that it was only children who were in some way vulnerable who were
affected by the vaccine. The vulnerabilities referred to might explain why such events
occasionally occurred in close temporal association with this and indeed other vaccinations as
well, but it did not show that any brain damage or epilepsy that ultimately resulted was due
to the vaccine as opposed to the underlying pathology.
In the last analysis it seemed that if pertussis vaccine could on very rare occasions cause
permanent brain damage in some children it must do so because of some vulnerability or
susceptibility on the part of the child. That did not help to establish the hypothesis.
His Lordship had come to the clear conclusion that the plaintiff had failed to satisfy him on
the balance of probability that pertussis vaccine could cause permanent brain damage in young
children. It was possible that it did; the contrary could not be proved. But in the result the
plaintiff's claim must fail.
His Lordship said that even if he had found in favour of the plaintiff on the preliminary issue
any plaintiff would face insuperable difficulties in establishing negligence on the part of the
doctor or nurse in administering the vaccine. Such a claim would have to be based on the
grounds that the vaccination had been given in spite of certain contraindications. (It will be
clear from the foregoing that several references have been made, from well before
this case, to such warnings.)
Appearances: Stanley Brodie QC and Jacqueline Beech instructed by Teacher Stern & Selby for
the plaintiff; Nicholas Underhill instructed by Hempsons for the doctor; Anthony Machin QC
and Michael Spencer instructed by Davies Arnold & Cooper for the Wellcome Foundation
who were joined as defendants.
Post-publication ADDENDUM
A Statutory Instrument 2007 No. 1931 was made on 5th July 2007 and came into force on 12th July
2007
PUBLIC HEALTH: The Vaccine Damage Payments Act 1979 Statutory Sum Order 2007.
This provided for an increase in the maximum payment to be made under the Act as follows:
1. For the purposes of the Vaccine Damage Payments Act 1979 the statutory sum is 120,000.
2. The Vaccine Damage Payments Act 1979 Statutory Sum Order 2000 is hereby revoked.

30

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A Comprehensive Report on Brain Damage caused by DPT Vaccination c1950-1970

Alan Challoner MA (Phil.) MChS 9 April 2003

The National Childhood Encephalopathy Study 1976

Advent of adverse reactions following vaccination

Cytokines and vaccine-induced brain damage

(ii) as a result of vaccination-induced oedema 35

(i) delineate the neuropathological substrate and

UPDATE Mercury is an extremely poisonous metal, a powerful neurotoxin which has

Strangely and despite the above the NHS Choices website:

The Injection Site60

Non-specific effects of vaccines 62-63

Encephalopathy not due to an identifiable cause, occurring within 7 days of a prior

Alan Challoner MA (Phil.) MChS 9 April 2003

Comments on the scientific evidence quoted in Counsels Advice

Other issues at the workshop: The incidence of post-vaccine encephalopathy is difficult to

Comments on the Appendix of Lord Brennans September 2001 Advice

SCIENTIFIC EVIDENCE NOT INCLUDED IN COUNSELS ADVICE

Contraindications for DPT Vaccine Medscape Pediatrics 4(1), 2002. 2002

Redhead K, et al. The activity of purified Bordetella pertussis components in murine

A mouse model for encephalopathy induced by pertussis immunisation has been

Ehrengut W at Institute of Vaccinology and Virology, Hamburg, Germany states, "Bias

1) Notifications of post-immunisation adverse events,

Administration of pertussis vaccine, consisting of whole-killed Bordetella pertussis

These two effects of B. pertussis appear to me mediated by different mechanisms and

A hyperacute form of experimental allergic encephalomyelitis (EAE) has been

From the Merck Manual

Adverse Effects of Pertussis and Rubella Vaccines (1991)

(1) the sudden onset of convulsions followed by coma and

78 Merck Manual http://www.merck.com/pubs/mmanual/section14/chapter180/180a.htm

Alan Challoner MA (Phil.) MChS 9 April 2003

REFERENCES (Noted in the text)

Berg JM. (1958) Neurological complications of pertussis immunization. British

Alan Challoner MA (Phil.) MChS 9 April 2003

Other papers worthy of consideration

Alan Challoner MA (Phil.) MChS 9 April 2003

Walker AM. "Neurologic events following diphtheria- tetanus-pertussis immunisation," Pediatrics

Alan Challoner MA (Phil.) MChS 9 April 2003

Reports of cases in the case series, or by clinicians of encephalopathy (inflammation of the

Alan Challoner MA (Phil.) MChS 9 April 2003

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