vaccine victims

VACCINE VICTIMS

Proving Your Case to the Special Masters

Sandra Cassidy Esq.

"...he no longer looked at his parents, nor looked at the revolving ceiling fan,
nor laughed at his toy.”
six month old Dustin Barton case number 91 1594V

Dedicated to my son Daniel who I love more than all the stars in the sky

The purpose of this book is educational only.
It is not intended to constitute legal or medical advice.

Copyright ©
Sandra Cassidy Esq.
June 2004 Buffalo, New York
All rights reserved

This writing may not be reproduced
without the express permission of the author
(716) 481-5542

Introduction

Since the September eleventh tragedy everyone has heard of the 9 11 fund established to compensate victims of the bombing of the World Trade Center. But few have heard of the vaccine fund created over ten years ago to compensate victims of another national tragedy-- our vaccine policy.

Congress created the vaccine fund to pay for injury and death to those who are vaccine victims. The victim must first win their case through the National Vaccine Injury Compensation Program a pseudo litigation process. The National Vaccine Injury Compensation Program, or NVICP, was created in 1986 when Congress acknowledged that the vaccines were causing permanent neurological injuries to children and the vaccine manufacturers threatened to stop production under the coming threat of lawsuits. The fund was created to “quickly and generously”--and quietly-- compensate injured victims and to preclude state court lawsuits by preempting state jurisdiction.

Few are aware that you can not sue any vaccine manufacturer in any court in the United States for a vaccine related injury unless you first bring an NVICP petition before the Special Masters within 36 months of the date of injury. There is no infant tolling –that is, the 36 months does not wait for the infant to grow up--and a regular state or federal court claim is prevented if a timely petitioned has not first been filed with the NVICP. It is truly a time of the essence remedy that prevents you from doing anything anywhere else if you miss the boat.

Unfortunately too many parents learn of it too late, or if they learn in time they usually cannot find an attorney who has any knowledge of the procedure or willingness to take the case. More cases are lost than won at the NVICP but state and federal remedies may be easier – especially with the flood of information now generated regarding these injuries.
Since win or loose you have to first petition the Vaccine Court in order to later have your day in regular court, it makes sense to me to just do it yourself. Most states have tolling of the statute of limitations, so once you have timely filed and argued your petition you have the luxury of time on your side and you have preserved your day in your state’s court.

This handbook is an educational tool to guide you in doing just that. This book is not intended to substitute for legal advice.

How the Book is Arranged
While editing this book it was suggested that I make a simpler version ‘for parents to read.’ My response was that is exactly how parents of vaccine injured children got into this mess in the first place. They were given a one page cartoon version of the vaccine risks and dutifully consented to their child's shots without a complete explanation of the risks and without a complete understanding of the precautions. This book is not a “simpler version.”

Part One provides information about the NVICP and a discussion of what type of information has been required by the Special Masters to prove a vaccine injury. Part Two presents summaries of each petition and decision rendered by the Special Masters between 1997 and 2000. This part is intended to assist you in finding decisions that match your child’s shots and symptoms. Part Three reviews the medical articles that are cited in the decisions. The Appendices provide lists of common symptoms of vaccine injury, names of common medical tests performed to detect vaccine injuries and a copy of the NVICP with the original vaccine table and all revisions. Websites are provided to request a copy of the vaccine court’s checklist of petition filing procedures, petition forms and court rules together with the simplified petition for autism claims.

While parents of vaccine injured children are whirling in a frantic attempt to recover their child, preserving their legal rights is the last thing on their mind. It is my hope that this book will help parents know whether their child has suffered a vaccine injury, help them timely file their petition, help them preserve their day in court, and obtain justice for their child.

Part One
What do vaccine petitions attempt to prove?

The National Vaccine Injury Compensation Program (NVICP) was created by Congress to provide quick and generous compensation to those injured by vaccinations. The Fund provides money damages to those who prove a vaccine related injury in the United States Court of Federal Claims in Washington, D.C. In the 'vaccine court' as it is sometimes called, decisions are made by appointed individuals called Special Masters and procedures are less formal than a 'regular' court. For example, the federal rules of evidence do not apply and often testimony is given by phone or by tape recording. Under the NVICP the Petitioner's compensation for the pain and suffering experienced as a result of the injury is limited to $250,000 but unlimited for medical care expenses.

If petitioner wins he can either accept the money and be precluded from going to a state
court where compensations for pain and suffering is not limited, or can reject the
money and go on to sue in state court. If petitioner looses he may appeal the NVICP
decision. But in all events, win or lose, before any state court litigation can commence anywhere
against any vaccine manufacturer for injuries to the vaccinee, the Petitioner must bring a
vaccine petition in the U.S. Federal Court of Claims within 36 months of the injury.

A petition must provide the simple proof that:
1. Petitioner received the vaccination within the United States

and
2. Incurred at least $1,000. of unreimbursed medical expenses and
3. Filed the petition within 36 months of the date of injury

Once these simple facts are established by petitioner, the sole remaining issue is medical proof that the vaccine caused the injury. This proof can be very complicated. Cases are won or lost over the tiniest detail. For example, a case that seemed otherwise winnable was lost because the infants mother testified that she saw a pulse in her baby's bulging fontanelle (soft spot). While the bulge indicated increased intracranial pressure indicative of encephalopathy, the government expert testified that a pulse would not be visible if indeed the brain was really swollen. The case was lost.

Because causation is difficult to prove, the NVICP "gives" petitioner a presumption that the vaccine did cause the injury when certain things are first proven. These certain things are contained in a list, or table of symptoms referred to as the vaccine table. If these symptoms manifest within certain time limits for certain vaccines, the petitioner receives a rebuttal presumption that the vaccine caused the injury. If petitioner proves these certain symptoms within these certain time limits and receives the presumption that the vaccine caused the injury the case is referred to as 'on the table'. Petitioner will win "table" injuries unless the federal government proves that a 'factor unrelated' to the vaccine caused the injury. If petitioner makes no attempt to prove all the certain symptoms within certain time limits as facts in the vaccine table, but instead chooses to proceed with whatever medical proof they have, then petitioners case is called 'a cause in fact claim'.

Proving a case 'on the table' has never been easy. Some of the most tragic cases go uncompensated. For example, when very severe symptoms are present within the time

requirements for them to present themselves according to the table, the child is usually dead. The Court has an often-repeated standing rule that "death alone is not a table injury" and the Masters routinely hold against the Petitioner for lack of proof. Generally the baby died too fast for anyone to observe the signs and symptoms listed in the table. If death is witnessed, parent’s testimony is often considered to be a description of ‘agonal’ signs, that is, the usual signs accompanying the dying process, not symptoms of vaccine injury.

In 1995 revisions to the vaccine table wrought many changes in NVICP litigation which made it even harder to meet a table definition. For example, the new stringent table definition for encephalopathy, (now called ‘serious neurological event’) is required to accompany any seizure in order for the seizure disorder to be recoverable. A serious neurological event requires that within 3 days of vaccination petitioner suffers an unexplained loss of consciousness for 24 hours (responds if at all only to loud voice, shows absent or decreased eye contact, does not recognize people, and is severe enough to require hospitalization even if not hospitalized) and 1/2 hour of convulsions (or if less than 1/2 hour than followed by 2 hour coma or paralysis, or followed by other neurologic signs not previously present) and which lasts 24 hours or more (or if child less than 18 months old this decreased level of consciousness persists beyond 24 hours and can not be attributed to postictal (after seizure) state. Additionally the less stringent definition of 'residual seizure disorder' was removed in 1995 as a recoverable category. Seizures can still be 'on the table' but only as a 'serious neurological event' that is accompanied by encephalopathy as defined above. Hypotonic hyporesponsive episode (collapse) was also defined in a more restrictive way by the revisions and is now called anaphylactic shock collapse.

Now most petitioners do not even attempt to obtain the presumption of cause by jumping through the table’s hoops. 'Off table' claims, also called cause in fact claims, now make up 90% of all program cases. At the same time Congress constricted the table definitions it added more vaccines to the vaccine schedule, including Hepatitis B. Special Master Golkicwicz notes in the case called Stevens that all 267 Hepatitis B cases are cause in fact claims.

As vaccine cases became harder to win, happenings nationally and internationally increased public awareness of vaccine risks and the role vaccines play in national biological security. The attack on the World Trade Center followed by terrorist’s use of anthrax placed all Americans in fear of mass infection and mass immunization. Prime Minister Tony Blair's public refusal to vaccinate his child made front-page news.

At the same time public awareness of the dangers of thimerosal was rising the Institute of Medicine published the Immunization Safety Review Committee Report which focused on the dangers of mercury in the vaccine preservative thimerosal. Thimerosal, banned in Canada and Europe has been in use in America since the 1930's and is linked to autism symptoms. The Environmental Protection Agency has declared recently that a fully vaccinated American infant carries an unsafe body burden of mercury. The FDA has "recommended" that manufacturers stop using thimerosal. State court litigation over thimerosal was dismissed in May 2002 against the vaccine manufacturer ruling that such litigation must begin in the vaccine court. The ruling specifically held that mercury is not an 'adulterant' unintentionally added to the vaccine (a finding which would have permitted the case to proceeding state court) mercury claims are not an exception to NVICP pre emption and original jurisdiction and these claims must begin with NVICP claims. (Owens v. American Home Products Corp., 2002 WL 992094 (S.D. Texas May 7, 2002) Although the danger of mercury and its link to autism is beyond the scope of this book,I would direct the readers to the Defeat Autism Now (DAN) protocol at www.autism.com if your child has been poisoned.

With widespread publicity about thimerosal and anticipating three to five thousand NVICP claims each month, the Office of Special Masters has declared a two year halt on all decisions while the Justice Department and a small team of lawyers who regularly represent petitioners study causation. (See Appendix M Autism General Order #1 filed July 3, 2002 by Chief Special Master Gary J. Golkiewicz). As the Immunization Safety Review Committee's Report indicates, “studies proving vaccines cause autism are lacking” so it is unclear how the office of Special Masters intends to accumulate evidence the scientists have not yet produced. Meanwhile, several bills in the House of Representatives have made their way to committee including HR1287. This bill provides changes to the NVICP but was not passed by the Senate. The bill would give petitioners more time to bring their petition and would make petitions easier win.

Clearly the Justice Department is feeling the coming wave of petitions. Special Master Golkiewicz in the case called Stevens for the first time refers to vaccine litigation as 'toxic tort' and indicates that 'toxicology' and ‘components’ of a vaccine will direct the future of vaccine injury litigation with the new mercury debate.

In fact, beginning with the Stevens case the Masters take a completely different approach. They recognize that petitioners no longer try to prove the table injury because the presumption of cause is essentially no longer attainable and petitioners know it. Instead they are coming at the vaccine court simply to jump the hoop to regular court where political momentum is gaining for real victories. In response the Masters are essentially writing their lists of required proof outside of the vaccine table and now are halting process altogether by calling a moratorium. This move reflects the Master's frustration with a program originally designed to provide a quick and generous resolution to injured vaccinees which, as a result of the table constrictions, forces petitioner to ignore the table and approach the NVICP as full litigation. After Stevens, the medical issues become much more detailed, there is a drop of general medical terms such as 'encephalopathy' and a replacement with very specific allegations of vaccine injuries, namely demyelinating diseases and autoimmunity.

Demyelination : The future.

The days of general allegations of brain disease or encephalopathy are over. Encephalopathy at its most primitive level simply means a change in behavior: fussiness, irritability or perhaps not communicating. Science is providing the causal connection between specific demyelinating diseases and vaccines and argument centers now on whether demyelination is static or can actually progress and recur.

Demyelination can be caused by inflammation resulting from an autoimmune response which occurs when the body mistakes itself for a foreign thing and attacks its own central or peripheral nerve sheaths called myelin basic protein (MBP). If you can visualize stripping the insulating plastic coating off of electrical wiring you can picture demyelination. Myelin is referred to as 'white matter' because it looks white on the standard MRI. It is located on the outside of the brain and the inside of the spinal cord. It develops slowly in an infant and is responsible for nerve conduction and messages. The myelin sheath which covers the neurons is stripped during demyelination. Stripped myelin actually sends impulses faster, and the neurons loose capacitance (the ability to hold an electrical charge) thus preventing proper signal transfer. Demyelination injures children by leaving demyelinated nerves or thinner and less effective myelin if remyelination occurs. Lesions may be left on their brains or spinal cord and swelling is always seen, particularly in the case of measles which contains a myelin matrix protein similar to myelin basic protein and is known to trigger demyelination. In fact preventing demyelination is exactly why the measles vaccine was invented.

Demyelination can cause global brain injury, mental retardation, developmental delay, speech loss, vision loss, loss of sphincter and bladder control, paralysis, seizures, and death. How does the body get confused and begin to attack itself? What causes the confusion? How demyelination occurs, or the mechanism of demyelination, is not yet proven. There are several theories which all agree that by molecular mimicry or homology (similarity in structure between myelin and proteins of implicate viruses) or some other process, T cells sensitized to the injected vaccine also attack the child's myelin basic protein (MBP). However it happens, one thing is clear ; “The last ten years of research shows that T-cell response is not as specific as we used to think.” Scott-Sheppard

Peripheral Nerve Myelin Destruction and the Immune Response

Because most cases of vaccine induced peripheral nerve demyelination involve a child who receives a vaccine while experiencing a recent or ongoing upper respiratory infection, a theory called 'the double hit theory' has been proposed as explaining the cause. This theory suggests that the child's ongoing infectious B cell immune response and the complement process somehow contributes to T cell mediated demyelination. Some information on B cell immunity, T cell immunity and the complement process is required for understanding.

T cells and B cells are both lymphocytes. Lymphocytes are a type of white blood cell. They develop from stem cells in the bone marrow. The 'B' in B cell immunity comes from the fact that the B lymphocyte is bone marrow dependent. B lymphocytes arise from precursor cells that continue to differentiate in the bone marrow. The 'T' in T cells comes from the fact that T cells are thymus dependent. T lymphocytes arise from precursor cells that migrate from the bone marrow to the thymus where they undergo further differentiation. The thymus is located over the base of the heart, it helps develop T lymphocytes in the fetus and later in the infant for a few months after birth, thereafter it has no function in the body's immune function. T and B cells continually circulate. Seventy percent of circulating cells are T lymphocytes, sensitized T lymphocytes have memory to re-attack a foreign invader. The remainder are B lymphocytes,
these have no memory.

The body's B cell immune response is called "humoral immunity" and it has no or limited memory to "re attack" the same substance later. Humoral immunity is carried out by B cell produced antibodies called immunoglobulins. Ig stands for Immunoglobulin. These antibodies can combine with and eliminate foreign substances. There are 5 types of immunoglobulins: IgM (the largest), IgG (G or gamma responds to most infections), IgA, IgD, and IgE (appears in larger amounts in the blood of allergic people). Humoral immunity lasts only four months or so.The complement process augments the effects of the direct action of B cell
antibodies. It is made up of about 25 body chemicals that work together to complement
the action of humoral immunity. Complement proteins cause the blood vessels to become
dilated then leaky. Each component takes its turn in a precise chain of steps known as the
complement cascade. The end product is a cylinder inserted into and puncturing a hole
in the cell's wall, fluids and molecules flow in and out and the cell then swells and
bursts.

T cells generally can be one of four types:
1.cytokine (T 1) which is sensitized by antigens (foreign bodies or toxins) presented by microphage, to absorb and destroy that particular foreign substance
2. suppressor (T 2) which turns off the T 1
3. helper T cells (T 3)
4. natural killer (NK) T cells which roam and kill anything foreign without specificity.
Sensitized T 1 cells do have memory and it is this fact that forms the basis of immunization. Live attenuated or whole killed virus is injected into the person and T 1 cells are sensitized to the foreign agent just enough to create memory cells but not enough to create the disease in the person. This process is called cell mediated immunity. Sensitized T cells can produce more of that particular sensitized T cell later when presented with that particular antigen.
A fifth type of T cell is described in the literature as capable of implicating itself in an auto immune response against myelin basic protein where ones own body attacks its own myelin sheath. It is a t cell clone. It reacts to Myelin Basic Protein. Human myelin is a recognized candidate as a trigger to this T cell clone based on observations in animal experiments. That is why MBP is often referred to as an auto-antigen. This amazing statement from the cases Rogers and Johnson seems directly out of a science fiction movie:

"T cell clones that specifically recognize MBP are in the lymphoid organs of all mammalian species... These clones are driven to proliferate by exposure to MBP, and after expansion, the antigen activated T cells migrate as blasts through the circulation and across venules into the central nervous system (CNS). These T cells in the brain attract monocytes which enter the CNS parenchyma, (essential parts of an organ) transform in to macrophages, (cells that kill and eat) and are the final vectors of myelin destruction."

How things migrate across –that is, how things that do not belong in the brain or central nervous system get past the barricade that nature created, is not well understood. How does it happen? In Breaching the Blood Brain Barrier Elaine Tuomanen describes the barrier this way: Whereas the walls of blood vessels elsewhere in the body are fenestrated, like stone walls with crannies, those of the vessels of the brain resemble a mortar sealed brick obstacle. This so called blood brain barrier offers free passage to glucose and a few other select substances but fends off intruders, whether friend or foe. For example, the brain alone remains inaccessible to chemotherapy. However spies may infiltrate a line no army could breach. Certain bacteria engage in such deception, slipping through the blood brain barrier to infect the central nervous system and the cerebrospinal fluid. When these bacteria pass the barrier and reach a certain number, the brain side of the barrier releases a hormone like substance called cytokines these hormones force the barrier to let in the white blood cell lymphocytes encouraging inflammation which causes brain swelling and defaces the cellular architecture of the brain and supporting tissues. When the bacteria is killed by the invading white blood cells, the bacterium shatters, the body's defenses then mistake the shrapnel for a burst of bacterial growth and respond by setting off more cytokine alarms which bring in more white blood cells through the open barrier. The white blood cells now ensconced in the brain, enhance the production of hormone alarms and accelerate the disruption of the barrier. In cases of meningitis, use of penicillin to kill and break apart the bacteria together with the steroid oxidanac to simultaneously freeze the immune response to the dead pieces of bacteria mistakenly considered to be bacterial proliferation, remarkably reduces death by 100% Breaching the Blood Brain Barrier Elaine Tuomanen, Scientific American V.28 page 80 84 1993.

The Institute of Medicine and the National Childhood Encephalopathy Study say
Pertussis causes Severe Acute Neurological Illness

Whole cell pertussis vaccine causes seizures, and while it is not established that it causes chronic brain damage, the Institute of Medicine has conceded this possibility based on the National Childhood Encephalopathy Study (Institute of Medicine, 1994).

Much of the risks of vaccines has centered on whether the child is injected with a virus that is whole cell or attenuated that is alive or dead. But does dead or alive toxoid matter?

Attenuated virus vaccines are intended to produce a mild and harmless infection with subsequent immunity. However, even under ideal circumstances symptoms of the natural disease and its known neurologic complications may develop in vaccine recipients.

Dead organisms do not reproduce their natural disease, but are alleged to injure the nervous system by a toxic or an allergic mechanism. Pertussis, also called whooping cough, is the P in DPT which stands for Diphtheria, Pertussis Tetanus.

Creating Vaccine Toxoid out of a deadly toxin has been accomplished by various methods over the years with the aim of breaking down the cell in order to make it less dangerous but retaining enough to be recognized by the body so as to elicit the T cell memory response. Methods of toxoid creation include sonicating that is rupturing the virus with sound waves and also by freeze drying. The cell, so treated, is then preserved to prevent putrefaction by treating it with phamaldahyde or glutaraldehyde which binds, by oxidation, certain parts of the protein but allows it to still be recognized by the body.

Understanding that the process of vaccine creation may not lessen its danger can best be seen in Pertussis. The acellular Pertussis vaccine contains several components. One component is filamentous Hemagglutinin (FRA) which is basically innocuous. It is a protein that appears on the hairs that cover whooping cough bacteria (pertussis) and is one of the signals the human body responds to. By presenting the hair to the patient you can induce a protective state prior to the patient acquiring the actual disease. It has no toxic component but rather is an immunogen, it is only aimed at producing protective immunity. The next component is endotoxin, it is this component that is reduced by 1000 fold in the acellular version of DPT called DPaT. This reduction corresponded to a 90% reduction in collapse type adverse reactions and seizure. The last component is the pertussis itself, it is called exotoxin. The amount that exotoxin was reduced in the acellular version (DPaT) is 'proprietary information' of the vaccine manufacturers and is not disclosed. It is believed to be reduced by 50% however Pertussis is still present. Regardless of the method of Toxoid creation exotoxin that is pertussis remains, and, according to Dr. Kevin C. Geraghty an immunologist who testified in the Herkert case "pertussis is pertussis is pertussis."

The National Childhood Encephalopathy Study (NCES) is the largest study of neurologic injury from DPT ever conducted. It found a causal relation between DPT and seizures. The study did not have a separate category for fever as a symptom and therefore each Special Master has their own separate view as to whether fever is or is not required to prove a pertussis or tetanus injury. Proof of fever is a required symptom for a causal connection to be made according to Special Masters Abell in the case Terran, Golkicwicz in the case Salmon and Master Millman in the case Clements . Master Millman goes so far as to say "there is no convincing evidence DPT can cause seizure without fever". However in the case Almeida Master French notes that although NCES did not distinguish between febrile (fever) and afebrile (no fever) seizures, its study concluded that children with seizures and no fever were apparently at even greater risk. Almeida also notes that the 1994 study concluded that DPT can cause seizure without fever. It was only the 1991 Institute of Medicine follow-up report to the original National Encephalopathy Study which said fever must be present, and that was a ‘limited’ study.

The Mechanism by Which Tetanus and Pertussis Crosses the Blood Brain Barrier
To cause Acute Brain Damage

“Regardless of its mechanism the biologic plausibility of acute brain damage caused by pertussis vaccine is beyond doubt” (Master French Almeida). Under the NVICP the exact mechanism of demyelination is not supposed to matter as long as "the injury is medically plausible and the facts of injury follow in a logical sequence consistent with the timetable that medicine provides, and no other explanation is plausible". In other words proof of a 'logical sequence' requires an analysis of mechanism.

In the case of tetanus, officially known as tetanospasmin, it has been proposed that a small amount of tetanus toxoid, attaches itself to the cell of peripheral nerves at the same time an immune response is mounting against tetanus toxoid. Peripheral nerves then interact not directly by crossing the blood brain barrier but rather by synaptic connections between the peripheral nerves and the central nervous system. This is called retrograde transport. The immune response which is directed against the tetanus toxoid then can become directed against the central nervous systems myelin basic protein sheath. In Scott Shepard other experts claim retrograde transport of toxoid to the CNS can not happen because when the toxoid is made it is converted from toxin to toxoid which 'links its chains and thereafter it can not be taken up by a cell'. However if one molecule survives such attachment could occur. Although each batch is tested on mice before it is distributed, experts note that if just one molecule is not converted to toxoid then that is considered a 'bad batch'. The case goes on to say that “that isn't supposed to happen".

As noted previously in the case of Pertussis the conversion to toxoid does not significantly affect the presence of pertussis (exotoxin) which is still present and, admittedly one exotoxin could cause death (Scott, Sheppard and Herkert ) Notably, Pertussis has a specific virulence or adjuvant property which causes profound increases in lymphocytes, in fact its former name was lymphocytosis promoting factor (LPF) and it was used in experiments just because it had this quality. Pertussis also has the ability to open up blood vessels and cause them to leak and allow the lymphocytes into the site of inflammation. Additionally it effects cytokines which are chemical messengers in the family of interferons and interleukins which direct, amplify, potentiate and suppress the overall immune system functions. "Pertussis is a know major factor that exerts a range of effects on the immune system including the enhancement of Ig A, E and G production hypersensitivity reactions and the induction of experimental autoimmune diseases." International Immunology 1998 May 10 (5): 651 662. Ryan M.; McCarthy L., Rappoul, R. Mahon BP; Mills KH

Special Master French, in Almeida, finds that the explanation of Dr. Kinsbourne on the crossing of the blood brain barrier meets the high ‘scientific certainty’ test required in Federal Court and not required in vaccine court. In Almeida, both Dr. Kinsbourne, the petitioner’s expert, and the court recognize that "regardless of the details of its mechanism, the biological plausibility of acute brain damage caused by pertussis vaccine is beyond doubt" (citing Institute of Medicine 1991 study).

Peripheral Nerve Demyelination

Peripheral neuropathy involves demyelination of the peripheral nerves, that is, it strips myelin of the nerves responsible for movement and sensation in the limbs, face and trunk and the autonomic responses of the vagal nerve. The mechanism of peripheral nerve demyelination is compared to an animal experiment called Experimental Allergic Encephalomyelitis (EAE). It has been found that what happens to animals in EAE happens exactly the same way in the clinical course of the human demyelination disease called peripheral neuropathy. Peripheral neuropathy has several forms including acute and chronic. These forms are called acute inflammatory demyelinating polyradiculoneuropathy or AIDP also known as Guillain Barré Syndrome (or GBS) and the chronic form or chronic inflammatory demyelinating polyradiculoneuropathy or CIDP.

In Lawson Special Master Millman takes note that the EAE study does not provide a causal link between a peripheral nerve demyelination and tetanus or pertussis because the EAE used measles. However, Master Millman acknowledges that tetanus has been 'related to' acute inflammatory demyelinating polyradiculoneuropathy.

The EAE experiment used measles because measles contains a matrix protein which shares homology to the myelin basic protein. In the EAE experiment animals immunized with this Matrix Myelin Basic Protein developed a multiple sclerosis (MS) like disease. MS is another demyelinating disease that has been compared as similar to AIDP and GBS. In the experiment the animals injected with myelin basic protein develop an inappropriately excessive proliferation of T cell responses (cloning) that attack and destroy the brains myelin. Signs and symptoms of MS then follow.

In Scott-Sheppard the court describes how this proliferation of T-cell clones ends up attacking the hosts own body. The court notes that "the last ten years of research shows that T-cell response is not as specific as we used to think." Instead when a macrophage presents an antigen (foreign body) to a T cell cytokine, it presents it as an antigen presenting molecule (APM), and it presents the antigens amino acid protein band (also called epitope) on a particular molecule called a major histo compatibility molecule so that a T cell will recognize the proper response to that protein.

The immune system will continue to respond as long as it perceives, through the antigen presenting cells, that the protein that it recognizes is present and associated with an infection. A response against self then can occur when the foreign agent shares homology with the myelin basic protein of the host, that is, the amino acid band of the infectious agent is similar to the MBP of the host nervous system. This creates molecular mimicry and leads to an auto immune response.

In another study called the Utz Biddison study AIDP was compared to multiple

sclerosis (MS). In that study scientists measured responses from identical twins to the injection of tetanus. Two sets of twins were used. The first set of twins did not both have MS; the second set did each have MS. The first set, one with and one without MS, reacted differently to the injection of tetanus, implying an environmental factor over a genetic one in the expression of MS and implicating tetanus. The study explains that the set of identical (monozygotic) twins both with multiple sclerosis (referred to as concordant) reacted identically to injected tetanus toxoid and to injected myelin basic protein. However, "remarkably” genetically identical twins one with MS and one without MS (referred to as discordant) reacted differently: "stimulation with tetanus toxoid induced the selection of distinct Va chains in the two discordant twins”. MS has been likened to AIDP and transverse myelitis both with causal connections to DPT. See: Utz, Biddison etc. Letters to Nature V.364 p.243 1993. Note: In my personal communication with a pediatric neurologist at Mayo Clinic in 2002 I learned that the Mayo Clinic is receiving 5000 new MS case inquiries each year.

Another experimental model for AIDP (Guillain Barré Syndrome or GBS) is Waksman and Adams 1955 study called Experimental Allergic Neuritis or EAN. In that experiment a monophasic inflammatory disease of peripheral nerves was repeatedly induced by immunization with any peripheral nerve material from any mammalian or avian species. After a 2 week latent period the clinical picture shows ataxia (clumsy gait) and weakness. Relapses by reimmunization have shorter incubation period and the intensity of EAN is directly proportional to the amount of neurotogenic immunogen (peripheral nerve material) given. Cyclosporin was found to protect against and ameliorate symptoms in guinea pigs. Nerve conduction test revealing a nerve block preceded evidence of demyelination. In fact demyelination was shown to peak after clinical recovery has begun. As discussed, most AIDP patients have a prodromal event such as an infection and a "double hit" mechanism seems to be involved specifically requiring complement activation by the prodromal. This prodromal plays a pathogenic role in initiation of immune mediated myelin damage.

Whatever the mechanism of demyelination may be, the Special Masters Millman, French, Golkicwicz and Abell each take the position that injury from demyelination should be recoverable whether manifested as an autoimmune response as with measles or tetanus as described above or manifested as acute disseminated encephalomyelitis (ADEM) demyelination caused as a result of swelling) or manifested as transverse myelitis demyelination caused by swelling that cuts across the spinal cord.

Hepatitis B, MMR, Pertussis, Tetanus and Demyelinization

In Stevens, Master Golkicwicz acknowledges that Hepatitis B can cause demyelinating disease; in Tufo, Master Millman says that the incubation period for demyelination with MMR is 2 13 days; and in Johnson she acknowledges that tetanus toxoid can cause acute disseminated encephalomyelitis and sets out standards of proof of a vaccine related ADEM injury as follows:

1. Following vaccine child suffers demyelination with relation back to the date of the vaccine as related in the medical documentation.
2. A plausible mechanism for injury exists, that is, the medical literature shows the vaccine is associated with demyelination.

3. There is an immunological challenge showing an auto or immune mediated response.
4. The illness occurs within the time frame shown in the medical literature.

In Rogers Master French granted petitioners award finding tetanus demyelinates in 4 21 days or as soon as 2 hours or as late as 29 days post vaccine. Master French found transverse myelitis was related to the tetanus vaccine and also could be analogized to acute inflammatory demyelinating polyradiculoneuropathy and to multiple sclerosis. In Scott Shepard Master Abell agreed that tetanus related demyelination is plausible, but in that case proof was lacking. In Lawson tracheal tube hemorrhage was deemed the direct cause of the death of Jennifer Lawson who was found slumped over after her tetanus shot and whose brain showed enlarged lateral ventricles. She did not die until two years later and Master Millman rejected the possibility that demyelination can progress. As a result, Special Master Millman would not refer to demyelinating diseases as an 'autoimmune disease' but only as an 'auto mediated condition'. That is, it comes into existence as a result of immunomodulation gone wrong but does not persist in time.

In Time or Space

The vaccine court seems to have accepted that Measles, Tetanus, Pertussis and Hepatitis B causes demyelination. The debate now is whether demyelination occurs only in space that is the injury is 'static' or 'monophasic' or whether it may also occur in time or be 'progressive'.

It has been argued that demyelination can progress and become chronic by a process

called epitope spreading. Epitope spreading occurs when tissue around the response is released and is taken up by the antigen presenting molecule and is also presented to the T cell for destruction. The consensus at this time among the Special Masters seems to be that vaccine induced demyelination injuries are static. This debate has its own distinct terminology which gives only static monophasic demyelination the term "demyelinating disease" and refers to it as automediated. Claims of progressive demyelination are categorized separately as auto immune disease and labeled "dys-myelinating disease'.

In the case of Rys vant Erve, the Justice Department (who represents the Federal Government in all NVICP cases), had appealed the amount of an award and the federal judge to whom he appealed returned the case to the Special Master Hastings and ordered the static-progressive debate to be examined.

Pursuant to that order Special Master Hastings in the case Rhys vant Erve on remand reversed himself and denied the award he had previously granted to the petitioners. Special Masters Hastings found petitioners four MRI's revealed progressive loss of white matter and he related this to an unknown metabolic prenatal event or condition. Petitioner had not attempted to argue that progressive demyelination is possible and recoverable. Instead he argued that the injury was static and that he was clinically the same and was not deteriorating. He lost his original award and the case established that progressive “dys-myelination” is not a vaccine injury.

In Lawson (on remand 2000) the possibility of progressive demyelination was presented by Dr. Vera Byers, a researcher for Immunex Corporation.

Master Millman seemed to discredit Dr. Byer's testimony referring her as a 'professional witness' although she was new to the vaccine court and, unlike some other experts who routinely testify before the vaccine court, had never appeared there. Master Millman rejected Dr. Byers evidence on progressive demyelination and accepted respondent's position that progressive demyelination is really 'dys-myelination' " meaning “the myelin was never right to start with and then began to fall apart.” The court goes on to say Byers was wrong when she stated that vaccine reactions in the brain result in progressive, rather than static, disease ...{and}... She was wrong when she said DPT leads to CNS demyelinating illness".

Dys myelinating or myelin that was 'never right to start with' is argued by the Justice Department as a defense to these claims by sometimes presenting statistics that most infants in a category have an “in born error” of some sort. In Tersen the Department argued that many premature infants have periventricular leukomalacia (PVL) which the Department claimed caused this infants progressive demyelination. The Court rejected the argument deeming it to be ‘idiopathic’, that is, based on statistics only and not on actual tests of this child. (See and compare Barton.)

However in Peripheral Neuropathy Vol III by P.J. Dyck a non specific but progressive demyelination is recognized: A slowly progressive demyelinating but noninflammatory neuropathy has been found to be associated with high titers of IgM antibody to Myelin Associated Glycoprotein (MAG)." Anti MAG antibody will cause demyelination when injected inter neurally into feline nerve. Anti MAG antibodies have been found in AIDP patients with IgM antibody titers that are said to wax and wane over the course of the disease.”

The above finding is non specific. Similar antibodies are found in multiple sclerosis, myasthenia gravis, and systemic lupus erythematosus. Approximately 3% of patients with AIDP have one or more relatively sudden relapses. Of relapsing cases, relapses will occur more than once and up to 5 times in one case. Intervals in between are inconsistent and can be up to 30 years apart and clinical symptoms are the same as the initial course. Recovered and completely asymptomatic patients who have had AIDP continue to show mild but definite lymphoid infiltrates in nerve months or years after complete clinical recovery. This finding suggests that subclinical disease smolders on in a significant portion of recovered cases. "It is probable, therefore, that clinical recurrences represent flare ups of an indolent, clinically silent, ongoing process." Peripheral Neuropathy Vol III by P.J. Dyck p. 1461, 1471

Part Two

The Case Notes
How have other vaccine petitions been decided?

The following represent one paragraph summaries, or case notes, of the facts and decisions of National Vaccine Injury Compensation Program Cases published from 1997 through 2001.They are intended to direct readers to cases that may be similar to there own. The case notes do not give anything but a brief idea of the decision. The full text must be read and can be printed on-line from the U.S. Federal Court of Claims website, www.uscfc.uscourt.gov under the heading Special Masters. I would suggest reading Liable (2000) first as it has a comprehensive overview.

Because children with vaccine injuries often have more than one injury, the case notes are arranged first by type of injury, then by vaccine. The categories of injuries begin with the most frequent or broadest category to which other injuries are added. For example, encephalopathy would be the broadest category followed by encephalopathy with seizures then encephalopathy with seizures as infantile spasms. Within each injury category the suspect vaccine will be listed as a heading. Each case that falls into that category then is summarized and quotes from cases that conceptualize the injury are highlighted.

Terms that are often repeated have been abbreviated to shorten things up as this chapter is intended as a quick reference to direct the reader to the cases which may relate to the injury they are researching. "D" means the petition was denied and “G” means it was granted. Because the word vaccine is repeated over and over I have simply abbreviated with the letter "v". Only the petitioner’s attorney is listed not the respondent's as the respondent’s attorney is always an attorney within the United States Justice Department and the respondent is always the Department of Health and Human Services. The petitioners last name is the "case name" and it is followed in parenthesis by the name of the Special Master who decided the case then by the case number and the date of the decision. Experts are listed for both the petitioner and the respondent where possible, and respondent's expert is identified with an "R”. The index lists all cases alphabetically with their page reference.

As will be seen, few cases are won. The winning cases turn on three facts:
1. Relation of injury to vaccine is stated in the medical record or relayed by several eyewitness accounts;
2. The injury is noted to have occurred within hours or up to three days after the shot (15 days after the MMR), 10 days to 6 weeks is allowed for any shot if the injury is acute neuropathy
3. The proof of injury is captured by appropriate testing

ENCEPHALOPATHY

"Encephalopathy would manifest itself in a quiet child who is obtunded (dull) and sleepy, with nuchal (neck) rigidity and high pitched cry" Chiaravalle

DPT (Diphtheria, Pertussis, Tetanus)

"Whether Dr. Guggenheim believes DPT can cause permanent brain damage is irrelevant since Congress obviously believes that it can" Copeland 90 867V at p.5

Shyface (French) 95 0272V 12 13 97 D (G on appeal)
Native Indian who spoke little English, baby sick on day 3 after v., dead on day 4, table strictly enforced which required symptoms within 3 days. Table injury denied. Cause in fact (CIF) evidence presented by Respondent of e coli; Court decided baby could have died from a factor unrelated to the vaccine (e coli). Vaccine as a cause stands in “equipoise with e coli cause but no better.” Petitioners’ proof failed. Reversed on appeal US Court Appeals 165 F3d 1344 (1999) Curtis R. Webb, Esq. Twin Falls Idaho
Dr. William C. Torch

Sheridan/Williams (Golkiewicz) 94 1005V 12 10 97 D
Petitioner argues decreasing head percentile circumference since vaccine to death at age
6. Respondent argues that baby had congenital defect hypoplasia thinning of the corpus
callosum . No documentation of congenital defect presented. Court finds DPT "can cause neurologic injury up to 7 days post vaccine". Symptoms occurred outside of this time frame. One day earlier and the court would have presumed causation.
Sandra B. Ribes, Esq. Baton Rouge Louisiana
Dr. Kevin C. Geraghty

Holihan (Hastings) injury conceded, lost earnings hearing 95 3 99V 1 19 99 G
Hastings calls petitioners expert Dr. Kinsbourne 'cogent and helpful.' Kinsbourne rejects
'7 days' as outside time limit for manifestation of symptoms says limit of National Childhood Encephalopathy Study (NCES) is 3 days or forget it (NCES required symptoms within 7 days but particularly in first 72 hours). Child lost 20 points in IQ Wechsler pre school primary scale of intelligence revised (WPPSI R), effected skills; auditory memory gross and fine motor all effected.

Mary Frankhart, Esq. Long Beach California
Dr. Moyer neuropsychologist
Dr. Marcel Kinsbourne professor at New School for Social Research a non medical
school with focus on organic basis for psychological problems NY, NY

Pittman (Millman) 91 457V 5 22 98 D

Dead day after v. baby cried continually eyes open looked in pain tears falling down cheek
would not fall asleep. No bulging fontanelle (soft spot) no loss of consciousness (LOC)
Boyd McDowell III, Esq. Chicago Il

Rhys Vant Erve (Hastings) 92 34 IV 12 3 98 G then D.
Petitioner wins but Respondent presents new evidence and is granted remand to reevaluate evidence. Hastings reverses decision. Says all genetic. 4 MRI's show progressive deterioration of white matter (myelin sheath), because it is progressive cannot be v. related, v. related demyelination is a static injury therefore this injury must be metabolic. But petitioner argued he had stopped regressing clinically.
Leroy Toiliver, Esq. Atlanta GA
Dr. Marcel Kinesbourn
Dr. Jan Mathisen
R: Dr. Fitz
R: Dr. Gale

Ralgy (Wright) D
Master Wright dismisses Respondent's motion for summary judgment (meaning a request for a ruling for you because the facts are so clearly in your favor) and orders a fact finding hearing for each side to submit medical proof. Respondent moved for summary judgment saying the doctor needs personal knowledge of facts and had none. 42 United States Code 300aa section 13(a)(1) requires records or medical opinion or court must dismiss but doctor need not have personal knowledge of facts (need not be a treating physician can be hired just to review the record and render an opinion)
Dr. Thomas A. Schwellca

Riggs (French) 95 0295V 8 5 97 D
Sick baby gets v. dead next day, mom sees pulsating bulging fontanelle court accepts
doctor view that increased intracranial pressure would hide the pulse and mom wouldn't
see pulse. 2 weeks prior to v. had upper respiratory infection.
David Dalton, Esq. Norfolk Virginia

Priest (Millman) 90 134V 12 7 98 G on table
V#2, 3 days later ER, comatose, hot, cyanotic (blue), lethargic, CT ventricular
enlargement (meaning brain damage permanent). Respondent argues carnitine not normal
therefore mitochondrial metabolic disorder. Court says carnitine is always abnormal in
encephalopathy.
Attorney?

Francis (Millman) 99 0186V 8 31-00 D
Eleven days after v. unresponsive in ER, found sepsis secondary to strep infection. Expert gives no basis for his opinion
Lawrence R. Cohen, Esq.
Dr.Michael Goodman

Tersen (Millman) 99 341V 4 27 00 D
Shock collapse, anaphylaxis. Respondent argues significant aggravation of pre existing
periventricular Leukomalacia (PVL). Born very compromised PVL causes spastic
quadriplegia, motor deficits, hearing defect, retinopathy, cognitive defects and seizures.
After DPT Petitioner “was doing what she was doing before only more of it,” mental status
did not change, effect of anaphylaxis only lasted 6 months. "This is not an easy case to
decide".
Don Russo, Esq. Miami Florida

ENCEPHALOPATHY with seizure

MMR (Measles, Mumps, Rubella)

Connor (Millman) 90 3327V 5 5 98 on table G
Prior toe walking (neurological symptom) v. given at 17 months, same day arm
and face twitch, eyes roll back, drooled, stopped talking, 6 days later first seizure, 4 days
later second seizure, 22 days later third seizure, afebrile clonic shaking, eye rolling, stiff,
staring episodes. CT normal. Table proven: afebrile seizure within 15 days of v. plus 2
more seizures within a year, unknown mitochondrial metabolic disturbance alleged by
respondent does not meet factor unrelated burden.
Curtis Webb, Esq.
Dr. Thomas Schweller board certified pediatric neurologist

R: Dr. Samuel J. Horwirz

Aalders (Millman) 90 3473V 6 23 98 D
Eyes roll back, arms stiff, scream, grand mal seizure, coma 2 weeks, roseola, abnormal
EEG. Doctor letter regarding cause written 30 years after injury. Documents indicate 5
days after v. had symptoms.
Lousi J. Cohn, Esq. Lauderhill Florida
Dr. Marcel Kinsbourne

Lurtz (French) 90 1703 6 4 98 G
Mom and neighbor witness symptom within time required in vaccine table (referred to as “table time”), strange yell and strange grimace within 4 hours of v. lasting 5 seconds. No medical
documentation. One month later in emergency room with seizure, 7 years later, coma.
CT and MRI showed generalized cerebral atrophy not apparent on prior imaging.
Johnathan Sobel, Esq. Beachwood California

Ellis (Millman) 96 437V 6 12 98 D
MRI normal, has random eye movement but has prior condition torticollis (lazy eye) For table proof must show focal and diffuse neurological signs within 5 15 days of MMR including
inconsolable screaming, bulging fontanelle, and increased intracranial pressure or changes lasting 6 hrs in level of conscious with or without seizure plus low fever under 102. Here no rash no fever.
Harvey L. Morton, Esq. Lubbock Texas

Wehmeyer (Abell) 90 2923V 10 3 97 D
Encephalopathy within 15 days of shot vs. congenital renal artery stenosis. MRI shows
focal lesion therefore may be hemorrhage from hypertension due to kidney failure . In
true encephalopathy MRI has global effect not focal .
Paul Speziale III, Esq. Lodi NJ
Dr. David Romano nephrologist
Marcel Kinesbourne pediatric neurologist
William Schwartz pediatric neurologist University Pennsylvania Medical
School
R: Dr. Mary Ann Guggenheim

DPT (Diphtheria, Pertussis, Tetanus)
Bumanlag (French) 90 3673V 1 22 97 D
Within 3 days of v. increasing fussiness for 5 weeks. "mothers memory cannot be relied

upon." Brought to ER with jerky arm, lost use, 5 weeks post v. Petitioner's own doctor says cause is an "educated guess". CT could be infarct stroke vascular accident.
Shirley H. Fraser, Esq.

Terran (Abell) 95 451V 1 23 98 D
Born with meningocele lump (congenital hernia in which the meninges protrudes
through opening in the skull or spine). v. #3 afebrile (no fever) seizure several seconds
long to 50 minutes in length, same day ER, doctor diagnosed encephalopathy but no
clouded level of consciousness. With DPT seizure, must be febrile and within 7 days. Must
have altered consciousness within 7 days or over 30 minute seizure or seizure followed
by coma for 2 hours or followed by paralysis or other neurological signs not previously
present lasting 24 hours or more. Here no fever, no altered consciousness.
Andrew W. Dodd Torrance California
R: John Menkes, Esq. (consultant for Committee on Adverse Reactions for Institute of
Medicine)

Clements (Millman) 90 484V 7 30 98 D
V#3 at age 6 months next day afebrile clonic tonic full body seizure, ER
EEG normal, 4 months later another seizure. Then gets MMR, 4 days after MMR has
another seizure, 2 months later another seizure. Has 75 seizures between 6 mo and 3 yrs
old. At age 3 in coma. No fever with any seizure.
Victor Harding, Esq. Milwaukee
John H. Menkes

R: Robert I Bauman
Jordan (Millman) 91 0113V 2 23 98 D
Cyanotic at birth, given phenobarbital. Birth EEG showed excessive amount of diffuse
delta activity during sleep with multifocal sharp transients consistent with mild to
moderate encephalopathy and congenital abnormalities. Dysmorphic features: telecanthus, low set ears posteriorly rotated, short nose, broad nasal ridge, micrognathia (small jaw), wide anterior
fontanelle and sutures. V#1 with Pertussis no seizure, v#2 w/o Pertussis EEG shows
hypsarrhythmia (hallmark of infantile seizure and encephalopathy) ACTH (adrenocorticotropic hormone) given; EEG moderate diffuse slow wave showing moderate diffuse
encephalopathy, baby dead 5 months later. Pre exist seizure aggravated within table time
but no " relentless decline" as required in significant aggravation cases. Significant aggravation cases are those children with preexisting problems made worse by the vaccine. For proof of significant aggravation of pre existing condition need : 1. current condition worse than previous 2. onset of worsening w/in table time and 3. v led relentlessly to current condition. Here number
3. fails.
Richard Gage, Esq. Cheyenne, WY
Marcel Kinsbourne New School University NY, NY

O'Connell (Millman) 96 63V 2 2 98 D
Twitching before DPT. Big family history of seizures. Birth hypertelorism (abnormal
width between two paired organs especially eyes). V.#2 next day ER shaking left arm right
leg, 30 twitches, no eye rollup, staring spells, flat fontanelle (no bulge), 101.5 temperature
discharged next day. No third v. back at ER within 2 days with 30 minute unconscious seizure
(status epilepticus), but there is no medical record of 30 minute seizure. Eight more ER visits within next 3 months these were flat fontanelle, color pink. remained alert but had sudden jerking of arms and legs, sudden darting of eyes, and just before episode would become irritable and arch back. Head droops, bends at the waist. Diagnosed with benign myoclonic seizures of infancy. MRI small left temporal lobe myelination was borderline normal. Questionable fever. Brian A. O'Connell, Esq.
Wellesley MA Dr. Marcel Kinsbourne
Dr. Elizabeth C. Dooling pediatric neurologist Massachusetts General
Dr. James J. Rivrello neurologist
R: Dr. Gerald Fenichel

Barton French 91 1594V 5 2 00 G
Death Certificate says seizure disorder. Respondent argues periventricular leukomalacia
(PVL) loss of white matter in corpus callosum with lesions that cause lower extremity
spasticity. Post vaccine symptoms all based on eyewitness account, not medical record.
Neurologically normal from birth until 2 months v#1 scream cry v#2 fever scream, call
doctor told colic, doctor did not see child, v#3 fever and lowered response, change in
personality, head floppy, stared into space, recurring repetitive movements.
Robert Moxley, Esq. Cheyenne WY
Dr. Marcel Kinsbourne
Dr. Roy Strand neuroradiologist
R: Dr. Rita Lee pediatric neurologist

SEIZURES

DPT (Diphtheria, Pertussis, Tetanus)

Lord (French ) 90 1630V 8 21 97 G on table
V#l, 3 days later ER, rapid labored breathing, coma like state, vomiting, hypotonicity (loss of muscle tone) tonic clonic seizure, deep coma, critical. Discharged 14 days later, deaf, hyper, low speech, got worse and worse, at 22 doesn't talk. Respondent argues Reyes Syndrome which looks like vaccine encephalopathy but patient has liver dysfunction which is common in Reyes. Respondent argues Reyes is a factor unrelated or inborn error of metabolism, Court rejects. Anthony Bettar, Esq. Syracuse NY

Langford (Millman) 91 0521V 8 21 98 G
V#2 same day leg jerks, deviation of eyes, no fever, alert in emergency room. Granted on
table, adjourn to submit medical records regarding screaming.
Robert T. Moxley, Esq. Cheyenne WY

McMurry (Millman) 95 682V 6 26 97 G
Seizure disorder without encephalopathy, but immunization records tipped scale in Petitioner’s favor. Two weeks prior to v#3 finished antibiotics. V#3, 5 hours later ER, 101 fever, arm twitch,
seizing 40 minutes, EEG and CT normal. Tonic clonic generalized seizure, given phenobarbital. Immunization records state "she had DPT seizure same day as vaccine no more DPT". Respondent argues pre existing condition of robertsonian translocation (genes not paired) court deems this of no merit as other family members have it without consequence.
Dr. Fenichel (on advisory commission on childhood vaccines and Institute of Medicine member) says DPT can cause fever that triggers seizure but can not cause neurological problems absent encephalopathy, this trigger vs. cause argument is rejected.
Sherry K. Drew, Esq. Chicago IL
Dr. Marcel Kinsbourne
R: Dr. Gerald Fenichel

Kirby (French) 91 160V 12 2 97 D
Vaccine related illness did not culminate in death, v. followed by 'tic' the same day.
Within 1 month had 3 hour seizure (status epilepticus) then mental retardation (MR).
Later developed acute lymphoblastic leukemia needed chest tube, suffered
pneumothorax. Death was “multifactorial.”
Douglas D. Potus, Esq. Selah Washington
Dr. Marcel Kinsbourne
Dr. Adam S. Hill hematologist
R: Dr. Rita Lee pediatric neurologist
R: Dr. Gregory H. Reamon pediatric oncology, hematology

Goodwin (Hastings) (date and case number unknown) D
Premie sick baby gets v. drooling, seizure. No proof within 3 days "all fully explained by his prematurity and prior symptoms” basic lack of documentation
Dr. Lawrence Chin
R: Dr. Arnold Gale

Salmond (Golkicwicz) 91 123V 12 16- 99 D
Pre NVICP act vaccine (1979) V. on April 4th 1979 in May 1979 had blinking, staring to left,
jerking arm, EEG normal. Residual Seizure Disorder (note: this category was removed from vaccine table injury in 1995) defined as: no seizure before v., first seizure within 3 days of v., 2 more within a year. Can be focal motor, petite or grand, myoclonic, tonic, clonic, but NOT
afebrile. Petitioners own doctor denies vaccine as cause.
Curtis Webb, Esq. Twin Falls Idaho

Castillo (Wright) 95 0652V 7 19 99 D
On same day as v. has seizure goes to ER, followed by dramatic loss of speech, later
very aggressive, hyper, poor writing, chronic ear infection, pharyngitis, bronchitis,
conjunctivitis, upper respiratory. No medical record of any post ER problems.
Seizure alone not table injury for which a presumption may be gained need
encephalopathy.
Curtis R. Webb, Esq. Twin Falls Idaho

Lagrand (Millman) 97 0692V 6 18 98 D
V#3 jerky movements within 24 hours myoclonic jerks arms legs no specific pattern, tonic flexing left upper arm, fist clench, EEG abnormal. No loss of consciousness. MRI left temporal lobe atrophy. Dead one year later. Questionable roseola. Court says no encephalopathy, seizure without more shows no causal connection to vaccine.
E. Paul Gibson, Esq. Charlestown SC

Lewis (Hastings) 95 728V 6 14 99 D
Within 4 days of v. unusual leg arm movements one time. Respondent argues premature
apnea. Big seizure next month. For cause in fact proof of encephalopathy must show
significant neurological symptoms this means that within 7 days of v. acute
encephalopathy unexplained loss of consciousness (LOC), ½ hour of convulsions or less
than 1/2 hour if followed by 2 hour coma, or paralysis or other neurologic signs not
previously present and lasting 24 hours. Single subtle seizure is not acute neurological
event.
J. Bradley Horn, Esq. Vienna Virginia
Dr. Mark R. Geier

Oetting (French) 95 0785V 6 11 99 G
Within 4 days of v#1 increased fever constant grating moaning cry, less eye contact, less
alert, limp 15 minutes. V#2 same day still, pallor, arm movements, limp. ER next day.
ER records say immunization reaction is blotchy rash and failure to develop speech.
Respondent says congenital multifocal seizure disorder but doesn't prove.
William J. Pauzauskie, Esq. Topeka KS
Dr. Jerome Murphy
Dr. Mark Geier
R: Dr. Molofsky

Muller (Millman) 90 2724V 6 23 98 D
V#3 same day muscle spasms. One babysitter’s testimony of table time symptom is not
sufficient proof (but compare mom plus neighbor testimony found sufficient
proof in Lurtz ). Need fever, excessive screaming, inconsolable cry, insomnia, altered
affect, excess irritability.
T. Carey Wicker III, Esq.
Dr. Kinsbourne pediatric neurologist
Dr. Mark Geier

Liable (Hastings) 98 120V 9 7 00 G
The case has the most medical citations and is very significant case to an understanding
of current NVICP litigation. Liable lists the factors that NCES used to include a child in the study also called 'case child' factors. They are as follows:
A "case child' is a child between the age of 2 and 25 months who is admitted to the
hospital between 1976 and 1979 with one of the following diagnoses:
1. Acute or subacute encephalitis, encephalomyelitis or encephalopathy
2. unexplained loss of consciousness
3. Reye syndrome
4. convulsions with a total duration of more than half an hour or followed by coma
lasting 2 hours or more or followed by paralysis or other neurological signs not
previously present and lasting 24 hours or more; or
5. infantile spasms (West syndrome).

The NCES data indicated that children vaccinated with DPT had a risk of experiencing a "severe acute neurological illness" in the 7 days following vaccination. This risk is about 3.3 that is over 75 % chance that there is a causal connection (75% more risk than a non vaccinated child would experience these symptoms in the same 7 day period).

The child in this case within 5 hours of V#3, has questionable fever, unusual movements, is rushed back to the pediatrician then to the hospital where the child has 30 60 minute seizure. Next month more seizure, and developmental delay. Master Hastings gives cause in fact standards for off table encephalopathy. They are:
1. Good pre vaccination health
2. within 7 days (note: not 3 days) the petitioner would have been reported to NCES
(see 'case child' standards.)
3. chronic dysfunction and
4. no other cause (petitioner must give some proof that there is no other cause then
respondent has burden)
Paul C. Quinn, Esq. Philadelphia PA
Dr. S. Charles Bean Pediatric Neurologist
R: Dr. John T. MacDonald

Almeida ( French) 96 0412V 1 5 00 G
Petitioner won with no fact witness just affidavits. Had one prior seizure, then same day as v#3 had a 45 minute seizure, rushed to emergency CT, EEG, spinal all negative, couldn't stop seizure with Valium. Later episodes of unresponsiveness interpreted by doctors as seizure was confirmed by neurologist. Hospitalized many times later with status epilepticus. Respondent argues fever required and child had none. Court discusses fever requirement saying NCES did not distinguish regarding fever. 1994 IOM report said DPT can cause a seizure without fever. Only 1991 IOM report said child must have fever and it was a “limited study.” Court says Dr. Kinsbourne's evidence regarding toxoid crossing the blood brain barrier is “scientifically reliable” and meets Daubert the federal case setting the reliability standard for admitting scientific evidence. The court finds that "regardless of its mechanism the biologic plausibility of acute brain damage caused by pertussis vaccine is beyond doubt “ citing IOM report of 1991. Court found significant aggravation of prior seizures, only one brief seizure before v., and following v. has intractable seizures.
Ronald C. Homer, Esq.
Dr. Marcel Kinsbourne
R: Dr. Joel Herskowitz Dr. Robert T. Baumann

Gruber (Golkiewiez) (case#?) 12 22 98 on table G
V#2 brief eye blinks, V#3 same day ER medical record says "no further Pertussis
MMR withheld " jerking of arm, EEG myoclonic seizure, continuous eye blinking, eye
deviation, funny mouth movement, little bit of body jerk to the right, fine motor
problems, at age 4 status epilepticus (uncontrollable seizures) wheelchair bound
mentally retarded. Severe myoclonic epilepsy (SME) seen on videotape. Court found
significant aggravation of SME.
Timothy B. Salor, Esq. Cantor Ohio
Dr. Tracy A. Glauser
R: Dr. MaryAnn Guggenheim

Gancz (Abell) 91 178V 2 15 00 G
Lay evidence regarding exact date of onset held more valid because family followed Jewish calendar with many celebrations, and those days were more in their memory, seizure onset occurred on one of those dates.
Clifford Shoemaker, Esq. Vienna Virginia

Gibson (Hastings) 98 782V 10 30 00 D
Upheld Respondents argument that a factor unrelated to the vaccine caused the injury of
SADH (syndrome of inappropriate secretion of antidiuretic hormone-- you retain water
and sodium level drops). No regular seizures, no disability.
Mark Anderson, Esq. Fort Worth TX

SEIZURES with infantile spasms
Infantile spasms are age dependent seizures occurring between 3 and 8 months
regardless of the cause Suel page 3
Infantile spasms are a particular type of afebrile (no fever) seizure with jackknife
movements of arms and drawing up of legs, characterized by EEG hypsarrhythmia
which is defined as a 1 to 2 per second spike and wave pattern of high voltage
prominent in all leads, prognosis is poor.

MMR

Reitz (Millman) 90 1344V 4 21 98 G on table
Hospital medical records show "crying, head banging over past month, eyes rolled back, staring, head bobbing, arms would fly up" v#3 same day fever vomit excessive sleep head banging from then on. Called doctor, told it's normal reaction. V#4 same day head drooped to tray, eyes closed, foam came out of mouth, emergency room (ER) did not believe mom, pediatric neurologist diagnosed infantile spasm, gave ACTH (adrone corticotropic hormone), 17 days later in ER with possible seizure, one month later abnormal EEG shows diffuse encephalopathy.
Joseph Elliott, Esq.
Berge (Millman) 90 3705V 3 30 98 G on table
Found table encephalopathy and seizure disorder and current condition of chronic
encephalopathy. V#1 questionable myoclonic seizure same day. Head circumference goes from 50th percentile to 3rd percentile in her 12th to 28th month. By 2 years profound developmental delay, level of one month old. Infantile spasms confirmed by EEG. Parasomnia (head banging) although head dropping is more typical of seizures. EEG is hypsarrhythmia pattern (multifocal sharp waves and slow waves are hallmark of encephalopathy and infantile spasms). Court recommends check of cerebral spinal fluid (spinal tap) when encephalopathy first starts, it will show abnormal immune reaction (white blood cells in cerebral spinal fluid).
E. Drew Britcher, Esq. Morristown N.J.
Dr. Marcel Kinsbourne
Dr. Gerald Schulman
Dr. Valeriano
R: Dr. A.G. Meisfin
R: Dr. Edwin H. Kolodny
R: Dr. Irving Fish
R: Dr. Isabelle Rapin
R: Dr. M. Harold Fogelson
R: Dr. Michael Kohreen

DPT

Wilkerson (Wright) 90 0822V 2 24 98 G (previously) life care plan hearing denied.
The day after v. had grand mal seizure, never recovered.
Joseph Elliott, Esq.
Jenkins (Wright) 90 3717V 5 23 99 D
V on 3 11 fever, fussy, 3 16 jerking, but in ER "looks happy" no tests, no fever. ER again, EEG abnormal hypsarrhythmia diagnosed with infantile spasm, generalized jerking of extremities and staring. Static encephalopathy diagnosed 3 years later. Diagnoses of infantile spasms qualifies child to be reported to NCES but ultimately infantile spasms were excluded from those injuries NCES found to be caused by DPT.
Dr. Mark Geier

Hoag (Golkiewicz ) 94 67V 6 10 98 D
Significant aggravation of preexisting infantile spasms not proven to have occurred within 3 days of vaccine. V then same day called health department because crying, but medical record says child is well without complaints, 10 days later taken to ER, seizure. Court says 'TV show influenced mom.'
Dr. Marcel Kinsbourne
R: Dr. John MacDonald pediatric neurologist

SEIZURE with tuberous sclerosis
Tuberous sclerosis (TS) is a genetic condition of tuberin and harmartin presenting abnormal glial and nueral cells that tend to calcify during childhood and can be a site of seizure activity if located in the brain. All tuberous sclerosis cases proceed as significant aggravation of a prior condition cases in which there must be a showing that the current condition, TS, is worse than the previous condition and the onset of the worsening was within table time and there was a “relentless decline” See Jordan

DPT (Diphtheria, Pertussis, Tetanus)

Turner Robert (Millman) 90 3409V 8 18 98 D
Whining, fever low brief, and fussiness, not significant magnitude or duration to be a
symptom.
Scott Bronn, Esq. Houston Texas
Dr. Marcel Kinsbourne
R: Mary Ann Guggenheim
R: Dr. Robert Lamm

Gallagher (Millman) 95 191V 8 18 98
Adjourn to submit medical records Medical record made 6 mo after v#2 says stiff, eye roll back, since 4 months after the date of v#2. tightening of arms and legs.
Robert T. Moxley, Esq. Cheyenne WY

Henkel (Millman) 90 3314V 8 31 98 D
Mom changed story to doctors, Master Millman questioned credibility.
Edward Allen, Esq. Fredericksburg VA
R: Dr. Mary Anne Guggenheim pediatric neurologist

Ulicny (Millman) 95 198V 3 29 99 D
4 days after v. myoclonic jerks mild short twitches is consistent with severe case of TS
TS is predominant cause, not vaccine. Dr. Marcel Kinsboume "I do not go beyond 72
hours in linking DPT to a seizure"
Robert T. Moxley, Esq. Cheyenne, WY
R: Dr. Mary Ann Guggenheim
R: Dr. Marcel Kinsbourne

Hulbert (Millman) 90 1335V 2 20 01 D
Form fruste (mild expression) of TS with very limited intracranial expression only one tuber or maybe two tubers and are subcortical (the region beneath the cerebral cortex), No rapid and steady decline post vaccine. (Note: Tuberous Sclerosis 3rd edition by Gomez says one tuber is the average.)
Robert Moxley, Esq. Cheyenne WY
Dr. Manuel Gomez
Dr. Robert Zimmerman Children's Hospital of Pittsburgh Pennsylvania neuroradiologist
(137 page curriculum vitae wrote many books on imaging and TS)
R: Dr. Roy D. Strand
R: Dr. Max Wiznitzer clinical pediatric neurologist Case Western School of Medicine
Behavioral neurology especially autism 60 70 patients per week

Flanagan (Millman) 90 1126V 8 4-00 D
Government will prevail on argument that TS is a 'factor unrelated' to the vaccine if seizures occurred in absence of post vaccine symptoms such as high fever, insomnia, inconsolable crying. 23 tubers found two years after v . Child was circling, extremities jerking, head eyes turn to right, hits head with hand, throat gurgle, eyes dart, loss of bladder control, frequent nausea, right arm jerks, diffuse insistence (viscosity) this all points to TS not vaccine.
Robert Moxley, Esq. Cheyenne WY
Dr. Marcel Kinsbourne
R: Dr. Gregory L. Holmes pediatric neurologist epilepsy and electromyography (nerve
conduction) Harvard Medical School
R: Dr Manuel Gomez Mayo Clinic retired (Arizona)
R: Dr. Peter Huttenlocher University of Chicago

Turner Robert Cleveland (Millman) 90 3490V 5 30 00 D
Most people with TS seize in the first year of life, petitioner not significantly worsened
Scott Brown, Esq. Houston Tx
Dr. Marcel Kinsbourne
R: Dr. Mary Ann Guggenheim

Moody (Millman) 91 393V 5 30 00 D
Child has tubers, v#3 throws arms out, jump startle, head would drop, arms would fly up, has no speech, functions today at age 16 like a two year old. Spasms within table time but without other symptoms of v reaction claim fails.
Robert F. Moxley, Esq. Cheyenne WY

Kouba (Millman) 90 3524V 5 30 00 D
Same as Moody
John H. Bass, Esq. El Reno OK

Barnes (Millman) 92 0032V 5 3 00 D
Same as Moody and Kouba
John Shannon, Esq. Skaneateles New York

SEIZURES with encephalopathy and tuberous sclerosis

MMR (Measles, Mumps, Rubella)

Evans (Millman) 90 3142V 7 15 97 G
Petitioner never seized before MMR, even though susceptible, had seizure within 10 days
of MMR with trunk rash.
Richard Gage, Esq. Cheyenne, WY
Dr. Marcel Kinsbourne
R: Dr. Phillip Lesser TS expert
R: Michael Pollack TS expert

DPT (Diphtheria, Pertussis, Tetanus)

Suel (Millman) 90 935V 9 18 97 G
Respondents argue if 8 or more tubers child would inevitably be symptomatic, Appellate Court rejected this. Child has poor social interaction, oppositional and aggressive behavior, poor self help skills, 10 yrs old still not toilet trained. One time rolling back eyes within table time this equals infantile spasm caused by DPT. A TS child is more likely to manifest infantile spasms and if repetitive they can damage the brain, eyes rolling back and up in indicative of a myoclonic seizure. Autism is a behavioral profile and a symptom of TS, TS is one of the 3 or 4 common causes of autism. MRI shows 5 lesions, repetitive seizures do lasting brain damage to infants.
Richard Gage, Esq. Cheyenne WY
Dr. Manuel Gomez
Dr. John McDonald pediatric neurologist

Copeland (Millman) 90 867V 5 30 00 D
MRI #1 normal, MRI 1991 6 tubers, MRI 1998 shows 10 tubers (due to better detection methods). If seizure is afebrile and unaccompanied by vaccine symptoms the fact that seizure follows vaccine will not sustain award, must have vaccine symptoms.
Robert Moxley, Esq. Cheyenne WY
Marcel Kinsbourne
Dr. Robert A. Zimmerman
R: Mary Anne Guggenheim University of Colorado School of Medicine
R: Dr. Peter Kellaway world expert on infantile spasms
R: Manuel Gomez the world's expert on TS (Suel at p.2) Gomez testified in 1991 that "DPT may trigger (bring on) seizures in children with TS." The court notes that Dr. Gomez in testimony given at an Omnibus (general) TS hearing in 1996 97 "came to the opposite conclusion he previously articulated due to subsequent medical studies and his own earnest wish to testify truthfully" Copeland page 3 . Dr. Gomez left the Mayo Clinic near this time.

DEMYELINATION

MMR (Measles, Mumps, Rubella)
Fedelalla (Millman) (cases number and date unknown) D
Adult rubella shot, then diagnosed with Guillain-Barré Syndrome also known as acute inflammatory demyelinating polyradiculoneuropathy (AIDP). There are no epidemiological studies connecting rubella to GBS over background rates.
Sylvia Chin Kaplan, Esq. Boston Mass
R: Dr. Barry Amason

Trojanowicz (Golkiewiez) 95 215V 7 1 98 D
Normal five year old has v. one week later collapsed from Chronic Inflammatory
Demyelinating Polyradiculoneuropathy (CIDP). "Failed to analogize CIDP to AIDP (one is acute sudden, one is chronic progressive). CIDP is not a table injury. No epidemiological studies. This is a time space argument the Court may connect demyelination and MMR but not if demyelination is progressive or chronic that is, over time.
Ronald C. Homer, Esq. Boston Mass
Dr. Charles Bean

Tufo (Millman) 98 108V 3 2 01 G
14 year old looses bowel and leg control within 12 hours of v. Diagnosed with acute disseminated encephalomyelitis (ADEM) with atrophy at nerves T6 through T12. Given intravenous immunoglobulin (IVIG) to boost passive immunity. White blood cell count of 15,000 suggesting infectious process, 50% of children with ADEM have previous infectious process (prodromal) prior to receiving vaccine. Measles is most common cause of ADEM. In fact that is why the vaccine was invented. ADEM is monophasic with no recurrence. The lesions of ADEM involve dissemination in space not in time. "T cell clones that specifically recognize myelin basic protein MBP fare in the lymphoid organs of all mammalian species. These clones are driven to proliferate by exposure to MBP and after expansion
the antigen activated T cells migrate as blasts through out the circulation and across
venules into the CNS. The T cells in the brain attract monocytes which enter the central
nervous system parenchyma, transform into macrophages and are the final vectors of
myelin destruction." "MMR can cause ADEM”
Sylvia Chin Kaplan, Esq. Boston Mass
Dr. Ben Renfroe
R: Dr. Barry G.W. Amason University of Chicago

DPT

Chiaravalle (Millman) 90 3307V 1 7 98 D
Opisthotonic attacks (refusing to support weight, head and heels bent backwards body bowed forward) were not enough proof. To diagnose ADEM need to have spinal tap, CT and MRI.
Pro se (represented themselves)
Dr. Alyn L. Benezette
R: Dr. M. Arnold Fogelson

Lawson (Millman) Original case filed 99, dismissed, appeal, remand 90 2455V
2 14 00 D
Normal skull x ray, CT mildly enlarged lateral ventricles, profound mental retardation non ambulatory, cardiac arrest then intubated, tube rupture, death. Vaccine cannot cause progressive demyelination, she had 'dysmyelination' and did not die until 2 years after v. additionally, tube rupture was the direct cause of death not the vaccine.
Ron Homer, Esq. Massachusetts
Dr. Vera Byers immunologist
R: Dr. Max Wiznitzer

Johnson (Millman) 99 0186 8 31 00 G
14 year old ADEM (acute disseminated encephalomyelitis) within 12 days of v. white matter lesions and loss of bladder control. Millman says ADEM is not auto immune but immune mediated. ADEM defined as an immune mediated disorder directed against antigens resulting in inflammation and damage to the myelin sheath, can have a 40% incidence of relapse.
Douglas 0. Meystre, Esq.
Dr. Spencer G. Weig
R: Dr.Subramaniam Sriram

Herkert (Millman) 97 518V 1 19 00 G
Quadriplegic infant following DPaT vaccine. DPaT (acellular pertussis) is a 1000 fold reduction of the endotoxin, however exotoxin (which is the pertussis) is reduced by only about 50%. Both sides agree petitioner has transverse myelitis (lesion on spinal cord from swelling) but argue whether it is caused by a prior vaccine. v#2 crying lethargic told to give Tylenol. V#4 listless, throw up, limp, rash on palm of hand, deep tendon reflex depressed, ER spinal tap shows elevated protein in cerebral spinal fluid (127 should be 12 60). Diagnosed with transverse myelitis and quadriplegia. Three doctors suspected the limp episode is hypotonic hyporesponsive episode (now called anaphylaxis), it can occur from hours to 2 3 days post vaccine. You don't have transverse myelitis in an immunologically normal child (cites 9 articles). Pertussis depresses the immune defenses, causes vascular permeability that leads to spinal edema, ties up the lymphatic responses which otherwise would make antibodies.
Dan Donnelly, Esq. Garrison, New York
Dr. Mark Geier
Dr. Kevin Geraghty

Rogers (French) 94 0089V 9 1 00 G
Case of first impression (first of its kind) involving tetanus and transverse myelitis vs. multiple sclerosis. Petitioner has tetanus vaccine for employment physical and develops cold feet and
numbness and swelling in legs. Diagnosis AIDM (acute inflammatory demyelination) an
"MS like" post vaccinal myelitis (myelitis means inflammation) of the spinal cord. Nine months later was in a wheelchair. By the following year had optic neuritis, MRI shows lesions and
abnormal myelin. Spinal Tap showed IgG in CNS evocative of MS. Expert Dr. Levin
analogizes acute inflammatory disseminated polyradiculoneuropathy (AIDP) to MS
and says all is implicated with tetanus. Dr. Amason disagrees says they are different
demyelinating disorders but agrees they are the same at the cell level. Court says there is no need for laboratory proof (laboratory proof standard is 95%) nor epidemiological studies nor Daubert. Standard to be met is feasibility. The Institute of Medicine (IOM) found a feasible relationship between tetanus and multiple sclerosis.
Ronald C. Homer, Esq.
Dr. Alan Levin American Board of Allergy and Immunology
R: Dr. Barry G.W. Amason

Scott Sheppard (Abell) 97 0449V 11 16 00 D
Death. Special Masters Abel accepts that tetanus can cause demyelination but finds lack
of proof because went to hospital prior to vaccine and respondent argues Petitioner has
Devic’s disease instead. But P.J. Dyck in Peripheral Neuropathy Vol III 3rd ed. at chapter
80 says transverse myelitis (demyelination across spinal cord) and Devic’s are the same, Devic’s not separate disease.
Ronald C. Homer, Esq.
Dr.Derek Smith board certified neurologist Massachusetts General Hospital, Brigham
Woman's Hospital Boston Massachusetts, also professor at Harvard Medical School also
conducts research in demyelination.
R: Dr. Rammohan
HEPATITIS B

Stevens (Golkiewicz) 99 594V 3 30 01 D of Petitioners motion for summary
judgment (this is not a denial of the petition). Within 12 days of v#1 numbness tingling; within 12 days v#2 fatigue, MRI showed ‘multiple sclerosis like' demyelination. IOM has determined Hepatitis B can cause transverse myelitis (demyelination of spinal cord). This is the first time this author read a case where a petitioner moved for summary judgment putting the respondent (Federal Government) to the task of presenting their medical position of lack of causation.
Stevens sets out its own standards for proof stating that if the following is shown then Daubert's scientific certainty (although not required in "vaccine court") is satisfied:
Prong #1 plausible injury
Prong #2 medical community is ‘seeing’ and ‘reporting’ ‘a suspected or potential
association’ with the alleged injury in relation to the vaccine
Prong #3 the vaccinee in fact suffered the injury which is associated with prong #1 & 2
Prong #4 medically acceptable temporal time relationship between the vaccine and onset
Ron Homer, Esq. Boston Mass

ANAPHYLAXIS

DPT (also HiB, Polio and Hep B)

Guerra (Millman) 00 535V 11 15 01 D
V. then same day made a noise ‘like a cat’, 2 days later on a respirator, rupture pneumothorax, ER, purple, couldn't breath looked like dying, sister had a viral infection 10 days earlier petitioner well until vaccine. Receives immuno gamma globulin 3 times per week.

Petitioner's expert was reprimanded by the state of Florida for poor practice also not board certified. Significant aggravation of pre existing hypogammaglobulinemia, (has less gamma globulin) not found. Insufficient proof especially from petitioner’s doctor.
Sina Negahbani and George M. Nachwalter Miami Florida
Dr. Nficheal Geraidi not board certified in any specialty

HEMOLYTIC ANEMIA

Hemolytic Anemia or Hemophagocytic Lymphohistiocytosis is an auto immune disorder where pertussis toxoid binds antigenetically to the erythrocyte (red blood cells) then antibodies against pertussis also attack the red blood cell

DPT (also HiB and Polio)

Brown (Millman) 99 044V 8 3 00 G
8 days after v #3 of DPT Hib polio combination, child is dead. Both Petitioner's doctor
and Respondent’s doctor agree it was hemolytic anemia but differ as to whether it was
immune modulated or auto immune disease.
Curtis Webb, Esq. Twin Falls Idaho
Dr. Ralph Shapiro director Midwest Immunology Clinic
R: Gregory Reaman Pediatric oncologist and hematologist

HEARING LOSS

Lunn (Hastings) 97 436V 2 17 00 D
Profound hearing deficiency. No reaction v#1 or 2 but v#3 two day fever, crying, seemed
different, more clingy. Although lay belief that fever causes hearing loss there is no proof.
Robert Danzi, Esq. Westbury N.Y.
Dr. Richard Etra
R: Dr. David Tunkel

PANCREATITIS

MMR
Platt (Hastings) 93 264V 12 1 00 D
Two prior similar episodes of abdominal pain in a year. “Mumps in wild form does
sometimes cause pancreatitis” need 12 25 day incubation his was within 24 hrs.
Clifford Shoemaker, Esq.
Dr. Mark Geier obstetrical geneticist Maryland Virginia worked at NIH
Dr. Joseph Bellanti Georgetown University School of Medicine Immunology and
Pediatrics
R: Dr. John Bacon University of Maryland Immunologist
R: Dr. John Sever George Washington University School of Medicine, pediatrics

Part Three
The medical Articles
Arguing your case will require an understanding of the injury and proof that your child suffered that injury. The injuries caused by vaccines have been reviewed, the following is an overview of the medical articles referred to in various cases, or which represent my research into authors cited in the cases.
There are only two categories of injuries : seizures and demyelination. Demyelination effects nerve transmission by stripping the myelin from the nerve sheath resulting in a array of problems including developmental delay, retardation, paralysis, blindness and death. Damage to myelin can be caused by inflammation from an immune response to the virus. Seizures can be caused by localized lesions resulting from demyelination. Demyeliation can be caused from inflammation from an ongoing immune response in the central nervous system.

Seizures
There are many medical articles cited in the NVICP cases regarding seizures. Since the amendment to the vaccine table, seizure disorder alone without signs of brain injury are not recoverable. The following is an overview of journal articles cited in the cases regarding seizure. A brief list of definitions of medical terms is in the Appendix.

“A hand may suddenly fling out, a shoulder may shrug, the foot may kick...”
Seizures and Epilepsy in Childhood A Guide for Parents John Freeman M.D. p.67
“Many types of seizures and epilepsy go undiagnosed for years.”
Principles of Neuroepidemiology Tracy Batchelor, Merit E. Cudkowicz
Chapter 8, at p. 153
“An EEG has a 50% chance of not picking up what it is looking for”
Tersen 99 341 V p. 19

The following is derived from Neonatal Neurology Consensus and Controversy in the Clinical Management of Neonatal Seizures Clinics In Perinatology 16:485 500 (1989)
Classifying seizures is necessary because of the danger of using epileptic drugs with encephalopathy based 'non epileptic' seizure. If it is a 'subtle seizure' or ‘non epileptical' seizure it is likely "...evidence of forebrain depression, and giving drugs that further depress brain function may be deleterious." At 493. Therefore: ... an electroclinical classification of neonatal seizures was proposed.

Where the EEG shows abnormal electrical activity at the time of the person’s physical movement then it is classified as a seizure: Focal clonic seizures, focal tonic seizures (characterized by tonic eye deviation or asymmetric tonic posturing), and some myoclonic seizures occur in close association with EEG electrical activity. (p. 487) Epileptic neonatal seizures include focal clonic, focal tonic and some myoclonic seizures. (p. 497)

Clinical events occurring without a consistent relationship to EEG seizure activity include generalized symmetric tonic posturing, some myoclonic jerking, and most behaviors currently considered to be subtle seizures (oral buccal lingual tongue movements, random eye movements, nystagmus, progressive movements such as pedaling, rowing and stepping, complex purposeless movements, and rotary arm movements) These last behaviors have been referred to as motor automatisms (p. 487,490,497) Both epileptic seizures and non epileptic events may be associated with infection.
... when the forebrain is depressed, brain stem centers are disinhibited, and primitive reflexes may occur spontaneously or be evoked by stimulation. The non epileptic seizures may be identified by their response to tactile stimulation and to restraint. They may be evoked by stimulation, demonstrating temporal and spatial summation and irradiation of the response (features characteristic of reflex physiology). The seizure may be suppressed by restraining or repositioning the affected limb. Non epileptic seizures such as generalized tonic posturing and motor automatisms are most often seen in infants who are lethargic or obtunded, who have depressed and undifferentiated background EEG activity, whose CNS dysfunction may be caused by encephalopathy or infection and who have poor short term outcomes. (p. 497)

Therefore, if the EEG is normal and movements can be restrained or elicited and are of the following type: tonic posturing, oral buccal lingual movements, ocular signs, tonic eye deviation, progressive movements such as pedaling, rowing and stepping and complex purposeless movements they may be non epileptic seizures also called subtle seizures; motor automatisms or brain stem release phenomena.

But considering that the EEG fails to detect what it is looking for 50% of the time, repeated long term ambulatory EEG is often necessary, additionally PET scan has determined the cause of 90% of previously 'cryptogenic' (cause unknown) seizure like activity.

The following is gleaned from Severe Myoclonic Epilepsy in Infants 2nd ed. (1992) Charlotte Dravet, Chapter entitled Epileptic Syndromes in Infancy

“... the post vaccine tape shows a child who was having almost continual brief seizures. He found it 'very hard to watch those videotapes, because I saw that she was having so many seizures, and I knew Mom didn't recognize them at the time’” Gruber (p 5) 12-22-98

In severe myoclonic epilepsy (SME) there is a high percentage of family history of same. All began before one year of age, 25% began with febrile convulsive seizure. If they begin as myoclonic seizure it begins as a partial seizure (limited to limb or head) rather than generalized and appears without fever (afebrile) days to weeks before the first convulsive seizure, or just before the convulsive seizure. Afebrile seizures occurred either after vaccination or during infectious episode. Generalized myoclonic seizure could be massive, involving whole muscles, particularly axial ones leading to hurling of objects held by the child and to falling. Intensity was variable sometimes being barely discernible.

Coinciding with the onset of myoclonus is slowing down of psychomotor development from second year, associated with refusal behavior making learning difficult. Metabolic disease tests normal, neuropathology was rarely contributory: generally normal CT and normal MRI, normal even when repeated. EEG is usually normal at onset with later EEG's showing spikes and slow waves in 20 cases. Those that were normal remained normal throughout study (11 years).

All patients had variable mental retardation "We must underline that this mental deficiency seems to develop between the second and the sixth years but to remain constant thereafter. SME is resistant to treatment.

From Clinical Pediatric Neurology A Signs and Symptoms Approach Gerald M. Fenichel Third Edition
What is a Tic?
The younger the age at onset of a nonfebrile (no fever) seizure of any type the more likely that the seizure is symptomatic (has an identifiable cause) rather than idiopathic (no identifiable cause)… prolonged ambulatory EEG is needed to detect electrical activity (p. 19) hypsarrhythmia is the usual pattern recorded on EEG during early stages of infantile spasms (p.20) In benign myoclonus of infancy … the spasms occur in clusters frequently at mealtime … last only 3 months and none are present after two years old. (p.21) Compare tics: tics are never incorporated into a voluntary movement and can be accurately described and reproduced by an observer. Tics disappear in sleep, seizures do not, in fact seizures may increase during sleep. The mean age of onset for Tourette’s tics is 6 7 years of age and new tics may replace old ones.

Infantile Myoclonic Seizures, Baird & Borofsky (1957)
Infantile Spasms
What do infantile spasms look like? Sudden lightening like contractions of the flexor muscles of the trunk which may be accompanied by abrupt flexion of the arms on the chest and flexion of the thighs on the trunk. Forearms may be retracted and pulled to either side of the head so the seizure may resemble the so called startle reflex in young infants. A sharp cry may precede or accompany the seizure. The face may assume a momentary blank or shock like expression. These are mass myoclonic movements ... rather than spontaneous jerky movements of the healthy newborn.

EEG shows Hypsarrhythmia (Greek Hypsi high meaning mountainous) a one to two per second spike and wave pattern of high voltage prominent in all leads. They are random, may vary from moment to moment in duration and location, they are never rhythmic or repetitive or highly organized.

In one study of infantile spasms, most infants have first seizure prior to first birthday, about half had normal development up to seizure, nearly all had developmental quotient of less than 50% on the Gessell standards the rest were severely retarded and only one child with hypsarrhythmia was known to have IQ within normal range. (Compare Seizures and Epilepsy in Childhood by John Freeman M.D. Says 20% of children with infantile spasm are normal in later development.)

Twenty-seven children in one test group had developmental deficiency from birth, 24 in second group did not. In the previously normal group there were nine cases of seizures following DPT vaccination. ...The capability of these children to relate to their environment is much more limited in later life.

“it is possible that DPT could be responsible for this convulsive disorder …the association may be more frequent than is generally recognized … a symptom of {vaccination} insult … it followed so closely that a cause and effect would have to be considered … Pertussis immunization should be considered as an etiological possibility”
Pediatrics 1: 48 7 (1948), B. K. Byers, E C. Moll, Chapter Encephalopathies

In Adverse Effects of Pertussis and Rubella Vaccines A Report of the Committee to Review the Adverse Consequences of Pertussis and Rubella Vaccines, Christopher P. Howson from the Division of Health Promotion and Disease Prevention at the Institute of Medicine, (National Academy Press, Wash. D.C, 1991) found 80% of infants with infantile spasms have hypsarrhythmia whereas this pattern is seen only in 4% of cases with other types of epilepsy. (p.65)

The Study of Neurologic Illness in Children (SONIC) on August 1, 1987 in Washington and Oregon found a six fold increased risk of infantile spasms among children immunized with DPT.

In Seizures Following Childhood Immunization by D.G. Hirtz, (J.Pediatrics, 102: 14 18 1983) it states that ‘In our study only one child experienced a long term handicap, and this was of moderate severity occurring in a child who had prolonged focal seizures following DPT immunization.

The following is from Nature and Rates of Adverse Reactions Associated with DPT and DT Immunizations in Infants and Children by Christopher L. Cody ( Pediatrics Vol. 68 No. 5 November 1981). The frequency of severe reactions associated with pertussis containing vaccines (DPT) has been incompletely studied, especially in the United States. The frequency of these reactions is uncertain, despite numerous reports of toxic reactions in the literature for over 40 years .... There have been few controlled prospective and/or blind studies .... The more serious reactions described following pertussis immunization include convulsions, infantile spasms, hypotonic hyporesponsive episodes (collapse or shock like episodes), encephalopathy, permanent neurologic damage, and death. This study involved 84 DT and 15,752 DPT immunizations given to children 0 to 6 years of age who were prospectively studied for reactions occurring within 48 hours following immunization (note: not 7 days –particularly looking at the first three days-- as used in the National Childhood Encephalopathy Study). The study supports the conclusion of others: that the benefits of pertussis immunization far outweigh the risks.

Demyelination

"…decreasing {head} circumference (indicating failure of brain growth) coincided exactly following the shots, from normal to ‘falling off the chart’. ...this factor alone is evidence of the occurrence of an acute brain injury ... These factors convince the court that Owen sustained a vaccine related injury to the brain...”
Owen Burman (p. 14) Dr. Michael Nigro pediatric neurologist, Childrens Hospital Michigan

National Childhood Encephalopathy Study A Ten Year Follow Up BMJ 307:6913 (Nov. 1993) p. 1171 1176. Two independent scientific reviews of the National Childhood Encephalopathy Study...both ... concluded that the evidence was consistent with a causal relation between diphtheria, tetanus and pertussis vaccine and acute encephalopathy... The present study, moreover offers a more robust assessment... Our results, therefore, provide good evidence that ... {the illnesses reported}... can have lasting sequelae as measured by various indices of brain function. ... although children with severe acute neurological illnesses resulting in death or later dysfunction had a significant excess risk of recent {DPT} immunization when compared to controls, this does not prove that the vaccine was the sole cause or even the prime cause of either the illness or the adverse outcomes in these cases... {But} ... This proportion was significantly greater than would have been expected by comparison with their matched controls showing a relative risk of 3.7 . Note : In epidemiological studies evidence showing a 2 fold increase of risk is a 50% probability of a causal association between DPT and the injury stated; a relative risk of 3 means a 75% probability of a causal association.

Demyelinating Disease In General
Peripheral Neuropathy 3rd ed. P.J. Dyck (1992) Chapter 80Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP). In certain instances a demyelinating process may be confined to the spinal cord (transverse myelitis TM); in others demyelinating within the cord may comprise but a part of a more widespread process within the central nervous system. (acute demyelinating encephalomyelitis ADEM or acute inflammatory demyelinating polyradiculoneuropathy AIDP also called Guillain Barré syndrome GBS). At times a demyelinating process that appears, on clinical grounds, to be restricted to the spinal cord may, by special testing or autopsy, prove to be more widespread. For these reasons we have chosen to orient the discussion that follows toward the basic pathogenic mechanisms that underlie demyelination itself regardless of its site within the neuraxis (introduction and p. 1455)

Handbook of the Spinal Cord, C.M. Helgason & B.G.W. Arnason (1987) Chapter 17 Demyelinating Diseases Affecting the Spinal Cord
By convention, a group of conditions known as the demyelinating diseases has been set apart from other entities in which myelin loss occurs. The so called demyelinating diseases share an inflammation component. ( itis indicates inflammation)

The following are different names for the same underlying demyelinating process called Perivenous Encephalomyelitis or PVE :
1. Acute disseminated encephalomyelitis (ADEM)
2. Postinfectious encephalomyelitis
3. Postvaccinal encephalomyelitis
4. Transverse myelitis (TM)

PVE most commonly follows acute upper respiratory infection. PVE usually begins abruptly, headache and delirium followed by lethargy and coma, seizures at onset are not infrequent, stiffness of neck and other signs of meningeal irritation may be present as well as fever. Flaccid paralysis of legs or all four limbs may be present. In some cases patients present with purely spinal cord syndrome (transverse myelitis) or Devic’s syndrome (characterized by acute ascending myelopathy accompanied by bilateral (sometimes unilateral) optic neuritis ... (author indicates devices may be a precursor to multiple sclerosis and not a separate disease)... rarely what would appear to be the same process may occur in patients with multiple sclerosis on the background of a very recent antecedent respiratory illness.

When the spinal cord is involved tendon reflexes are lost initially but become hyperactive subsequently, sphincter control is almost invariably lost, spinal fluid shows increased protein and lymphocytes are present. Diagnosis is straight forward if there is a history of rabies or smallpox vaccination or measles .... How or why measles might sensitize to Myelin Basic Protein is unclear. PVE is still encountered following rubella.. and rarely following mumps.

AIDP Acute Inflammatory Demyelinating Polyradiculoneuropathy ( also called Guillain Barré Syndrome)

“... in our present state of knowledge, the basis for diagnosis {of GBS} is descriptive…”
Description
AIDP is "a paralytic disease of unestablished etiology major complaint is weakness " Gross symptoms are: Myelin stripped, inflammation, edema within nerves. Cellular infiltrates (proteins, white blood cells and lymphocytes that shouldn't be in the cerebrospinal fluid), lesions, conduction block (major complaint is weakness due to conduction block and axonal degeneration) even fully recovered patients frequently show permanently slowed nerve conduction velocity.

Stages
Early stage: myelin retraction at node of Ranvier
Midstage : frank myelin breakdown (detached terminal myelin loops adjacent to node proceeds towards centrally situated Schwann cells and as myelin sheath degenerates, segmental demyelination that is ovoid (egg shaped) formations and phagocytes of myelin debris by macrophages becomes increasingly prominent.
In severe (or fatal stage): lesions and denuded axons that is axonal degeneration in addition to segmental demyelination.

Remyelination
During repair of segmental demyelination, Schwann cells produce Nerve Growth Factor (NGF) how this is triggered is unknown. The "new" internodes are more lightly myelinated than the ones they replace and uniformly less myelin than originally. Axon volume is reduced by 50 % in denuded axons in demyelinating neuropathies. This accounts for a conspicuous increase in the density of microfilaments and microtubules as well as for wrinkling of the axolemma (cylinder sheath of nerve fiber) Normal myelin investment favors fluid retention within the axon.

Onset, symptoms, treatment, recovery and residua:
When diagnosing AIDP (GBS) it is common to find preceding disorders or procedures such as surgery or mycoplasmal infections. These are called the prodromal. Two thirds of patients have an antecedent acute infectious illness that usually clears up by the time neuropathic symptoms begin. The most common prodromal is upper respiratory infection with fever, 10 20 % have acute dysenteric episode, (20% have Campylobacter infection and recent episode of diarrhea) less commonly low back pain is reported.

Prodromal Viral Infection and AIDP
AIDP is generally following a upper respiratory infection. An association is established for: Cytomegalovirus, Epstein Barr Virus and HIV. An association is probable for: Measles and an association is doubtful for: Mumps and Rubella (1 in 5000 of these 4% were AIDP)

For hepatitis B 30 cases see Stevens at page 37 39 which indicates the Institute of Medicine found a biologic plausibility between hepatitis B and demyelinating diseases (including transverse myelitis).
Tetanus: the IOM’s 1994 report does not find it probable 'by the high confidence level required by laboratorian standards' (i.e. 95%) that the tetanus toxoid vaccination causes multiple sclerosis … the court in Stevens finds that it is possible that the DPT vaccine can cause ADEM (acute disseminated encephalomyelitis)

For a non viral prodromal infection an association is common for Mycoplasma pneumoniae (shown by elevated levels of serum IgM and red blood cell called agglutinins). The time between prodromal infection and onset of AIDP symptoms is
1 3 weeks or as long as 6 weeks
average 11 days
range of 3 to 36 days.
90% of cases have evolved in 4 weeks then plateau for up to 90 days then show satisfactory recovery in 80% of cases in 4 6 months. Severe cases show gradual improvement over 2 years.

A Prospective Study of Acute Idiopathic Neuropathy Antecedent Events J.B. Winer, I Neurol, Neurosurgery, Psychiatry 51:613 18 1988. At least half the reported cases of Guillain Barré Syndrome (GBS) have been preceded by infections or other antecedent events during the few weeks before the neuropathy, 38% had preceding respiratory infection within the prior month, 17% had gastrointestinal infections.

Symptoms
Major complaint is weakness, from mild ataxia (tremor and clumsiness), numbness tingling hands feet, to total paralysis of every cranial and motor nerve. Usually begins in legs. Symmetric pattern is usual but seldom absolute. Reflex loss. (can be retained but rare) facial weakness unilateral (one side) if bilateral is asymmetric. Sixth cranial nerve involvement may result in diplopia (double vision) sometimes ophthalmoplegia, (optic nerve paralysis) swallowing chewing affected, weak jaw opening power, external urethral sphincter involvement but retention more common. A consistent rule is that weakness of shoulder elevation and neck flexion parallels diaphragmatic weakness and respiratory failure, 30 % had pain (charley horse like) especially thighs at night. Generalized myokymia or facial myokymia (twitching) can be a rare prelude to AIDP.

Diagnosis
1. Clinical (above)
2. Autonomic function testing big component of diagnosis
3. Nerve Conduction testing
4. Laboratory

Autonomic tests
Often abnormal sympathetic or parasympathetic functioning:, no fright response, abnormal heart rhythms, fainting, well known increased sensitivity of peripheral sympathetic endings to denervation, parasympathetic over activity characterized by generalized warmth, profound weakness, facial flushing, tightening sensation in chest and may present following Valsalva maneuver (hold nose closed, forcibly exhale), Loss of thermal regulation, Inability to sweat, bouts of excessive sweating, blood pressure may be extremely labile, loss of gastric acidity associated with vagal nerve damage (orange bowel movement).

Treatment
Immuno globulin plasma exchange begun early pursued vigorously 3 5 treatments over 7 10 days with 3 3.5 liters being exchanged at each treatment. Continuous flow machines give better results than intermittent flow machines no consensus on how severe before recommend exchange (can't walk?). One exchange can give rapid response suggesting it is a blood component like circulating IgM antibody to a myelin component.

Recovery
Incomplete recovery may include simple footdrop up to chair bound existence. Studies show cyclosporine will protect against EAN experimental allergic encephalomyelitis (a possible model for AIDP) in guinea pigs if given prior to disease and lessens deterioration if given after the appearance of neurologic signs. Following cessation of cyclosporine treatment EAN relapses. Cyclosporine inhibits production of IL 2 and important signaling molecule for T cell proliferation and exerts a major effect on CD4 positive T cells.

No association of GBS with immunization could be demonstrated ... although it is of interest that multiple immunizations were a feature of the history of three GBS patients … it is possible that the number of GBS patients surveyed (100) was not sufficient to detect vaccine associated cases (p. 617). Homology (similarity in structure) between myelin components and short sequences of proteins in implicated viruses is one possibility by which T cell mediated damage of myelin might take place. Sequence homologies between myelin basic protein and different virus proteins have been reported. (p.618).

AIDP with Measles Mumps Rubella
Lee P.R. Arthritis and Rubella Br Med J 2:925 (1962)
Guillain Barré Syndrome After Measles, Mumps and Rubella Vaccine Lancet 343:60
(1994). AIDP is thought to be an immune mediated disorder affecting the peripheral nerves associated with virus including measles mumps rubella cytomegalovirus, polio, Hib, hepatitis B (etc.) In one case study a 16 month old girl begins falling over, clumsy, becomes progressively more weak and unable to stand without support, and within 10 days after immunization she has generalized weakness and no reflexes. Spinal tap showed raised cerebrospinal fluid protein concentrations and electrophysiology (nerve conduction tests) were consistent with peripheral neuropathy. She was treated with IVIG and tube feeding and after 4 weeks began to walk again. It is a rare association, but we believe MMR immunization was the probable trigger for the development of GBS in this child.

Guillain Barré Syndrome After Rubella A.A. Saeed Postgraduate Med. J. 54:333 334
(1978)
"Lest we think that neuropathy is a new complication of rubella, we call the readers attention to an author's comment in 1940: “I said to one of the patients that this complication was not
given by the authorities, and was crestfallen when she told me that it was described as a complication of rubella in her household book of herbal remedies. "

GBS also called polyneuropathy developing 6 days after rubella infection in 26 year old woman. Within a week after rubella exposure suffers from increasing weakness of upper and lower limbs, two weeks prior had a rash which started on face and spread to body lasting 48 hours. Calf muscles painful and tender. No sphincter involvement. She deteriorated, and was given ACTH (adrenocorticotropic hormone) with improved neurological state. She was discharged in 2 weeks and fully recovered at 8 weeks. The test for rubella is called hemoagglutination inhibition test which shows specific IgM antibody which appears after primary rubella and persists for about 4 weeks, this test confirms the diagnosis.

Peripheral Neuropathy following Rubella Immunization Am J Dis Child 127: 684 88
(1974) William Shaffner
There are two general types of symptoms: Pain in arms in the morning which lasts a week with no recurrence, or pain in legs in the morning with reluctance to extend legs fully and walking in a crouching gait this subsides during the day but lasts longer and may recur. The interval between immunization and the onset of neuritic (inflammation of nerves associated with GBS) symptoms ranges broadly from 7 to 99 days. (p 686 comment par. #6). A previous study JAMA 314: 2287 2292 (1970) by A.W. Kilroy demonstrated two syndromes following rubella immunization and indicates a mean latent interval of about 40 days which is supported by this review. The most striking difference between the neuropathy following natural rubella and that following immunization is the interval between the infection and the onset of the neuropathy. With immunization the time between immunization and the onset of neuropathy is variable but relatively long (7 99 days) Whereas the interval following natural infection is usually short with neuropathy beginning while the exanthem (Greek Eruption) is still evident.

Children with post rubella neuropathies were watched for 32 months. Nerve conduction tests showed neuropathy (note however that normal values for nerve conduction velocity have been recorded during periods of active neuropathy). Rubella hemagglutination inhibition titers and sucrose gradient serum protein fractionation was carried out to detect the presence of specific rubella IgM antibodies. 6% had recurrences, 31 % had minor complaints that included features of their initial syndromes (such as leg aching at bedtime, right wrist aching, paresthesias in legs, pain behind both knees, mild crouching gait, inability to straighten legs, requiring him to walk on tiptoes one morning for two hours). Major recurrences also included 'catchers crouch' (crouching gait) 70 days after vaccination with live attenuated rubella virus. This happened again at three later times. In the second case of recurrence morning pain behind the knees lasted 30 minutes with crouched gait, tiptoe walking and prolonged velocities on nerve conduction test.

Two cases of Guillain-Barré Syndrome and Encephalitis After Measles Brit Med Journal
G. Lidin Janson 2: 572 (1972)
Natural measles: symptoms within 5 days of exanthem. Rash, pain in arms and legs, unable to walk, CSF protein risen to 760 mg/100 ml electrophoresis indicated massive damage to the Blood cerebral spinal fluid barrier (Blood Brain Barrier).

Chronic Arthopathy After Rubella Vaccination In Women False Alarm JAMA 278: 594 (1997)
No major permanent joint disability to women given rubella immunization.

Guillain Bare Syndrome Following Administration of Live Measles Vaccine C Grose Am J Med 60: 441 43 (1976) C. Grose
10 month old receives live measles, second DPT and second trivalent oral polio vaccine (OPV). One day later became febrile and refused to drink, developed hypotonicity (loss of muscle tone) especially in legs and depressed deep tendon reflexes. 19 year old received live MMR and within a week was unable to stand, weakness spread to upper limbs and face. Time interval for onset of symptoms was less than a week. These cases suggest an occasional role for measles virus (both vaccine and wild strains) in the pathologic process which leads to demyelination. These cases again emphasize the need to carefully document the neurologic diseases which follow infections with live viral vaccines. Of utmost importance are serums obtained during the acute and convalescent periods for appropriate viral antibody titers.

AIDP with Hepatitis B

Postmarking Surveillance for Neurologic Adverse Events Reported after Hepatitis B Vaccine Am J. Epidemiology 127: 337 (1988)
Only acute inflammatory demyelinating polyradiculoneuropathy was reported significantly more than expected (p.344). However, our data would suggest that, if an association exists between Hepatitis B vaccine and Guillain Barré syndrome the risk may lay predominantly after the first dose.
Concludes it would be illogical for homosexual men or health care workers to refuse the Hepatitis B vaccine. But no conclusion is drawn regarding safety to others.

AIDP with DPT

Peripheral Neuropathy Third ed. P.J. Dyck (1992) Chapter 80 Acute Inflammatory Demyelinating Polyradiculoneuropathy (p. 1446)
"We conclude that ... based on the cases of Pollard and Selby, AlDP recurrence with tetanus toxoid are probable"

Pollard, J.D. and Selby, G.: Relapsing Neuropathy Due to Tetanus Toxoid. Report of case. J. Neurol. Sci., 37:113, 1978.
Pollard and Selby described a 42 year old man with three episodes of Guillain-Barré syndrome (AIDP) each following administration of tetanus toxoid.

Eur. J Pediatr 15 5:2 1996 p. 136 138 Relapsing Acute Encephalopathy J. Mancini
On admission to the hospital {with} acute encephalitis ... At that time the mother confided the boy had had DPT vaccination 2 weeks before the first signs of illness … Five years later that boy was again admitted to the hospital … 10 days after subsequent DPT vaccination ... EEG disclosed slow waves ... diagnosed with acute disseminated encephalomyelitis ... The precipitating, factor of both episodes was DPT vaccination ... Acute transverse myelitis has been reported after DT ... Whittle E. Robertson NRC 1977 transverse myelitis after diphtheria, tetanus and polio immunization BMJ 1:1450 145 1.

The repetition of adverse events in our patient suggests a cause and effect relationship between DPT vaccination and the involvement of the central nervous system ... Pollard and Selby described a 42 year old man with three episodes of Guillain Barré each following administration of tetanus toxoid. As in their case, the relapsing post vaccination complications in our patient strongly suggest a cause and effect relationship between the vaccination and neurologic complications.

Conclusion

Neurological damage from vaccines is rare, but so are your children. Parents’ willingness to vaccinate depends on their belief, that they are doing only a good for their child. They believe that they are injecting “medicine” rather than live or modified virus and they believe that permanent harm is so remote as to be virtually impossible. The survival of the national vaccine policy requires parents to be presented with simpler versions which understate the full potential for lasting damage to their child. Without this approach parents, like England's Prime Minister Tony Blair, would choose to forego the risk of vaccination hoping instead that society, and their child, will remain virus free by the inoculations of other people’s children. Predictably under such a scenario the vaccination program would be placed in jeopardy. However, a vaccination policy which depends on simplified information in order to gain parental consent is a policy which needs revision. It is hoped that writings such as this one will bring needed information to parents and, in turn, influence those representatives in federal government to respect parents enough to provide a vaccine policy which can operate with full and adequate informed consent.

For those parents who now know that their child was injured by a vaccine, and who may spend the rest of their lives wondering why they did not fully understand the risks, why they did not see the signs, why they got the second or third shot, and why it's too late now to do anything about it I can only say 'tell others'. For those for whom it is not too late, I hope this book has helped.

APPENDIX A

Post Vaccine Symptom Chart as Reported in the Cases

Fever
Projectile vomiting
Loss of consciousness
Excessive sleeping or prolonged sleeping
Hypotonicity
Lethargic
Obtunded or dull
Change in growth percentile of head/weight/length
Unusual large or unusual small head
Stiff neck
high pitched cry
Excessive and strange sounding crying
Inconsolable crying
Sudden cries and deep long sleep where child cannot seem to be aroused
Head banging (parasomnia)
Staring episodes
Excessive drooling
Jerking movements (clonus)
Opisthotonos head and heals bent backward and body bowed forward.
Jerking arms and legs

Sounds m, b and p sound like “f”, there may be sixth cranial nerve involvement
Pink disease allergic reaction to mercury (neurotoxin) cheeks and tip of nose are pink
Mercury Poisoning has not been discussed in any NVICP case, but it will be in the future.
Note: for a complete discussion of symptoms of mercury poisoning see Autism a Unique
Form of Mercury Poisoning. Albert Enayati, B.S., Ch.E, M.S.M.E.; Theresa Birstock,
Heidi Roger, Lyn Redwood, R.N., M. S.M., C.R.N.P., Woody McGinnis, M.D.
Discussing the possible symptoms of Mercury Poisoning from thimersol, the Mercury
preservative in vaccines.
Fasciculations; involuntary twitching of muscle fiber can be seen under the skin does not
cause a movement of a joint.
High stepping and misplacement of feet
Pre existing conditions which may increase child's risk of adverse affects from vaccine
hypopigmented macules (in tuberous sclerosis:TS) white spots hard to see without a wood lamp (medical device)
forehead plaque (TS) looks like whiteheads or acne
ashleaf spots (TS) leaf shape white in lineal orientation on trunk
repeated or chronic infection
odynophagia (painful swallowing) may suggest neurologic dysfunction
viscosity (diffuse insistence)
Signs of polyneuropathy:
Catchers crouch, behind the knee pain, leg or arm weakness,
Vagal nerve autonomic damage
absence of "fright" reaction,

loss of sweating, bradycardia or tachycardia (fast/slow heart rhythm low gastric acidity (orange bowel movement)
Repeated contractions of the ankle/wrist
Bilateral sustained clonus (rhythmic contractions)
Face twitches
Loss of eye contact
Loss or diminished response or only responds to loud voice
Doesn't seem to recognize familiar people or things
Bulging fontanelle with no visible pulse
Cyanotic (blue color)
Clonic Rhythmic movements followed by Tonic phase (clenching or contracting)
Head drooping with or without bending at the waist
Head bobbing
Rapid eye blinking
Eyes roll back in head
Labored breathing
Animal like screaming
rash
Random eye movements (opsoclonus)
Deviation of gaze staring to the left or right
Loss of speech

Slumping over Roseola Jackknife movements of arms and leg symmetrical jerking of the limbs Joint pain Muscle group pain especially thigh asymmetrical paralysis/weakness Rubbery legs Facial weakness Enlarged spleen/liver (hemophagocytic lymphohistiocytosis] Ryabdomyolysis (carnitine deficiency) Toe walking

APPENDIX B

Frequently Used Medical Terms

Perioral surrounding the mouth
Febrile fever
Afebrile without fever
Lyses decomposition
Form fruste an atypical especially a mild or incomplete form as of a disease or anomaly
Anoxic complete lack of oxygen
Clonic slower rhythmic characterized by rhythmic jerking with an occasional stiffening
known as the tonic phase.
Tonic contracted and sustained
Myoclonic brief shocklike contraction of the muscle groups.
Myoclonus sudden jerky movements that may result from seizure, during sleep or from
A movement disorder that is not a seizure. All look the same no matter what
cause; very fast and jerky
Status epilepticus uncontrollable seizure lasting 30 minutes or more
Opsoclonus random eye movements frequently associated with severe encephalopathy
Rhabdomyolysis a carnitine deficiency with muscle weakness and some mental
confusion, this is present in almost every encephalopathy
Generalized seizure starts on whole surface of brain
Tuberous sclerosis – clinical signs are: hypo (less) pigmented macules (neither raised nor depressed discolorations), forehead plaque, facial angiofibroma, ash leaf sots generally shows up by age 6
Infantile seizures occur between 3 8 months of age, jackknife arm/leg movements, trunk jerks
with hypsarrhythmia EEG (slow wave and spike of 1 2 seconds), poor prognosis for majority, slow step like decline to MR.
SME severe myoclonic epilepsy
Hypotonicity lack of muscle tone
Robertsonian translocation genes not paired
Dysmorphic deformed features such as:
Telecanthus increased distance between inner canthi (angle at either end of the slit
between the eyelids)
Low set ears posteriorly rotated
Short nose
Broad nasal ridge
Micro abnormal flexion of the palmar creases (palm of hand)
Micrognathia small jaw especially lower
Wide anterior fontanelle and sutures (soft spot)
Hypertelerorism abnormal distance between two paired organs especially eyes
Cyanotic dark blue
Hypsarrhythmia EEG 1 2 second spike then slow wave pattern present on all Leads. It is the hall mark of encephalopathy and seizures associated with infantile spasms. Majority develop normally then slow down, loose ground and become severely retarded

Bells Palsy unilateral facial paralysis probably due to swelling and compression of 7th cranial nerve
Ptosis drooping
Ophthalmoplegia paralysis of optic nerve
Ataxia clumsy gait
Areflexia no reflex
AIDP acute inflammatory demyelinating polyradiculoneuropathy also called Guillain-Barré Syndrome or GBS (AIDP and CIDP are the same, one is acute one is chronic)
Myelopathy change in spinal cord, non specific lesion, in contrast to inflammatory lesion which is called myelitis
Artifact in radiologic films something that is produced by the technique not actually a part of the anatomy
Myokymia generalized twitching can occur with autonomic insult, AIDP, and is also seen in cases of persons treated with gold therapy for rheumatoid arthritis, gold is a neurotoxin
Nosology science of descriptive classifying of disease
Ictal laughter giggling associated with seizure also see facial flushing and pupil dilation

APPENDIX C

Diagnostic Tests Mentioned in the Cases

For Seizures:
ROUTINE MRI (magnetic resonance imaging)

FLAIR MRI: (fluid-attenuatedd inversion recovery imaging) especially to look for tubers: gadolinium contrast, views include axials and coronals, T2, T I with magnitization transfer.

Video EEG (electroencephalograms) EEG Hypsarrhythmic spike and slow wave suggests infantile spasms and diffusely slow background and absent alpha rhythm suggests global encephalopathy, there are many other patterns of seizures.

PET (position emission topography with 2 deoxy 2 f 18F floro D glucose (FDG) see J. Child Neurology 1:44 48 (Jan. 1996) 90% of cryptogenic seizures become symptomatic (are defined and located) using PET

Demyelination: (TK AIDP IFBS, CIDP, ADEM):
CT enlarged bilateral ventricles

MRI see enlarged lateral ventricles, migration of myelin, diffuse changes

SPINALTAP LUMBAR PUNCTURE (Cerebral spinal fluid recovery of Organism Specific Antibody Index (OSAI) look for elevated protein, WBC (white blood cells), or IgG

to 50 per mm3 have been recorded but there can be none during initial attack but present on recurrence or vice versa. This points up the fallacy of refusing to entertain the diagnosis of AIDP
when more that a few cells per mm3 are found in the CSF. Peripheral Neuropathy Vol III
Dyck at p 1474. High level of vaccine toxoid in spinal tap.

ELECTROCARDIOGRAM
T wave changes are the most prominent abnormalities (flat or inverted in the lateral leads, increase QRS voltage are also seen)

BLOOD WORK serum immunoglobin levels may be elevated (precedent infection) {sera from AIDP patients sometimes proves capable of destroying myelin in organotypic tissue culture this is relatively specific to AIDP} C9 component of complement is said to be elevated in more than 50% of cases

ELECTROPHYSIOLOGIC TESTS
Helpful in detecting proximal sensory and motor conduction abnormalities as well as defective cranial nerve conduction.
electromyography (EMG) Nerve conduction tests
Multifocal conduction block, slow nerve conduction Velocities (NCV) with prolonged distal and F wave latencies and varying degrees of denervation {shows widening of the paranoidal gap, segmental demyelination and axonal damage) lack of F waves shows GBS.

Blink reflex studies (over half AIDP patients in Massachusetts General Hospital study had abnormal blink reflex, abnormalities prolonged RI or R2 latencies)

SEP Somatosensory evoked potential abnormal in cases of very proximal root involvement

BAEPs brain stem auditory evoked potentials prolonged wave I-III interwave latencies
TESTS OF AUTONOMIC DYSFUNCTION (Vagal nerve involvement:)
SSR sympathetic skin response (sweat tests) absent in 13 of 17 patients with peripheral neuropathy tested

R R interval or beat to beat variations, an index of parasympathetic neural activity
Abnormal cardio vascular responses present in 10 of 15 patients in one study

Tilt table may show defective sympathetically mediated vascular tone (Late response)

Sinus Stimulation tachycardia test carotid (arteries from aorta to head and neck) with direct carotid sinus stimulation if there is a response than vagal conduction is in tact, if no response direct vagal damage.

Bradycardia (slow heart rate)

The combination of atrophy (no growth or withering) and fasciculations (twitchy movements without causing movement of a joint) is strong evidence for denervation Clinical pediatric Neurolo Gerald Fenichel, M.D. p156

DEVELOPMENTAL DELAY

Developmental milestones:

4 months social smile, puts hands together, laughs. Holds head up at 90 degrees, sits with head steady, rolls over

6 months reaching for objects, turning to a voice

By age 2 children have learned to combine at least 2 words, understand more than 250 words and follow many simple verbal directions Clinical Pediatric Neurology Gerald Fenichel, M.D. at p 119

Head growth:
Normal head growth in the term newborn is 2 cm per month for the first 3 months, 1 cm
per month for the second 3 months, and 0.5 cm per month for the next 6 months. Clinical
Pediatric Neurology Gerald Fenichel, M.D. p 93. Normal head circumference at birth
followed by failure of normal head growth usually indicates a secondary microcephaly

(brain was forming but a disease process impaired further growth) Clinical Pediatric Neurology Gerald Fenichel, M.D. p. 376. Failure of normal brain growth removes the force keeping the cranial bones separated, and they fuse prematurely.

APPENDIX D

List of Injuries Commonly Asserted In the Petitions

ENCEPHALOPATHY general name meaning brain disease now referred to primarily as DEMYELINATING DISEASE and includes:

1. ACUTE DISSEMINATED ENCEPHALOMYELITIS (acute inflammation of brain and spinal chord)

2. TRANSVERSE MYELITIS (inflammation ascending and descending the spinal cord) process may also involve brain.

3. ACUTE or CHRONIC INFLAMMATORY DEMYELINATING POLYRADICULONEUROPATHY(Demyelination effecting the peripheral nerves) also called GUILLAIN-BARRÉ SYNDROME

HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS (HEMOLYTIC ANEMIA) (Auto immune response to self red blood cells, may involve thrombocytopenic purpura a decrease or an increase in production of platelets) effect is a reduction in the growth of oxygenated tissue and life threatening bleeding into brain or gastrointestinal track) also called EVANS SYNDROME

THROMBOCYTOPENIA (auto immune attack on self platelets)

SEIZURE

INFANTILE SPASMS occur between 3 8 months, jackknife lightening like movements of arms and drawing up of legs

HYPOTONIC HYPORESPONSIVE EPISODE (ANAPHYLAXIS) (shock collapse)

ARTHRITIS

POLIO

HEARING LOSS

OPTIC NEURITIS (damage to nerve of the eye)

PANCREATITIS (inflamed pancreas)

FATIGUE SYNDROME

FACTOR UNRELATED MEDICAL CONDITIONS frequently asserted by the attorney for the Department of Health and Human Services (respondent) to lessen the injury or to assert a different cause of the injury. The following is a list of frequently claimed factors unrelated:

AGENESIS (failure to develop) OF CORPUS COLLOSUM

Benign nature of SEIZURES: recurrent seizures do not necessarily damage the brain. As a rule a single 1 3 minute seizure will not cause developmental problems (Connor)

TUBEROUS SCLEROSIS a preexisting condition. Petitioner must show significant aggravation of this condition that is, a worsening of symptoms and relentless decline, as a result of the vaccine. Petitioner must show a vaccine reaction such as fever, crying, screaming and local reaction at injection site. 8 9 tubers is used as the cut off to argue that the child had so many tubers their seizures were inevitable.

INFANTILE SPASMS victim must have a dramatic developmental decline, (most but not all children experience such with infantile spasms but up to 20% may have normal development). If there is no dramatic decline, then Petitioner is left with just seizures which must now meet the definition of ‘serious neurological event’ that is they must be accompanied by the following: within 3 days of vaccination petitioner suffers an unexplained loss of consciousness for 24 hours (responds if at all only to loud voice, shows absent or decreased eye contact, does not recognize people, and is severe enough to require hospitalization even if not hospitalized) and 1/2 hour of convulsions (or if less than 1/2 hour than followed by 2 hour coma or paralysis, or followed by other neurologic signs not previously present) and which lasts 24 hours or more (or if child less than 18 months old this decreased level of consciousness persists beyond 24 hours and can not be attributed to postictal (after seizure) state.. Infantile Spasms were not included as causally related to DPT in the National Childhood Encephalopathy Study.

CYTOMEGALOVIRUS infection which can be easily cured in a immunocompetent person but if active or resolving when DPT or DpaT given can result in transverse myelitis.

HYPERTENSIVE CEREBRAL HEMORRHAGE if lesion is focal and MRI does not show diffuse changes consistent with encephalopathy it may be a hemorrhage

METABOLIC DISORDER respondent general allegation of ‘metabolic disorder’will fail it must be specific, provide tests of child and show an actual causal relationship or it is considered an "idiopathic claim" and will fail.

PERIVENTRICULAR. LEUKOMALACIA: PVL is observed as an abnormal lesion deep within the developing brain next to the ventricular system in which the white matter or tissue of the brain (the leuko) becomes morbidly softened due to failure of blood flow, preventing the brain from completing its development in that area. PVL generally happens between 26 and 34 weeks of gestation. PVL is demyelination commonly associated with premature babies, it effects corpus callosum and has sequela of spastic quadriplegia cerebral palsy, motor deficits, hearing loss, retinopathy, cognitive defects and seizures (Barton, Tersen ). It must be shown that the child has PVL, the fact that PVL is statistically higher among premies will not support this factor unrelated claim. Respondent must have actual test of the child.

MULTIPLE SCLEROSIS chronic inflammation in the CNS involving loss of the myelin sheath and underlying axonal damage. The most common of a number of immune-mediated demyelinating diseases pathogenesis unknown, thought to be result of toxins, medications or viruses which trigger this autoimmune response. Special Master French in Rogers has recognized that MS can be analogized to AIDP (Acute Inflammatory Demyelinating Polyradiculoneuropathy) popularly called Guillain-Barré Syndrome or GBS.

APPENDIX E
Terms of Art

Terms of Art (these are phrases the court uses frequently in making its analysis. They represent cumulative truths based on prior vaccine court case law (precedent).
Term of art Interpretation
Stands in equipoise but no better
Your proof has failed
Leaves no footprints
No vaccine injury ever leaves irrefutable proof of injury
Relentless decline
Needed to prove your case of significant aggravation of a pre-existing condition
Can? Did?
To prove ‘cause in fact’ you must show it can happen (that it is medically plausible, i.e.: for DPT injuries ask would the child have been reported to NCES?) and show that it did happen. Medical record or eyewitness testimony. Testifying doctor need not be treating doctor.
Daubert is merely an aid not a prescription
you don't need epidemiological double blind peer reviewed studies to prove causation as is required by the case Daubert in Federal Court.

Federal rules of evidence do not apply
decision can be based on a witnesses, medical record, or opinion of non treating doctor (you do not need treating doctor but treating doctor's process of differential diagnosis has a medical certainty similar to a scientific certainty).

Factor Unrelated -----------
To rebut the presumption of cause granted to petitioners (if petitioner establishes a table claim) Respondent must present proof that the injury was caused by something else--a factor unrelated to the vaccine. This shifts the burden back over to petitioner. A factor unrelated must be specific or it will be considered a general claim of a condition. A general claim will be denied as idiopathic that is, unknown unexplained, unidentifiable or based on statistics. As nearly all cases are now cause in fact claims this 'factor unrelated' term is not seen as frequently, rather, the medicine surrounding this argument will be found in petitioners arsenal as proof that there could be no other cause.

Inborn error of metabolism
Your child was born defective. This is respondents 'back up' factor unrelated. See Rhys Vant Erve where respondents made a general allegation of inborn error of metabolism claiming it resulted in progressive demyelination (ie: continuing deterioration of the victim). This general allegation was enough for Master Hastings to reverse himself pursuant to respondents motion for reconsideration and deny an award he had previously granted to petitioner thereby foreclosing claims of progressive demyelination which are now on the fore front of current argument.

Epidemiological studies Studies of the rate of disease or injury among populations. A Relative risk of 2 means there is a 50% probability of a causal relationship, relative risk of 3 means 75%. Laboratory proof means 95% probability of causal relationship.

The Special Masters

The following is my opinion of the Special Masters from reading the cases. It is not intended to suggest bias, nor represent advice.

French, LaVon E., pro petitioner
Abell, Richard B., pro petitioner
Millman, Laura D., medium pro petitioner. Requires a fever with DPT cases and rules against
petitioner where there are credibility issues.
Golkicwicz, Gary J., Chief Special Master, medium pro petitioner

Edwards, John F., unknown
Hastings, George L., Pro respondent
Sweeney, Margaret M., unknown

APPENDIX F

Web Sites and Phone Numbers

Office of Special Masters United States Court of Federal Claims (202) 504 2189:
www.uscfc.uscourt.gov
Respondent Secretary of Health and Human Services :
www.HRSA.gov
(click on the left at 'special programs' then on the bottom at NVICP)
Government Printing Office:
http://www.access.gov/

www.minds.com

Dr. Marcel Kinsburne:
newschool.edu/GF/PSY/faculty/kinsboume

thimerosal mercury information:
http://www.safeminds.org

Center For Disease Control
http://www.cdc.gov

Institute of Medicine
http://www.iom.edu

Government Bills
http://Alllaw.com

APPENDIX G

The United States Federal Court of Claims Guide to the
National Vaccine Injury Compensation Program.

Printed by Office of Special Masters United States Court of Federal Claims
(202) 504 2189 or www.uscfc.uscourt.gov

APPENDIX H
Rules of the United States Court of Federal Claims
(Vaccine Rules)

APPENDIX I
42 USC 300aa The National Vaccine Injury Compensation Program

This statute is the Compensation program itself. This original statute is in full force and effect but the vaccine injury table contained at section (14) has been revised twice.

The original vaccine injury table is located at (14) of this statute.
This vaccine injury table applies to petitions filed from the date of the Act’s enactment, November 14 1986, and up to the time this vaccine injury table was first revised on March 10, 1995.
The March 10, 1995 first revised vaccine injury table, is located in Appendix J.
Petitions filed after March 10, 1995 and before March 23 1997, the date of the second revision, refer to any revisions in the vaccine injury table in Appendix J.
Petitions filed after March 23, 1997 refer to any changes contained in the present vaccine injury table revision contained in Appendix K

APPENDIX J

Vaccine Table revisions applicable to petitions filed between
March 10, 1995 and March 23, 1997

APPENDIX K

Vaccine Table revisions applicable to petitions filed
on or after March 24, 1997

APPENDIX L

HR 1287 A Bill To Amend the Vaccine Injury Compensation Program

Appendix M

Autism General Order #1

OMG

SANDRA,

Post this blog again, this is excellent I must have missed it the first time around.