DENISE K. VOWELL, Chief Special Master.
On March 26, 2002, Kellie and Ron Miller ["Ms. Miller," "Mr. Miller," or "petitioners"] filed a petition on behalf of their minor daughter, A.H.M., seeking compensation under the National Childhood Vaccine Injury Act
Over the last four years, Mr. and Ms. Miller have modified their claim repeatedly, raising new theories and re-litigating old ones, but have failed to produce reliable evidence that any vaccine or combination of vaccines that A.H.M. received actually caused her condition. Accordingly, I hold that petitioners are not entitled to compensation and the petition is dismissed.
A.H.M.'s case, filed more than 13 years ago, was filed prior to the creation of the OAP. Beginning in 1997, but peaking numerically in 2002-03, thousands of petitions were filed alleging either that the measles, mumps, and rubella ["MMR"] vaccine or thimerosal, an ethyl mercury preservative used in multi-dose vials of vaccine, caused ASD. The sheer volume of petitions filed—more than 1,300 new petitions in 2002 alone—led to the creation of the OAP.
Following a series of meetings with an informal advisory committee comprised of petitioners' counsel representing many of the Program claimants plus legal and medical representatives of the Secretary of Health and Human Services, the Office of Special Masters ["OSM"] adopted a plan that would allow a period of discovery, followed by the selection and litigation of test cases on the theories of causation presented. Autism General Order #1 at 2-3. The conclusions reached on general causation in the test cases would be used to resolve the remaining individual claims. Id. at 3. Petitioners were allowed to "opt in" or "opt out" of the proceedings and future claimants could automatically "opt in" by filing the short form petition included as Attachment B to Autism General Order #1. Autism General Order #1 at 6-8.
Attorneys representing petitioners created the Petitioners' Steering Committee ["PSC"] to coordinate the OAP litigative effort. The PSC acknowledged that there was insufficient evidence at the time the OAP was created to prove vaccine causation, but averred that such evidence could be found through discovery and ongoing scientific investigations. Petitioners sought and received an extended period of time to conduct discovery and prepare to litigate test cases.
Nearly five years after the OAP was created, litigation in the test cases began. The PSC presented two different theories on the causation of ASD in two sets of test cases. The first alleged that thimerosal-containing vaccines and the MMR vaccine, in combination, could cause ASD (Theory 1). The second alleged that thimerosal-containing vaccines could cause ASD (Theory 2).
Decisions in each of the three Theory 1 test cases, which were tried in 2007, rejected petitioners' causation theories. Cedillo v. Sec'y, HHS, No. 98-916V, 2009 WL 331968 (Fed. Cl. Spec. Mstr. Feb. 12, 2009), aff'd, 89 Fed. Cl. 158 (2009), aff'd, 617 F.3d 1328 (Fed. Cir. 2010); Hazlehurst v. Sec'y, HHS, No. 03-654V, 2009 WL 332306 (Fed. Cl. Spec. Mstr. Feb. 12, 2009), aff'd, 88 Fed. Cl. 473 (2009), aff'd, 604 F.3d 1343 (Fed. Cir. 2010); Snyder v. Sec'y, HHS, No. 01-162V, 2009 WL 332044 (Fed. Cl. Spec. Mstr. Feb. 12, 2009), aff'd, 88 Fed. Cl. 706 (2009).
Decisions in the three Theory 2 test cases, which were tried in 2008, also rejected the causation theory presented. Petitioners did not seek review of the special masters' decisions. Dwyer, 2010 WL 892250; King v. Sec'y, HHS, No. 03-584V, 2010 WL 892296 (Fed. Cl. Spec. Mstr. Mar. 12, 2010); Mead, 2010 WL 892248.
An impressive body of medical and scientific evidence was adduced in the OAP test cases, with the three special masters who heard this evidence finding that the issue of vaccine causation was "not a close case." See, e.g., King, 2010 WL 892296, at *90 (emphasis in original); Snyder, 2009 WL 332044, at *198. Each of the three special masters independently determined that the medical theories advanced were not reliable and that the test case petitioners had failed to produce preponderant evidence of causation. The OAP test case litigation concluded in 2010, with the last Federal Circuit decision affirming the dismissal of the final Theory 1 test case.
With appellate review completed, orders were issued on a rolling basis to the remaining 4,800 petitioners, requiring them to inform the court whether they intended to dismiss their case or proceed on a different theory or with different evidence. Petitioners were cautioned that the special masters did not intend to re-litigate the test case theories, and that a reasonable basis to proceed would require either new evidence on the old theories or new theories of causation.
The original petition filed in this case claimed that A.H.M. had ASD and raised both of the theories of causation presented in the OAP.
Thereafter, at petitioners' request, their case was included in the newly-created OAP. Order, issued Aug. 8, 2002. The case was reassigned to Special Master George Hastings and, pursuant to the transfer order, stayed until the general causation issues raised in the OAP could be decided.
While the OAP test cases were being litigated, petitioners were ordered to file medical records to position their case for resolution after the test cases were resolved. Petitioners ignored the order issued on January 15, 2008, but complied with a similar order issued March 31, 2009.
In April 2011, after the final appellate decision in the test cases was issued, petitioners were ordered to inform the court whether they intended to proceed with their claim, either on a new theory of causation or with new evidence on one or both of the rejected causation theories. Order, issued Apr. 29, 2011. On July 18, 2011, petitioners filed the amended petition which now constitutes the operative petition for their vaccine injury claim.
The amended petition and theories raised in subsequent filings recharacterized A.H.M.'s injury as an encephalopathy rather than ASD, caused by vaccines which either triggered or aggravated a mitochondrial disorder. Nevertheless, petitioners have continued to rely on either or both of the causal mechanisms identified in the OAP.
As the filed medical records did not establish the diagnosis of a mitochondrial dysfunction claimed in the amended petition, and the affidavit of Dr. Amy Holmes, a treating physician,
A few weeks later, Mr. Cave stated he had not produced updated medical records establishing that A.H.M. had the claimed diagnosis of a mitochondrial dysfunction because he still had not located his clients.
On March 30, 2012, respondent filed a second Vaccine Rule 4 report addressing the amended claim. Respondent again recommended against compensation. Respondent's 2012 Rule 4 Report at 10. On August 23, 2012, respondent filed the expert report and CV of Dr. Max Wiznitzer. See Respondent's Exhibits ["Res. Ex."] A-B. The accompanying medical literature was filed as Res. Ex. A, Tabs 1-6.
A Vaccine Rule 5 status conference was held on October 12, 2012. Possible hearing dates were among the matters discussed.
At the beginning of the hearing, I noted for the record that petitioners were not present. At that point, Mr. Cave stated that they were not present because he thought the hearing was limited to expert testimony alone. Transcript ["Tr."] at 4. He added that if petitioners were to testify, he would have expected me to travel to petitioners' location because travel would have been burdensome for the parents.
Although I directed Mr. Cave to talk again with Ms. Miller and determine if she had anything to add to her affidavit (Tr. at 12-13), he did not request to have Mr. or Ms. Miller testify, telephonically or otherwise. Mr. Cave did not raise the issue of petitioners' testimony in petitioners' post-hearing memorandum. See Petitioners' Post-Hearing Memorandum, filed Dec. 16, 2013 ["Pet. Post-Hearing Memo"].
The only hearing witnesses were Drs. Cave and Wiznitzer. Based on discussions during the hearing involving diagnostic criteria for mitochondrial disorders, I filed a complete copy of the medical journal article discussed, N. Wolf & J. Smeitink, Mitochondrial disorders—A proposal for consensus diagnostic criteria in infants and children, NEUROL. 59 (9): 1402-05 (2002), Court Ex. I [hereinafter "Wolf & Smeitink, Court Ex. I"], after the hearing.
In their amended petition, petitioners claimed that A.H.M. suffers from mitochondrial dysfunction and a "progressive decrease in brain function with encephalopathy." Petition at 1. Petitioners identified the varicella vaccination received on June 4, 1999, and the MMR, oral polio ["OPV"], "DTP/Hib"
Petitioners and their expert have modified their claim on several occasions since filing the amended petition. In her initial expert report, Dr. Cave appeared to claim that different vaccines were causal. She asserted that A.H.M.'s mitochondrial dysfunction first manifested after vaccinations administered in November 1998 when A.H.M. was six months old,
Less than one month prior to hearing, petitioners argued for the first time that they also had proven a "Table" injury
In later filings, petitioners focused on a comprehensive off-Table injury claim involving mitochondrial dysfunction and encephalopathy. See Pet. Post-Hearing Memo at 5-8. They did not address the Table injury again but did "adopt and incorporate" the arguments set forth in their pre-hearing brief. Post-Hearing Memo at 1.
Petitioners' hearing presentation and post-hearing arguments were not well-developed or presented. In spite of my cautions during several status conferences and in orders that I did not intend to permit re-litigation of the rejected OAP test case theories, absent new evidence, Dr. Cave presented testimony about mercury, oxidative stress, and brain inflammation that had been heard and rejected in the OAP test cases, without producing any new evidence.
Technically, petitioners presented reports on causation from two physicians: one from Dr. Amy Holmes, filed with the original petition, and the more recent reports from Dr. Stephanie Cave. Although Dr. Holmes also offered an opinion regarding the cause of A.H.M.'s condition (see Affidavit, Pet. Ex. 7), she is better categorized as a treating physician in this case. As I informed petitioners in 2011, Dr. Holmes' affidavit was not sufficient to establish causation. See Order, issued July 28, 2011, at 1.
Doctor Holmes did not provide a supplemental report or testify at hearing. She did, however, treat A.H.M. from May 2000 until she retired in 2002. See Pet. Ex. 8; Tr. at 24. Thus, I viewed her statements regarding causation contained in the medical records and affidavit as the opinion of one of A.H.M.'s treating physicians and analyzed and weighed her opinion accordingly. See Pet. Exs. 7, 8 (affidavit and medical records).
One of the studies relied upon by the petitioners in the OAP test cases which compared mercury content of hair samples from autistic and non-autistic children was authored by Dr. Holmes.
Prior to attending medical school, Dr. Cave earned a Master's degree in clinical chemistry and taught clinical biochemistry for five years at Louisiana State University ["LSU"] in Baton Rouge. Tr. at 14-15; Pet. Ex. 12 at 1. She attended the LSU School of Medicine from 1979-1983 (id.) and completed her residency at the Earl K. Long Memorial Hospital in Baton Rouge from 1983-86 (Tr. at 15; Pet. Ex. 12 at 1). Since earning her medical degree, she has practiced family medicine and is currently in private practice as a family physician in Baton Rouge. Tr. at 16-17; Pet. Ex. 12 at 1. She is board certified in family medicine.
Her only training in several of the disciplines in which she offered expert opinions is from medical school classes and blocks of training during her family practice residency. Tr. at 15-16. Mr. Cave creatively referred to these blocks of training as "subspecialties," a term more appropriately applied to training in addition to, rather than as part of, residency training. Doctor Cave offered opinions grounded in several medical specialties in this case, including neurology, genetics, toxicology, mitochondrial disease, and immunology, all of which were clearly beyond her area of expertise.
The majority of Dr. Cave's patients are children who come to her for treatment after being diagnosed elsewhere with autism. Tr. at 17, 107. She estimated she has treated more than 10,000 children with autism since 1996. Tr. at 17; see also Pet. Ex. 12 at 1.
Doctor Cave's treatment of children with ASD involves, in her words, "normalizing" their "cellular chemistry." Tr. at 22. She still prescribes chelation to remove heavy metals in spite of the lack of any controlled study showing it can reduce ASD symptoms or cure autism. Tr. at 23, 74. During her testimony, she acknowledged that chelation agents do not cross the blood brain barrier, and thus cannot remove mercury from the brain. Tr. at 74. See also Dwyer, 2010 WL 892250, at *104.
Doctor Cave testified before a Congressional subcommittee hearing on the issue of mercury in vaccines. She also presented testimony to the Louisiana legislature regarding thimerosal and the MMR vaccine and their connection to autism. Tr. at 18; Pet. Ex. 12 at 6. She has spoken at numerous conferences regarding a relationship between autism and vaccines. She authored a book on vaccines published in 2001, which was revised in 2010, and authored several articles published between 2000 and 2008, but none appeared to involve original research. Tr. at 19-21; Pet. Ex. 12 at 6. In her book, Dr. Cave recommended a revised schedule for childhood vaccinations, with no vaccines administered until a child is four months old and administering the usual childhood vaccinations over a more extended period. Tr. at 58-62. She did not identify any research upon which her recommendations for the alternative vaccination schedule were based.
Doctor Wiznitzer earned his medical degree in 1977 from Northwestern University. Tr. at 116; Res. Ex. B at 1. He participated in a three year residency at the Cincinnati Children's Hospital and a one year child development fellowship at the Cincinnati Center for Developmental Disorders. Id. He then trained in child neurology at the University of Pennsylvania and completed a two year National Institutes of Health fellowship in disorders of cognitive or higher cortical function in children at the Albert Einstein College of Medicine. Tr. at 116; Res. Ex. B at 1-2. He is board certified in pediatrics, neurology (with special qualification in child neurology), and neurodevelopmental disabilities. Tr. at 116-17; Res. Ex. B at 5.
At the time of the hearing, Dr. Wiznitzer was employed as a pediatric neurologist at the Rainbow Babies and Children's Hospital in Cleveland, Ohio. Tr. at 115-16; Res. Ex. B at 1. He was also an associate professor at Case Western Reserve University, School of Medicine. Tr. at 116; Res. Ex. B at 2. His clinical practice is not exclusively devoted to autism treatment, but he sees many patients with ASD, and he routinely diagnoses autism spectrum disorders. Tr. at 117-18. Working with mitochondrial disease specialists, he also diagnoses mitochondrial disease. Tr. at 118.
Doctor Wiznitzer has authored or co-authored approximately 60 peer reviewed articles, many of which deal with ASD. He also peer reviews papers and serves on the editorial boards for various medical journals. Tr. at 117; Res. Ex. B at 6. Doctor Wiznitzer testified for the respondent in the Theory 1 OAP test cases and was described in the test case decisions as experienced, credible, and persuasive.
Doctor Wiznitzer testified that he reviews medical records for the Department of Vaccine Injury Compensation (DVIC) in Vaccine Act cases and, in some of those reviews, he has found that the child experienced a Table encephalopathy. Tr. at 209-10. He was a member of a panel that developed criteria for definitions for conditions such as encephalitis, multiple sclerosis, and acute disseminated encephalomyelitis for the Vaccine Adverse Events Reporting System. Tr. at 207.
Several issues concerning the backgrounds and possible biases of the witnesses that testified at the hearing emerged before and during the hearing.
Both Drs. Cave and Wiznitzer have previously provided opinions and testified in other vaccine injury cases. When petitioner's counsel, Mr. Cave, questioned Dr. Wiznitzer regarding the percentage of his income that he earns from testifying,
While I have considered Dr. Wiznitzer's compensation for his frequent appearances as an expert witness for respondent and the fact that he has authored opinions in additional cases in which his testimony was not required, virtually all witnesses who testify as experts are compensated. Both experts in this case have that common financial interest, regardless of the outcome of the case. In view of their extensive involvement in patient care, neither of these witnesses could be classified as a "professional witness."
However, Dr. Cave's practice appears to depend in large measure on her alternative medical approach to the treatment of ASD. Thus, she has a financial interest in establishing the bona fides of her treatment methods, in that mainstream physicians do not claim to prevent or cure autism. Doctor Cave does. Establishing, via a court decision, that vaccines can cause ASD or ASD-like symptoms could be expected to increase her book sales, as well as have a similar impact on her private medical practice. Thus her financial interest in the outcome of this case is likely greater than Dr. Wiznitzer's.
By any measure, except perhaps the sheer number of ASD patients seen, Dr. Wiznitzer's qualifications to opine on the causes of ASD and whether A.H.M. has ASD, or a mitochondrial dysfunction masquerading as ASD, far exceed those of Dr. Cave. Doctor Wiznitzer is more highly credentialed in relevant areas such as pediatrics and neurology than Dr. Cave. Then-Special Master (now Judge) Sweeney took note of the difference in qualifications of these same two experts in a prior case. See Nilson v. Sec'y, HHS, No. 98-797V, 2005 WL 6122524, at *9, 13-14, 20 (Fed. Cl. Spec. Mstr. Aug. 31, 2005), aff'd, 69 Fed. Cl. 678 (2006). Furthermore, Dr. Wiznitzer has conducted research on ASD and co-morbid conditions, has peer-reviewed publications on ASD and related topics, and has been awarded research grants in relevant fields; Dr. Cave has not.
Despite her lack of training, research, or board certification in relevant disciplines, Dr. Cave opined on a range of medical conditions, but offered little support for her opinions. In contrast to Dr. Cave's sweeping statements about causation (see, e.g., Tr. at 70-71) and opinions in areas in which she has neither the training nor the experience to opine credibly, Dr. Wiznitzer candidly acknowledged the limits of his expertise, often noting when he did not feel qualified to opine on a medical issue. The wide latitude afforded to an expert "is premised on an assumption that the expert's opinion will have a reliable basis in the knowledge and experience of his discipline." Daubert, 509 U.S. at 592.
A more significant problem with Dr. Cave's testimony was apparent from the time her first expert report was filed: she was retained to offer expert testimony in a case in which her son was counsel of record. I informed Mr. Cave of my concerns that this relationship might impact on Dr. Cave's credibility, but he elected to proceed with Dr. Cave as his expert witness despite them. See Order, issued Dec. 6, 2011, at 2, n.3.
Familial relationships alone may raise the issue of bias.
Doctor Cave's poor qualifications to opine as an expert and her familial relationship to petitioners' counsel do not preclude her appearance as a witness under the more flexible evidentiary standards in effect in Vaccine Act cases
A.H.M. was born in mid-May 1998 after an unremarkable pregnancy.
Numerous videos show A.H.M. as an alert and healthy infant who occasionally smiled at the person holding or filming her. See Titles 1-6.
At her nine month well-child visit on February 17, 1999, A.H.M. was assessed as having normal growth and development. She was pulling up to stand and saying "mama" and "dada." Pet. Ex. 4, p. 8. She received no vaccinations at this visit.
Shortly before her first birthday, A.H.M. was taken to the emergency room ["ER"] with vomiting, diarrhea, and a fever of 103.4° Fahrenheit.
A.H.M. visited her pediatrician a week later on May 19, 1999 for her one year well-child visit. Recorded milestones reflected that she was walking well and saying "mama" and "dada" with specificity. Pet. Ex. 4, p. 8. She was described as alert and active and assessed as a well-child with normal growth and development. Id.
Several undated videos appear to have been filmed at some point during the first half of 1999.
A.H.M. received the varicella vaccination recommended at her one year well-child visit on June 4, 1999, when she returned to the pediatric practice with her older brother. Pet. Exs. 4, p. 8; 5, p. 1. This vaccination is the first one petitioners alleged as causal.
On July 2, 1999, almost a month after the varicella vaccination, A.H.M. was seen for a rash on her legs, hips, and face that had begun about two weeks earlier. She also had a low grade fever, cough, and runny nose. Pet. Ex. 4, p. 7. She was described as alert and active with no fever and was diagnosed with an upper respiratory infection ["URI"] and contact dermatitis. Id. Although petitioners pointed to this rash as evidence that A.H.M. suffered a Table encephalopathy (Pet. Pre-Hearing Memo at 6-7),
In videos dated between July 18, 1999 and August 1, 1999, A.H.M. showed more pronounced abnormal behaviors: a lack of vocalization and eye contact, a failure to respond to others, and a fascination with objects. See Titles 11-16. Doctor Wiznitzer gave detailed testimony regarding A.H.M.'s behavior, describing it as "distinctly different" than the behaviors he had seen in previously recorded clips. Tr. at 133. He characterized the behavior as typical autistic behavior, but not evidence of an encephalopathy. Tr. at 135-37, 139-40. In the July 18, 1999 video, A.H.M. dropped the electrical cord she was holding and reached for the camera. See Title 12. Contrasting her behavior with that seen in Title 8 (recorded around Christmas 1998), Dr. Wiznitzer pointed out that A.H.M. paid more attention to the camera than the person filming. Tr. at 133. He described her behavior as being "distinctly different" from the behavior shown on Title 8. Tr. at 133. In the July 18, 1999 video, A.H.M. was babbling, but no discernable words could be identified. See Title 12.
In the July 19, 1999 video, A.H.M. pushed a plastic buggy on the deck while her father watched, her mother filmed, and her brother and three dogs played with a ball. See Title 13. She looked at the ball when her brother bounced it and at a toy lawn mower as he pushed it, but showed little interest in her brother or the dogs. See id. Doctor Wiznitzer commented on her lack of attention to those around her and noted that she had few vocalizations during the video. Tr. at 133-34.
The next three videos were filmed inside.
When A.H.M. returned to her pediatrician on August 10, 1999, for a cough and fever, Ms. Miller reported that A.H.M. had experienced colds off and on over the prior six weeks, a loose and productive cough for the last few days, fever, increased fussiness when lying down, and a decreased appetite. Pet. Ex. 4, p. 7. Her temperature at the visit was normal, and she was diagnosed with a URI and ear infection. Id. She failed to show for a follow-up appointment approximately a week later, suggesting that she had improved on treatment. Id.
In early September 1999, A.H.M. visited her pediatrician again for nighttime coughing. Id., p. 6. Her temperature was 100.5°, but she was alert and active. She was diagnosed as suffering from croup. Id.
At her next well-child visit on September 15, 1999, A.H.M. still had a cough and runny nose, but her cough was much better. Pet. Ex. 4, p. 6. At this visit, her parents reported a concern about her speech ("doesn't say much"). Id. Her pediatrician assessed her as having mild developmental and speech delay. Id. A.H.M., then 16 months old, could say four to five words, but she did not seem to understand or follow directions or otherwise indicate her wants and needs. She was not pointing to body parts. However, she walked and ran well, used utensils, and was loving and appropriately affectionate. Id. A.H.M. received the allegedly causal DTaP, Hib, OPV, and MMR vaccinations at this visit. Pet. Ex. 5, p. 1.
In medical histories provided almost ten years later, Ms. Miller claimed that A.H.M. suffered a sudden reaction to her September 15, 1999 vaccinations. She described this immediate reaction (occurring within eight hours of the vaccination (see Pet. Ex. 18, p. 8) as including a fever of 105° (see Pet. Ex. 20, p. 2). However, there is no evidence to support these claims in the contemporaneously-created medical records or in other histories provided during the almost ten year period following the vaccinations.
A.H.M. did not return to her pediatrician after the September 15, 1999 vaccinations until October 5, 1999, when she was seen for a croupy cough and a runny nose. The cough was described as the same one she had during the prior month. Pet. Ex. 4, p. 5. Her temperature was normal, and she was playful, active, and in no apparent distress. Id. At a visit on October 21, she was experiencing a low grade fever, not sleeping, and "still coughing all the time." Id. She had a slight fever (her temperature was 100° at the visit), and she was again described as playful and active. Her pediatrician assessed her cough as having an allergic component and increased her Zyrtec dosage. Id. By her next visit on October 29, she was "[d]oing alot (sic) better" but still had a loose cough during the day. Id., p. 4. Her illness (described as allergic rhinitis) was "much improved." Id. No concerns about any reactions to the September vaccinations were recorded at any of these visits. See id., pp. 4-5.
During her testimony, Dr. Cave pointed to these three visits in October 1999 as proof that A.H.M.'s health went "downhill" after her September 15, 1999 vaccinations. Tr. at 30.
At A.H.M.'s 18 month well-child visit on November 12, 1999, the "History of Present Illness" section (abbreviated on the form as "HPI") reflected that her parents were still concerned about her speech. A headnote on the form before the HPI section reflected "Speech + Hearing Evaluation — Not talking yet" as the reason for the visit.
A.H.M. received her First Steps evaluation in her home on December 10, 1999. Pet. Ex. 19, p. 1. Her mother was present and provided the case history. Her father later provided some additional information via telephone. According to the report, her parents' view of the problem was a "possible speech delay." Id. Ms. Miller reported that A.H.M. had achieved motor milestones at the appropriate ages. Id., pp. 1-2. The parents' reports of her language differed slightly from the contemporaneous records; petitioners reported that the use of "dada" had begun at 12 months of age, while the contemporaneous record of her one year well-child visit reflected that she was using both "mama" and "dada" with specificity (Pet. Ex. 4, p. 8) and an even earlier record reflected that she said both words at nine months of age (id.). Her vocabulary at the time of the evaluation was reported as three to four words. Pet. Ex. 19, p. 2.
The Battelle Developmental Inventory was administered during the home visit that day. This test assesses personal-social, adaptive, motor, communication, and cognitive skills. A.H.M. scored more than two standard deviations below the norm in every area of development assessed. Pet. Ex. 19, p. 2 (chart). A.H.M., then 18 months old, was, on average, functioning at the level of a nine month old infant. Her lowest score was in communication, where she was observed to function at an age-equivalent of six months. Her strongest performance was in motor skills, with an age-equivalent score of 13 months. Id. She qualified for participation in the First Steps early intervention program. Id., pp. 5-6. Additional testing and evaluation were recommended. Id., p. 6.
Specific observations during the evaluation included a failure to respond to familiar names, such as "Where's mama?"; inconsistent response to her own name; engaging in parallel play without initiating contact with her brother; a focus on television or videos; failing to attempt to stack blocks or place rings on a post; a lack of response to simple verbal commands; humming instead of babbling or using jargon; a lack of gestures (other than lifting her arms to be held); a lack of pointing to desired objects; repetitive play; and failing to reach around a barrier to obtain a toy. Pet. Ex. 19, pp. 2-5.
After the First Steps evaluation, Ms. Miller met with A.H.M.'s pediatrician the same day. She reported that a possible diagnosis of "PDD" was mentioned, and that additional testing would be performed. Pet. Ex. 4, p. 3.
In two undated videos filmed about the same time as the First Steps evaluation (Christmastime 1999), A.H.M. was playing with toys. Titles 17-18. These were the last of the videos that Dr. Wiznitzer discussed at the hearing. See Tr. at 136. He described A.H.M. as awake and alert and noted that she played with and manipulated objects in her environment. However, he commented that she ignored the people around her and their attempts to get her attention. Tr. at 135-36. He characterized A.H.M.'s behavior as demonstrating "selective awareness." Tr. at 136.
An in-home speech and language evaluation took place approximately a month later on January 20, 2000. Pet. Ex. 19, p. 7. A.H.M. followed simple directions when they were accompanied by gestures but, without the gestures, she could not do so. She did not understand verbs in context. Id., p. 8. A.H.M. communicated nonverbally by pushing, pulling, and pointing. Id. She used jargon and said "no" during the evaluation. Based on her parents' assertion that she could use the words "mama," "daddy," and "why," they were also included in scoring the extent of her vocabulary. Id., pp. 7-8. A.H.M. scored higher on the Preschool Language Scale testing administered at this evaluation than she had on the First Steps testing. At 20 months of age, A.H.M.'s auditory comprehension was at a 12 month level, her expressive communication was scored at a 15 month level, and her total language skills were assessed at the 14 month level. Id. She was assessed as having mild delay in both receptive and expressive language. Speech therapy was recommended. Id., p. 9.
The language evaluation was followed about a week later by a developmental intervention assessment. Pet. Ex. 19, pp. 10-14. Her fine and gross motor skills appeared to be at age level. Per parental report, A.H.M. could perform cognitive tasks such as identifying some body parts and the neighbor's dog, but she was unable to identify objects in a book. Id., p. 11. A.H.M. showed good eye contact but little interaction with the evaluator. Id., p. 12. She "jabbered a lot," repeating the same vocal patterns over and over, but said few understandable words. Id., pp. 12-13. Ms. Miller's main concerns were centered on A.H.M.'s language development; she reported that A.H.M. did not use many words or communicate her wants and needs very effectively. Id., p. 13. With regard to sensory processing problems, the evaluator reported no "red flags" but added that she "did notice [A.H.M.] wave her fingers, some paper, and a few other things in front of her face." Id., p. 13. A.H.M. "usually had something in each hand and she frequently rubbed her thumbs on the object." Id., p. 12. Developmental intervention was recommended "based on parental concerns, her language delay, and her lack of interaction" with the examiner. Focus on functional play skills was recommended. Id.
On February 2, 2000, A.H.M. was evaluated by an interdisciplinary team at the University of Louisville's Child Evaluation Center ["CEC"].
During the evaluation at the CEC, A.H.M. was hard to engage, and showed reduced eye contact and scant shared enjoyment. Pet. Ex. 6, p. 2. She used jargon, but no identifiable words.
Laboratory testing, including genetic testing, metabolic disease screening tests (including tests for storage disorders and urine organic and amino acid screening), and blood testing for lead and thyroid function, was performed as part of the CEC evaluation. Pet. Ex. 6, pp. 15-35. The only abnormality detected on testing was a mild elevation of glycine.
During the February 2, 2000 CEC evaluation, A.H.M. had nasal congestion and fluid in her left ear. Pet. Ex. 6, p. 2. She visited her pediatrician the next day for treatment and was diagnosed with an ear infection. Pet. Ex. 4, p. 3. At this visit, A.H.M. was reported to have 12-15 persistent words, to repeat words, and to have "lots of jargoning." Id. The report of 12-15 persistent words was likely an overestimate, as no identifiable words were heard at the CEC evaluation the prior day and the assessment of her language expression at the CEC reflected that she was not saying fifteen meaningful words, used gestures rather than talking, did not imitate words overheard in conversation, could not ask simple questions, and could not name five to seven familiar objects on request. Pet. Ex. 6, p. 5.
She visited her pediatrician in March and again in April for vomiting and diarrhea. Pet. Ex. 6, p. 2. Fevers of 99.9° and 100° were recorded in conjunction with her ear infection in February and gastrointestinal illness in March respectively, but no fever was recorded in April. At the March visit, her pediatrician discussed the milk and wheat free diet "prescribed by [the] CEC," commonly referred to as a gluten-free, casein-free ["GF/CF"] diet.
The next videos appear to have been filmed after these evaluations, as they show A.H.M. interacting with a therapist. See Titles 19-20. A.H.M. pointed to the card requested by the therapist and mimicked the therapist's actions in making a toy squeak. Title 19. In the second video, the therapist called A.H.M.'s name several times and rolled a ball to get her attention. A.H.M. babbled expressively but uttered no discernable words. Title 20.
On May 23, 2000, A.H.M. saw Dr. Holmes in Baton Rouge, LA, for the first time. In the notes from the office visit, Dr. Holmes observed that A.H.M.'s eye contact was "not good," her interaction was "poor," and her behavior was "zoned out." Pet. Ex. 8, p. 8. In the HPI section of the form, Dr. Holmes wrote "no talking," but also indicated that A.H.M. had "some expressive language, decent receptive." Id. Her parents also reported that she had "chronic diarrhea" but when they removed fruit juice from her diet, it stopped. Doctor Holmes' impression was that A.H.M. had "probable ASD" and "irritable bowel." She wanted to rule out "neurotoxicity." Id. She instructed A.H.M.'s parents to continue the GF/CF diet and administer Epsom salt baths. Id., p. 7. She also ordered a number of tests and diagnosed A.H.M. with neurotoxicity, nutritional deficiency, mineral deficiency, and irritable bowel. Id.
A.H.M.'s parents signed a consent form that acknowledged that some of the treatments and tests offered by Dr. Holmes were not used by the majority of doctors in the community and were not considered part of the standard of care. Pet. Ex. 8, pp. 22-23. The tests ordered by Dr. Holmes included "urine organix profile," plasma amino acids, hair analysis for "toxic" and "essential" metals, and stool analysis. Id., pp. 16, 18, 20-21. After receiving A.H.M.'s test results, Dr. Holmes determined there was "presumptive evidence of heavy metal toxicity" due in part to what she characterized as increased amounts of heavy metals in A.H.M.'s hair. Id., p. 10. However, the level of mercury in A.H.M.'s hair (.21 mcg/g) was within the laboratory's reference range (id., pp. 20). In spite of this normal level, Dr. Holmes informed petitioners about "Autism + Mercury" and recommended they begin "mercury chelation."
A.H.M. also was treated and monitored by Dr. Jeffrey Wampler
Initially, Dr. Wampler was hesitant to begin chelation. In email to Dr. Holmes, Ms. Miller indicated Dr. Wampler would "not be doing anything" until testing confirmed A.H.M. was "lead or mercury toxic," at which time "chelation may be attempted." Pet. Ex. 14, p. 101. After a July 7, 2000 call with Dr. Holmes, Dr. Wampler agreed that A.H.M. could begin chelation. Id., p. 99.
The urinary metals testing was performed by Doctor's Data laboratory, a testing facility that performed similar tests on the children in the OAP test cases. King, 2010 WL 892296, at *80, 82. As I noted in Dwyer, 2010 WL 892250, at *182 n.687, concerns about this laboratory's testing methods have been raised, particularly with regard to comparisons of metal levels found during chelation to reference ranges established in non-chelated individuals. The results reported for A.H.M. in Dr. Wampler's and Dr. Holmes' records were difficult to interpret. No baseline testing for urinary mercury (or other metals) was performed.
Without a baseline, it is difficult to assess the significance of the first "post provocation" (after chelation) test result, which showed a level of 11.8 micrograms (expressed as "03bcg/g creatinine" on the test report) per grams of creatinine on July 26, 2000.
Other testing in the summer of 2000 found normal immunoglobulin levels and one slightly high test involving liver function, but the results were otherwise not remarkable. Pet. Ex. 2a, pp. 25-26, 30-33. The only test of significance for the issues in this case was a serum lactic acid test performed on July 31, 2000. Although it was ordered by Dr. Wampler (id., p 143), Dr. Holmes requested it because she wanted to rule out a possible mitochondrial disorder, based on a high urine lactate level on an earlier test (see Pet. Ex. 8, p. 10). A high blood or cerebral spinal fluid ["CSF"] lactate level may indicate a mitochondrial disorder, but may also be elevated due to a struggling child or the use of a tourniquet to obtain the sample. A.H.M.'s lactate level was low. Pet. Ex. 2a, p. 146; see also Wolf & Smeitink, Court Ex. I, at 1404 (high serum lactate is a metabolic abnormality that may be indicative of mitochondrial disease).
In email messages to Dr. Holmes, Ms. Miller reported improvements but also complained of "excessive `stimmy'" behavior in August 2000 (Pet. Ex. 8, p. 70) and some regression in behavior, to include an increase in temper tantrums in May 2001 (id., p. 38). In April 2001, Ms. Miller asked Dr. Holmes about a treatment she had found on the internet, FGF2 therapy.
A.H.M. visited Dr. Aguilar during the summer of 2001. See Pet. Ex. 8, p. 31. From the email correspondence between Dr. Holmes and Ms. Miller, it appears Dr. Aguilar commented that A.H.M.'s brain was "not the brain of an autistic child." Pet. Ex. 8, p. 32. He agreed that the cause of A.H.M.'s condition could have been mercury, but also considered the possibility of a lack of oxygen during birth. Id. In her email response, Dr. Holmes wondered "what the EEG[
After the summer 2001 visit to Dr. Aguilar, Ms. Miller emailed Dr. Holmes indicating she was overnighting a report from Dr. Aguilar and forwarding a letter she wrote to DrAmysKids,
The records reflect that Dr. Holmes and Ms. Miller sought assistance from several airlines in October and November 2001 for second trip to see Dr. Aguilar but there is no evidence A.H.M. saw him again. Pet. Ex. 8, pp. 110-13.
A.H.M. saw Dr. Holmes only twice, first on May 23, 2000, and again in November 6, 2001, when A.H.M. returned to Baton Rouge to receive a secretin injection.
The last two videos were not dated. Based on A.H.M.'s appearance and the piles of leaves, they could have been recorded in the fall of 2000 or 2001. See Titles 21-22. In the first video (Title 21), A.H.M. was sitting in the leaves, feeling their texture. In the last video (Title 22), she was running around and playing apart from the other children and adults. She occasionally looked up as the other children and adults made noise, and glanced at an older woman who called her name, but she ignored a Frisbee that the woman threw to her. Id.
A.H.M.'s later treatment records are quite sparse. She apparently became a patient of Dr. Jeff Bradstreet in 2003, upon referral from Dr. Holmes, who had retired.
For routine care, A.H.M. was seen at Sharonville Pediatrics from late 2002 through early 2005. A well-child visit in late 2002 and several visits for illnesses (bronchitis, sinusitis, an ear infection, pharyngitis, and URI) throughout 2004 and 2005 are reflected in these records. Pet. Ex. 15, pp. 1-5.
A.H.M. saw a new pediatrician, Dr. Jonathan Mumma, on May 14, 2009 for a checkup prior to moving to Florida in June 2009. See Pet. Ex. 18. That fall, A.H.M. was referred for an autism spectrum evaluation by her new middle school in Florida. See Pet. Ex. 20. The report from the evaluation listed A.H.M.'s diagnoses as "Asperger's Syndrome" and attention deficit hyperactivity disorder. The background section indicated that A.H.M. was receiving special education services from her school in Ohio. Id., p. 1. This record is incomplete, stopping mid-sentence and the conclusions reached by the evaluators are unknown. Id., p. 6. A.H.M. was reported to exhibit several symptoms typical of autism, such as self-stimulating behavior, difficulty with a change in routine, and sensitivity to sound. Id., p. 5.
These two more recent records contain the first mention of a sudden reaction to A.H.M.'s September 15, 1999 vaccinations. When providing a medical history to Dr. Mumma, Ms. Miller claimed that A.H.M. received her 15 and 17 month vaccinations at one time and suffered a reaction eight hours later. Pet. Ex. 18, p. 8. During A.H.M.'s ASD evaluation for the new school district in Florida, Ms. Miller claimed the reaction was immediate and included a fever of 105°. She stated that A.H.M. "began saying single words with communicative intent at 14 months of age and then at 17 months [A.H.M.] stopped talking all together and did not speak again until about the age of 3." Pet. Ex. 20, p. 2.
Both physicians testified about A.H.M.'s symptoms and the conclusions they drew from the medical records and other evidence.
Doctor Cave claimed that A.H.M. exhibited symptoms of encephalopathy following her June 4, 1999, vaccination and that these symptoms became more severe after her September 15, 1999 vaccinations. Tr. at 26-27; see also Pet. Post-Hearing Memo at 2. Claiming that the "worst injury" was caused by A.H.M.'s September 15, 1999 vaccinations (Tr. at 33), Dr. Cave testified that A.H.M. regressed after the June 4, 1999 varicella vaccination, had more illnesses after the September 15, 1999 vaccinations, and was no longer talking by November 1999 (Tr. at 27).
She described A.H.M. as having words and a lot of playful behavior before the June vaccination, and then compared A.H.M.'s condition before that vaccination to her appearance at the initial visit with Dr. Holmes, which occurred almost a year later. Tr. at 29. Doctor Cave mentioned the specific symptoms of poor eye contact, "zoned out" behavior, chronic diarrhea, and lack of speech noted by Dr. Holmes as evidence of encephalopathy and regression. Tr. at 25, 29-30. She also relied upon Ms. Miller's claim of a sudden reaction to the September 15, 1999 vaccinations as evidence that A.H.M. experienced a vaccine-related encephalopathy. See Tr. at 88-89.
Doctor Cave was not precise in her use of the terms "regression" and "encephalopathy." At times, she appeared to be using the term "encephalopathy" in the context of the severe, acute encephalopathy described in the Vaccine Injury Table. See, e.g., Tr. at 25; see 42 C.F.R. 100.3(b)(2) (definition of a Table encephalopathy found in the Qualifications and Aids to Interpretation ["QAI"]). At other times, she and Mr. Cave used the term more generally, but she never really defined it. Tr. at 32-33, 63, 76.
Doctor Wiznitzer opined that A.H.M. did not suffer an encephalopathic reaction or a developmental regression in response to her vaccinations. Tr. at 120-22; Res. Ex. A at 7. Distinguishing between regression and stagnation,
When testifying about the absence of an encephalopathic condition in A.H.M., Dr. Wiznitzer clarified that he was referring to an "acute encephalopathy" rather than the more general use of the term. "Encephalopathy" simply means "there's something wrong with the brain." Tr. at 138. Doctor Wiznitzer explained that although both "autism" and "encephalopathy" are terms reflecting a problem with the brain, they are not interchangeable. Tr. at 230-31. According to Dr. Wiznitzer, there is no diagnostic entity of "encephalopathy with autistic features." Autism is a separate diagnostic entity with specific diagnostic criteria, and all the required criteria must exist before the diagnosis can be assigned. Tr. at 231. Doctor Cave made the point that the majority of the children with autism would be considered to have some degree of encephalopathy (Tr. at 270), but this would be in the broad, general use of the term, rather than in the sense of the child having an acute encephalopathy. And, according to Dr. Wiznitzer, the correct diagnosis for children who meet the ASD diagnostic criteria would, nevertheless, be autism, not encephalopathy. Tr. at 230-31.
He described three main developmental patterns seen in children with ASD. Tr. at 127-29. He opined that A.H.M.'s pattern of development fit nicely in the most common group. These children appear to be developing normally until approximately six to twelve months of age when they start showing "deviations" from the normal social, language, and play behaviors. Tr. at 128-29. He described this phenomenon as a failure "to turn on certain centers in the brain," much like the failure to flip a switch at the appropriate time. The resulting difference becomes more apparent over time, and in part of this group of children, development stagnates. Tr. at 129-30. Although some children with ASD regress or lose skills that they once demonstrated, he opined that A.H.M. showed no evidence of regression. Tr. at 136-37.
Doctor Wiznitzer also observed that there was no sign A.H.M. suffered the impairment of consciousness alleged by petitioners and Dr. Cave. Tr. at 138-39. Rather, he maintained A.H.M.'s lack of eye contact and response to others was selective behavior indicative of autism and not evidence of impairment in consciousness or a lack of responsiveness to her environment. Tr. at 139. Summarizing the video evidence submitted, he testified that the videos showed a change in A.H.M.'s social behavior and language beginning in the summer of 1999, but not the regression or loss of skills or the impairment of consciousness that Dr. Cave asserted had occurred. Tr. at 137.
In summary, after reviewing the entire record and weighing the experts' testimony, I conclude that the symptoms and behaviors that Dr. Cave relied upon for her conclusion that A.H.M. regressed did not occur as she described them. Although A.H.M.'s impairments, including loss of some eye contact, stagnation in language and social development, and lack of response to her name, could be termed an encephalopathy in the broad use of the term, A.H.M. never experienced an acute encephalopathy, much less one that meets the strict Table definition.
With regard to the mitochondrial disorder diagnosis made by Dr. Cave based on medical records alone, I summarize the relevant testimony and report and the conflicting testimony of Dr. Wiznitzer. I discuss the diagnostic criteria Dr. Cave used, and make factual findings regarding whether A.H.M. had the symptoms relied upon by Dr. Cave, either at all or to the degree required by the diagnostic criteria. I ultimately conclude that there is insufficient evidence that A.H.M. actually has either a mitochondrial disorder or mitochondrial dysfunction.
Conflicts between the events described in contemporaneous records and those described in documents prepared or testimony given several years later are common in Vaccine Act cases. Two general legal principles guide the resolution of conflicts between contemporaneous records and later-adduced evidence. The first is that the absence of a reference to specific symptoms in a medical record does not conclusively establish the absence of symptoms during that time frame. See, e.g., Murphy v. Sec'y, HHS, 23 Cl. Ct. 726, 733 (1991), aff'd, 968 F.2d 1226 (Fed. Cir. 1992) ("[T]he absence of a reference to a condition or circumstance is much less significant than a reference which negates the existence of the condition or circumstance" (citation omitted)).
The second principle addresses the degree of reliance commonly accorded to contemporaneous records. Special masters frequently accord more weight to contemporaneously-recorded medical symptoms than those recounted in later medical histories, affidavits, or trial testimony. "It has generally been held that oral testimony which is in conflict with contemporaneous documents is entitled to little evidentiary weight." Murphy, 23 Cl. Ct. at 733 (citation omitted); see also Cucuras v. Sec'y, HHS, 993 F.2d 1525, 1528 (Fed. Cir. 1993) (medical records are generally trustworthy evidence). Memories are generally better the closer in time to the occurrence reported and when the motivation for accurate explication of symptoms is more immediate. Reusser v. Sec'y, HHS, 28 Fed. Cl. 516, 523 (1993). Inconsistencies between testimony and contemporaneous records may be overcome by "clear, cogent, and consistent testimony" explaining the discrepancies. Stevens v. Sec'y, HHS, No. 90-221V, 1990 WL 608693, at *3 (Fed. Cl. Spec. Mstr. Dec. 21, 1990).
I find that A.H.M. did not have a sudden or dramatic reaction to either the June 1999 varicella vaccination or the September 1999 combination of vaccinations. She did not have a fever caused by these vaccinations.
Doctor Cave testified that petitioners had an unrecorded meeting with A.H.M.'s pediatrician shortly after the September 1999 vaccinations. She relayed that petitioners were told by the pediatrician that the reaction was not vaccine-related. See Tr. at 88. However, Dr. Cave offered no explanation for the lack of documentation for this meeting or for petitioners' failure to mention it to any other physician (including Dr. Holmes). She "thought" that the report of this meeting was in the CEC records (Tr. at 89), but the CEC records (Pet. Ex. 6) do not reflect any mention of the September 1999 vaccinations, much less a reaction to them. A.H.M. had multiple pediatric visits for illness in the two months after the September 1999 vaccinations, but none of the records from these visits attribute the illnesses, which were apparently allergic in nature, to the September vaccinations.
Ms. Miller's later reports of A.H.M.'s vaccinations and reactions thereto contain numerous assertions that are contradicted by, or inexplicably missing from, the contemporaneous medical records, including the extent of A.H.M.'s vocabulary, the abrupt loss of all language, and the presence of a high fever. While I do not question Ms. Miller's veracity, her recollection of events occurring many years earlier is clearly flawed. Thus, Dr. Cave's reliance on these reports, made about 10 years after the events in question, is misplaced.
One of A.H.M.'s treating physicians, Dr. Wampler, specifically questioned Ms. Miller about any reaction to the September 1999 MMR vaccination. He reported that "[A.H.M.'s] mother said that there was really no high fever or other systemic reactions at the time the MMR vaccine was taken" but only a regression in speech shortly after vaccination. Pet. Ex. 14, p. 6. The fact that this report by a treating physician, who thought the MMR vaccine could cause autism, was made in a letter to petitioners' former attorney of record (see Pet. Ex. 14, pp. 4-8), is particularly telling, as Dr. Wampler was clearly looking for evidence of a vaccine reaction or regression to explain A.H.M.'s ASD.
I find that A.H.M.'s health in the two months after the September 15, 1999 vaccinations was not significantly different from her health in the months prior to those vaccinations.
Doctor Cave pointed to the three "sick visits" in October 1999, as evidence that A.H.M. had "many sick visits," that her health "generally went downhill," and that she was chronically ill with respiratory and other problems after receiving the September 15, 1999 vaccinations. Tr. at 27, 30. She testified that this demonstrated an "insult to the immune system at the very least." Tr. at 30. Precisely what point Dr. Cave was making with regard to A.H.M.'s encephalopathy, regression, or any mitochondrial disorder by these claims of increased illnesses was never articulated.
The evidence does not support Dr. Cave's assertions about increased ill health after the September vaccinations. A.H.M. had been suffering from coughs, colds, and low grade fevers throughout the summer and fall. See Pet. Ex. 4, pp. 5-7. Her pediatrician attributed these illnesses to an ear infection, URI, and allergies. See id. After her Zyrtec dosage was increased on October 21, 1999, she returned to the doctor only once more (on October 29) and was described as "much improved." Id., p. 5. A.H.M. did not visit her pediatrician for illness again until February 2, 2000 when she was diagnosed with another ear infection. Pet. Ex. 4, p. 3.
With regard to A.H.M.'s receptive and expressive language skills, I make the following factual findings:
a. A.H.M. was saying "mama & dada" at nine months of age. She was using these words in reference to her parents at twelve months of age.
b. She gained words over the summer after receiving the varicella vaccination in June 1999. She had four to five words at the time of her September 15, 1999 vaccinations. In November 1999, she had the same number of words.
c. As early as September 1999, petitioners were concerned about A.H.M.'s speech.
d. There is no reliable evidence of a regression in speech, defined as a loss of words previously used, in the five months after her September 15, 1999 vaccinations.
e. Although some records contain notations such as "not talking yet," the same records, taken as a whole, reflect some speech, just not the level of speech expected in a child of A.H.M.'s age at the time the record was created.
f. As reflected by her pediatric records, A.H.M. had a mild developmental and speech delay in both September and November 1999.
g. During the period from November 1999 through January 2000, A.H.M. had a vocabulary of three to five words at any given time, including "mama," "dada," "why," "no," and "Dusty."
h. It is unlikely that A.H.M. had 12-15 words in February 2000.
Doctor Cave's testimony about A.H.M.'s language demonstrated a lack of familiarity with and a selective reading of the information contained in A.H.M.'s records. She initially testified that A.H.M. had acquired 12 to 15 words prior to the alleged causal vaccinations and thereafter stopped talking. She pointed to the medical records from November 1999
Doctor Cave ignored other entries in the two records she referenced which indicated the description of "not talking" did not equate to lost speech or no words. Doctor Cave claimed an entry in the November 12, 1999 records that A.H.M. was "[n]ot talking yet" (Pet. Ex. 4, p. 4) was proof that A.H.M. had lost speech since the September 1999 vaccinations. This assertion not only ignores the qualifier "yet," which, read literally, would indicate that she had not been talking previously. It also ignores the remainder of the office visit notes, which reflect that the concern about A.H.M.'s speech was ongoing and that she was "not making progress." Id.
Doctor Cave also pointed to Dr. Holmes' intake interview from May 2000 (Pet. Ex. 8, p. 8) as proof that A.H.M. had lost words after the September 1999 vaccinations. Tr. at 96. Even assuming her assertions to be correct, this note, written in May 2000, can hardly be said to follow closely the allegedly-causal September 1999 vaccinations. Doctor Cave's assertions were not correct. Although the note indicated that, by history, A.H.M. had "no talking," this entry was immediately followed by "some expressive language." Pet. Ex. 8, p. 8. Read together, these entries are consistent with the reports from the fall of 1999, both to the pediatrician and to the Early Steps evaluators. A.H.M. had some vocabulary, but was not talking the way her parents expected. Doctor Holmes' entries are likewise consistent with the CEC reports. February 2, 2000, one day before the visit to the pediatrician where this report was made, A.H.M. had a speech and language evaluation which reflected the use of only a few words. See Pet. Ex. 6, p. 5.
Nowhere in the contemporaneous records is there a report that A.H.M. stopped talking or lost words. As Doctor Wiznitzer testified (Tr. at 121-22, 124), none of A.H.M.'s treating physicians noted a regression in speech or any other skills.
The video evidence reflects that A.H.M. did not often talk or use discernable words, but the videos recorded both before and after the allegedly causal vaccinations are remarkably similar regarding the extent of A.H.M.'s expressive communication. See Tr. at 137 (Dr. Wiznitzer's testimony).
With regard to other symptoms and their onset, I make the following factual findings:
a. There is no evidence of any other type of developmental regression after the September 1999 vaccinations. Although A.H.M. began displaying more behaviors consistent with ASD, symptoms of ASD had begun to manifest in the summer of 1999. The additional ASD-type behaviors, including changed play and eye contact, did not include the loss of skills previously displayed.
b. Doctor Cave's assertions about a developmental regression were based on a selective reading of the medical records. Her contention that A.H.M. "went from words to no words, from eye contact to no eye contact, from playful behavior to zoned out behavior" (Tr. at 90; see also Tr. at 69-70) were hyperbole. What happened to A.H.M. was not a loss of skills; it was the progression of atypical behavior patterns commonly seen in ASD. No treating physician, not even Dr. Holmes, diagnosed a regression of skills.
c. A.H.M. exhibited symptoms of social deficits common in children with ASD, such as poor eye contact, failure to respond to her name, ignoring others, and a fascination with specific objects, as early as July 1999. Even in the five months after the September 1999 vaccinations, eye contact was not non-existent; it was selective and less extensive than the eye contact seen in a typically developing child.
d. A.H.M. was not unresponsive to her environment; she was selectively responsive. She paid more attention to objects than people. However, she was capable of interaction and remained affectionate with her parents.
e. No treating physician who evaluated A.H.M. in the winter and spring of 1999-2000 diagnosed her as encephalopathic. Although her poor eye contact and lack of social interaction with people could be characterized, in the broad use of the term, as an encephalopathy, A.H.M. never experienced an acute encephalopathy as defined by the Vaccine Injury Table.
f. These behavioral symptoms manifested over the summer of 1999, at a time period when it is expected that deficits in social behaviors (behavioral symptoms) typically become apparent. See Johnson, Res. Ex. A, Tab, 1 at 8-9. As Dr. Wiznitzer testified, the deviations in development generally begin around twelve months of age. Tr. at 129-30, 136-37.
No treating physician or specialist ever diagnosed A.H.M. with a mitochondrial disorder, mitochondrial disease, or mitochondrial dysfunction. Prior to Dr. Cave's initial expert report, the only mention of a mitochondrial disorder anywhere in the evidence filed was a comment by Dr. Holmes that an elevated urinary lactate might be indicative of a mitochondrial disorder, and a suggestion that a serum lactate level be obtained. See Pet. Ex. 8, p. 10. She repeated both this comment and the suggestion that a serum lactate level be obtained in a June 19, 2000 letter to Dr. Wampler. Id., p. 24 Serum lactate testing performed in July 2000 in response to this suggestion was essentially normal. Pet Ex. 14, p. 121 (reporting lactic acid as low in a blood sample drawn on July 31, 2000). Nevertheless, ostensibly applying the Morava criteria discussed below, Dr. Cave diagnosed A.H.M. with a mitochondrial disorder. Tr. at 44; see also Pet. Ex. 11-a at 7-8 (citing the scoring checklist found at Pet. Ex. 11-a, Tab 11); Pet. Ex. 35 at 1-2.
The Morava criteria were formulated as a simplified "bedside version" of the Nijmegen mitochondrial disease criteria used in diagnosing children.
The Morava diagnostic criteria are divided into three sections, with scoring limitations for each section, as well as in the subsections that form Section I, the clinical criteria. Section II covers metabolic and imaging studies, and Section III, the findings on muscle biopsy (morphology). No more than 4 points may be awarded in each section. As A.H.M. did not have a muscle biopsy, only Sections I and II of the Morava criteria are discussed.
Section I covers the three basic clinical presentations in mitochondrial disorders: muscular (Section I.A); central nervous system ["CNS"] (Section I.B); and multisystem disease (Section I.C). The total point score allowed in Section I is a maximum of 4 points, with no more than 2 points each allowed in Sections I.A and I.B, and a maximum of 3 points in Section I.C. The maximum score from Section II is 4 points, with each test or syndrome-like presentation limited to 1 or 2 points. See Morava, Pet. Ex. 26, Table, at 1824 [hereinafter "Morava Table"]. A score of 8-12 points results in a diagnosis of a definite mitochondrial disorder, 5-7 points a probable mitochondrial disorder, 2-4 points a possible mitochondrial disorder, and 1 point identifies someone unlikely to have a mitochondrial disorder. Id.
The Morava Table simply lists symptoms, such as "exercise intolerance," "seizures," or "GI tract" (in Section I) and lists tests such as "elevated lactate" or "ethylmalonic aciduria" (in Section II) without any explanation of the parameters of the criteria. However, the references in the Morava article to the MDC (Nijmegen) criteria, with reference 5 citing to the Wolf & Smeitink article (Court Ex. I), reflect an adoption of the parameters found in that article and the www.neurology.org website's supplemental materials, a portion of which were filed as Pet. Ex. 25. During the hearing, Dr. Wiznitzer testified that the more detailed Wolf (Nijmegen) criteria were the source of the Morava criteria. Tr. at 148-49; see Res. Ex. D, Tab 1.
Doctor Cave's lack of understanding of the Morava criteria is best illustrated by her initial expert report and score sheet. Using the list of symptoms and tests appearing on the Morava Table, she scored A.H.M. as having 8 points, to arrive at a "definite" mitochondrial disorder diagnosis.
At the hearing, Dr. Cave testified that she awarded 5 points in Section I, again exceeding the maximum points allowed in that section. In Section II, she awarded 2 points (this time reflecting the correct amount) for an elevated lactate level and 1 point for an elevated ethylmalonic acid level. Tr. at 39. She did not award any points for the elevated lactate/pyruvate ratio that she had scored in her expert report. For the first time, she awarded 2 points for elevated urinary tricarboxylic acid ["TCA"]
Her difficulty in following the scoring criteria was not limited to math errors or remaining within the score system parameters. Each time she opined on the application of the Morava Table to A.H.M., she arrived at a different total or used different symptoms.
What Dr. Cave determined to be symptoms matching the lists appearing in Section I of the Morava Table reflected a fundamental misunderstanding of the nature of the symptoms involved in mitochondrial disorders and how such disorders are diagnosed. She also ignored or misunderstood the requirements for awarding points for metabolic and imaging studies in Section II.
In her expert report and at the hearing, Dr. Cave awarded points for exercise intolerance, muscle weakness, developmental delay, regression (loss of skills), and gastrointestinal disease as clinical symptoms scored in Section I of the Morava Table. Pet. Ex. 11-a, Tab 11; Tr. at 35-44 (cites from transcript). After the hearing, Dr. Cave apparently eliminated the points she awarded for regression,
In her post-hearing report, Dr. Cave reduced the score on Section II to 3 points, 1 point for elevated ethylmalonic acid and 2 points for elevated tricarboxylic acid. Id.; Pet. Ex. 35 at 1. She eliminated the points she had awarded previously for elevated lactate (or lactic acid)
Doctor Cave's post-hearing rescoring, necessitated by evidence demonstrating that A.H.M. did not have the symptoms or test results required by the Morava diagnostic criteria, reduced A.H.M.'s point total to 5, a "probable" mitochondrial disorder under the Morava scoring system. However, respondent's expert, Dr. Wiznitzer, had previously challenged the factual basis for, or Dr. Cave's interpretation of, most of the remaining symptoms or test results for these 5 points. I resolve the factual issues largely in favor of Dr. Wiznitzer's testimony, although I note that Dr. Wiznitzer's scoring was not without some of the same problems that Dr. Cave demonstrated.
Doctor Wiznitzer testified that A.H.M. did not suffer from a mitochondrial disorder. Tr. at 140. Often referencing the more detailed explanation for these categories provided by the Wolf (Nijmegen) criteria, he challenged every point awarded by Dr. Cave except the 1 point for developmental delay (Tr. at 155-56). His scoring would place A.H.M. in the category of an unlikely mitochondrial disorder (Pet. Ex. 11-a, Tab 11 at 2).
Although Dr. Cave lowered A.H.M.'s point total to 5 after the hearing, she maintained this score was sufficient to support her opinion on causation as it placed A.H.M. in the range of probable mitochondrial disorder. Pet. Ex. 35.
I find that proper scoring of the Morava criteria in this case results in a diagnosis of, at best, a possible mitochondrial disorder, and the more reliable score would place her in the "unlikely" category. A.H.M.'s developmental delay was the only symptom that met the clinical Morava/Nijmegen criteria, accounting for 1 point.
I find that A.H.M. did not have muscle weakness meeting the requirements under the Morava criteria. Except in the case of a young infant, this criterion requires reduced muscle power.
Post-hearing, Dr. Cave continued to maintain that A.H.M. displayed muscle weakness (Pet. Ex. 35 at 1), based on a reference to hypotonia in A.H.M.'s pediatric records (Pet. Ex. 6, p. 9). As Dr. Wiznitzer explained, low muscle tone (hypotonia) is not the same as muscle weakness. Tr. at 155, 180. She acknowledged that she had reviewed the Nijmegen (Wolf) article filed as Court Ex. I (Tr. at 36), but had apparently never looked at the supplemental materials referenced in the article. Those materials were filed post-hearing by respondent. Res. Ex. D, Tab 1. These supplemental materials fully supported the testimony of Dr. Wiznitzer that hypotonia alone in a toddler is not sufficient to meet the diagnostic criteria of "muscle weakness."
Differentiating between muscle tone and muscle strength, Dr. Wiznitzer described muscle tone as the idle state of a car engine, which "tells you nothing about how fast the car can run" (Tr. at 153), and muscle strength as the car's horsepower (Tr. at 154). He pointed to the portion of the CEC evaluation indicating A.H.M. had diminished muscle tone but adequate muscle strength. Tr. at 153; see Pet. Ex. 6, p. 2. He added that, according to the Wolf criteria, muscle tone or hypotonia could be used to fulfill the criteria of muscle weakness as claimed by Dr. Cave but only until the child is six months old. Tr. at 154-55; see Res. Ex. D, Tab 1 at 1. He then quoted the examples provided in the Nijmegen criteria for a child less than six months of age, explaining that "head lag on traction" involved a baby whose head lags or falls back when you pull her up from the arms; "poor head control" involved a baby whose head falls in different directions when placed in a seated position; "slip through" involves a baby who, when picked up, falls through the adult's arms; and "frog-like posture" as an infant whose legs fall into a frog-like position when placed supinely. Tr. at 154-55. A.H.M. displayed none of these classic indications of muscle weakness.
Thus, Dr. Wiznitzer concluded that no points should be awarded for muscle weakness. I agree.
In her post-hearing report, Dr. Cave awarded points for elevated levels of TCA (2 points) and ethylmalonic acid (1 point) based on the results of testing ordered by Dr. Holmes in May 2000. Tr. at 41-42.
These elevated levels were detected in urine testing ordered by Dr. Holmes in May 2000 and conducted by MetaMetrix.
Doctor Wiznitzer considered the MetaMetrix test results to be suspect because similar testing by the University of Chicago had produced normal results in February and April 2000, several months earlier and, thus, closer in time to the allegedly causal vaccines. Tr. at 140-42; see Pet. Ex. 16, p. 24 (February 2000 test results); id., p. 35 (April 2000 test results).
Mr. Cave cross-examined Dr. Wiznitzer about his reliance on the University of Chicago testing, noting the results were simply a summary, rather than a report identifying the specific organic acids tested and the results for each, unlike the MetaMetrix results.
MetaMetrix performed urine organic acid testing in November 2000 and March 2001, during the time period when A.H.M. was undergoing chelation. Pet. Exs. 8, pp. 174, 179 (test results), 9, 25; 27, 35 (references to chelation during these time frames); 14, pp. 99, 105, 111, 122 (reference to chelation and laboratory tests from July through late October 2000 reflecting that urine tests were performed "post provocation," a reference to chelation). The November test for ethylmalonate showed a level of 49.4, more than 10 times the reference range and more than seven times the May 2000 result. The TCA testing results were mixed. Several organic acids were within the reference ranges, three remained high, and one was well below the reference range reported. Id., p. 179.
The March 2001 test reported an ethylmalonate level of 5.1, above the reference range, but much closer to the May 2000 results rather than the November 2000 results. The TCA testing results were also mixed in March 2001, but they were very different with regard to specific acids. Pet. Ex. 8, p. 174. The chart below reflects the extremely wide variation in results reported in the three tests performed by MetaMetrix:
A.H.M.'s clinical presentation justifies the award of only 1 point. The point total for the metabolic and imaging studies is a closer call, but without a rational explanation for the highly variable results, I find it difficult to attach much weight to MetaMetrix's findings of high ethylmalonic acid and TCAs. That uncertainty, particularly in view of the University of Chicago laboratory tests reporting essentially normal results,
Even if I thought points should be awarded, A.H.M.'s total under the Morava criteria would increase from only 1 to 4 points for the MetaMetrix test results. This amount still is not sufficient to raise her score to the range for a "probable" mitochondrial disorder, taking her from "unlikely" to "possible."
In her post-hearing report, Dr. Cave reiterated a point she made during her testimony: that mitochondrial dysfunction may exist in individuals who cannot be diagnosed with mitochondrial disease. Pet. Ex. 35 at 1-3. She described this dysfunction as lacking the genetic basis present in mitochondrial disorders, and contended that medical studies demonstrate that those with ASD diagnoses have more mitochondrial dysfunction than typically developing children. Her post-hearing report implied that mitochondrial dysfunction is a milder form of a mitochondrial disorder. See id. at 2. She did not explain how there can be a mild form of a genetic disorder that lacks any genetic basis.
Doctor Cave and petitioners, however, provide no evidence that A.H.M. suffers mitochondrial dysfunction other than a score under the Morava criteria insufficient to establish she suffers from a mitochondrial disorder. No treating doctor ever diagnosed A.H.M. with mitochondrial disorder, disease, or dysfunction. Doctor Holmes was the only treating doctor to mention the possibility of a mitochondrial disorder and, given the serum lactate testing results, dropped the issue.
There is simply no evidence that A.H.M. showed any sign or symptom that her mitochondria were dysfunctional. In her post-hearing report, Dr. Cave did not point to any test results (other than the MetaMetrix urine organic acids results discussed above) that suggested that A.H.M.'s mitochondria had diminished function. In citing to medical journal articles that she claimed demonstrated that children with ASD had markers of mitochondrial dysfunction (Pet. Ex. 35 at 1, referring to an unspecified literature review by Rossignol and Frye
I conclude that there is insufficient evidence in this record to establish that A.H.M. suffered mitochondrial disease, disorder, or dysfunction.
There are two ways to establish entitlement to compensation under the Vaccine Act's no-fault system. First, petitioners may demonstrate that A.H.M. suffered a vaccine-specific injury listed on the Vaccine Injury Table within the requisite time period set forth in the Table (a "Table injury"). To prove a Table injury, petitioners must show that the first symptom or manifestation of the onset...of any such illness, disability, injury, or condition...occurred within the time period after vaccine administration set forth in the Vaccine Injury Table." Shalala v. Whitecotton, 514 U.S. 268, 270 (1995) (quoting 42 U.S.C. §11(c)(1)(C)(i)). In such cases, causation is presumed. See 42 C.F.R. § 100.3.
Second, petitioners may demonstrate by preponderant and reliable evidence that an injury was caused in fact or significantly aggravated by a vaccine listed on the Table ("actual causation" or "causation-in-fact" or "significant aggravation"). See § 11(c)(1)(C); see also Moberly v. Sec'y, HHS, 592 F.3d 1315, 1321 (Fed. Cir. 2010) (causation in fact claims); W.C. v. Sec'y, HHS, 704 F.3d 1352, 1357 (Fed. Cir. 2013); Loving v. Sec'y, HHS, 86 Fed. Cl. 135, 144 (2009); Hennessey v. Sec'y, HHS, No. 01-190V, 2009 WL 1709053 at *40 (Fed. Cl. Spec. Mstr. May 29, 2009), aff'd, 91 Fed. Cl. 126 (2010) (significant aggravation claims).
To prove actual causation, petitioners must demonstrate by preponderant evidence: "(1) a medical theory causally connecting the vaccination and the injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason for the injury; and (3) a showing of a proximate temporal relationship between vaccination and injury." Althen v. Sec'y, HHS, 418 F.3d 1274, 1278 (Fed. Cir. 2005); see also Grant v. Sec'y, HHS, 956 F.2d 1144, 1148 (Fed. Cir. 1992); Hines v. Sec'y, HHS, 940 F.2d 1518, 1525 (Fed. Cir. 1991); de Bazan v. Sec'y, HHS, 539 F.3d 1347, 1351-52 (Fed. Cir. 2008); Caves v. Sec'y, HHS, 100 Fed. Cl. 119, 132 (2011), aff'd per curiam, 463 Fed. Appx. 932, 2012 WL 858402 (Fed. Cir. 2012) (holding that each Althen factor must be established by preponderant evidence). The applicable level of proof is the "traditional tort standard of `preponderant evidence.'" Moberly, 592 F.3d at 1322 (citing de Bazan, 539 F.3d at 1351; Pafford v. Sec'y, HHS, 451 F.3d 1352, 1355 (Fed. Cir. 2006); Capizzano v. Sec'y, HHS, 440 F.3d 1317, 1320 (Fed. Cir. 2006); Althen, 418 F.3d at 1278).
Petitioners' assertions regarding the factual predicate for their claims are so far removed from the facts of this case that I could deny petitioners' claims on that basis alone. However, I elect to discuss their poorly articulated Table claim and their causation in fact case. Under the facts of this case, it was unreasonable to maintain that A.H.M. experienced a Table encephalopathy.
To establish a Table encephalopathy, petitioners must demonstrate A.H.M. suffered an "encephalopathy" as defined by the QAI section to the Vaccine Injury Table within five to fifteen days of her MMR vaccination or within seventy two hours of her DTaP vaccination.
According to the QAI, a vaccinee is considered to have suffered a Table encephalopathy if the vaccinee manifests an injury encompassed in the definition of an acute encephalopathy within the appropriate time period, and if a chronic encephalopathy is present for more than six months after the immunization. 42 C.F.R. § 100.3(b)(2).
An acute encephalopathy is "one that is sufficiently severe so as to require hospitalization (whether or not hospitalization occurred)." 42 C.F.R. § 100.3(b)(2)(i). For a child younger than 18 months of age,
A chronic encephalopathy is defined in the QAI as "a change in mental or neurologic status, first manifested during the applicable time period [that] persists for a period of at least 6 months from the date of vaccination." 42 C.F.R. § 100.3(b)(2)(ii). If a person returns to a typical neurologic state after suffering an acute encephalopathy, he or she is not presumed to have suffered residual neurologic damage and "any subsequent chronic encephalopathy shall not be presumed to be a sequela of the acute encephalopathy." Id.
"The symptoms associated with an acute encephalopathy are neither subtle nor insidious." Waddell v. Sec'y, HHS, 2012 WL 4829291, at *6 (Fed. Cl. Spec. Mstr. Sept. 19, 2012). As noted in Waddell, "[t]he hospitalization requirement underscores how serious the symptom presentation must be after vaccination to merit classification as a Table encephalopathy." Id. at *7 (citing to Revision of the Vaccine Injury Table, 60 Fed. Reg. 7,685, 7,687 (Feb. 20, 1997) (preamble to final rule) ("[W]e did not intend that hospitalization be viewed as an absolute requirement to establish an acute encephalopathy, but rather as an indicator of the severity of the acute event.").
In contrast, "encephalopathy"
There is nothing in the record to indicate A.H.M. suffered any reaction to the DTaP and MMR vaccines she received on September 15, 1999, much less an encephalopathy as defined in the QAI section to the Vaccine Injury Table. Certainly, she did not suffer an acute encephalopathy within the time periods required by the Vaccine Injury Table. See 42 C.F.R. § 100.3(a)II.B and III.B.
In their pre-hearing memorandum, petitioners list as proof of A.H.M.'s encephalopathy the rash A.H.M. experienced in July 1999, the speech delay noted just prior to vaccination on September 15, 1999, and the concerns noted during A.H.M.'s February 23, 2000 evaluation. See Pet. Memo at 5-7. Not only do these symptoms and concerns not qualify as proof of encephalopathy, but the record does not show that any of these conditions began or were significantly aggravated in the time periods set forth for the MMR and DTaP vaccines. In fact, both the rash and speech delay occurred before A.H.M. even received these vaccinations. Although A.H.M. developed a rash within a few weeks of the varicella vaccination she received in June, since there is no Table injury associated with that vaccine, any reaction is irrelevant to the Table injury claim.
Even if petitioners could establish the symptoms and behavior they describe occurred or were significantly aggravated during the appropriate time frame, they fail to constitute an encephalopathy "sufficiently severe as to require hospitalization." 42 C.F.R. § 100.3(b)(2)(i). Petitioners argue that A.H.M.'s autistic symptoms are sufficient to establish that she suffered the decreased level of consciousness that is required to establish an acute encephalopathy in a child younger than 18 months. See 42 C.F.R. § 100.3(b)(2)(i)(A). There is a difference, however, in the various symptoms and behaviors autistic children often exhibit and the clinical signs listed in the QAI. See 42 C.F.R. § 100.3(b)(2)(i)(D).
For example, A.H.M.'s inconsistent response to her name (see, e.g., Pet. Ex. 19, p. 3) is not equivalent to the decreased or absent response to the environment enumerated in the QAI. See 42 C.F.R. § 100.3(b)(2)(i)(D)(1). To meet the lack of response described in the QAI, a child must not respond, or respond only to a
Likewise, A.H.M.'s lack of eye contact is not equivalent to the decreased or absent eye contact listed in the QAI. See 42 C.F.R. § 100.3(b)(2)(i)(D)(2). To meet the QAI description, a child must fail to gaze on family members as well as other individuals. See id. At times, A.H.M. showed good eye contact such as that noted at her January 26, 2000 evaluation. See Pet. Ex. 19, p. 12. At other times, she showed a lack of eye contact with others but good eye contact with family members. See Pet. Ex. 20, p. 3.
Finally, although A.H.M. sometimes exhibited a lack of response, there is nothing to indicate she failed to recognize familiar people and things. See 42 C.F.R. § 100.3(b)(2)(i)(D)(3). A.H.M.'s autistic symptoms alone do not qualify as any of the clinical signs of the decreased level of consciousness required by the QAI, which clearly requires symptoms which are more intense and consistent than those A.H.M.displayed and which manifested during the very specific time periods provided.
Doctor Wiznitzer eloquently explained this difference during the hearing. He testified that the lack of eye contact needed to satisfy one of the clinical signs of an acute encephalopathy stems from a lack of visual function because the brain is not awake and alert. Tr. at 211-12. The signals coming into the eye are "not processed in any manner because there's an impairment in consciousness." Tr. at 213. The information comes into the brain but is not processed. Id. In contrast, the autistic child is receiving and processing information but is being selective in how she responds. Tr. at 213-14. This child is not making eye contact due to an impairment in social behavior, not because she is failing to process the visual information. Tr. at 214. An autistic child has a deficit in socialization and social communication. Tr. at 217. She will respond to her favorite TV show but not to her name. This behavior is different than that of a child experiencing acute encephalopathy.
A.H.M.'s condition after receiving the MMR and DTaP vaccinations does not meet the requirements established by the Vaccine Injury Table for encephalopathy. Because petitioners failed to demonstrate that A.H.M. suffered a Table injury, they can prevail only on an actual causation claim.
The Federal Circuit has set forth three factors petitioners must establish to prove causation in off-Table cases. See Althen, 418 F.3d 1274, 1278 (Fed. Cir. 2005). Althen requires petitioners to provide: "(1) a medical theory causally connecting the vaccination and the injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason for the injury; and (3) a showing of a proximate temporal relationship between vaccination and injury." Id. All three prongs of the Althen test must be satisfied by preponderant evidence. De Bazan v. Sec'y, HHS, 539 F.3d 1347, 1351-52 (Fed. Cir. 2008); Caves v. Sec'y, HHS, 100 Fed. Cl. 119, 132 (2011), aff'd per curiam, 463 Fed. Appx. 932, 2012 WL 858402 (Fed. Cir. 2012) (finding that "[w]hen a petitioner seeks to demonstrate causation in fact by meeting the three Althen requirements, each of those requirements must be proven by a preponderance of the evidence"). Petitioners may satisfy this evidentiary burden by relying either on "medical records or medical opinion." Althen, 418 F.3d at 1279 (emphasis in original).
A petitioner is not required to establish identification and proof of specific biological mechanisms, as "the purpose of the Vaccine Act's preponderance standard is to allow the finding of causation in a field bereft of complete and direct proof of how vaccines affect the human body." Althen, 418 F.3d at 1280. The petitioner does not have to show that the vaccination was the sole cause, or even the predominant cause, of the injury or condition; showing that the vaccination was a "substantial factor"
Although a petitioner cannot be required to show "epidemiologic studies, rechallenge, the presence of pathological markers or genetic disposition, or general acceptance in the scientific or medical communities to establish a logical sequence of cause and effect,"
Causation is determined on a case by case basis, with "no hard and fast per se scientific or medical rules." Knudsen v. Sec'y, HHS, 35 F.3d 543, 548 (Fed. Cir. 1994). Close calls regarding causation must be resolved in favor of the petitioner. Althen, 418 F.3d at 1280; but see Knudsen, 35 F.3d at 550 (when evidence is in equipoise, the party with the burden of proof fails to meet that burden).
Althen requires that a petitioner in an off-Table causation case present a reliable medical theory by which a vaccine can cause the injury in question. Althen, 418 F.3d at 1278. This first prong of Althen's three-part causation test has also been characterized as the equivalent of the "Can it cause?" inquiry used in toxic tort litigation. See Pafford v. Sec'y, HHS, No. 01-165V, 2004 WL 1717359, at *4 (Fed. Cl. Spec. Mstr. July 16, 2004), aff'd, 64 Fed. Cl. 19 (2005), aff'd, 451 F.3d 1352 (Fed. Cir. 2006). The medical theory must be a reputable one, although it need only be "legally probable, not medically or scientifically certain." Knudsen, 35 F.3d at 548-49. Theories of causation must be reliable as well. Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579, 590 (1993); Moberly, 592 F.3d at 1324.
Althen's second prong requires a logical sequence of cause and effect between the vaccine and the injury. It has been characterized as addressing the "Did it cause?" or specific causation query. See Pafford, 2004 WL 1717359, at *4. Circumstantial evidence and medical opinions may be sufficient to satisfy this requirement. Capizzano, 440 F.3d at 1325-26. Opinions of treating physicians may also provide the logical connection. See Andreu v. Sec'y, HHS, 569 F.3d 1367, 1376 (Fed. Cir. 2009); see also Moberly, 592 F.3d at 1323; Capizzano, 440 F.3d at 1326.
The third Althen factor requires a proximate temporal relationship between the allegedly causal vaccine and the injury suffered. The requirement of temporal connection necessitates a showing that the injury occurred in a medically or scientifically reasonable period after the vaccination, not too soon (see de Bazan, 539 F.3d at 1352) and not too late (see Pafford, 451 F.3d at 1358). Merely showing a temporal connection between a vaccination and an injury is insufficient, standing alone, to establish causation. Grant, 956 F.2d at 1148. A temporal relationship, even when coupled with the absence of any other identified cause for the injury, is not enough to demonstrate probable cause under the Vaccine Act's preponderance standard. Moberly, 592 F.3d at 1323 (citing Althen, 418 F.3d at 1278).
To satisfy the first prong of the Althen test, petitioners must provide "a medical theory causally connecting the vaccination and the injury." Althen, 418 F.3d at 1278 (quoting Grant v. Sec'y, HHS, 956 F.2d 1144, 1148 (Fed. Cir. 1992)). Although petitioners are not required to provide an exact mechanism for their theory, the medical theory must be a reliable one. Knudsen, 35 F.3d at 548 ("This `logical sequence of cause and effect' must be supported by a sound and reliable medical or scientific explanation."). Petitioners must prove the existence of this medical theory by a preponderance of the evidence. Broekelschen v. Sec'y, HHS, 618 F.3d 1339, 1350 (Fed. Cir. 2010). In other words, petitioners must show that it is more likely than not that the received vaccine
In her expert reports, Dr. Cave asserts the vaccines A.H.M. received caused A.H.M. to suffer mitochondrial dysfunction resulting in autistic symptoms (which Dr. Cave called an encephalopathy) (see Pet. Ex. 11-a at 8) or caused a regression and encephalopathy which was more pronounced in A.H.M. because she suffers from mitochondrial dysfunction (see Pet. Ex. 11 at 1). Doctor Cave switched with abandon between these variations of her theory. When asked on cross examination to clarify her theory of causation, Dr. Cave answered, "I think it's the metal toxicity from the vaccine mainly that caused the mitochondrial disorder, and it manifested in behavior and regression." Tr. at 76. She claimed, however, that her theory would be sufficient even without the presence of mitochondrial dysfunction. Tr. at 86.
Doctor Cave provided few details about and little support for her theory. The medical literature offered by Dr. Cave either did not indicate what she claimed or did not provide support for her theories. She referred to oxidative stress on several occasions but failed to explain how the vaccines A.H.M. received could have caused oxidative stress sufficient to result in the damage she describes.
Doctor Cave also labeled A.H.M.'s condition immunocytotoxicity. See id. at 8. She stated that "[t]he mitochondrial dysfunction combined with the glial cell excitotoxicity from a toxin like MSG (Varicella vaccine) as well as the metals, affecting developing neurons-altering their function and development." Pet. Ex. 35 at 3. Except for the added element of mitochondrial dysfunction and the expansion of toxins to include MSG and metals other than mercury, this theory was discussed during the OAP Theory 2 test case litigation. See, e.g., Dwyer, 2010 WL 892250, at *27. Many of articles and studies that Dr. Cave claimed as support for her theories were discussed in the OAP litigation.
Doctor Cave testified that she based her definition of oxidative stress on the work of Jill James, Ph.D. and Richard Deth, Ph.D. Tr. at 101. Doctor Deth's opinions and testimony were thoroughly analyzed in the theory 2 OAP test cases and determined to be lacking.
Doctor Cave also identified the work of Drs. Burbacher, Vargas, and Hornig as supportive of her theories. See Tr. at 52-55, 262-63. For example, she cited Dr. Vargas's study as "reporting the neuroactivation and neuroinflammation in the brains of patients with autism."
The new studies referenced by Dr. Cave share similar flaws and shortcomings. Discussing the articles involving MSG, Dr. Wiznitzer testified that the dosages administered were 10,000 and 54,000 times higher than what A.H.M. received via vaccination.
Although Dr. Cave acknowledged that the Poling claim was compensated as a Table injury for which causation is presumed, she cited the Poling case report, Pet. Ex. 34, as supporting her theory of causation.
The Poling child was diagnosed with a mitochondrial disorder after muscle biopsy and experienced a regression within the Table injury time frame; neither of these factors is present in A.H.M.'s case. I note that the Frye & Rossignol article filed post-hearing as Pet. Ex. 36 discussed the controversy raised by the Poling case (id. at 2) and expressed doubt that the proposed causal mechanism (metabolic decompensation in a child with an underlying mitochondrial disorder as the result of fever) would apply in cases of mitochondrial dysfunction rather than mitochondrial disease. Id. There was no evidence that A.H.M. actually experienced a fever after either her June or September vaccinations, other than a report first made about a decade later by Ms. Miller.
Although petitioners are not required to provide proof of a biological mechanism for their theories, petitioners must demonstrate that the theory or theories proposed are reliable. See Moberly, 592 F.3d at 1324. They have failed to do so. Doctor Cave's background, training, and experience are inadequate to validate the theories she cobbled together from the scientific and medical literature she cited. Her reports, testimony, and other evidence do not constitute preponderant evidence that vaccines can cause autism or mitochondrial dysfunction, or mitochondrial dysfunction masquerading as ASD.
To satisfy the second prong of the Althen test, petitioners must establish a "logical sequence of cause and effect showing that the vaccination was the reason for the injury." Althen, 418 F.3d at 1278. In other words, petitioners must show that the received vaccine actually
In this case, no treating doctor, other than Dr. Holmes, opined that A.H.M.'s injuries were caused by the vaccines she received, and Dr. Holmes' opinion was based on her belief that the thimerosal found in vaccines caused A.H.M.'s injuries, the theory considered and rejected in the OAP test cases.
This case is not a close call. There is nothing in the record, other than the assertions of petitioners and their expert, to establish A.H.M. suffered from encephalopathy, regression, or mitochondrial dysfunction, elements which are crucial to establishing causation. Without a fever and evidence of a mitochondrial decompensation, they cannot establish facts that parallel even their expansive reading of the Poling case as one involving actual causation rather than a Table encephalopathy. The basic requirements of the theories advocated by Dr. Cave are not present in this case. Thus, even if I accepted Dr. Cave's theories as reliable, petitioners have not shown A.H.M.'s vaccinations caused her injuries. Petitioners have failed to establish a logical cause and effect in this case.
Finally, when proving that a vaccine was the cause of an injury, petitioner must also show "a proximate temporal relationship between vaccination and injury." Althen, 418 F.3d at 1278. Petitioner must prove "that the onset of symptoms occurred within a timeframe for which, given the medical understanding of the disorder's etiology, it is medically acceptable to infer causation-in-fact." De Bazan v. Sec'y, HHS, 539 F.3d at 1352. Failure to provide a proximate temporal relationship will result in a denial of compensation. Id. at 1353.
The medical records and videotape in this case show a child exhibiting the traditional symptoms of autism. The correlation in timing relied upon by petitioners and Dr. Cave is not supported by the record in this case, certainly not regarding A.H.M.'s September 15, 1999 vaccinations. Although the onset of A.H.M.'s autistic behaviors coincide somewhat with the first vaccination alleged as causal (the varicella vaccination), the onset and developmental pattern A.H.M. exhibited is common for children with ASD. Moreover, the only "toxin" petitioners allege is contained in the varicella vaccination is MSG and the evidence petitioners submitted regarding MSG and ASD was extremely weak. There is no evidence that A.H.M.'s symptoms or behaviors appreciably worsened after the September vaccinations.
Petitioners claimed both a Table and non-Table injury but have failed to prove any of their claims. After considering the record as a whole, I find that petitioners have failed to establish entitlement to compensation. The petition is dismissed. The clerk shall enter judgment accordingly.
To avoid confusion between medical records and other filings, medical records are cited throughout this decision using a page number format, e.g., "Pet. Ex. 5, p. 1." Other exhibits and filings, including motions, expert reports, briefs, and journal articles, are cited using an "at" format, e.g., "Petition at 3."
The test case evidence showed that the brain damage caused by the measles virus was "an entirely different type of damage than is found in autism." Id., at *93. Moreover, Dr. Kinsbourne's "excess glutamate theory lacked any evidentiary basis, as there was no evidence of excess glutamate in autistic children. Id. at *93.
During the Theory 2 test case litigation, petitioners offered an additional theory presented by Dr. Richard Deth, that the mercury in TCVs affected biochemical processes causing metabolic problems which produced oxidative stress. Dwyer, 2010 WL 892250, at *27. He opined that this oxidative stress affected "neuronal function in the areas of attention and cognition." Id. I concluded that respondent's experts on oxidative stress were far more qualified to opine on vaccinations and oxidative stress than Dr. Deth. Id. at *13-15. I ultimately concluded that the theories advanced involving mercury and oxidative stress to be "illogical, contrary to the weight of the evidence, and, ultimately, unpersuasive." Id. at *165.
I informed petitioners that, based on the test case decisions, they needed to provide "different evidence or theories not presented in the test cases" in order to proceed. Order, issued Apr. 29, 2011, at 2. Throughout this proceeding, petitioners and their expert continued to rely on theories offered and fully litigated in the OAP test case litigation. Doctor Cave was even less qualified to opine on oxidative stress caused by vaccines than Dr. Deth, and ultimately proffered little that was new or different from the matters presented in the OAP test cases, other than her mitochondrial dysfunction theory.
Id., pp. 9-10.
Res. Ex. D, Tab 1, at 1. A.H.M. did not meet these criteria, as her hypotonia was not evident in the newborn to six months of age period, and she did not show a lack of strength or delayed motor milestones.
