Full opinion text
AMENDED MEMORANDUM AND ORDER WEBBER, District Judge. This matter is before the Court following a Daubert hearing upon defendant’s Motion in Limine to Exclude Plaintiffs’ Experts [Document # 170] and defendant’s Motion for Summary Judgment [Document # 211]. In both motions, defendant challenges the qualifications of plaintiffs’ experts on causation, Dr. Kenneth Kulig and Dr. Denis Petro. Defendant claims that both experts must be excluded, because they do not meet the test of scientific reliability set forth by the Supreme Court in Daubert v. Merrell Dow Pharmaceuticals, 509 U.S. 579, 113 S.Ct. 2786, 125 L.Ed.2d 469 (1993). If such experts are excluded, defendant claims, plaintiffs’ case must fail, because plaintiffs will be unable to present any evidence of causation in this case. In addition, defendant argues that it is entitled to partial summary judgment on plaintiffs’ failure to warn claim due to the learned intermediary doctrine. Finally, defendant claims that plaintiffs’ claim for punitive damages must fail on the facts of this case. Having considered the arguments advanced by the parties at the hearing, the Court concludes that defendant is entitled to summary judgment, because plaintiffs’ evidence of causation fails the test for scientific reliability set forth in Daubert. I. STANDARDS GOVERNING MOTIONS FOR SUMMARY JUDGMENT. While defendant styled its initial motion with respect to plaintiffs’ experts as a Motion in Limine, defendant seeks summary judgment in the event that its Motion in Limine is granted. Thus, the Court will undertake its analysis in this matter under the standards governing motions for summary judgment. The standards applicable to summary judgment motions are well settled. Pursuant to Federal Rule of Civil Procedure 56(c), a court may grant a motion for summary judgment if all of the information before the court shows “there is no genuine issue of material fact and the moving party is entitled to judgment as a matter of law.” See Celotex Corp. v. Catrett, 477 U.S. 317, 322, 106 S.Ct. 2548, 91 L.Ed.2d 265 (1986). The United States Supreme Court has noted that “[s]ummary judgment procedure is properly regarded not as a disfavored procedural shortcut, but rather as an integral part of the federal rules as a whole, which are designed to ‘secure the just, speedy and inexpensive determination of every action.’ ” Id. at 327, 106 S.Ct. 2548 (quoting Fed.R.Civ.P. 1). In order to obtain summary judgment, the moving party must demonstrate “an absence of evidence to support the non-moving party’s case.” Celotex, 477 U.S. at 325, 106 S.Ct. 2548. Once the moving party carries this burden, the nonmoving party must “do more than simply show there is some metaphysical doubt as to the material facts.” Matsushita Elec. Indus. Co. v. Zenith Radio Corp., 475 U.S. 574, 586, 106 S.Ct. 1348, 89 L.Ed.2d 538 (1986). The non-moving party may not rest on allegations or denials in the pleadings, but “come forward with ‘specific facts showing that there is a genuine issue for trial.’ ” Id. at 587, 106 S.Ct. 1348 (quoting Fed. R.Civ.P. 56(3)). In analyzing summary judgment motions, the Court is required to view the facts in a light most favorable to the non-moving party, and must give the non-moving party the benefit of any inferences that can logically be drawn from those facts. Matsushita, 475 U.S. at 587, 106 S.Ct. 1348; Buller v. Buechler, 706 F.2d 844, 846 (8th Cir.1983). Moreover, this Court is required to resolve all conflicts in favor of the non-moving party. Robert Johnson Grain Co. v. Chemical Interchange Co., 541 F.2d 207, 210 (8th Cir.1976). The trial court may not consider the credibility of the witnesses or weigh the evidence. White v. Pence, 961 F.2d 776, 779 (8th Cir.1992). II. DISCUSSION. This case concerns the use of a drug called Parlodel, which has been utilized in the past by some women, like plaintiff Tina Glastetter (Glastetter), for the prevention of postpartum physiological lactation. The plaintiffs in this action, Glastetter and her husband, Steven Glastetter, bring this product liability action against defendant Novartis Pharmaceuticals Corporation (“NPC”), formerly known as Sandoz Pharmaceuticals Corporation, alleging that Glastetter suffered an intracerebral hemorrhage following her ingestion of Parlo-del. Glastetter delivered a child on August 2, 1993. On day 13 of a 14-day course of Parlodel drug therapy, she became symptomatic and on August 17,1993, she was taken to a hospital where she was diagnosed with an intracerebral hemorrhage. Glastetter was 36 years old at the time of this second cesarian section delivery. Bromocriptine mesylate (“bromocrip-tine”) is Parlodel’s active ingredient. Plaintiffs will attempt to establish that Parlodel caused the injury at issue in this case through the testimony of expert witnesses. At this time, defendant has presented the issue of these witnesses’ qualifications to testify under the standards set forth by the Supreme Court in the case of Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579, 113 S.Ct. 2786, 125 L.Ed.2d 469 (1993). Defendant argues in both its motions that plaintiffs have failed to come forward with sufficient reliable evidence to demonstrate that Glastetter’s intracerebral hemorrhage (“ICH”) could be and was caused by defendant’s drug Parlodel. Defendant claims that plaintiffs’ experts admit that their hypotheses have not been tested and validated using the scientific method and that there is no epidemiological evidence supporting their theories. In addition, defendant claims that plaintiffs’ experts admit that they rely upon evidence such as case reports, temporal proximity, animal studies, and inferences based on other drugs to support their hypotheses. Defendant claims such evidence fails under the requirements of Daubert. Also, defendant argues that plaintiffs’ experts have no reliable means of ruling out other possible causes of the ICH at issue in this case. In Daubert, the United States Supreme Court confronted the issue of the proper standard for evaluation of expert testimony by trial judges in light of Federal Rule of Evidence 702. In Daubert, the Supreme Court began by noting that Rule 702 superceded the Frye test, which required courts to exclude all “expert” evidence that was not derived from generally accepted principles or theories. See Jau- requi v. Carter Manuf. Co., Inc., 173 F.3d 1076, 1081 (8th Cir.1999) (citing Frye v. United States, 293 F. 1013 (D.C.Cir.1923) and Daubert, 509 U.S. at 586, 588-89, 113 S.Ct. 2786). Rule 702 provides as follows: If scientific, technical, or other specialized knowledge will assist the trier of fact to understand the evidence or to determine a fact in issue, a witness qualified as an expert by knowledge, skill, experience, training, or education, may testify thereto in the form of an opinion or otherwise. While the Supreme Court found that Rule 702 altered the Frye test in that “general acceptance” was no longer an “absolute prerequisite to admissibility,” the Court “emphasized that trial courts must still screen proffered expert testimony for relevance and reliability.” Jaurequi, 173 F.3d at 1081 (citing Daubert, 509 U.S. at 588-89, 113 S.Ct. 2786). The Court noted that the adjective “scientific” in Rule 702 “implies a grounding in the methods and procedures of science” while the word “knowledge” “connotes more than subjective belief or unsupported' speculation.” Daubert, 509 U.S. at 589-90, 113 S.Ct. 2786. After setting forth this interpretation of Rule 702, the Supreme Court focused much of the remainder of its opinion in Daubert to the issue of how a trial court should determine the reliability of scientific “expert” testimony. Jaurequi, 173 F.3d at 1081-82. The Court noted that in determining whether proposed evidence is valid, trial courts should consider the following factors: (1) whether the underlying theory or technique can or has been tested; (2) whether the theory or technique has been subjected to peer review and publication; (3) whether the technique has a known or knowable rate of error; and (4) whether the theory or technique is generally accepted in the relevant community. Id. (citing Daubert, 509 U.S. at 593-94, 113 S.Ct. 2786). However, the Court made clear that these four factors are not exclusive, and that the trial court has flexibility in adapting its analysis to the particular facts of the case before it. Id. (citing Daubert, 509 U.S. at 594-95, 113 S.Ct. 2786). In General Elec. Co. v. Joiner, 522 U.S. 136, 118 S.Ct. 512, 139 L.Ed.2d 508 (1997), the Supreme Court made clear that rulings on the admissibility of evidence pursuant to Rule 702 under these principles are entrusted to the discretion of the trial court. In addition, in Kumho Tire Co., 526 U.S. at 152, 119 S.Ct. 1167, the Court emphasized the importance of the trial judge’s gatekeeping role in analyzing proffered testimony of experts. The Supreme Court decisions involving Federal Rule of Evidence 702 make clear that in evaluating testimony pursuant to Rule 702 in this case, this Court must consider the relevancy and the reliability of the proposed expert testimony. Blue Dane Simmental Corp. v. American Simmental Assoc., 178 F.3d 1035, 1040 (8th Cir.1999) (citing Kumho Tire Co., 526 U.S. at 147, 119 S.Ct. 1167); see also Jaurequi, 173 F.3d at 1082 (quoting Daubert, 509 U.S. at 594-95, 113 S.Ct. 2786, for the proposition that the “polestar ... must always be ‘scientific validity — and thus the evidentiary relevance and reliability — of the principles that underlie a proposed submission’ ”). In making the determination of whether the proffered expert evidence is reliable in this case, this Court is guided by the four Daubert factors set forth supra, as well as any other factors that might fit this particular case. Applying such factors in this case, the Court concludes that the opinions of plaintiffs’ expert witnesses fail to meet the reliability-requirements of Rule 702. In this case, it is clear that plaintiffs’ proffered expert witnesses are imbued with “technical, or other specialized knowledge,” but it is equally clear that any opinions they have to offer for a jury’s consideration are inadmissible, since they cannot “assist the trier of fact to understand the evidence or to determine a fact in issue,” because they are not qualified to testify to general causation in regards to cause and effect of Parlodel and intracerebral hemorrhage. Because such opinions are not admissible, and plaintiffs are unable to establish causation without it, defendant is entitled to summary judgment’ for the reasons that follow. The plaintiffs’ experts in this case, Dr. Dennis Petro, a board-certified neurologist, and Dr. Kenneth Kulig, who is board certified in toxicology and emergency medicine, are both presented with impressive credentials. Kenneth William Kulig, M.D., is licensed to practice medicine in Colorado. A practicing physician for twenty-two years, Dr. Kulig received a B.S. Degree from Michigan State in 1972 followed by a M.D. Degree from Wayne State Medical School in Detroit in 1978. His internship was in internal medicine and his residency was in emergency medicine. He did a two-year fellowship in clinical toxicology at the University of Colorado. He was affiliated with both the Denver General and the Rocky Mountain Poison Center in Denver for ten years. In 1991, he went to Porter Hospital in Denver where he established a private practice where he remains to this date. Dr. Kulig has published at least one journal article related to Parlodel. Dr. Petro received his M.D. degree at Penn State University. He completed his residency in neurology at the Hershey Medical Center. He was employed at the Food and Drug Administration, Washington, D.C. in 1977, where he reviewed drug applications relevant to neurologic disorders, specifically, those that pertained to analgesics and drugs of abuse. When he started with the FDA, Parlodel was an investigation drug, i.e., it had not yet been approved for Parkinson’s Disease, After leaving the FDA, he continued part-time employment with the FDA as a consultant and became employed by the New York State Department of Health. He then worked in the field of development of neu-rologic drugs in a division of American Home Products. Thereafter, he was employed by Pfizer Pharmaceuticals. He then went to the Nassau County Medical Center on Long Island to run the Neuro-logic Department Research Program. From there, he want to the Fidia Pharmaceutical Company in Washington, D.C. He left that firm and became a consultant in the area of development of new drugs. Since 1980, he has been a member of The American Heart Association’s Stroke Council. He has published medical articles in peer-reviewed journals. In this case, both experts set forth what they described as their methodology for diagnosing the cause of the injury at issue in this case. Both experts referred to their methodology as “differential diagnosis.” The Court believes that the court in Hall v. Baxter Healthcare Corp., has set forth the proper definition of “differential diagnosis” as used and explained by Dr. Kulig and Dr. Petro in this case: Differential diagnosis is a patient-specific process of elimination that medical practitioners use to identify the ‘most likely’ cause of a set of signs and symptoms from a list of possible causes. 947 F.Supp. 1387, 1413 (D.Or.1996). Discussing their use of differential diagnosis, both experts explained that they analyzed Glastetter’s case, including relevant medical records, looked at possible “other” causes of her ICH, such as her weight and history of smoking, and concluded, at the end of the process, that Parlodel caused such injury. According to Dr. Kulig, when Glastetter presented at the hospital 13 days after delivery of the child, she developed an “excruciating headache,”. A CT scan revealed an intracere-bral hemorrhage — blood in the brain tissue causing some motor paralysis and speech difficulty. He concludes that she suffered a bleeding-type stroke, as opposed to a “dry stroke” or ischemic-type stroke. Dr. Kulig notes that Glastetter took Parlodel after her first delivery in 1981 with no adverse reactions. However, it is Dr. Ku-lig’s opinion that Glastetter’s intracerebral hemorrhage was caused by the drug Parlo-del. He outlines his “scientific method” that led him to this conclusion as follows: Your Honor, this is basically what I call the scientific method for analyzing adverse drug reactions. I’ve talked to many people. I’ve heard many lectures on the subject. I’ve read textbooks on this. To me, this is not a mysterious approach that only a few select people can understand. This is common sense and it’s what is done on a daily basis by physicians, scientists, regulatory agencies, and drug manufacturers, and I believe that this is the approach that was used by Sandoz itself in analyzing cases of possible adverse drug reactions reported to it at their Drug Monitoring Centre in Basle, Switzerland. The approach is basically, you learn what you can about the patient, then you learn what you can about the drug in question, and then you put all that information together and ask the question, Was the drug in question the cause of ADR [Adverse Drug Reaction]? When you, first of all, learn what you can about the patient, you review the medical records. If you have the patient in front of you, you would do a history and physical, or an H and P. And you would ask many questions about their past history, what drugs they’ve been on in the past, what drugs they’re on now. Are there any risk factors for stroke? If it’s a stroke patient, was there a family history of stroke? Do they have hypertension? Et cetera. You may want to do some laboratory testing, do some blood work. If the patient, for example, had a hemorrhagic stroke, you may want to make sure that they don’t have a bleeding disorder, so you would do some clotting studies in the patient. In order to find out what kind of stroke they had, if it was a stroke patient, you might want to order some x-rays, including CAT scans, MRIs, angiograms, whatever is clinically warranted in that patient, and this is what’s called the “patient workup” basically. You may want to examine some specific heart tests to determine if the cause of the patient’s stroke originated in the heart. If it was an embolic stroke, meaning a blood clot traveled from someplace going up into the brain, a common source of that, it would be the heart. Where a blood clot may form in the heart, a little piece of it may break off and travel to the brain causing an ischemic stroke. The way you determine that is to look at the heart itself, commonly with an echocardiogram. Finally, you’d want to interview people who know the patient. If the patient has had a stroke, they may not be able to give you a very good history because they may be confused or even unable to speak. So you would want to interview family members or friends of the patient. I would ask them questions about prior drug use. Street drug abuse is always important. Is this person a known cocaine abuser or an amphetamine abuser? And sometimes the patient won’t tell you that, but you may get that information from a friend or family member. So basically, again, it’s learn what you can about the patient. If you don’t have the ability to interview the patient, you can still look at the medical records, you can read reports or depositions given by treating physicians to learn more, you can read the deposition of the patient themselves to help fill in some of the gaps that invariably occur in the medical record. Secondly, the approach is to learn what you can about the drug in question, and that might begin with the package insert, but you can certainly also look at textbooks. Looking at the family of drugs from which the drug originated is important. That doesn’t tell you automatically that the drug must act like other family members, but it gives you an idea of what the expected side effects might be. If you know the side effect of aspirin, for example, and there’s a drug that is an aspirin derivative, one might conclude that you would expect the side effects of that derivative to be like aspirin. It may or may not be true, but it’s a good place to start. Computerized searches. With the internet capability today, it’s very easy to very quickly get hundreds of articles on a given drug, and pulling that information off of the internet is often important. Epidemiology, if it exists, is important It’s unusual for there to be epidemiology involving adverse drug reactions. In this case there is some, and I will talk about that in a few moments, but clearly epidemiology is important. One must examine that scientifically to determine if it’s valid epidemiology and if the conclusions are supported by the data presented. Case reports have their place. Contrary to what’s been represented, I don’t have — I don’t believe that case reports prove causation. On the other hand, if there are no case reports, if no one has ever see a case of a stroke from a drug where it’s been alleged maybe a drug caused it, who would ever think that the drug could cause it if it’s never been seen? So case reports are important. The analysis of the case report is important as well, especially if it’s published in a peer-reviewed journal and other people have the opportunity to critique the case report and even exclude it from publication if it’s too far out scientifically- Case series means more than one case report published together. Rechallenge and dechallenge information is just critical, especially involving a very rare adverse drug reaction. If you have a given case where the patient develops an adverse drug reaction, they get better when the drug is withdrawn, and they’re rechallenged with the same drug and they develop the exact same phenomenon that can be objectively measured, that’s critical to the thinking that the drug was the cause of the reaction in that particular patient. It’s not proof necessarily, but it’s powerful evidence, and regulatory agencies, as well as manufacturers, place a very heavy emphasis on rechallenge information. Clinical trials are important, but it’s important to keep in mind that when a drug comes to market, there may have only been a few hundred or at most a few thousand patients who have received that drug in clinical trials, meaning pre-market trials where the drug is being tested to see if it’s effective and if it’s safe. If the adverse effect in question is very rare, if it only occurs in one in 5,000 patients, it would be unusual to see it in the clinical trials. But nevertheless, that information can be important. Animal studies are important. Again, it would be inappropriate to rely solely on animal studies, but if you do have animal studies, for example, showing a given drug is a vasoconstrictor in animals, that is evidence that it could be a vasocon-strictor in man. Vol. I: 68-73 (Kulig) (March 20, 2000). Dr. Kulig later continued to address the issue of causation by the differential diagnosis method as follows: ... Finally, we come to the bottom line. Was the drug in question a cause or the cause or a substantial factor in the development of the adverse drug reaction? My approach and, again, the generally accepted approach, is first of all to formulate a differential diagnosis. What else could be the cause in this patient? Did this patient have a head injury? Did this patient have an arteriovenous malformation, an anatomical defect in the brain that was the result — excuse me, that was the cause of the stroke as opposed to postulating a drug being the cause? And we’ll go through a differential diagnosis in just a moment in this particular case. Then you attribute an appropriate weight to the various components of the medical evidence. The medical evidence could include, involving the drug Parlo-del, is Parlodel a vasoconstrictor? Does Parlodel cause vasospasm? Has Parlo-del been associated with stroke in human beings? Is there animal evidence that Parlodel is a vasospastic agent? Do the pharmacokinetics of the drug lend themselves to saying it makes sense, that it’s plausible the drug was the cause? And again, I’m not saying that any of these components individually leads one to draw that conclusion, but in compilation of all of the evidence involving all of these components, one might be able to reach a conclusion. Many scientists and physicians end right there, Your Honor. They say, I’ve seen enough. I’m willing to say that in Patient X, the drug caused the adverse drug reaction. I’ve taken it even one step further and I use the Bradford-Hill criteria, which is outlined in detail in my affidavit. It’s my representation that the Bradford-Hill criteria are generally accepted criteria for analyzing causation, both for drugs and for nondrugs such as chemicals. The toxicologic community, my peers, use Bradford-Hill extensively. When a paper is presented at our scientific meeting, it is not uncommon for people to say, I believe causation exists because I’ve applied the Bradford-Hill criteria and here’s what my analysis shows. In the case of Sandoz, they used a different criteria, they used the Karch Lasagna criteria. Many of the principles overlap; they’re quite similar. But what I’m saying, Your Honor, is that it is appropriate to use an outline, a construct, a logical construct to say, I believe cause and effect exists because of all of this, but in addition, I’ve taken the extra step and applied a published, generally accepted criteria to the analysis. You may not agree with everything I have to say about that analysis, you may interpret the evidence differently, but at least I’m willing to lay it on the line and say, Here is my thought process; here is the evidence I’ve looked at and why I believe cause and effect exists. And the Bradford-Hill criteria, in my opinion, it’s a generally accepted scientific methodology for the analysis of adverse drug reactions. Vol. I: 77-79 (Kulig) (March 20, 2000). Dr. Kulig also explained that in his differential diagnosis, he ruled out arteriove-nous malformation (AVM), an aneurysm that is essentially an outpouching of an artery, as the cause of Glastetter’s injury, concluding that the neurosurgeon removed a clot and surrounding tissue which was submitted for pathologic analysis. His view is that Glastetter’s treating physicians would have been able to diagnose AVM by objective tests, “To the best of their capabilities.... ” Vol. I: 93-95 (Ku-lig) (March 20, 2000). In his differential diagnosis, Dr. Kulig also ruled out hypertension as a cause of Glastetter’s stroke. He notes that she was never treated for hypertension. He observes that “her first recorded blood pressure was during the elevate — evolution of her stroke, recorded during the critical period where she was becoming quite ill from her stroke and evolution and it’s certainly possible that the blood in her brain was causing the blood pressure elevation.” Vol. I: 99-101 (Kulig) (March 20, 2000). Similarly, Dr. Kulig also looked at coaqulo-pathy, i.e., consideration of whether her blood was clotting properly. Her blood-clofting tests, he concludes, were unremarkable. Vol. I: 101-102 (Kulig) (March 20, 2000). Dr. Kulig also ruled out infection as a cause of the Glastetter stroke, finding no evidence of infection in the medical records. Likewise, he testified that he found no evidence of venous thrombosis — excessive blood-clotting — in Glastetter. Dr. Kulig also ruled out vasculitis — inflamation of blood vessels — as a cause of Glastetter’s stroke. Vol. I: 102 (Kulig) (March 20, 2000). Dr. Kulig believes that Glastetter’s stroke was an arterial event rather than a venous event because a craniotomy — brain surgery to evacuate the blood clot with a suction machine — -was necessary. “That is very unlikely to be a venous bleed, in my opinion,” he stated. Dr. Kulig also ruled out brain tumor as a cause of the Glastet-ter hemorrhagic stroke, primarily on the basis of the radiographic studies and tissue samples from the surgery. Dr. Kulig next considered the effect of other drugs as a probable cause of Glastet-ter’s stroke. In reviewing the case, he considered drugs such as cocaine, methamphetamine, courmadin, heparin and aspirin overdose. He testified that no evidence indicates that any other drugs contributed to Glastetter’s stroke. Vol. I: 103-106 (Kulig) (March 20, 2000). Dr. Kulig also recognized that Glastetter was postpartum with a history of headaches and sinusitis. He observed a history of migraine headaches by noting that she “does have a five-year history of intermittent vertex throbbing headaches.' These headaches were associated with nausea and vomiting in addition to photophobia and sonophobia, and if she were able to sleep in a dark room, she would often wake up with a complete resolution to the headache. Each attack would last about two hours and she would have no more than two monthly. The headaches were getting progressively worse since about one year ago.” Vol. II: 87-88; 90-91 (Kulig) (March 20, 2000). He is not sure if the history of migraine headaches pre-dated the cesarian section birth, but concludes that migraine headaches do not cause in-tracerebral hemorrhage, and if she had migraine headaches, it did not cause her stroke. He testified that there is evidence that migraine headaches can cause ischemic strokes where blood vessels can clamp down so that brain tissue no longer receives blood, but that is different than hemorrhagic stroke. He stated that in general, he does not believe there is an association between migraine headaches and hemorrhagic stroke, and he does not believe there are any epidemiologic studies verifying such association. Vol. II: 87-88; 90-91 (Kulig) (March 20, 2000). He ruled out migraine headaches as a cause of Glas-tetter’s stroke. Vol I: 106-108 (Kulig) (March 20, 2000). In conducting his differential diagnosis, Dr. Kulig also recognizes that Glastetter smoked a pack of cigarettes each day for about six years before her stroke. He is aware of an epidemiologic study showing increased risk of hemorrhagic stroke in cigarette smokers. Also, when he was asked whether cigarette smoking causes vasospasm, he answered, “I think the nicotine in cigarette smoke can cause some element of vasoconstriction. Whether or not it actually causes the pathologic condition vasospasm, I’m not sure.” In addition, when he was asked about Berger’s disease in heavy smokers, he stated, “That’s generally where you see it, yes.” He also stated that “only in a very rare, very susceptible individual who is a heavy smoker,” one might find that “cigarette smoking causes Berger’s disease through the mechanism of vasospasm.” In the same line of questions, he acknowledged that vasospasm can be so severe that it causes gangrene and digit amputation. He confirmed that a physiological mechanism for vasospasm could be responsible for some cases of otherwise itcopathic in-tracerebral hemorrhage. Vol. II: 99-101 (Kulig) (March 20, 2000). Regarding such medical or scientific evidence as to the relationship between smoking and hemorrhagic stroke, Dr. Kulig testified that there “is some evidence that that occurs.... Her short smoking history, although a pack a day is a pretty heavy habit, I think did not cause her stroke because there was no evidence for atherosclerosis on her angiogram, which is one of the reasons smoking may be associated with stroke to begin with. Her blood vessels were clean.” Vol. I: 108-110 (Kulig) (March 20, 2000). While Dr. Kulig did not concur that Glastetter was “clinically obese” when she became pregnant and at the time of her stroke, he confessed that she was “heavy” — “overweight.” He says he’s seen some evidence that suggests obesity is a risk factor for stroke. Vol. II: 92-94 (Ku-lig) (March 20, 2000). While he observed that Glastetter was overweight with a cholesterol of 201 which is “minimally elevated,” he said this did not cause her stroke. Vol. I: 111 (Kulig) (March 20, 2000). The last factor Dr. Kulig considered in his differential diagnosis was the postpartum status of Glastetter. He recognizes the existence of multiple studies performed on strokes in the postpartum period, and that some have concluded that there is an increased risk of stroke. He questions the results of the studies, because the larger studies have not examined whether women were eclampsic or whether they were on Parlodel. He testified that if eclampsia is ruled out, or if medication use is ruled out in the postpartum period, “it is not at all clear that there’s this greatly elevated risk of stroke in the postpartum period specifically.” However, he states that he recognizes that eclampsia is a disease occurring only in the immediate postpartum period, and that it is characterized by severe elevations of blood pressure as well as significant edema or swelling of the body, with protein being found in the urine in excessive concentration. He stated that it “can result in stroke if the blood pressure elevations are excessive.” However, Dr. Kulig is not convinced that cesarian section represents an increased risk for stroke. He stated that it “just seems to me to be totally unscientific to say that an epidemiologic study shows that the postpartum period by itself is a risk factor and Parlodel therefore, is not when the study did not examine whether or not the women were on Parlo-del.” However, he is not specific in his exclusion of surgical delivery as a cause in this case, and he recognizes some risk of stroke from general anesthesia. Vol. I: 97-99 (Kulig) (March 20, 2000). However, notwithstanding his apparent disagreement with respect to the conclusion that women in the postpartum period, especially women who had cesarian sections, are at risk of stroke, Dr. Kulig indicated that he considered such risk in his differential diagnosis. He stated that “[w]hether or not I believe that to be true, I did consider cesarian section in her and ruled that out as a cause of her stroke.” Glastetter’s 1993 delivery was by cesarian section, but Dr. Kulig concluded that she was not preeclamptic during her 1993 pregnancy. While he did note that in Glastetter’s 1981 pregnancy, she had “some blood pressure elevations,” and that her physician found “toxemia,” which he says is another word for “eclampsia or preeclampsia,” he stated that Glastetter reported no significant elevations in blood pressure in her 1993 pregnancy. Vol. I: 95-96 (Kulig) (March 20, 2000). After discussing his consideration of all these factors, Dr. Kulig concluded his differential diagnosis exercise by saying that it was his “opinion that the intracerebral hemorrhage in Mrs. Glastetter was caused by the drug Parlodel.” Vol. I: 111-116 (Kulig) (March 20, 2000). Following Dr. Kulig’s testimony on direct examination, defendant inquired in regards to his conclusions on cross-examination. Cross-examination of experts is very important in determining whether their testimony is reliable or relevant. Cross-examination of plaintiffs’ expert witnesses in this case is particularly instructive. Dr. Kulig demonstrated frequent episodes of poor or selective memory, and his answers, when challenged, demonstrate the unreliability of his conclusions. Dr. Kulig had much trouble remembering the testimony he has given in many prior cases which involve Parlodel. When reminded of answers he previously gave under oath, which confirm in most cases the responses sought from counsel in cross-examination, Dr. Kulig frequently responds that the testimony occurred a long time ago. Dr. Kulig’s opinions are not based upon scientific studies but are, in the final analysis, reposed in the realm of “may cause” or “possibly could cause.” With respect to his conclusions about the postpartum period in his differential diagnosis, Dr. Kulig was asked on cross-examination if he agreed that the postpartum period is a period of increased risk for stroke in the general female population, and he at first responded, “I’m not sure the period itself is the cause as opposed to things that can happen during that period being the cause, such as drug use or ec-lampsia.” He was asked if he had given another answer in a deposition in a prior case against Sandoz to this question, “You’re not aware that there is an increase of stroke in postpartum women as opposed to women who are not prepartum?” His reported answer was, “I am willing to say that pregnancy and delivery are risk factors for the development of stroke.” Vol. I: 120-123 (Kulig) (March 20, 2000). Dr. Kulig acknowledged familiarity with the Kittner Study published in the New England Journal of Medicine in 1996, a peer-reviewed article reporting the relative risk of intracerebral hemorrhage at a point during the six-week period after delivery, with an increased risk of more than 28 times the risk for a woman not in the postpartum period. The relative risks were adjusted for age and race. The paper reports an increased risk of intracere-bral hemorrhage postpartum statistically significant at the 95% confidence interval. After shown the Kittner paper with its conclusion that “A causal role for a preec-lampsia and eclampsia does not fully explain the much stronger associations with stroke found for the postpartum state than for pregnancy itself,” and when asked if it was his opinion that preeclampsia and ec-lampsia account for a significant percentage of postpartum stroke, Dr. Kulig said he did not think he ever made such a statement, but that preeclampsia and ec-lampsia account for some percentage of stroke postpartum, and that Parlodel does not cause preeclampsia or eclampsia or eclampsic stroke or eclampsic seizure. He admitted that blood volume decreases from the time of delivery to the end of the postpartum recovery. He was unwilling to agree on a specific percentage of blood volume decrease but testified, “And there is probably some range that may include 50 percent, but I would be reluctant to accept that figure as being true.” Vol. I: 124-130 (Kulig) (March 20, 2000). In addition, Dr. Kulig admitted that he was not familiar with any study which shows Parlodel affects the coagulating factors of blood. He admitted that he was familiar with a postpartum epidemiology study published by Dr. Lanska in 1998, which looked at postpartum stroke and showed an increased risk of stroke postpartum. The report was reviewed in a journal called Neurology. Like Dr. Kulig, Dr. Petro also relied upon differential diagnosis in reaching his conclusions in this case: Q: Doctor, what methodology have you used in reaching your opinions with regard to the itiology of Glastetter’s intra-cerebral hemorrhage? A: Well, in general issues, you use certainly the scientific method, but as part of the practice of medicine, the practice is to use — the classic technique is to use the technique of differential diagnosis. “You begin with horses and you end up with zebras.” Vol. I: 61 (Petro) (March 21, 2000). Like Dr. Kulig, Dr. Petro excluded possible risk factors of stroke in his differential diagnosis. He concluded that Glastet-ter did not have chronic hypertension. Her hypertension in the emergency room, he concludes, is complicated to evaluate “because obviously she’s evolving an event that can either cause the transient rise in hypertension, just because of the stress of having a brain hemorrhage. That’s clearly obvious.” He also mentions other factors relevant to autoregulation in the brain which may impart in terms of a presser effect, and he says there are cases where patients on Parlodel in the postpartum period develop hypertension. Vol. I: 64 (Petro) (March 21, 2000). Dr. Petro also ruled out AVM as a cause of Glastetter’s stroke. After first noting that he recognizes that they are of varying sizes, he noted that a large or medium AVM would appear on tests and “would be seen at the time of the craniotomy.” He recognizes that crypto-genic AVM, which Barnett references as invisible AVM which bleeds, leaves no residual to be seen, meaning there would not be 100% exclusion of something that is both invisible and leaves no remnants. As he stated, “[tjhere’s no way to essentially rule out an invisible vascular malformation.” Also, he notes that Glastetter’s multiple radiological studies showed no evidence of AVM. The neurosurgeon who performed the craniotomy evacuated the material in the area. The pathology showed no finding of arteriovenous malformation. Vol. I: 64-68 (Petro) (March 21, 2000). In his differential diagnosis, Dr. Petro also ruled out all other drugs as a cause of the intracerebral hemorrhage other than Parlodel. He acknowledges that she had taken analgesics, but he noted that there is no indication she had taken other prescription medication. He concluded there was no evidence of infection, tumors, inflammation or vasculitis to explain the hemor-O & o £ CD Ph o 3 ho o c3 O o In conducting his differential diagnosis, Dr. Petro also recognizes the difference between a risk factor and a cause. As he observed, “there’s really a distraction between factors which may or have some connection that is distant to the event versus the actual precipitation of the event by some causal agent.” Dr. Petro also recognizes other risk factors, noting that “some of them include things such as use of other drugs, use of — certainly other things such as tobacco use, certainly nowadays it’s caffeine use, and many, many other factors. Also, race, issues of race, and also obesity, cholesterol levels, et cetera, et cetera.” When asked whether Glastetter’s smoking history was the cause of her hemorrhage, he responded, “my opinion is it was not a factor. It was not a causative factor in her hemorrhage.” In expanding his answer, he said there were “a whole series of factors associated with chronic smoking over long periods of time. So that’s to be considered more likely in older patients.” He testified that there is a relationship between smoking and atherosclerosis, but from laboratory tests, he concluded that no evidence indicated she had atherosclerosis. Vol. I: 70-73 (Petro) (March 21, 2000). Dr. Petro also ruled out caffeine as a causative factor, because he believes that there has not been a consensus in terms of neurologic findings that it plays a role in stroke. He also believes that obesity was not a factor in Glastetter’s stroke. Because she was 36-years old, he contrasts her with women in the sixty-year range, explaining that obesity in combination with diabetes and hypertension work together to “perhaps have an influence.” In a 35-year old, premenopausal female, “that’s not a significant factor.” Vol. I: 73 (Petro) (March 21, 2000). Dr. Petro also ruled out cholesterol measurements as a causative factor for Glastetter’s hemorrhage. He noted that he thinks low levels of cholesterol may be a risk factor. Vol. I: 75 (Petro) (March 21, 2000) (emphasis added). In addition to the foregoing, it did not appear that Dr. Petro believed that Glas-tetter’s postpartum period was a causative factor for her intracerebral hemorrhage. He testified, “Yeah, I think just in a sentence these kind of questions is to look at what are recorded in neurologic treatises, and when I look at the standard treatises that are in neurology and I look at the postpartum period, I don’t see that as any particular factor, certainly as presented in the standard treatises that I use.” Vol. I: 75 (Petro) (March 21, 2000). Thus, plaintiffs’ experts indicated that their conclusions with respect to the likely cause of Glastetter’s ICH, to the exclusion of other causes, were reached through a scientific process known as differential diagnosis. As plaintiffs note, other courts have embraced differential diagnosis as a sound scientific methodology. See Westberry v. Gummi, 178 F.3d 257, 262 (4th Cir.1999) (noting that “[differential diagnosis, or differential etiology, is a standard scientific technique of identifying the cause of a medical problem by eliminating the likely causes until the most probable one is isolated” and that such technique “has widespread acceptance in the medical community, has been subject to peer review, and does not frequently lead to incorrect results.”) (citations and internal quotations omitted); Heller v. Shaw Industries, Inc., 167 F.3d 146, 155-56 (3d Cir.1999); Hose v. Chicago Northwestern Trans. Co., 70 F.3d 968, 973 (8th Cir.1995) (noting that “ruling out alternative explanations for injuries is a valid medical method”) (citation omitted). In addition, defendant does not contest plaintiffs’ use of a differential diagnosis. Concluding that differential diagnosis is a sound scientific methodology, however, does not end the Court’s inquiry. As the court in Hall noted, “differential diagnosis does not by itself prove the cause, even for the particular patient.” 947 F.Supp. at 1413. The Hall court emphasized that while differential diagnosis is important and an accepted methodology with respect to issues of “specific causation,” such diagnosis may not be helpful with respect to “general causation:” The process of differential diagnosis is undoubtedly important to the question of “specific causation.” If other possible causes of an injury cannot be ruled out, or at least the possibility of their contribution to causation minimized, then the “more likely than not” threshold for proving causation may not be met. But, it is also important to recognize that a fundamental assumption underlying this method is that the final, suspected “cause” remaining after this process of elimination must actually be capable of causing the injury. That is, the expert must “rule in” the suspected cause as well as “rule out” other possible causes. And, of course, expert opinion on the issue of “general causation” must be derived from scientifically valid methodology- Id. at 1413 (citations and internal quotations omitted). Plaintiffs’ experts also indicate that the differential diagnosis is not helpful in assessing general causation. When asked if differential diagnosis as applied to a specific patient cannot establish general causation, between the exposure and the disease end point generally, Dr. Kulig said differential diagnosis in a specific patient “has nothing to do with general causation except for the items in the differential diagnosis are probably accepted by the physician as being shown to be general causes of the condition in question. We just have to find out now in a given patient if that’s the operative process.” When asked if he testified in a prior case in 1997 to the question, “can differential diagnosis as applied to a specific patient establish general causation between the exposure and the disease end pont generally?,” he answered, “No.” Dr. Kulig also testified that a differential diagnosis is designed to answer questions in a specific patient “and that’s all it really can do.” Vol. II: 77-78 (Kulig) (March 20, 2000). When asked whether general causation between “a drug and a disease cannot be established by a process of differential diagnosis, is that correct?,” Dr. Kulig said, “Well, it’s not — it’s not designed to do that. It — it—a differential diagnosis is designed to be used for a specific patient which is not what general causation concerns, as you know.” Vol. II: 80 (Kulig) (March 20, 2000). Similarly, Dr. Petro was asked if he understood the difference between general causation and specific causation. He agreed that general causation means whether substance A can cause Effect B. He also agreed that before it can be concluded that bromocriptine did cause intra-cerebral hemorrhage in Glastetter, it must first be known that bromocriptine can cause intracerebral hemorrhage, generally. Vol. I: 101-102 (Petro) (March 21, 2000). Thus, while plaintiffs’ experts testified that in performing differential diagnosis in this case, they ruled out other possible causes of Glastetter’s ICH, the experts and plaintiffs must also come forward with evidence “ruling in” Parlodel as a possible cause of ICH. If no evidence suggests that Parlodel can cause ICH in humans generally, then the Court does not believe that plaintiffs’ experts conclusions that Parlodel caused ICH in Glastetter, as evidenced by their use of differential diagnosis, passes the reliability standards under Daubert and its progeny. See National Bank of Commerce v. Daw Chemical Co., 133 F.3d 1132 (8th Cir.1998) (affirming exclusion of evidence under Daubert when plaintiffs failed to demonstrate that proffered expert testimony had a valid scientific foundation, “because it was not based on accepted scientific methodology for determining whether a chemical agent can cause birth defects in humans”); Brumbaugh v. Sandoz Pharmaceutical Corp., 77 F.Supp.2d 1153, 1155, n. 1 (D.Mont.1999) (noting that specific causation is only material “if plaintiff can demonstrate general causation between Parlodel and her injury”). In their papers and at the hearing, plaintiffs came forward with the following evidence supporting their claim that Parlo-del can cause, ICH: (1) peer reviewed articles, texts, and treatises; (2) multiple human dechallenge and rechallenge studies and reports; (3) an epidemiology study on stroke and Parlodel, which plaintiffs admit is “underpowered and thus partially flawed” in their Memorandum in Opposition; (4) determinations by the FDA that Parlodel is unsafe because of stroke and other vasopastic risks; and (5) allegedly hidden internal company admissions by Sandoz concluding that Parlodel can cause such conditions, including information related to animal studies. Having reviewed this evidence, heard the testimony from plaintiffs’ experts, and considered plaintiffs’ arguments in their papers and at the hearing, the Court does not believe that this evidence is sufficient to establish the reliability of plaintiffs’ proffered expert testimony. A. CASE REPORTS ARE NOT RELIABLE IN ESTABLISHING CAUSATION. At the outset, the Court notes that plaintiffs’ experts’ reliance on ease reports is not sufficient to make their causation opinions rehable under Daubert. Plaintiffs’ experts indicated at the hearing that they have reached their conclusions based, at least in part, upon numerous case reports or individual case studies. Much of Dr. Kulig’s support for his causation conclusions comes from case reports, which he describes as “important.” More specifically, Dr. Kulig refers to two cases where women were taking Parlodel, and, in his opinion, had adverse drug interactions. He claims such cases prompted the writing of his report. The first woman he saw was a postpartum patient taking Parlodel for lactation suppression who developed “a very bad headache while taking the drug ... and was given Midrin, which is a common headache medication.” She was released, then returned in “critical condition ... in ventricular tachycardia.... She apparently did not suffer a myocardial infarction, however, but she was in preinfarction condition.” The neurologist who was involved in treating this patient related to Dr. Kulig a case history of a woman taking Parlodel for lactation suppression who developed a headache and was given a drug before she had a stroke, while on both medications. The day after her stroke, she had an angiogram which showed “widespread diffuse vasospasm on the an-giogram.” A repeat angiogram performed several months later was normal. “It was my belief that the condition was that she was on one or both drugs that I had mentioned, Parlodel with or without the [other drug], that was clearly causing spasm and the subsequent stroke. So the analogies between this — that case and Mr. Glastetter were clear to me. Be that as it may, I published both cases together.” That publication, Bromocriptine — Associated Headache, Possible Life-Threatening Sympathomimetic Interaction, was received as plaintiffs’ exhibit 1400. Thereafter, these patients contacted attorneys who contacted Dr. Kulig. He then associated himself with these patients as an expert witness in litigation involving Parlodel. Vol. I: 57-59 (Kulig) (March 20, 2000). Like Dr. Kulig, Dr. Petro relied, in part, on case reports to reach his conclusions. At the hearing, he indicated that he has reviewed clinical trials for Parlodel in the course of litigation where he has served as an expert witness. He testified concerning a particular patient’s case report under controlled conditions where the patient was under consistent observations of a treating physician and was monitored for new signs and symptoms and for regulation of medication. Soon after initiation into the study, she developed profound hypertension. Dr. Petro testified that hypertensive encephalopathy is a potential precursor to an intracerebral hemorrhage; however, the patient was dropped from the program, and the reports of these clinical trials were summarized to the FDA, but this patient’s encephalopathy was not referenced in the summaries. Vol. I: 30-35 (Petro) (March 21, 2000). In addition, while Dr. Petro worked with the FDA, he made a report concerning adverse drug reactions with Parlodel and the Parkinson’s indication in 1979. He noted three deaths in the Parlodel group, two attributed to myocardial infarction and one from intestinal obstruction and gangrene. Caution was suggested in use of bromocriptine in patients at risk for cardiovascular disease. He commented that the literature and sponsor study demonstrate neuropsychiatric complications (hallucinations, confusion, psychosis) and cardiovascular effects (vasospasm, arrhythmia, myocardial ischemia, etc.), which limit the usefulness of bromocrip-tine in elderly patients with Parkinson’s disease. He suggested continued surveillance for adverse toxic reactions, with particular attention to patients with vascular disease, hepatic impairment or hematologic disorder. He concluded that the three deaths suggest “some ergotism in the study population.” He recommended approval of the Parlodel indication, subject to appropriate surveillance, at a time when he was a consultant with the FDA. Sandoz was then required to list ergotism and symptoms of ergotism in the package insert for the Parkinson’s indication for Par-lodel. Vol. I: 19-24 (Petro) (March 21, 2000). In addition, he observed that Dr. Davoi-sin reported a Parkinson’s Disease patient developing pallor and painful sensations in the fingers which disappears when the drug was withdrawn and resurfaced after a period of time when Parlodel was reintroduced to the patient. Vol. I: 19-24 (Petro) (March 21, 2000). Dr. Petro also relied on other published case studies that he expressly mentioned at the hearing, including some discussed by the Court infra The Court does not find that the case reports support the reliability of plaintiffs’ experts’ testimony. As defendant notes, a number of courts have concluded that case reports are not a scientifically reliable basis for a causation opinion. See generally Allison v. McGhan Med. Corp., 184 F.3d 1300, 1316 (11th Cir.1999) (noting that “case studies pale in comparison” in the face of “population-based epidemiological studies” and that district court did not abuse its discretion by discounting expert’s “reliance on case reports in the face of the overwhelming contrary epidemiological evidence presented”); Hollander v. Sandoz Pharmaceuticals Corp., 95 F.Supp.2d 1230, 1235-38 (W.D.Okla.2000) (noting that “case reports have been repeatedly rejected as a scientific basis for a conclusion regarding causation”) (citing In re Breast Implant Litigation, 11 F.Supp.2d 1217, 1228 (D.Colo.1998); Willert v. Ortho Pharmaceutical Corp., 995 F.Supp. 979, 981 (D.Minn.1998)); Pick v. American Med. Sys., 958 F.Supp. 1151, 1161-62 (E.D.La.1997) (noting that “courts have frequently rejected case studies as an insufficient basis to decide causation when they lack control groups” and that “the individual reports cited must be shown to be independently reliable under Daubert before they can be admitted”); Haggerty v. Upjohn Co., 950 F.Supp. 1160, 1164 (S.D.Fla.1996) (citing Casey v. Ohio Medical Products, 877 F.Supp. 1380, 1385 (N.D.Cal.1995), for the proposition that “while case reports may provide anecdotal support, they are no substitute for a scientifically designed and conducted inquiry”). Such case reports are not reliable, because normally, such reports “record nothing more than a temporal association between an exposure and a particular occurrence,” and are therefore less reliable than epidemiological studies, because “[ejpidemiologists use their population studies to eliminate the chance associations and confounding factors, which inherently infect anecdotal reports, to determine whether a statistically significant positive association exists.” Wade-Greaux v. Whitehall Labs., 874 F.Supp. 1441, 1453 (D.Vi.1994); see also Hollander, 95 F.Supp.2d at 1237-38 (noting that the problem with case reports and adverse drug experience reports is that “they are not controlled studies and do not eliminate confounding variables,” which means that “the reported effect or injury could be due to some other cause than Parlodel”). Dr. Kulig apparently has recognized these flaws with case reports, as he testified at the hearing in this matter that case reports “do not establish causation” and that he did not believe “that case reports prove causation.” Vol. 1:71, 138. He admitted that “case reports by themselves do not prove causation and I would never attempt to do so.” In his prior testimony in a case in New York, Dr. Kulig gave testimony in response to the question, “Doctor, on a more general level, can a cause-and-effect relationship be established with a disease as common as breast cancer in humans without just showing an association through a controlled study?” His answer there was “no.” When asked, “Can it be shown with case reports?”, he said, “no.” Vol. I: 134-139 (Kulig) (March 20, 2000). He also admits that clinical trials would be a very small component of the entire list of evidence that he would consider, and he would not say that clinical trials in isolation prove anything. He stated that he believes that case reports are traditionally viewed as the least vigorous form of proof of a hypothesis or validation of a theory, and he testified at an earlier hearing that he would put case reports as his least important evidence of causation. Moreover, Dr. Kulig testified in an earlier case that a single case report is uncontrolled, and he confesses that relative risk factors cannot be derived from case reports. He acknowledges that he is not giving the Court an estimate of Parlodel’s risk based on case reports. He agrees that case reports and temporal associations taken together are unlikely to give proof of causation. In a prior hearing, Dr. Kulig was asked the following question, “Sir, do you agree with FDA’s caveat number one that for any given case report there is no certainty that the suspect drug caused the reaction?” He answered by stating, “I would agree with that.” Dr. Kulig testified he is not saying that vetro evidence proves that Parlodel causes stroke. Vol. II: 26; 28-38; 41; 72 (Kulig) (March 20, 2000). In addition, while plaintiffs in this case, like the plaintiffs in Hollander, emphasize that a number of the case reports include dechallenge/rechallenge information, Dr. Kulig testified that while such evidence is “powerful,” he also stated that “it’s not proof necessarily,” Vol. 1:72, and that such dechallenge/rechallenge reports are not controlled except in “a very loose sense.” Vol. II:44. Thus, in light of the case law discussing case reports and the testimony of plaintiffs’ experts, this Court, like the Hollander court, does not believe that the case studies in this case are sufficient alone to “establish the requisite causation, as they fail to take into account the postpartum incidence of stroke and other factors.” 95 F.Supp.2d at 1237-38. Therefore, the case reports, including the re-challenge/de-challenge studies, are not sufficient to establish the reliability of plaintiffs’ experts’ causation opinions. B. PLAINTIFFS’ MAY NOT SHOW CAUSATION MERELY BY PRESENTING TESTIMONY AND OTHERWISE DEMONSTRATING THAT OTHER ERGOT ALKALOIDS CAUSE HYPERTENSION OR BY PRESENTING PUBLISHED WORK BASED UPON CASE STUDIES IN THE ABSENCE OF EVIDENCE ESTABLISHING THAT PARLODEL CAN CAUSE INTRACEREBRAL HEMORRHAGE Plaintiffs and their experts have come forward with evidence they claim indicates an “association” between bromocriptine and vasoconstriction in some parts of the body and under certain conditions. Dr. Kulig says that bromocriptine is a vasocon-strictor, that bromocriptine and pergolide share some common properties with the parent family of ergot compounds, including digital vasospasm, and that bromocrip-tine is on the differential diagnosis for myocardial infarction. Vol. I: 83-85 (Ku-lig) (March 20, 2000). He concludes that vasospasm is ergotism and ergotism is va-sospasm; however, he testified that just because bromocriptine is an ergot does not mean it causes vasoconstriction. Notwithstanding such testimony, he believes, apparently for other reasons, that there is clear and convincing evidence that bronco-criptive causes myocardial infarction and that such evidence can be used, “that, therefore, it appears that bromocriptine possibly could cause stroke as well because the physiologic mechanism is identified. You would have to have some evidence, as well, but again, you’re looking at a toxicologic syndrome of ergotism where these things happen together from the same drug.” Vol. II: 72-73 (Kulig) (March 20, 2000). However, Kulig does not know the mechanism by which bromocriptine causes seizure. He believes it to be a vasocon-strictive phenomenon. However, his conclusion lacks scientific support. He relies upon his conclusion, which is about to be published in a textbook, that bromocriptine is not generally