package inserts did specify the general type of side effect -- corneal abnormalities and iritis -- that led to the demise of Golod's eye. However, with respect to the corneal problems, the inserts indicated that the side effects were temporary and resolved after Tegison was discontinued. Golod has produced evidence that the corneal effects were not temporary in her case but persisted and worsened after Tegison was discontinued.
Although the package insert warns of iritis, there is no indication that cases of iritis had been persistent or severe, or could lead to permanent visual impairment. Golod has introduced evidence that her iritis was unusually severe and resistant to standard topical and systemic corticosteroid treatment.
The Tegison Patient Information states that a patient may develop "eye irritations" and that a patient should "check with [her] doctor to determine if any change in the amount of [her] medication is needed." The patient leaflet also contains a capitalized warning that Tegison "may cause some more serious side effects, including . . . blurred vision . . . persistent feeling of dryness of the eyes" and that these may be signs of "more serious" side effects which "if left untreated" could possibly result in permanent effects. However, the Patient leaflet does not specify what these "more serious" and "possibly permanent" effects are.
Plaintiffs contend that the language Hoffmann used to describe possible adverse effects did not effectively convey the seriousness of those effects. "It is basic that a warning 'must be commensurate with the risk involved in the ordinary use of the product.'" Martin, 83 N.Y.2d at 11 (quoting Cooley v. Carter-Wallace, Inc., 102 A.D.2d 642, 645, 478 N.Y.S.2d 375 (4th Dept. 1984)) Thus, the language of a warning must be "direct, unequivocal and sufficiently forceful to convey the risk." Martin, 83 N.Y.2d at 11.
It cannot be said, as a matter of law, that the Tegison warnings adequately disclosed a risk of permanent corneal deterioration or severe iritis which could result in the permanent and complete loss of vision. A reasonable juror could conclude that the patient leaflet, which is the most strongly worded of all the warnings issued by Hoffmann, implies that if the patient is "treated," i.e., visits an ophthalmologist, there will be no permanent effects. Thus, the Tegison warnings lack emphasis, clarity and a sense of urgency commensurate with a risk of total and irreversible loss of vision.
Hoffmann contends that because it warned of adverse effects on the cornea and iris, some of which Golod did experience in her left eye in 1988 and 1989, and some of which she experienced to a lesser degree in her right eye prior to 1990, that it is entitled to summary judgment. However, it is the permanent and complete blindness resulting from the severe and permanent deterioration of her cornea and severe and persistent iritis in 1990 for which Golod seeks damages, whether or not she may have suffered other milder effects of which Hoffmann warned.
Hoffmann's adequate warning of milder ophthalmic risks associated with Tegison use did not absolve it of a duty to warn of more severe permanent ones of which it knew or had reason to know. The decision in Erony is instructive. In that case, although the package insert advised physicians and patients to keep the drug out of the reach of children and warned that the drug could cause severe hypoventilation requiring medical treatment, the court held that a reasonable jury could find that the warnings were incomplete because they did not state that oral ingestion could cause hypoventilation serious enough to result in death. Erony, 913 F. Supp. at 200. Similarly, although the warnings here stated that Tegison could cause ocular abnormalities, they did not state that these abnormalities could lead to permanent blindness. See also, Hermes v. Pfizer, Inc., 848 F.2d 66, 68 (5th Cir. 1988) (warning of temporary "extrapyramidal symptoms" did not excuse duty to warn of permanent symptoms of same type).
Hoffmann cites a number of cases in which warnings were held adequate as a matter of law. In each of those cases, the warnings identified the precise adverse effect suffered by the plaintiff and the seriousness of that effect. In Martin, for example, the defendant's drug caused plaintiff to become depressed and eventually suicidal. However, the package insert for the drug at issue explicitly warned that the drug could induce depression, that the depression could persist after the drug was discontinued, and that the depression could be severe enough to result in suicide. 83 N.Y.2d at 11, 15. See also Eiser v. Feldman, 123 A.D.2d 583, 583-84, 507 N.Y.S.2d 386, 387(1st Dep't 1986) (plaintiff who experienced visual blockage in eye adequately warned where package insert, PDR and patient literature regarding drug expressly stated possibility of blindness or partial visual blockage); Wolfgruber v. Upjohn Co., 72 A.D.2d 59, 423 N.Y.S.2d 95 (4th Dep't 1979), aff'd, 52 N.Y.2d 768, 436 N.Y.S.2d 614, 417 N.E.2d 1002 (1980) (no liability where manufacturer warned in package insert and PDR of risk of diarrhea and/or colitis, "the precise malady incurred by plaintiff"); Glucksman v. Halsey Drug Co., 160 A.D.2d 305, 553 N.Y.S.2d 724 (1st Dep't 1990) (no liability where plaintiff suffered "bilateral aseptic necrosis of the femoral head" after ingesting prednisone, and PDR and package inserts expressly listed this specific condition as possible adverse reaction, but physician knowingly chose not to warn patient).
Accordingly, because there is evidence that the Tegison warnings did not adequately convey the possibility of the ocular injuries actually suffered by Golod, summary judgment may not be granted on the basis of the adequacy of the warning of those injuries.
B. Whether HoffmannKnew or Should Have Known of the Dangers of Tegison
Hoffmann next contends that it had no duty to warn of the serious and irreversible ophthalmic effects suffered by Golod because these effects were not reasonably foreseeable at the time Golod was taking Tegison.
A pharmaceutical manufacturer has a duty to warn of dangers of which it knows, or in the exercise of reasonable care, should have known. See Martin, 83 N.Y.2d at 8; Lindsay v. Ortho Pharmaceutical Corp., 637 F.2d 87, 91 (2d Cir. 1980). The manufacturer has a duty to adequately test its drugs. See Enright v. Eli Lilly & Co., 77 N.Y.2d 377, 387-88, 568 N.Y.S.2d 550, 555-56, 570 N.E.2d 198 (1991) (manufacturers should not "enjoy immunity from liability stemming from their failure to conduct adequate research and testing prior to marketing of their products"). Moreover, a drug maker has a "continuing obligation" to "keep abreast of knowledge of its product as gained through research, adverse reaction reports, scientific literature and other available methods." Baker v. St. Agnes Hospital, 70 A.D.2d 400, 406, 421 N.Y.S.2d 81, 85 (2d Dept. 1979); accord Lindsay, 637 F.2d at 91.
Golod contends that Hoffmann should have known of the danger of permanent blindness because Adverse Experience Reports and FDA computer printouts summarizing reports of adverse reactions for both Tegison and Accutane should have alerted Hoffmann to the risk of permanent blindness.
Hoffmann urges that these documents are inadmissible, and thus may not be considered on this motion. See Fed. R. Civ. P. 56(e); Maier-Schule GMC, Inc. v. General Motors Corp., 154 F.R.D. 47, 59 (W.D.N.Y. 1994) (nonmoving party may not rely on inadmissible evidence to avoid summary judgment). Hoffmann contends that these documents are hearsay not within an exception. However, the reports are not hearsay, because they are offered not as proof of the fact that Tegison caused the reported blindness, but as evidence that Hoffmann was on notice of potentially serious optical side effects, and thus "should have known" and warned of such a risk. Hoffmann also attacks the reliability and relevance of the reports, contending that they are merely anecdotal reports and that Golod has not demonstrated that the incidents they relate are sufficiently similar to her experience to be relevant. While the reports may not be sufficiently reliable or relevant to be admissible on the issue of causation, see Wade-Greaux v. Whitehall Laboratories, 874 F. Supp. 1441, 1481 (D. V.I. 1994), aff'd, 46 F.3d 1120 (3d Cir. 1994), they are relevant to Hoffmann's awareness of potentially serious ophthalmological effects and the possible need to conduct further research into them. Cf. Deluca v. Merrell Dow Pharmaceuticals, 791 F. Supp. 1042, 1050 (D. N.J. 1992) (Drug Experience Reports cannot be used to prove causation, but may be "stimulus for further study"), aff'd, 6 F.3d 778 (3d Cir. 1993).
Hoffmann also contends that evidence of the side effects of Accutane should not be admitted because there is insufficient evidence that the side effects of Accutane and Tegison are similar. However, there is enough evidence in the record of similarities in side effects among the retinoids to permit consideration of Hoffmann's experience with Accutane on the issue of whether Hoffmann should have known of the potential for serious ophthalmological effects of Tegison. The package insert notes that Tegison's adverse event profile is similar to other Vitamin A compounds. Dr. Barasch's testimony also provides some evidence that Vitamin A derivatives, including Tegison and Accutane, have similar side effects. Hoffmann's own witnesses have conceded that there are some similarities in the side effects caused by retinoids. See Basko, 416 F.2d at 426-27 (where evidence "fairly established" that two drugs produced same idiosyncratic side effect, question of whether warning as to either drug was adequate was for jury); but see Hoffmannv. Sterling Drug, Inc., 374 F. Supp. 850, 862 (M.D. Pa. 1974) (rejecting evidence of side effects of drug in same chemical family, on grounds probative value of such evidence was outweighed by jury confusion and waste of time on collateral issue of similarity).
Hoffmann also contends that this evidence, even if admissible, does not support the contention that it failed to warn of foreseeable risks. The cursory descriptions contained in these reports may be rather thin evidence of the foreseeability of irreversible blindness from long-term Tegison use, particularly in light of the fact that the one long-term study of Tegison available at the time did not find any risk of blindness.
However, they do indicate that blindness and other permanent or persistent ocular symptoms have occurred in patients using Tegison and related compounds, and thus raise a question of fact for trial as to whether Hoffmann had sufficient information to give rise to a duty to warn of such effects. See Hermes, 848 F.2d at 68 (FDA computer printout of adverse drug reaction reports supports jury finding that defendant had knowledge of side effects sufficient to trigger duty to warn); Basko, 416 F.2d at 426 (whether risk of retinopathy was either knowable or reasonably foreseeable at a time when plaintiff was still taking drug was for jury); See Bukowski, 185 A.D.2d at 33-34 (testimony of defendant-manufacturer's witness that incidence of corneal ulcers resulting from use of defendant's product was less than 1/1000% did not support summary judgment in favor of defendant on issue of failure to warn where plaintiff presented clinical reports, adverse effect abstracts and other information).
On a motion for summary judgment, it is not the Court's role to weigh evidence, but only to determine whether there is an issue of fact for trial. Anderson v. Liberty Lobby, Inc., 477 U.S. 242, 249, 91 L. Ed. 2d 202, 106 S. Ct. 2505 (1986). Accordingly, summary judgment will not be granted on the ground that the harm that befell Golod was unforeseeable.
C. Failure to Warn as Proximate Cause
A plaintiff suing a prescription drug manufacturer on a failure to warn theory must prove that the failure to warn was a proximate cause of the plaintiff's injury. See Glucksman, 160 A.D.2d at 307; Bravman v. Baxter Healthcare Corp., 984 F.2d 71, 75 (2d Cir. 1993); Erony, 913 F. Supp. at 200. Thus, the plaintiff must generally demonstrate that had appropriate warnings been given, the treating physicians would not have prescribed or would have discontinued use of the drug. See Krasnopolsky v. Warner-Lambert Co., 799 F. Supp. 1342, 1347 (E.D.N.Y. 1992) (treating physician's statement that he would prescribe drug even if adequately informed severs causal relationship between failure to warn and plaintiff's injury).
Defendants contend that any inadequacy of its warning was not a proximate cause of Golod's injuries because Dr. Grossman, who prescribed Tegison for Golod, has testified that he believes Hoffmann's warnings are adequate despite Golod's blindness and has not changed his practices in prescribing Tegison since her injury.
However, unless a physician's claim that she would have prescribed a drug even if adequately warned is self-disserving, the credibility of such a claim is generally a jury question not to be resolved on a motion for summary judgment. See Bravman, 984 F.2d at 75. Here, because Dr. Grossman is not a defendant in this action, his statement is not self-disserving in any meaningful way.
Moreover, Dr. Grossman's affidavit is ambiguous. He has not stated that even if he was warned of a risk of permanent blindness, he would still have continued Golod on Tegison despite her initial eye complaints. Instead, he has expressed an opinion that the Tegison warnings are adequate. This may be because he believes that Tegison does not cause blindness, rather than because he thought the warnings were adequate even if Tegison does cause blindness. His further statement, that he has not changed his prescribing practices with respect to Tegison, may simply reflect his belief that the warnings were adequate. It does not amount to an assertion that he would have prescribed the drug to Golod in the face of a risk of blindness.
In addition, Dr. Oksman, Golod's ophthalmologist since 1988, knew that she was taking Tegison and has indicated that he would have recommended that she cease using the drug if the PDR had warned of the risk of permanent ocular adverse effects. Thus, even if Dr. Grossman would have continued prescribing Tegison, another of Golod's physicians would have recommended that she stop.
Accordingly, a question of fact remains regarding whether Hoffmann's alleged failure to warn was a proximate cause of her continued ingestion of the drug.
IV. Causation of Injury
Golod has produced the opinion testimony of three ophthalmologists, Drs. Friedman, Oksman, and Barasch, who concluded that Tegison most likely caused her injury. All three formed their opinions, in whole or in part, by ruling out other likely causes of Golod's ophthalmological condition.
Hoffmann contends that these opinions are insufficient to create a genuine issue of material fact on the issue of whether Tegison caused Golod's injury.
In McCullock v. H.B. Fuller Co., 61 F.3d 1038, 1043-1045 (2d Cir. 1995), the Court held that it was proper for the trial court to admit the opinion of plaintiff's expert physician that the plaintiff's throat ailment was caused by inhalation of the defendant's product and sustained the jury's verdict for the plaintiff on the basis of this causation evidence. The defendant argued that because the expert "could not point to a single piece of medical literature" stating that its product caused the specific injury suffered by plaintiff, and because the expert came to his conclusion as to medical causation by using "differential etiology", that the expert's opinion should have been excluded. "Differential etiology" is the process by which the cause of a disease or condition is determined by considering and eliminating other possible causes.
The Second Circuit held that the expert physician, who was an experienced medical doctor practicing in the specialty of ear, nose and throat for approximately thirty years, was sufficiently qualified to give expert testimony on a throat ailment and its causes. Moreover, the Court reasoned that with respect to the expert's methodology, it was not necessary that there be textual authority to support his opinion in order for that opinion to be put before the jury.
The Court noted that the doctor based his expert opinion on:
a range of factors, including his care and treatment of [plaintiff]; her medical history (as related by plaintiff and derived from a review of medical and surgical reports); pathological studies; a review of the manufacturer's product warnings; the doctor's training and experience; and the use of a scientific analysis known as differential etiology (which requires listing possible causes, then eliminating all causes but one); and references to various scientific and medical treatises.
61 F.3d at 1044.
The Court stated, that "faults in [the expert's] use of 'differential etiology' as a methodology, or lack of textural authority for his opinion, go to the weight, not the admissibility of his testimony." Id. (citing Daubert v. Merrell Dow Pharmaceuticals, 509 U.S. 579, 113 S. Ct. 2786, 2798, 125 L. Ed. 2d 469 (1993)). Accord, Maiorana v. U.S. Mineral Prods Co., 52 F.3d 1124, 1136 (2d Cir. 1995) (reversing district court's grant of judgment as a matter of law and holding that district court improperly undertook weighing of scientific evidence).
Moreover, in Lappe v. American Honda Motor Co., Inc., 857 F. Supp. 222 (N.D.N.Y. 1994), aff'd, 101 F.3d 682, (2d Cir. 1996), the court noted that "weaknesses in the methodology and investigation of [a] particular expert might lead the trier of fact to discount his opinions" but "Daubert only prescribes judicial intervention for expert testimony approaching the outer boundaries of traditional scientific and technological knowledge." 857 F. Supp. at 228.
Here, Hoffmann contends that because they have provided no "reliable scientific support" for their opinion that Tegison causes corneal abnormalities and iritis, the ophthalmologists' opinions should be rejected. However, like the expert physician in McCullock, their opinions raise an issue of fact for trial. Their opinions on causation are based upon their collective training and experience; Golod's medical history, including the reports and records of her physicians; the hospital records; various scientific and medical abstracts and treatises; the Tegison package insert and PDR; and certain reports issued by defendant to the Drug Advisory Committee of the FDA, including test reports conducted by defendant. Although these sources do not definitively prove causation or establish a mechanism of toxicity, they are a sufficient basis upon which to base a medical opinion. The fact that these physicians are unable to describe the mechanism by which Tegison caused its adverse effects is irrelevant. The mechanisms of both therapeutic and toxic effects of drugs are often unknown. As indicated in the PDR and package inserts, Hoffmann does not know the mechanism by which Tegison produces its therapeutic effects, but the documentation of its efficacy by clinical trials suffices to support a claim that it causes those beneficial effects. Just as the mechanism of efficacy need not be known to support a claim that Tegison causes abatement of dermatological symptoms, so the mechanism of toxicity need not be known to support an inference of causation based on accepted clinical methods of diagnosis.
Like the expert physician in McCullock, Drs. Barasch, Friedman and Oksman used a scientific analysis known as differential etiology or differential diagnosis to rule out other possible causes of Golod's injuries, leaving Tegison as the most likely etiologic agent. This methodology is accepted in this Circuit and other jurisdictions. See McCullock, 61 F.3d at 1044; McEwen v. Ortho Pharmaceutical Corp., 270 Ore. 375, 414, 528 P.2d 522, 541 (Or. 1974) (causation adequately proved by expert who, after considering and discounting various diseases which also could have caused the condition, concluded that plaintiff's detachment of and holes in her retina were caused by ingestion of defendant's drug).
Hoffmann contends that Golod's experts' testimony should be discounted because they did not consider and exclude all possible causes for Golod's ocular problems. Specifically, they contend that various of the doctors failed to consider and rule out psoriasis, psoriatic arthritis or a viral infection as the causes.
However, Dr. Barasch has testified that he considered and ruled out all of these possible causes. Although Dr. Friedman did not specifically rule out psoriatic arthritis at the time Golod was in the hospital, he has testified subsequently that he is aware of the ocular effects of both psoriasis and psoriatic arthritis and still considers Tegison the most likely cause of Golod's condition. Although he was hesitant to rule out a viral infection conclusively because he did not see the lab report on an Anterior Chamber tap ("AC tap") to determine if there was virus present in the fluid behind the cornea, he knew the test was done and assumed that it was negative because he did not hear otherwise. Dr. Oksman's testimony also establishes that he considered and ruled out a viral cause based on the results of the AC tap.
Moreover, to the extent that these physicians did not fully consider and rule out all possible causes, such deficiencies in the application of the method generally go to the weight of the evidence. See McCullock, 61 F.3d at 1044. It is for the jury to determine the weight to be given to the ophthalmologists' conclusions, after thorough cross-examination and the presentation of contrary evidence. Furthermore, under New York law "a plaintiff need not disprove every possible ground of causation suggested by the manufacturer in order to prove causation." Tinnerholm v. Parke Davis & Co., 285 F. Supp. 432, 440 (S.D.N.Y. 1968), aff'd in relevant part, modified on damages, 411 F.2d 48 (2d Cir. 1969). When there are several risk factors that can explain a plaintiff's injury, the plaintiff must provide some evidence of why those other causes are in applicable. See Wheat v. Pfizer, Inc., 31 F.3d 340, 342-43 (5th Cir. 1994). Here, Golod's physicians considered and ruled out the most likely alternative causes on various grounds. They ruled out a viral etiology by testing ocular fluid for the presence of viral agents. They ruled out psoriasis and psoriatic arthritis because Golod had not experienced ocular symptoms before taking Tegison, despite a 17-year history of the disease, and because they had never seen a case of such extreme ocular problems caused by psoriatic conditions.
Hoffmann also points out that Dr. Penny Asbell, an ophthalmologist at Mt. Sinai, and Dr. Leslie Kerr, a rheumatologist at Mt. Sinai, attributed Golod's ophthalmic symptoms to her underlying psoriatic arthritis, rather than to Tegison. This disagreement among experts presents a factual question for jury determination. It does not negate the other physicians' opinions.
Accordingly, questions of fact with respect to causation remain for the jury.
V. Barasch's Theory of Causation
In Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579, 113 S. Ct. 2786, 125 L. Ed. 2d 469 (1993), the Supreme Court assigned district judges a "gate-keeper" function in determining whether scientific evidence is admissible. The court fulfills this function by "ensuring that an expert's testimony both rests on a reliable foundation and is relevant to the task at hand." Id. at 597. In announcing this rule, the Court abandoned the Frye test, which had required that scientific evidence have general acceptance in the relevant scientific community in order to be admissible, in favor of a more flexible rule that was more lenient in permitting expert testimony. Id. at 588-89. The Court stated that "vigorous cross examination, presentation of contrary evidence, and careful instruction on the burden of proof are the traditional and appropriate means of attacking shaky but admissible evidence." Id. at 596.
Under Daubert, "scientific knowledge" implies that the expert arrived at her conclusion using the methods and procedures of science and that the conclusion is "more than subjective belief or unsupported speculation." McCullock, 61 F.3d at 1043-44 (quoting Daubert, 509 U.S. at 590. A district judge is to consider a variety of factors in determining whether an expert's proffered testimony is admissible as "scientific knowledge," including: (1) whether the theory has been or can be tested; (2) whether the theory has been subject to peer review or been published; (3) when a particular technique is used, that technique's known rate of error; and (4) the extent of acceptance of the theory in the relevant scientific community. Daubert, 509 U.S. at 593-94.
Hoffmann contends that Dr. Barasch's theory of prolonged Tegison toxicity resulting from the continuous release of Tegison or retinol from the liver and fatty tissues does not pass muster as scientific evidence under Daubert. This argument was made in connection with the summary judgment motion. However, because Golod's causation evidence is sufficient to survive summary judgment without Dr. Barasch's toxicity theory, it will be treated as a motion in limine to exclude testimony on this theory at trial.
As an initial matter, Dr. Barasch's testimony that Tegison is stored in the fat and the liver appears to have support in the medical literature. At his deposition, Dr. Barasch quoted a published study stating that "After continuous administration, etretinate and its active metabolite accumulate in fat and plasma, and half-lives increase as a function of duration of treatment." There is also little question that the toxicity of Tegison persists for some time after the patient stops taking the drug. Because of potential teratogenicity, Hoffmann advises that women not become pregnant for two years after the cessation of Tegison therapy. There is also scientific support for the proposition that vitamin A derivatives produce ocular side effects, including corneal abnormalities and, less frequently, iritis. However, the scientific literature indicates that these effects are temporary and relatively mild.
The novel aspect of Dr. Barasch's hypothesis is his proposition that the release of Tegison or its metabolite from storage in body tissues, in combination with continued oral ingestion of Tegison, can raise the concentration of circulating Tegison to extremely toxic levels and that such levels of Tegison persist and cause more extreme ocular consequences than previously noted. He contends that so long as the concentration of Tegison in circulation is less than the concentration in the fat and liver tissues, stored Tegison is released into circulation, elevating blood Tegison levels above the level that oral ingestion alone would produce. The elevated levels are purportedly more toxic to the eye than lower levels. Dr. Barasch also proposes a mechanism for the ocular toxicity of Tegison. He claims that Tegison, like vitamin A, causes abnormal changes in epithelial cells in the eye and that the dead epithelial cells block secretion of oils and mucus, two components of tears, into the eye. The loss of these components leads to dry eye syndrome. When the eye is dry, the cornea begins to break down. Moreover, Dr. Barasch claims that Tegison acts to directly break down and erode the corneal epithelium, in the same manner that it breaks down other epithelial cells. Because Tegison remains in the body for such an extended period of time, Dr. Barasch surmises that the dry eye syndrome and corneal breakdown continue even after Tegison is discontinued, thus leading to more severe consequences than occur with use of retinoids with shorter half-lives.
Dr. Barasch has provided no direct scientific evidence to support these novel aspects of his theory. From what appears in the record, the hypothesis has not been previously advanced in the scientific literature or otherwise been subjected to peer review, such as through a grant application process. Moreover, there is no evidence that Dr. Barasch's theory has achieved any acceptance (or rejection) in the medical community.
There is no evidence that the hypothesis has been formally tested by clinical trials, in animal studies, or otherwise. While, Dr. Barasch's hypothesis may be "testable" or "falsifiable" by experimental or epidemiological techniques, see Daubert, 509 U.S. at 593 ("a key question" is whether hypothesis can be falsified), he has not indicated how such testing might be practically undertaken using current scientific methods. A court should not be charged with determining how a study testing a hypothesis would be conducted, since the proponent of challenged scientific evidence bears the burden of demonstrating its admissibility by a preponderance of the evidence. Daubert, 509 U.S. at 592 n.10.
As a result, although Dr. Barasch's theory may be biologically plausible, it does not constitute "scientific knowledge" within the meaning of Daubert. Instead, it is, at most, scientifically-grounded speculation: an untested and potentially untestable hypothesis. Although there may be circumstances in which a scientific hypothesis that is, practically speaking, untestable, would nevertheless be admissible, perhaps because of general acceptance in the scientific community, this is not such a case. "The courtroom is not the place for scientific guesswork, even of the most inspired sort. Law lags science; it does not lead it." Rosen v. Ciba-Geigy Corp., 78 F.3d 316, 319 (7th Cir. 1996).
Accordingly, unless Golod comes forward with additional support for Dr. Barasch's theory of ocular toxicity prior to trial, he will not be permitted to testify as to that theory.
For the reasons set forth above, Hoffmann's motion for summary judgment is hereby denied. In addition, the proffered testimony of Dr. Barasch with respect to his hypothesis as to the biological mechanism by which Tegison caused Golod's injuries will be excluded at trial unless further scientific support for the hypothesis is adduced prior to trial.
The parties will appear for a pretrial conference on May 28, 1997 at 4:30 PM, or such other date as may be convenient for counsel.
It is so ordered.
New York, N. Y.
May 20, 1997
ROBERT W. SWEET