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CASE NO. 5625 CRB-7-11-2
COMPENSATION REVIEW BOARD
WORKERS’ COMPENSATION COMMISSION
AUGUST 16, 2012
GREENTREE TOYOTA LINCOLN-MERCURY
The claimant was represented by Philip F. Spillane, Esq., Allingham Spillane, L.L.C., 54 Bridge Street, New Milford, CT 06776.
The respondents were represented by Heather K. Porto, Esq., Pomeranz, Drayton & Stabnick, L.L.C., 95 Glastonbury Boulevard, Suite 216, Glastonbury, CT 06033-4412.
This Petition for Review from the January 24, 2011 Finding and Dismissal of the Commissioner acting for the Seventh District was heard on December 16, 2011 before a Compensation Review Board panel consisting of Commissioners Scott A. Barton, Amado J. Vargas and Stephen B. Delaney.
SCOTT A. BARTON, COMMISSIONER. The claimant has petitioned for review from the January 24, 2011 Finding and Dismissal of the Commissioner acting for the Seventh District. We find no error and accordingly affirm the decision of the trial commissioner.1
The trial commissioner made the following factual findings which are pertinent to our review. On May 17, 2005, the claimant, who was employed as a car salesman, was struck in the head by a closing SUV door. The impact knocked him to the ground and he sustained a cut on his forehead above the right eye. A co-worker drove the claimant to a medical facility where he received stitches to his forehead. The claimant did not lose consciousness. The claimant testified that on June 19, 2005, he developed problems with the vision in his right eye. If he covered the left eye and looked only through the right eye, “he saw a shadow around the periphery of the objects that he viewed.” Findings, ¶ 5. When he tried to look through both eyes, he could see “clearly, but he saw two additional replications of the object he was looking at, one at ‘two o’clock’ and one at ‘eight o’clock.’” Id. When he looked through his left eye only, his vision was clear. The claimant testified that prior to his head injury on May 17, 2005, he had never had any problems with his eyes and had never had an eye examination.
On June 19, 2005, the claimant went to New Milford Hospital Emergency Room and underwent a CT scan, the results of which were normal. The claimant was discharged that evening. On June 21, 2005, the claimant saw Christopher R. Reynolds, M.D., an ophthalmologist, who reported that the claimant was complaining of both binocular and monocular diplopia (double vision). Dr. Reynolds opined “that the claimant’s binocular diplopia suggested that the claimant had superior oblique muscle palsy and that the monocular double vision was probably due to an early cataract.” Findings, ¶ 9. Dr. Reynolds found no evidence that that claimant was suffering from any strabismus (a misalignment of the eyes).
On January 22, 2007 and January 31, 2007, the claimant sought treatment with Robert T. Spector, M.D., a neuro-ophthalmologist, who on March 27, 2007 issued a report stating that the claimant’s visual fields were normal but “the claimant’s muscle balance examination demonstrated left fourth nerve palsy which was particularly evident when the eyes, as well as the head, were placed into certain positions.”2 Findings, ¶ 11; see also Claimant’s Exhibit A (March 27, 2007 report of Robert T. Spector, M.D.). Dr. Spector also noted that when the claimant was looking straight ahead, he demonstrated displacement of the left eye in that it was higher than the right eye. Dr. Spector opined that the claimant had “suffered a job-related concussive injury that ‘probably hit the fourth nerve somewhere around the brainstem, or as the nerve left the brainstem, which unfortunately resulted in a strabismus that has yielded double vision (diplopia).’” Findings, ¶ 12, quoting Claimant’s Exhibit A (March 27, 2007 report of Robert T. Spector, M.D.).
On January 3, 2008, the claimant was evaluated by Stephen A. Mathias, M.D., an ophthalmologist, who opined that the claimant was suffering from a right superior oblique palsy and that the most likely cause of the claimant’s double vision was a “decompensated congenital superior oblique palsy brought about by fatigue, illness, anxiety, medication or aging.” Findings, ¶ 15; see also Claimant’s Exhibit A (January 25, 2008 report of Stephen A. Mathias, M.D., p. 1). Dr. Mathias did not believe that the claimant’s decompensation was caused by the head injury but stated that it was “possible” that the injury might have caused the decompensation to occur “sooner than would be expected.” Id.
On April 15, 2008, Andrew J. Levada, M.D., an ophthalmologist, performed a respondents’ medical examination on the claimant. Dr. Levada rendered a preliminary diagnosis of right superior oblique palsy which the doctor opined “could have been” caused by the head injury. Claimant’s Exhibit A (April 15, 2008 report of Andrew J. Levada, M.D., p. 3). Dr. Levada indicated that while the palsy could account for the claimant’s intermittent binocular double vision, it did not explain the monocular double vision, and he recommended the claimant undergo a neuro-ophthalmology exam. The claimant then saw Yanina Kostina-O’Neil, M.D., an ophthalmologist, for a second respondents’ medical examination on May 1, 2008. Dr. Kostina-O’Neil essentially concurred with the diagnosis of a “subtle” right superior oblique palsy and agreed that the palsy would not explain the claimant’s monocular double vision. Claimant’s Exhibit A (May 1, 2008 report of Yanina Kostina-O’Neil, M.D., p. 6). Dr. Levada again evaluated the claimant on May 20, 2008 and still could not determine what was causing the claimant’s monocular diplopia; the doctor opined that there was a “remote possibility” that the claimant had nuclear sclerosis cataracts in both eyes but could not relate that condition to the work-related injury. Claimant’s Exhibit A (May 20, 2008 report of Andrew J. Levada, M.D., p. 1).
At his deposition on March 12, 2010, Dr. Levada testified that the claimant had probably suffered with right superior oblique palsy for most of his life and that the injury on May 17, 2005 caused his brain to lose the ability to compensate for the palsy resulting in vertical diplopia. Dr. Levada reported that his office conducted a synoptophore examination which revealed irregularities in the claimant’s vision suggestive of a longstanding adaptation to a head tilt and an abnormal partial suppression of images. Dr. Levada opined that the claimant may have had the head tilt adaptation since childhood and that people can decompensate for this condition even in the absence of physical trauma. The doctor testified that the claimant had the equivalent of 100% loss of vision in one eye because the binocular diplopia could be relieved by covering one eye, and attributed this loss of vision to the claimant’s injury.
The claimant underwent another respondents’ medical examination on June 1, 2009 with Darron A. Bacal, M.D., an ophthalmologist. At his deposition on January 6, 2010, Dr. Bacal concurred that the diagnosis of the claimant’s mild concussive injury could produce binocular double vision but questioned whether the claimant was suffering from a fourth nerve palsy because such a condition usually affects both eyes. Dr. Bacal also noted that the injury of May 17, 2005 was not severe enough to cause a fourth nerve palsy in that this condition “is usually associated with a loss of consciousness, which did not occur in the claimant’s case.” Findings, ¶ 21, citing Respondents’ Exhibit 2, pp. 13, 17, 36. Dr. Bacal indicated that the claimant’s small, vertical strabismus diagnosed by several doctors one month after the injury was not evident when Dr. Kostina-O’Neil performed her examination on May 1, 2008 and had completely resolved by the time Dr. Bacal saw the claimant on June 1, 2009. Dr. Bacal did acknowledge that in Dr. Levada’s report of July 27, 2009, the doctor had reported observing a small strabismus in testing conducted in June and July 2009; however, Dr. Bacal “essentially dismissed it as deminimis [sic] in that the condition was so slight that the degree of misalignment that he measured would be within the range that a human being would be able to fuse those two images.” Findings, ¶ 23, citing Respondent’s Exhibit 2, p. 47. Relative to the claimant’s complaints of monocular diplopia, Dr. Bacal concluded that the claimant did not suffer from any condition which would cause monocular diplopia and monocular diplopia is “inconsistent with the stated mechanism of injury in that the claimant’s May 17, 2005 injury was suffered to the eyebrow area, and did not involve a direct injury to the eye itself.” Findings, ¶ 24, citing Respondents’ Exhibit 2, p. 19.
On September 17, 2009, the claimant underwent a Commissioner’s Examination with David M. Waitzman, M.D., a neuro-ophthalmologist. Dr. Waitzman concurred with the prior diagnosis of a fourth nerve palsy but opined that it had resolved and was not related to the May 17, 2005 injury. In his report of September 17, 2009, Dr. Waitzman stated that it is “an extreme stretch of the imagination to believe that his fourth nerve paresis actually occurred a month following the initial injury,” Findings, ¶ 25, because Dr. Waitzman’s research indicated that “the longest delay of the onset of diplopia would be three to four days.”3 Id. Dr. Waitzman noted that on the date of injury in question, the claimant did not hit his head or lose consciousness, and he subsequently did not complain of headaches or of being dizzy or disoriented. The doctor also testified that patients usually develop binocular diplopia in particular directions of gaze, not in all directions as this claimant reported.
In addition, Dr. Waitzman reviewed photographs of the claimant from childhood to adulthood and found no evidence of a head tilt; he therefore disagreed with Dr. Levada’s opinion that the claimant had a longstanding adaptation to tilting. The doctor also noted that the claimant also had normal three-dimensional vision. Rather, Dr. Waitzman opined that the claimant suffered an embolic stroke on June 17, 2005, which induced polyopia; he believed that the CT scan of February 1, 2010, which showed an area of infarction in the left cerebellar hemisphere, substantiated his theory that the claimant’s problems are more cerebral than ocular.4 Dr. Waitzman’s opinion was further buttressed by the findings of Dr. Kostina-O’Neil relative to the haziness that the claimant experienced in the center of each eye during the Amsler grid test, which haziness, according to Dr. Waitzman, was more consistent with a central nervous system problem than an ocular problem. Dr. Waitzman indicated that although the 2005 MRI did not show evidence of a stroke, it might have been so small as to go undetected; however, he did concede that this is a theory.5
The trial commissioner concluded that her ability to find the claim compensable was “compromised” by the delay between the date of injury and the development of the claimant’s reported double vision and the inconsistent and/or inaccurate medical histories contained in the record. Findings, ¶ A. The trial commissioner also found significant the fact that the claimant’s “primary advocate,” Dr. Levada, did not see the claimant until three years after the date of injury, could provide no proof for his theory of why the claimant decompensated following the injury, and in fact conceded that decompensation could have occurred absent any trauma. Id. Noting that “[w]ith few exceptions, the doctors’ opinions on diplopia causation were either equivocal or speculative,” Findings, ¶ B, the trial commissioner determined that the opinions of Drs. Waitzman and Bacal were most persuasive. Concluding that neither the binocular nor monocular diplopia were caused by the claimant’s work-related injury of May 17, 2005, the trial commissioner dismissed with prejudice the claims for compensation and permanent partial disability.
The claimant filed a Motion to Correct which was denied in its entirety, and this appeal followed. On appeal, the claimant contends that the trial commissioner’s reliance on the opinion propounded by Dr. Waitzman constituted error in that Dr. Waitzman’s opinion was not within reasonable medical probability. The claimant also challenges the trial commissioner’s factual findings with regard to Dr. Bacal’s opinion, asserting that the findings are inconsistent with the evidence presented and fail to include admitted and undisputed material facts.
The standard of deference we are obliged to apply to a trial commissioner’s findings and legal conclusions is well-settled. The trial commissioner’s factual findings and conclusions must stand unless they are without evidence, contrary to law or based on unreasonable or impermissible factual inferences.” Russo v. Hartford, 4769 CRB-1-04-1 (December 15, 2004), citing Fair v. People’s Savings Bank, 207 Conn. 535, 539 (1988). Moreover, “[a]s with any discretionary action of the trial court, appellate review requires every reasonable presumption in favor of the action, and the ultimate issue for us is whether the trial court could have reasonably concluded as it did.” Burton v. Mottolese, 267 Conn. 1, 54 (2003). “This presumption, however, can be challenged by the argument that the trial commissioner did not properly apply the law or has reached a finding of fact inconsistent with the evidence presented at the formal hearing.” Christensen v. H & L Plastics Co., Inc., 5171 CRB-3-06-12 (November 19, 2007).
We begin with the claimant’s allegations of error relative to the trial commissioner’s inferences regarding the opinion of Dr. Waitzman. The claimant contends that the trial commissioner’s dismissal of the claim constituted error because it hinged on a misplaced reliance on Dr. Waitzman’s theory that the claimant suffered a stroke, a theory for which Dr. Waitzman conceded he did not “have hard data to back it up.” Respondents’ Exhibit 3, pp. 34-35. As such, because the doctor’s opinion was based on “mere speculation and conjecture” and he “did not testify within reasonable medical probability that the diplopia was caused by a stroke it was improper for the commissioner to rely on his opinion as the basis for her ultimate conclusion that the claimant’s diplopia was not caused by the work injury.” Appellant’s Brief, p. 9. In addition, the claimant challenges the trier’s finding that the CT scan performed on the claimant on February 1, 2010 “substantiated” the doctor’s theory that the claimant suffered a stroke on June 17, 2005, pointing out that Dr. Waitzman never testified to this effect. Findings, ¶ 28. Having reviewed Dr. Waitzman’s testimony in its entirety, we are not persuaded by either of the claimant’s arguments in this regard.
In fact, our review of the record indicates that at his deposition of March 25, 2010, Dr. Waitzman provide a clear basis, independent of his theory that the claimant may have suffered a stroke, for the trier to reasonably infer that no causal connection existed between the injury of May 17, 2005 and the claimant’s binocular diplopia. For instance, Dr. Waitzman testified that the claimant’s case was “very confusing at the onset” in that the claimant was initially suffering from both binocular and monocular diplopia. Respondents’ Exhibit 3, p. 11. See also Claimant’s Exhibit A (April 15, 2008 report of Andrew J. Levada, M.D., p. 2). Although Dr. Waitzman agreed with the preliminary diagnosis of right fourth nerve palsy (which he explained was actually a right fourth nerve paresis), Dr. Waitzman described the injury as “relatively minor”, id., at 28, and also indicated that by the time he examined the claimant, the claimant’s binocular diplopia and right fourth nerve paresis had resolved and the claimant was experiencing monocular diplopia only. Id., at 11, 26. In addition, Dr. Waitzman testified that he found significant the fact that Dr. KostinaO’Neil had determined that the claimant’s double vision was not the result of any misalignment of the eyes when she examined the claimant on May 1, 2008.
Thus, although Dr. Levada reported finding evidence of binocular diplopia in July 2009, Dr. Waitzman disagreed, remarking that he and Dr. Levada had “a difference of opinion” on the issue and the deviation found by Dr. Levada was “tiny.”6 Id., at 22-23. Dr. Waitzman testified that he “disputed” Dr. Levada’s finding of binocular diplopia because the claimant was reporting double vision when he looked through his right eye only.7 Dr. Waitzman stated that he had found no physical evidence of binocular diplopia, and noted that the claimant’s field of binocular diplopia, as measured in the synoptophore examination conducted by Dr. KostinaO’Neil, was “all over the place” rather than confined to particular positions of gaze and, as such, also caused the doctor to doubt that the claimant was suffering from binocular diplopia. Id., at 55. Dr. Waitzman also testified that he disagreed with Dr. Levada’s opinion that the claimant’s initial binocular diplopia was due to a longstanding deviation for which the claimant had decompensated following the injury, likening that theory to “a glass that doesn’t hold water.” Id., at 28. Dr. Waitzman’s opinion in this regard was predicated on his own review of photos of the claimant which did not suggest that the claimant had been suffering from any “preexisting condition that would have been worsened” by having had this accident.8 Id., at 27. When queried as to whether he believed the claimant’s binocular double vision had resolved in light of Dr. Levada’s findings showing otherwise, Dr. Waitzman remarked that the difference of opinion between him and Dr. Levada could at least be partially attributed to the different histories given by the claimant to different physicians.9 Finally, at the conclusion of his deposition, Dr. Waitzman reiterated that even after reviewing the claimant’s test results, he would state within a reasonable degree of probability that the injury of May 17, 2005 was not the cause of the claimant’s current condition. Id., at 63.
Having reviewed the foregoing testimony from Dr. Waitzman, we find that the doctor provided a more than adequate basis, independent of his testimony regarding his theory that the claimant may have suffered a stroke, for the trier to properly infer that the claimant’s binocular diplopia did not arise out of or in the course of his employment. As such, we find no merit in the claimant’s contentions that the trial commissioner improperly based her dismissal of the claim on a medical opinion which was in any way speculative or outside the realm of reasonable medical probability. “Unless the medical testimony by itself establishes a causal relation, or unless it establishes a causal relation when it is considered along with other evidence, the commissioner cannot conclude that the [condition] arose out of the employment.” Murchison v. Skinner Precision Industries, Inc., 162 Conn. 142, 152 (1972).
We similarly reject the claimant’s charge that the trier erroneously concluded that Dr. Waitzman believed that the results of the February 1, 2010 MRI “substantiated” his theory that the claimant suffered an infarction on June 17, 2005. Findings, ¶ 28. At his deposition, Dr. Waitzman testified that the MRI findings of February 1, 2010 were “extremely important” in that they revealed “an area of infarction in the posterior or inferior cerebella artery distribution, which would be in the left cerebellar hemisphere. It’s the same vascular distribution that would supply blood to the occipital pole, which is where I would hypothesize this patient’s infarct might be.” Respondents’ Exhibit 3, p. 32. He therefore opined that because evidence of a stroke was not seen on the MRI taken in 2005, it must have developed after 2005. Dr. Waitzman also testified that he had found significant Dr. Kostina-O’Neil’s finding that the claimant complained of “haziness” in the center vision of each eye while undergoing the Amsler grid test, which complaint Dr. Waitzman ascribed to “damage to the pathways of the brain behind the crossing of the two optic nerves.” Id., at 14. In light of this test result, Dr. Waitzman concluded that the claimant had possibly experienced trauma, a stroke, a tumor or some other condition that had affected the central nervous system rather than the eye itself. Id., at 15. His theory was partially predicated on the fact that the claimant had a long-standing smoking habit; the doctor testified that his “hypothesis is that [the claimant] has a vascular disease involving the vertebrobasilar system, and most likely what happened on June 17, 2005, is, he had an embolic stroke, a small embolic stroke to the occipital parietal region.” Id., at 32.
There is no question that based on the foregoing testimony by Dr. Waitzman, the trier could have reasonably inferred that the doctor strongly believed several of the documented findings in this case, in combination with the claimant’s history as a smoker, supported his theory that the claimant may have suffered a stroke on June 17, 2005. Thus, while it may perhaps have been a slight overstatement for the trier to find that Dr. Waitzman believed this evidence “substantiated” his belief that the claimant suffered a stroke, the use of the word “substantiated,” rather than “supported,” is harmless error at most. This is particularly so in light of the fact that the trier, in her Finding and Dismissal of January 24, 2011, specifically stated that Dr. Waitzman acknowledged his hypothesis regarding the claimant’s possible stroke was a theory. Findings, ¶ 31; Respondents’ Exhibit 3, pp. 34-35. Moreover, as discussed previously herein, the balance of the doctor’s testimony provided a sufficient basis, independent of his discussions regarding his theory that the claimant suffered a stroke, for the trier to reasonably infer that the claimant’s binocular diplopia did not arise out of or in the course of his employment.
The claimant also challenges the trier’s findings with respect to the opinion propounded by Dr. Bacal, contending that the findings cited were inconsistent with the evidence and failed to include admitted and undisputed facts. Specifically, the claimant points to the trier’s findings relative to Dr. Bacal’s conclusion that the claimant’s vertical strabismus had resolved by the time both he and Dr. Kostina-O’Neil examined the claimant. The claimant points out that Dr. Kostina-O’Neil reported, and the trier so found, that as of May 1, 2008, the claimant was continuing to demonstrate symptoms of a “subtle” right superior oblique palsy which would suggest that the claimant was still suffering from binocular diplopia. Findings, ¶ 17; Claimant’s Exhibit A (May 8, 2008 report of Dr. Kostina-O’Neil, p. 6). The claimant also argues that even though Dr. Bacal initially testified at deposition that the claimant’s strabismic diplopia and fourth nerve palsy had resolved by the time he examined the claimant on June 1, 2009, when queried regarding the findings from an examination conducted by an associate of Dr. Levada’s on June 9, 2009, Dr. Bacal conceded that “you can’t conclusively say that the fourth nerve palsy has completely resolved.”10 Respondents’ Exhibit 2, pp. 55-56; Claimant’s Exhibit A (June 9, 2009 test results of The Eye Care Group). As such, the claimant maintains that “the commissioner’s reliance on Dr. Bacal’s opinions in support of her ultimate conclusions was misplaced in that it resulted from a misinterpretation of his testimony and a failure to find material, admitted and undisputed facts.” Appellant’s Brief, p. 11. We are not so persuaded.
The record indicates that when Dr. Bacal examined the claimant on June 1, 2009, he concluded that the claimant did not have binocular diplopia because there was no misalignment of the eyes and testing revealed that when the claimant’s left eye was occluded, the diplopia persisted. Respondents’ Exhibit 2, p. 33. However, when crossexamined at deposition regarding the results of the testing conducted by Dr. Levada’s office on July 1, 2009, Dr. Bacal acknowledged that the testing revealed full motility but also “an incredibly small vertical strabismus in straight-ahead position and straight down.” Id., at 46. Dr. Bacal described the result as “a very microscopic vertical deviation” and explained that “this very small vertical deviation doesn’t necessary have to produce diplopia because human beings, if the eyes are very, very slightly misaligned, can actually bring those two images together. And this degree of misalignment that he measured would be within the range that a human being would be able to fuse those two images.” Id., at 47. When queried as to whether such a small strabismus could cause binocular diplopia, he replied, “[i]t could. But what I’m saying is the deviation that he measured is basically as minute as you possibly can have.” Id. Dr. Bacal added that “[m]ost people would not experience diplopia with this tiny of a deviation unless you were extremely tired or fatigued.” Id., at 48. Dr. Bacal also observed that one set of tests performed by Dr. Levada’s office revealed “a very small amount of strabismus in straight-ahead position and down gaze, but all of the up gaze and the left gaze and the right gaze, there’s no strabismus. But then when you go the Exhibit 3, they’re reporting that there’s diplopia in up gaze and left gaze and right gaze. So, those two things don’t seem to coordinate.”11 Id., at 52.
Dr. Bacal testified that the results obtained by Dr. Levada’s office were not only inconsistent with his own findings but were also inconsistent with the findings of Drs. Waitzman and KostinaO’Neil. Id., at 53. As discussed previously herein, Dr. Kostina-O’Neil found “symptoms” of a subtle right superior oblique palsy but did not expressly report finding a strabismus. Claimant’s Exhibit A (May 1, 2008 report of Dr. Kostina-O’Neil). For his part, Dr. Waitzman testified that the testing conducted by Dr. Levada’s office in June and July 2009 revealed only a “really tiny” deviation which Dr. Waitzman did not deem medically significant.12 Respondents’ Exhibit 3, p. 23. In addition, when queried as to whether, in light of Dr. Levada’s test results, Dr. Waitzman still believed the binocular diplopia had resolved, Dr. Waitzman replied, “I will stand by what I have examined the patient for, and from what I’ve seen in the patient, I don’t find any evidence, physical evidence, of binocular double vision.” Id., at 55.
Our review of the trier’s findings relative to this issue indicates, contrary to the assertions of the claimant, that the trier adequately accounted for the discrepancy between the medical opinions of Dr. Bacal and Dr. Levada. The trier found that “Dr. Bacal acknowledged Dr. Levada’s observation of a small strabismus in his July 27, 2009 [report] but essentially dismissed it as deminimis [sic] in that the condition was so slight that the degree of misalignment that he measured would be within the range that a human being would be able to fuse those two images.” Findings, ¶ 23. The preceding discussion indicates that this finding accurately summarized and resolved the discrepancy between the opinions of Dr. Bacal and Dr. Levada relative to the results of the testing performed by Dr. Levada’s office in June and July 2009. This is particularly so in light of Dr. Waitzman’s remarks regarding these test results. Thus, although the trier’s finding that the claimant’s vertical strabismus had “completely resolved” by the time Dr. Bacal examined the claimant more accurately reflects the content of Dr. Bacal’s written report of June 5, 2009 rather than his deposition testimony of January 6, 2010, her subsequent finding addressing the de minimus nature of the strabismus accurately reflects the ultimate tenor of Dr. Bacal’s testimony. We therefore reject the claimant’s allegation that the trier erroneously relied upon Dr. Bacal’s opinion or in any way misinterpreted his testimony regarding Dr. Levada’s test results.13 Moreover, given that the trier ultimately determined that the claimant’s binocular diplopia was not related to the incident of May 17, 2005, the fact that said condition may have persisted when Dr. Levada’s associates examined the claimant in June and July 2009 is irrelevant.
We therefore reject the claimant’s contentions that the trier’s conclusions in this matter were predicated on either speculative testimony from Dr. Waitzman or an incorrect interpretation of Dr. Bacal’s testimony. The medical record in this matter clearly indicates that while there was some degree of overlap among the opinions of the various medical experts consulted in this claim, only Dr. Levada asserted within a reasonable degree of medical probability that the claimant’s injury of May 17, 2005 caused the claimant’s binocular diplopia.14 Claimant’s Exhibit B, pp. 15-16. However, Dr. Levada’s opinion was predicated on a theory of decompensation of a long-standing condition on the part of the claimant, and Dr. Levada himself testified that the decompensation could have occurred even in the absence of any trauma. Dr. Waitzman failed to find a causal connection between the injury of May 17, 2005 and the claimant’s binocular diplopia and dismissed Dr. Levada’s theory, at least in part on the basis of his review of old photographs of the claimant that did not reveal indications of a longstanding condition. Instead, Dr. Waitzman theorized that the claimant may have suffered a stroke. Both Drs. Waitzman and Bacal were troubled by the delay in the onset of the claimant’s symptoms, and Dr. Bacal likewise failed to find causation. As the respondents point out, “[s]imply because there is no agreed upon explanation for the cause of the ... diplopia does not mean that the commissioner simply has to jump to the conclusion that it is automatically related based on the fact that Dr. Levada concluded it was.” Appellees’ Brief, pp. 9-10. As such, we find the trial commissioner’s conclusions in this matter were well-supported by the record and reject the contentions of the claimant to the contrary. “It is the quintessential function of the finder of fact to reject or accept evidence and to believe or disbelieve any expert testimony. The trier may accept or reject, in whole or in part, the testimony of an expert.” (Internal citations omitted, emphasis added.) Tartaglino v. Department of Correction, 55 Conn. App. 190, 195 (1999), cert. denied, 251 Conn. 929 (1999).
The claimant also filed a Motion to Correct which was denied in its entirety. Our review of the proposed corrections indicates that the claimant is primarily engaged in reiterating the arguments made at trial which ultimately approved unavailing. We therefore find no error in the trier’s decision to deny the claimant’s Motion to Correct. As this board has previously observed, when “a Motion to Correct involves requested factual findings which were disputed by the parties, which involved the credibility of the evidence, or which would not affect the outcome of the case, we would not find any error in the denial of such a Motion to Correct.” Robare v. Robert Baker Companies, 4328 CRB-1-00-12 (January 2, 2002).
Having found no error, the January 24, 2011 Finding and Dismissal of the Commissioner acting for the Seventh District is hereby affirmed.
Commissioners Amado J. Vargas and Stephen B. Delaney concur in this opinion.
1 We note that a motion for extension of time and a motion for continuance were granted during the pendency of these proceedings. BACK TO TEXT
2 Darron A. Bacal, M.D., later testified that the notation in Dr. Spector’s report indicating that the claimant was suffering from nerve palsy in the left, rather than the right, eye was probably due to a typographical error given that all the other doctors who examined the claimant and diagnosed a nerve palsy attributed it to the right eye. Respondents’ Exhibit 2, p. 14. BACK TO TEXT
3 Administrative notice is taken of the September 17, 2009 Commissioner’s Examination provided by David M. Waitzman, M.D. See pp. 11, 12. BACK TO TEXT
4 The claimant underwent a second CT scan on February 10, 2010, after presenting at New Milford Hospital Emergency Room with vertigo and nausea which he reported had begun on January 28, 2010. We note that the record contains a report dated March 9, 2010, issued by Christian Leonardi, D.O., referencing this CT scan “which did show findings suggestive of a sub-acute stroke (likely less than 6 mos) that were not present from the scan from 6/19/05.” Claimant’s Exhibit C. BACK TO TEXT
5 Dr. Waitzman stated, “I think some damage to the occipital parietal area is the thing that makes sense in this case. Whether it’s a stroke or whether it’s a tumor or whether it’s trauma is unclear, and we don’t have physical evidence on an imaging study to back it up. So, yes, it remains a theory, and that’s as best as I can explain.” Respondents’ Exhibit 3, p. 35. BACK TO TEXT
6 Dr. Waitzman stated: “I understand what he’s saying, but I just disagree. I think that, based on my training and my experience with patients, this is not typical of patients who have binocular diplopia, even in patients who have this variation in their ability to fuse. This degree of a problem, which is really tiny, the degree of deviation we’re talking about is one diopter or less, and that means that the images are displaced one centimeter or one meter of viewing distance. So it’s a very tiny - a very tiny phoria or deviation.” Respondents’ Exhibit 3, p. 23. BACK TO TEXT
7 Dr. Waitzman testified that “the patient still experiences double vision, and, in fact, is most troubled by experiencing double vision when viewing through his right eye alone. That is the primary reason that I dispute these findings. I think he’s compensated for the findings that are present on this exam and that he’s never compensated and cannot compensate for the findings, in terms of his monocular vision.” Respondents’ Exhibit 3, p. 47. BACK TO TEXT
8 Dr. Waitzman conceded that the claimant could belong to the one or two percent of patients whose deviations are so minor that there is no compensating head tilt, but thought it was “highly unlikely.” Respondents’ Exhibit 3, p. 44. BACK TO TEXT
9 Dr. Waitzman commented, “I’ll say that I think the patient has given different histories to different physicians, it’s been documented multiple times throughout the record. So I don’t think it’s specifically the doctors that are at fault. I think it’s the history obtained from the patient that continues to change, and he does not provide the same story to every physician.” Respondents’ Exhibit 3, pp. 62-63. BACK TO TEXT
10 At Dr. Bacal’s deposition, the findings in question (“a very small exophoria and right hyperphoria in the straight ahead and down gaze,” possibly attributable to a residual of a fourth nerve palsy or some other etiology) are identified as the results of the testing performed by an associate of Dr. Levada on June 9, 2009 and are referred to as “Exhibit 2.” Respondents’ Exhibit 2, p. 55. Our review of the exhibits entered into the record reveals that Respondents’ Exhibit 2 is in fact the deposition of Dr. Bacal. Dr. Levada’s reports, including his report of July 27, 2009, were actually entered into the record as part of Claimant’s Exhibit A. However, it would appear that some portion of the testing performed on the claimant on June 9, 2009 by Dr. Levada’s office was previously marked as Claimant’s Exhibit 2 in a prior proceeding. These materials presumably provide the basis for the findings under discussion; however, these findings are not readily apparent. BACK TO TEXT
11 The results of the synoptophore examination conducted by Dr. Levada’s office on July 1, 2009 were submitted into the instant record as part of Claimant’s Exhibit A. It would appear that these test results were previously marked as Claimant’s Exhibit 3 in a prior proceeding. See footnote 10, supra. BACK TO TEXT
12 Dr. Waitzman based his opinion in this regard on the fact that the tests administered by Dr. Levada’s associates were designed to measure the maximum deviation between the eyes, as opposed to the double Maddox rod test administered by himself and Dr. O’Neil, which makes it more difficult for patients to fuse images because “they’re getting a line in one eye that’s red and a white line in the other eye. It’s extremely difficult to fuse those two images, and we found no evidence that this changed in any direction.” Respondents’ Exhibit 3, p. 48. BACK TO TEXT
13 Dr. Levada actually proffered his own explanation for the discrepancy in the test results, attributing the differences in the results between his initial exam and Dr. Kostina-O’Neil’s to “variability in the measurements.” Claimant’s Exhibit B, p. 19. Dr. Levada also explained that the symptoms of a strabismus can vary depending on whether the patient is fatigued or ill. Id., at 41. BACK TO TEXT
14 It should be noted that none of the doctors consulted in this matter identified the incident of May 17, 2005 as a contributing factor to the claimant’s monocular diplopia. In addition, although Dr. Spector did identify a possible causal link between the claimant’s injury and the diplopia, he reported that the claimant had “apparently” suffered a concussive injury which “probably” affected the fourth nerve, resulting in a strabismus. Claimant’s Exhibit A (March 27, 2007 report of Robert T. Spector, M.D.). BACK TO TEXT