Source: http://wcc.dli.mt.gov/D/Davis_M_FFCL.htm
Timestamp: 2019-04-21 06:19:25+00:00

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Summary: While working in the stationary department at Wal-Mart, claimant was injured when a paper shredder fell and struck the left side of her head. A CT head scan taken that day indicated no hemorrhage or lesions. However, she thereafter developed headaches, memory loss, unsteady gait, and other symptoms. Subsequent MRIs disclosed a mass on the right side of the brain which was larger with each subsequent MRI. Finally, approximately 18 months post-injury, claimant underwent brain surgery which disclosed an anaplastic astrocytoma, which is a glioma-type tumor. Although claimant's treating neurologists initially opined that the tumor was unrelated to her injury, during deposition they changed their opinions and testified that it was caused by the trauma. Claimant also called a non-treating neurosurgeon who testified similarly. However, another neurologist who had examined claimant, testified that there was no relationship between the trauma and the tumor. More importantly, Dr. Peter Burger, a neuropathologist on the faculty at Johns Hopkins, with 30 years experience in the field of brain tumors, testified on behalf of the insurer that that causation was not possible based on everything currently understood about glioma-type tumors, emphasizing in particular that brain tumors do not grow as quickly as would have been necessary in this case. He also testified there is no evidence suggesting trauma impacts or accelerates the growth of an existing tumor.
Held: Dr. Burger was far more qualified than all of the other medical witnesses in the area of brain tumors and their causation. His opinions were supported by medical literature and were persuasive.
Benefits: Medical Benefits. Claimant suffering from right-sided glioma-type brain tumor failed to persuade the Court her tumor was caused by work-related blow to the left side of her head, therefore she is not entitled to medical benefits for treatment of the tumor.
Causation: Medical Condition. Claimant suffering from right-sided glioma-type brain tumor failed to persuade the Court her tumor was caused by work-related blow to the left side of her head. The testimony of a tumor specialist, who was far more qualified than other testifying physicians, was persuasive that no link has been established between trauma and glioma-type brain tumors and that in any event glioma-type tumors develop slowly and could not have possibly developed in the short time in this case.
Evidence: Expert Testimony: Physicians. The testimony of tumor expert, with over 30 years experience and who is well versed in current medical research and literature as to cause of a brain tumor, is more persuasive than the testimony of far less qualified physicians.
Physicians: Conflicting Evidence. The testimony of tumor expert, with over 30 years experience and who is well versed in current medical research and literature as to cause of a brain tumor, is more persuasive than the testimony of far less qualified physicians.
¶1 The trial in this matter commenced on December 14, 2000, in Kalispell, Montana. Petitioner, Marilee Davis (claimant), was unable to be present but was represented by Mr. Garry D. Seaman. Respondent, Insurance Company of the State of Pennsylvania (Insurance of Pennsylvania), was represented by Mr. Donald R. Herndon. Through agreement of the parties, further telephone testimony was taken on January 25, 2001.
¶2 Exhibits: Exhibits 1 through 44, 46 and 47 were admitted without objection. Exhibit 45 was not offered.
¶3 Witnesses and Depositions: The parties agreed that the depositions of Robert Hollis, M.D., Ethan Russo, M.D., Bret D. Lindsay, M.D., and Douglas A. Nelson, M.D. shall be considered by the Court. Peter C. Burger, M.D., testified at trial on December 14, 2000. On January 25, 2001, Robert D. Schimpff, M.D., testified by telephone with the Court participating.
¶4A Whether the brain tumor leading to claimant's June 2000 surgery and responsible for her current medical condition and prognosis was caused or aggravated by the head injury she suffered on December 29, 1998, entitling her to benefits for medical expenses and disability.
¶4B Whether claimant is entitled to an award of costs and/or attorney fees.
¶7 Claimant reported the accident to her employer, which was insured by Insurance Company of the State of Pennsylvania. (Id.; Ex. 14 at 1.) A First Report of Injury was completed the day of the injury. Insurance of Pennsylvania accepted liability for the claim(1) but disputes liability for a brain tumor that was diagnosed a year-and-a-half after the injury. It alleges that the tumor is unrelated to the industrial accident.
Persistent left temporal headache and tenderness to touch there. She noted she was not as mentally sharp as usual. Often lost her train of thought. Got, quote, spaced out, unquote, on sitting. Sometimes felt sleepy, sometimes had difficulty sleeping. She stated that she lacked much of the intuitive sense that she had had previously and had been more emotional than usual, crying or easily losing her temper more easily.
Overall she felt she was improved since the prior visit. She was still having left temporal headaches occurring two to four times per week, which is somewhat less frequent than they had been previously. She was having what she called, quote, black out spells, unquote, which were brief, several second episodes, where she was unaware, was how she described it. When she would come to she would feel panicked and that she had been unaware. On average, these were occurring daily to every other day.
She said that these episodes had not improved since her last visit. She denied at that point weakness, numbness, tingling, or focal neurologic symptoms.
IMPRESSION: This is an abnormal EEG characterized by episodes of generalized dysrhythmic activity associated with hyperventilation as well as rare components of frontal sharp activity and focal left temporal slowing as well as occipital theta activity. This tracing is nondiagnostic in nature, but is highly suggestive of an underlying cerebral disturbance. The possibility of seizure disorder can not be excluded with this tracing alone and clinical correlation is advised. Other potential abnormalities would include vascular disease, degenerative processes and metabolic activity.
That her blackout spells were still occurring every other day to every day. She often - I believe she was back working at Wal-Mart at this point and she was doing inventory work and she noted that she was losing count when she was doing inventory work, which was atypical for her.
She noted that she was having brief memory loss episodes occurring several times daily. Her friends thought that she was getting worse. She often lost her train of thought in the midst of conversation. Still complained of left temporal headaches and tenderness. And she did state specifically at that time that all of these symptoms dated specifically from the date of her head trauma.
Marilee stated at that point that she seemed more off balance intermittently, the headaches were somewhat worse, still often relieved with aspirin. Her off-balance sensation was worse when she would look up and her symptoms were worse when she worked a long shift, the 11:00 a.m. to 8:00 p.m. shift. Her balance difficulties worsened in that situation.
When compared to the prior study of 2/26/99 there has been a slight, equivocal interval increase in the size of this lesion and it is better appreciated. Appearance is nonspecific but differential would include post-traumatic lesion, sequella of ischemia, inflammation and low-grade glioma. Clinical correlation is warranted and if indicated a repeat scan at the appropriate interval would be helpful in further evaluatin [sic] this lesion. No appreciable change in the size of this lesion.
The concern is that the right posterior temporal lesion appears to be growing in size subtly over the past eight months. The two primary differentials would be evolving contusion secondary to trauma and slowly growing glioma such as a low grade astrocytoma or low grade oligodendroglioma. Neither of the two neurosurgeons feel that biopsy or resection would be indicated yet as the lesion is quite small and it has demonstrated only very mild changes over the interval. We have hoped to obtain a functional scan either with SPECT or PET to help elucidate whether this is an area of encephalomalacia or if this represents neoplasm and the patient will be referred to Dr. Lynne Taylor in Seattle for a second opinion from a neuro-oncologist and, hopefully, functional scanning. Additionally, I will have her follow-up with Dr. Hollis for review of her case as well.
Closed head injury, post-concussive syndrome and intercerebral mass (? [questionable] Tumor vs. contusion). Through your office endeavoring to set up an appointment for her, she will go to Seattle for functional studies. If this proves to be a mass, then we will proceed with open biopsy/resection. If this proves to be a "cold" lesion then we will continue to watch it. If it is equivocal, I told her we would continue to watch.
a. History of closed head injury with post traumatic headaches and reported cognitive impairment.
b. Poorly circumscribed non-enhancing lesion in the right temporal parietal lobe just superior to the tentorium, of unknown etiology. Available evidence points away from an injury effect, given the lack of surrounding atrophy and slight interval increase in size. A repeat MRI is pending.
Marilee reports significant change in her neurologic symptoms with more difficulty with sequencing, disequilibrium and right temporal headaches. She does inquire with regard to the coincidence of head trauma and occurrence of her tumor and I discussed that I felt cause and effect were unlikely.
¶31 Claimant has treated with Dr. Lindsay following surgery. (Ex. 3 at 38-39.) She has undergone radiation and chemotherapy, as well as physical therapy. (Id.) Tragically, her prognosis is poor.
¶32 The issue raised by the claimant's petition is whether her tumor was caused or materially aggravated by her December 29, 1998 industrial accident. The record contains conflicting medical opinions regarding the issue.
¶33 The expertise of each of the physicians who rendered an opinion concerning causation is important to determining whose testimony the Court should give the most weight. I therefore preface my survey of each physician's opinions with a summary of his medical qualifications, beginning with Dr. Lindsay.
¶36 By the time of his deposition on October 12, 2000, Dr. Lindsay had changed his mind. He testified that "based on the temporal occurrence of the tumor and its rate of progression, and based on my understanding of the literature, I would say that it is more likely than not related to the trauma." (Lindsay Dep. at 15.) He explained what he meant by "temporal relationship:"
The fact that the lesion appeared to grow at a relatively slow rate initially and that growth rate would have been commensurate with beginning around the time of the trauma, so that one could easily suggest that the tumor or the neoplasm began growing around the time of the trauma, based on the evolution of the lesion on serial MRI scans.
¶40 As did Dr. Lindsay, Dr. Hollis gave great weight to the temporal relationship of the tumor to the trauma, i.e., to the fact that the tumor and her symptoms appeared to arise coincidentally with the industrial accident. He believed that the tumor and claimant's clinical symptoms both arose after claimant's December 1998 head trauma. (Id. at 21-22.) .
Right now we have only citations in the literature that suggest the possibility of development. Some of our older neurosurgeons that are no longer with us felt that relationship was stronger than has now been - that is now felt to be represented.
nothing in my earlier training in internal medicine and pediatrics to suggest that malignant gliomas occurred as a result of traumatic injuries.
¶44 Dr. Russo is a board certified neuorologist. There is nothing in the record to indicate that he has specialized training in glioma-type tumors.
was suffering from a condition called complex partial seizures, and that her medical complaints of blackouts and disturbed cognitive function occurring periodically were secondary to abnormal electrical activity which was being generated in her brain passing through a portion of the brain and causing disruption of her cognitive processes.
¶52 He also believed it was not clear that the abnormality on the February 1999 MRI was then an incipient tumor (id. at 64), as it "can be associated with a lot of different types of pathology, and the scans are in no way explicit with regard to what is causing that." (Id. at 25.) He thought it possible that it was evidence of injury from trauma, with the tumor developing later.
¶53 Dr. Schimpff discussed medical literature concerning the relationship between glioma-type brain tumors and trauma. According to the doctor, the literature contains anecdotal case reports of trauma inducting brain tumors and epidemiological evidence either showing no apparent association between trauma and gliomas or a weak association. (Id. at 21-22.) He also said that there is epidemiological evidence which appears to show an association between trauma and meningiomas. (Id.) Claimant, of course, had a glioma-type tumor, not a meningioma.
¶54 Dr. Schimpff articulated a possible mechanism by which trauma might cause the emergence of a glioma.
[W]hen a person has an injury to the brain, it can result in a type of scar, and the type of scar which occurs in the brain can be associated with a condition called gliosis.
And to try and keep it simple, gliosis simply refers to a reactive change which occurs in the astrocytes of the brain or other glial cells in the brain, and that reactive change is a change in the biology of the cells. The glial cells, the astrocytes, are sitting in the brain carrying out certain basic functions, but in the face of trauma, their biology changes. They can reproduce; that is, they can undergo cell division. There's all types of experimental work which shows that there's a change in the types of microbiologic substances which they produce. There can be change in growth factors. There can be a change in the type of metabolic activity which these cells undergo.
Because there is this reactive change which can occur as a result of traumatic injury, people have taken that one step further and said, "Gee, during this reactive change that occurs in these cells, could a certain percentage of patients, a small percentage or a subpopulation of patients, then go on to the development of uncontrolled cell division of the type which would then pathologically be identifiable?"
So that's sort of - I hope I didn't digress too much, but that's sort of a basic thinking which has gone on and been reported in the literature. That's the kind of thinking which I've indulged in thinking about this case, about the possibility that a reactive astrocytosis, secondary to a blow to the head and injury to the brain, could then, in a subpopulation of people, go on to establish actually a tumor.
¶57B Exhibit 49B is a 1998 anecdotal report of a case of a post-traumatic glioma. The latency period was two years (the tumor appearing two years after prior surgery which disclosed no tumor at the time). (Id. at 52, 56-57.) Dr. Schimpff was asked what in the article supported his opinion in this case and he referred to two things. The first was the introductory statement, "Trauma and scarring have been known to be predisposing factors for the development of meningiomas." (Id. at 53.) When counsel pointed out that the present case does not involve a meningioma, the doctor pointed out that the fact that there is a relationship between one type of brain tumor and trauma raises the possibility that a relationship could exist with respect to another type. (Id. at 53-54.) The second was reference in the article to a German experiment on rats which suggested "that under certain conditions cranial trauma may act as a cocarcinogen and enhance the rate of glioma formation in rats exposed to a potent carcinogen." (Id. at 54.) Dr. Schimpff had not read the German study and was relying on the report of it in the article in question.
¶57C Exhibit 47C is a 1989 journal article reporting an epidemiological study into risk factors for glioma. The study actually supports the proposition that there is no association between trauma and gliomas. It concludes "that head injury appeared not to be associated with glioma risk." (Id. at 58-59, emphasis added.) Dr. Schimpff, however, felt that the article overall supported his opinion because the mere fact of the study points out that there may be groups of people who on account of some exposure or biological susceptibility may be "susceptible to trauma as a trigger for glioma." (Id. at 58.) Dr. Schimpff's reasoning is illogical. The study, as he concedes, fails to find any relationship between the risk factors and subgroups identified by the authors and gliomas. The fact that some associative risk factors not identified in the study "might exist" is not proof that such risk factors in fact exist, it is merely an acknowledgment that lots of things are possible, or, as many experts concede in response to not-so-clever cross-examination, "Anything may be possible." The doctor's sloppy thinking, as manifested in his analysis of this article, is a factor I have considered in resolving the conflicting opinions rendered in this case.
A positive association between head trauma and glioblastomas was reported by Hochberg, but most studies have failed to support this finding [Choi 19, Annegers 20, Kurland 21, Codd 7]. No such association emerged in our series either, whether cerebral gliomas were considered as a whole or evaluated separately according to their malignancy; nor was any correlation found when mild traumas were distinguished from severe lesions.
¶57F Exhibit G added nothing since it was the same article as Exhibit B, thus Dr. Schimpff referenced only six articles.
¶61 Dr. Burger testified unequivocally that the claimant's tumor was not causally related to her head trauma. His opinions were based not only on his review of medical literature but also upon his extensive personal research and study.
Well, the articles can be summarized by saying that there are occasional cases where there is a patient that has a brain tumor that has a history of trauma, and these articles that were written would attempt to determine whether this was causally related. My review of the literature convinced me, which I already believed anyway, that these two things were not related in any way, shape or form. It's pure coincidence.
The concept is that, in brain tumors, like many others, by the time you see it on a scan, it's been there for years. It takes a long time for tumors to get to a certain stage.
This has been studied mathematically. If you take two cells, which are microscopic, and double them every so often, for a long time it doesn't get to be anything. Once it gets to be a certain size, doubling something that big becomes quite significant. When you see something, it's not like it just all of a sudden showed up. It's been there for awhile. When they first present, you're seeing things which, in a way, are in the late stages of the development.
It's actually very easy to explain. The CT scan is a much less sensitive test than MR by far. You would not expect to see this lesion on the CT when it was seen later in February. CT by today's MR standards is a pretty crude test. You cannot say that this was not there in December because it wasn't seen by CT. It wasn't a sensitive test . . . CTs are done for emergency, often for emergency purposes for head trauma, things like that.
But on patients having complex partial seizure as an expression of a tumor, I suppose trauma could do that. Some patients, it's never clear what the cause of it is, but it's a little bit out of my area of speciality.
¶72 I am not persuaded that claimant's brain tumor was caused by the head injury she suffered at Wal-Mart. Initially, I found the testimony of Drs. Lindsay and Hollis wholly unpersuasive. They both lacked any particular expertise concerning glioma-type tumors. Moreover, their literature review appeared cursory and they did not bother to print out or save their results. I was also unpersuaded by Dr. Schimpff's testimony. While he did some cancer research in the 1970s, he has been out of that field for more than 20 years and has been out of academia for the same time period. He has authored no articles in over 20 years and the medical literature he identified as supporting his opinions was limited to six articles which were either anecdotal or actually concluded that there is no proven link between trauma and glioma tumors. Dr. Schimpff's interpretation of two of the articles as supporting a relationship (see paragraphs 70C and 70D) strained credulity and undermined his credibility. Ultimately, it was clear to me that Dr. Schimpff failed to appreciate the standard for opinion testimony, confusing what is medically "probable" with what is medically "possible."
¶73 By far, the most persuasive testimony was that of Dr. Burger. Dr. Burger had far greater expertise than any of the other doctors, indeed he has decades of experience in tumor research, including gliomas, and has published extensively in the field. His testimony concerning the prevalent medical opinion regarding trauma and gliomas was persuasive; he had far greater familiarity with the medical literature on the subject and his interpretation of the articles which Dr. Schimpff said he relied upon is more consistent with the articles than was Dr. Schimpff's interpretation. But of even greater significance was his testimony concerning the latency period for gliomas, i.e., the time it takes for a glioma to develop into a detectable mass. He was unequivocal in stating that the claimant's glioma manifested itself far too quickly for it to have been triggered by trauma. The fact that the December 1998 CT scan did not disclose a tumor or other lesion does not undermine his opinion: Dr. Burger was not the only physician who pointed out that the CT scan is not as sensitive to tumors as is MRI and that the tumor could have been present but not detected by the scan. (See Drs. Russo and Schimpff testimony, ¶¶ 46, 56.) His analysis of the pathology slides from the tumor site disclosed no evidence of traumatic injury or lesion, thus undermining Dr. Schimpff's theory that the glioma could have developed from scar tissue caused by the trauma. Moreover, Dr. Burger testified that the February 1999 abnormality on the MRI "doesn't look like trauma on the film, and it gets bigger and ends up a brain tumor." (Tr. I at 66.) Finally, Dr. Burger also indicated that there is no credible scientific support for the notion that trauma accelerates the growth of a tumor.
¶74 The best case for a causal connection between the claimant's head trauma and her tumor is the temporal relationship between her injury and the tumor and symptoms. However, as Dr. Burger pointed out, temporal coincidences do not prove causation; it can be expected that in any population of people with brain tumors, some will have a history of head trauma even without a causal connection. The fact that claimant's symptoms followed her head injury does not provide a scientific basis for causation of the tumor. Moreover, some of her symptoms appear to have been caused by the head trauma, while others are due to the tumor.
¶77 The 1997 version of the Workers' Compensation Act applies to this case since that was the law in effect on the date of the injury at issue in this case. Buckman v. Montana Deaconess Hospital, 224 Mont. 318, 321, 730 P.2d 380, 382 (1986).
¶78 Claimant bears the burden of proving by a preponderance of the evidence that she is entitled to the benefits she seeks. Ricks v. Teslow Consolidated, 162 Mont. 469, 512 P.2d 1304 (1973); Dumont v. Wicken Bros. Construction Co., 183 Mont. 190, 598 P.2d 1099 (1979).
(1) Each insurer is liable for the payment of compensation, in the manner and to the extent provided in this section, to an employee of an employer that it insures who receives an injury arising out of and in the course of employment or, in the case of death from the injury, to the beneficiaries, if any.
¶80 Montana case law has also long held that testimony in the form of medical possibility does not by itself prove a claimant's entitlement to benefits. Matthews v. State Compensation Insurance Fund, 1999 MT 225, ¶ 15-17; Caekaert v. State Compensation Mutual Insurance Fund, 268 Mont. 105, 114, 885 P.2d 495, 501 (1994); Kramer v. EBI Companies, 265 Mont. 525, 533, 878 P.2d 266, 270 (1994) ("Mere medical possibility without supporting evidence is insufficient to establish compensability.").
¶81 In this case I am affirmatively persuaded that claimant's tumor was not caused or accelerated by the blow to her head occurring at Wal-Mart during December 1998. Therefore, respondent is not liable for medical bills or compensation benefits related to the tumor and subsequent surgery.
¶82 In her post-hearing brief, claimant cites several cases from other states for the proposition that cancer, including a brain tumor, is compensable if a workplace injury caused, accelerated, or aggravated a tumor. See, e.g., Reynolds Metals Co. v. Industrial Commission of Arizona, 98 Ariz. 97, 402 P.2d 414 (1965); United Electric Co. v. Myers, 134 So.2d 7 (Fla. 1961); Kling v. Central Lumbar & Millwork Co., 3 N.J. 151, 65 A.2d 772 (1949); Calabretta v. Lanorith, 90 App.Div.2d 608, 456 N.Y.S.2d 175 (1982); and additional cases noted in Petitioner's Brief in Support of Benefits at pages 16-18. Each of these decisions, of course, turns upon its own facts and medical testimony. As noted, on the record presented, and given current medical knowledge, I am not persuaded claimant's brain tumor was caused, accelerated, or aggravated by her work accident. I note that the most recent decision cited by claimant was decided in 1982, with the other decisions falling within the years 1939 through 1967. None of these decisions reflect current medical knowledge.
¶83 The questions presented for trial were whether claimant's tumor was related to her industrial accident and whether she is entitled to temporary total disability on account of the tumor. I have found adversely to her on those issues. However, since the issue was not presented, I do not determine whether she is entitled compensation benefits on account of her closed head injury, including the partial complex seizure disorder Dr. Schimpff believed to exist. Moreover, the evidence presented does not provide good guidance for determining whether absent the tumor she would be disabled.
¶84 Claimant's brain tumor was not caused or aggravated by her industrial accident. She is not entitled to medical or disability benefits on account of the tumor.
¶85 Claimant is not entitled to costs or attorneys fees.
¶86 Any party to this dispute may have 20 days in which to request a rehearing from these Findings of Fact, Conclusions of Law and Judgment.
¶87 This JUDGMENT is certified as final for purposes of appeal pursuant to ARM 24.5.348.
DATED in Helena, Montana, this 20th day of August, 2001.

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