Full opinion text
OPINION ON DAMAGES ENSLEN, District Judge. Plaintiffs in this action under the Federal Tort Claims Act (FTCA) are Dr. Walter Bergman and the personal representative of the estate of his late wife, Frances Bergman. Both Walter and Frances Bergman were among the “freedom riders” who traveled by bus into the South in May, 1961 to test a recent pronouncement by the United States Supreme Court that the Constitution required racial equality in interstate transportation facilities. Their encounter with a conspiracy of violent racism in Alabama was described in detail by this Court in an earlier opinion. Bergman v. United States, 565 F.Supp. 1353 (W.D.MI. 1983). That decision followed upon trial of the United States’ liability for the injuries plaintiffs suffered during their journey into Alabama. I held that the federal Government was negligent in failing to take steps available to it to avoid the violence, and concluded that, ... the United States’ failure to carry out its duties was a primary moving cause without which the physical injuries to the Freedom Riders would not have occurred. Moreover, the Plaintiffs suffered not only physical injury but also injury in the sense that they were deprived of the equal protection of the laws and their right to travel freely interstate. 565 F.Supp. at 1414. In addition to these rather obvious injuries, Plaintiffs contend that when Walter Bergman was beaten in Anniston, he suffered an injury to one of the arteries that supply blood to the brain. At trial in October, 1983 on the bifurcated issue of damages, Plaintiffs sought to prove that such an arterial injury, though essentially asymptomatic for several months, caused Dr. Bergman to sustain serious and permanent injury to a portion of his brain when he underwent an appendectomy some four months after the beating. The testimony presented to the Court during the five days of trial on damages focused almost exclusively on this causation question, and its resolution is the most difficult task before the Court at this final stage of the litigation against the United States. Plaintiffs seek damages for Walter Bergman’s permanently disabled condition since the operation, and for the toll that condition took on Frances Bergman during her lifetime. Plaintiffs also claim damages based on the events of the ride itself, including the beating, the fear and emotional injury they both suffered, and the Constitutional deprivations that they endured. Each plaintiff requests an award of one million dollars for these injuries, although they argue that in fact the value of their claims exceeds even that amount. In support of their damage claims, Plaintiffs presented the testimony of Walter Bergman and his present wife, Patricia Bergman. Dr. George Mogill, for many years the family doctor of both Walter and Frances Bergman, also testified on their behalf. In their efforts to prove a causal connection between the beating and Bergman’s brain damage, Plaintiffs relied largely on the testimony of their expert witness, Dr. John Gilroy. A specialist in neurology since 1960, Dr. Gilroy is Chief of Neurology at Harper Grace Hospital and Detroit Receiving Hospital in Detroit, consults at several other hospitals there, and is Professor and Chair of the Department of Neurology at Wayne State University. Through a deposition taken in 1983, Plaintiffs also introduced the testimony of the anesthesiologist involved in Bergman’s 1961 appendectomy, Dr. Raymond Sphire. The Government called two expert witnesses to contest Plaintiffs’ theory of causation. Dr. Oscar Reinmuth has been a neurologist for some 30 years, and is now Professor and Chair of the Department of Neurology at the University of Pittsburgh. Dr. Maurice Victor's background includes a decade of teaching at Harvard University, and. he has been a Professor of Neurology at Case Western Reserve University and Chair of the Department of Neurology at Cleveland Metropolitan General Hospital since about 1962. All of the extremely well-qualified experts relied on Dr. Gilroy’s report of an examination of Bergman early in 1983, and supplemented that information with medical records which were also received in evidence. Those records include extensive reports from Dr. Bergman’s 1961 hospitalization, and a thorough reevaluation of Bergman’s condition undertaken in 1975. A number of other exhibits were also received. In preparing this opinion, and weighing the sharply contrasting expert testimony, I have reviewed the entire record and considered the briefs submitted by the parties. Having done so, and having observed the witnesses and heard the evidence presented at the time of trial, I make the following findings of fact and conclusions of law, as required by Rule 52(a), Federal Rules of Civil Procedure (FRCP). I turn first to the most difficult and most controverted question of whether Dr. Bergman’s brain damage was proximately caused by injuries he received in Anniston, Alabama. I. CAUSATION The Beating in Anniston On May 14, 1961 the Trailways Bus carrying Walter and Frances Bergman, and other freedom riders, stopped in Anniston, Alabama. There, Walter Bergman was beaten into unconsciousness by a group of attackers who entered the bus carrying brass knuckles and clubs. Dr. Bergman recalled being floored by blows to the head and face, but once on the floor of the bus he quickly blacked out. Other witnesses provided details of the severe beating Bergman sustained. Schooled in nonviolence, Bergman had offered no resistance to the blows, but Isaac Reynolds testified that it “took something for them to beat him down to the floor where they began to kick and stomp him.” (TR L 89). Herman K. Harris testified that there were “two main guys” kicking Dr. Bergman, and that they “just kicked him and kicked, just kicked him * * Up, up his head and shoulders in the back. I thought maybe they would break his, bust his head, ...” (TR L 168). Another freedom rider, Ivor Moore, ended up on top of Bergman, and he was also kicked and stomped. According to Reynolds, the beatings lasted a total of maybe seven or eight minutes, then Bergman was picked up and thrown over several seats to the rear of the bus. At the time of the incident, Bergman was 61 years old. When Bergman regained consciousness, he was seated, and the bus was moving on its way to Birmingham. Both of his eyes were blackened from the blows he had received, and his jaw was so sore and swollen that he had to live on a liquid diet for several days. Bergman testified that he felt he had recovered his “normal sensibilities” when he came to. (TR L 525). He does not recall feeling dizzy, and he was aware of his surroundings. Over the next few days he had no visual problems, no headaches, suffered no further loss of consciousness, and did not feel faint. (TR D 296-297). He believed his wounds needed only time to heal, and he did not seek medical attention for his injuries. (TR D 296, TR L 535). The freedom riders, unable to continue their bus trip from Birmingham, flew to New Orleans where they stayed for a few days, participating in civil rights activities. The Bergmans then returned to Detroit, Dr. Bergman resuming work he had begun before the trip, on the grounds of their new home. Bergman testified that in April he had cleared a path up a hill from a creek on the property, and that after returning to Detroit he was taking pebbles from the creek bed and using them to cover the path he had already cleared. He testified that the work was fairly strenuous; the hill was steep enough to require five switchbacks, and Bergman was pushing the rocks up the trail in a wheelbarrow. His time that summer was divided between the work on his property and a busy schedule of civil rights activities, including speaking engagements and training events in the midwest and east. At trial, Dr. Bergman recalled that much later his wife told him that she had noted he had been dragging one of his feet slightly since the beating. The medical records contain reports of this “foot drop” and that Bergman had been acting somewhat “hazy” and had shown some personality change during the summer. It appears that this information came largely from Frances Bergman, although in one notation, a doctor states that “this peculiar demeanor was noticed by the physicians and later confirmed by the patient’s wife.” (Ex. 2, p. 201). A history taken by Dr. Mogill on September 16, 1961 noted that after the beating in Anniston, Bergman “was somewhat dizzy for sometime although there was no apparent sequelae of unusual moment.” (Ex. 2, p. 197). However, Bergman’s present recollection is that he did not suffer any dizziness during the summer of 1961, and he testified that he could not say whether he had in fact been somewhat “hazy” during the months following the beating. The secondhand reports in the medical record are the only evidence before the court of any possible sign during the summer of 1961 that the injury Bergman received in Anniston might be more serious than Bergman had at first believed. The Operation On September 15, 1961, Frances Bergman contacted Dr. Mogill and told him that Bergman had diarrhea and abdominal pain. The doctor prescribed some medication, but when Bergman’s symptoms were not relieved, Dr. Mogill arranged for him to be admitted to Grace Hospital in Detroit (now Harper-Grace). Dr. Bergman has no recollection of this event, but the hospital record reflects that he was admitted at 12:25 a.m. on September 16, 1961, with diarrhea and lower abdominal pain. The initial impression was acute gastroenteritis, and a possible partial bowel obstruction. However, by 4:30 p.m. on the 16th, consulting surgeons Miller and McLean concluded that an immediate appendectomy was indicated, (Ex. 2, p 213), and a post-operative report confirms that his appendix was indeed inflamed. (Ex. 2, p 222). Dr. Bergman was given some premedications, and at 5:00 p.m. a spinal anesthetic was started. According to the anesthesiology record, the surgery began at 5:10. Toward the end of the operation, Dr. Bergman suffered a drop in blood pressure, and for some period of time between 5:50 and 6:00 p.m., his heart stopped. The length of that cardiac arrest, and its significance in light of Bergman’s symptoms, are key elements to both the Plaintiffs’ and the Defendant’s view of the case, and are strongly contested. However, it is undisputed that although Dr. Bergman’s vital signs returned, he remained in a coma for several days, and suffered severe and permanent damage to the portion of his brain that controls muscle coordination. The hospital progress notes indicate that Bergman suffered convulsions and had problems with muscle coordination both while comatose and after he regained consciousness. Bergman testified that for fully a month after the operation, he had to be tied down when on a stretcher or in a wheelchair, because of the intensity of the shaking in his limbs, and his bed had to have sideboards to keep him from falling out. He began physical therapy on September 29, making some minimal progress. By November 11 he was able to get in and out of bed, and by December 15, he could feed himself, according to the progress notes contained in the hospital record. Bergman was discharged on December 16, 1961, with only a “guarded” prognosis for recovery of full muscle control. (Ex. 2, p. 212). For several weeks after leaving the hospital Bergman was unable to sit up on his own, and had to be bolstered in a sitting position with pillows. His testimony recounted the lengthy and difficult process of regaining the ability to do even such simple things as clapping his hands. A diary that Frances Bergman had kept (Ex. 23) indicates that it was not until the end of April 1962, that Bergman was able to write a letter, and that it was not until late May 1964 that he was regularly able to use the bathroom without assistance. The diary reflects a daily struggle in which Bergman would slowly and painfully progress and then regress. He had shaky days with persistent tremors, and steady days when he met with some success at standing or walking for minutes at a time. Although Bergman persisted in his attempts at walking, and in fact made some progress, he was never able to walk without either the aid of another person or some artificial support. In 1975, after having already suffered several falls, he was advised not to make further attempts to walk, given the likelihood of injury. Since that time, Bergman has reamined confined to a wheelchair. Dr. Gilroy examined Bergman in March, 1983 and found that he continues to suffer from a severe tremor in his limbs. He also has difficulty in speaking because of impaired articulation, a condition known as dysarthria. Dr. Bergman cannot stand or walk unaided, because of truncal ataxia, a nervous system condition in which the muscles are unable to make the minute adjustments required to balance and counteract gravity. Bergman’s movements are marked by what is known as an “intention trem- or”: when he tries to touch an object, for example, his arm overshoots and then over-corrects until finally reaching the target, in a kind of oscillating motion. While Dr. Bergman’s coordination remained severely impaired, his mental processes appeared to be making a swift recovery within a relatively short time after the operation. The September 17, 1961 progress notes indicate that Bergman appeared to respond slightly to loud calling, and by September 21, he was responding to suggestions and trying to communicate. The progress notes from the end of September reflect that Bergman’s speech was good and his thinking was clear. On October 2, it was noted that Bergman’s cerebration was improving, and he was mentally alert. Similar observations of clear mentation were made in May 1962 when Bergman was in the Rehabilitation Institute of Metropolitan Detroit, (Ex. 3, p. 24), and in 1975, by Dr. McHenry. A test administered to Bergman in 1975 indicated that he has an IQ in the superior range. Bergman recalled at trial that within a month after he regained consciousness, he was used to demonstrate to a class of medical students the sharp distinction between physical agility and mental capacity: while practically shaking off the hospital bed, he counted backwards rapidly from one hundred, by sevens. Plaintiffs’ Theory It is this marked contrast between Dr. Bergman’s intellectual ability and his in-coordination of movement that first caught the attention of Plaintiffs’ expert, Dr. Gilroy. This clinical picture, combined with evidence of cardiac arrest of only short duration, caused Dr. Gilroy to theorize a causal factor with an origin outside the walls of the operating room. An understanding of Plaintiffs’ theory and the medical testimony requires first an orientation to the anatomy of the brain. Here, the testimony focused on three major anatomical divisions: the cerebrum, the cerebellum, and the brainstem. The cerebral hemispheres include the large convoluted folds of matter at the top of the brain, and are concerned with higher functioning such as thought and memory, as well as hearing and vision. A smaller area of the brain, the cerebellum, lies beneath the cerebral hemispheres toward the rear of the skull cavity. This portion of the brain controls regulation of muscles of posture and allows a person to be stable by making the automatic adjustments necessary to combat gravity. Thus when we sit or stand, we do not sway, the head does not nod; the muscles are under automatic control. The brainstem is located in front of the cerebellum, and connects to the spinal cord. The upper portion, the pons, bridges the two cerebellar hemispheres. All of the pathways from the cerebral hemispheres v and cerebellum have to go through the brainstem to reach the spinal cord. Eye movement is programmed in the brainstem, and in the lower part, called the medulla, there are senders for automatic functioning such as maintenance of blood pressure and respiratory rate. The experts agreed that Dr. Bergman’s problems with coordination of movement and speech signify severe and permanent damage to the cerebellum. They agreed that if any cerebral impairment is present, it is only mild in degree. But while they agreed that in general terms it was a deprivation of oxygen — anoxia or hypoxia — during the operation that damaged Bergman’s brain, their theories diverged sharply when it came to the mechanism by which he sustained a sufficient amount of anoxia to account for his severe and permanent impairment. The seed of the experts’ dispute in this case is the report found in Bergman’s medical record that the cardiac arrest was estimated to have lasted only about one minute and 45 seconds. Blood flow to the brain through its arterial systems, like all blood flow, depends on the pumping action of the heart. The cessation of blood flow caused by a cardiac arrest deprives the brain of the vital oxygen and glucose it needs to survive, and results in permanent cell damage, but only if the cardiac arrest is of at least three to five minutes duration. The Government’s experts contended that Bergman’s condition can be explained by the lack of blood flow during the cardiac arrest. They argued that given Bergman’s residual symptoms, the one minute, 45 second estimate must be an error. Dr. Gilroy, on the other hand, advanced the position that because Bergman’s heart is reported to have resumed its beat within such a short time, the anoxia caused by that event was not enough by itself to cause the severe brain damage observed in Bergman. Dr. Gilroy found further support for this proposition in the predominantly cerebellar nature of Bergman’s injury. He testified that in his experience anoxia alone, no matter how long it deprives the brain of oxygen, does not produce a clinical picture of significant cerebellar damage and nonexistent or mild cerebral damage in a brain where the circulatory system had been functioning normally. Usually, Gilroy testified, there is major involvement of the cerebral hemispheres, with clinical signs of damage to that area of the brain as marked or more marked than the indications of damage to the cerebellum. Dr. Gilroy testified that in light of these considerations, there must have been some preexisting abnormality in the brain’s circulatory system that focused on the cerebellum and that was responsive not only to the cardiac arrest, but also to the period of low blood pressure which preceded it. Dr. Gilroy testified that the selective nature of the brain damage, resulting in a predominantly cerebellar syndrome, can only be reflective of damage to the arterial system which supplies blood to that specific area of the brain. Two main circulatory systems feed the brain with oxygen and glucose. The carotid arteries are the large vessels in the front of the neck, each palpable as a strong pulse. These two arteries have their origin in the main vessels in the chest, and each divides into two branches, one going into the face, and one — the internal carotid — going up into the brain through the base of the skull. The most important branch of the internal carotid, the middle cerebral artery, nourishes about two thirds of the cerebral hemispheres. In the territory of that artery are the areas controlling speech and orientation, and most of our thought processes. The other main system is the one that supplies the cerebellum. It is composed of two vertebral arteries that ascend close together in the back of the neck at either side of the spinal column, encased in lateral protrusions of the vertebrae called transverse processes. These arteries ultimately pass through the foramen magnum in the base of the skull and run up the medulla, joining at the base of the pons to form the basilar artery. In addition to supplying the cerebellum, this vertebral basilar system also supplies blood to the brainstem, part of the midbrain, and some of the internal structures of the brain, and often provides some supply to the occipital area of the hemispheres. Before joining to form the basilar artery, the vertebráis give off a branch which feeds the undersurface of the cerebellum. The basilar artery also gives off several branches as it runs up the brainstem. As Dr. Gilroy explained, the vessels of two of these branches interlace in the cerebellum, creating an area referred to as the “watershed.” There, blood supply is relatively poor and there is maximum damage when there is a reduction of blood flow, since blood flow tends to be least effective where there is a juncture of circulation. Under normal circumstances, the vertebral arteries are the sole source of blood supply to the cerebellum. However, two communicating vessels connect the carotid and vertebral basilar systems in a safety feature called the Circle of Willis. While blood from the carotid system may run backward to the base of the brain through this mechanism, it does not protect the brainstem or cerebellum. It does serve to protect the area supplied by the last branch of the basilar system, the occipital lobe. Thus, when there is a vertebral basilar problem, the entire cerebral hemispheres may be protected from damage. Given these principles of blood flow in the brain, Dr. Gilroy looked to the vertebral basilar system to find the mechanism that produced Bergman’s condition. In a report to Plaintiffs’ attorneys written after his examination of Bergman in March 1983 (Ex. 24), Dr. Gilroy concluded that the mechanism involved was blockage of a vertebral artery. He opined that Bergman would have survived such an occlusion with a marginally sufficient blood flow through the second vertebral artery, and would not have experienced any symptoms until the system was stressed by a drop in blood pressure. He posited that when Bergman suffered such an episode of hypotension during the operation, the reduced efficiency in circulation of the damaged arterial system resulted in inadequate blood flow to the cerebellum, causing permanent damage, while the normal carotid system continued to supply the cerebrum. Under this theory, Dr. Gilroy concluded that the damage in the cerebellum was then compounded by the cardiac arrest, which was too short in duration to affect the cerebral hemispheres. Dr. Gilroy theorized that the injury to the vertebral artery must have been caused by trauma at the time of the beating, since there was no other explanatory cause of vertebral basilar insufficiency in Bergman’s medical history and since Bergman had been healthy prior to going on the freedom ride. Dr. Gilroy’s examination of Bergman and the medical history he took at that time had revealed no indications of vascular disease which might have explained the posited vertebral artery occlusion. Prior to May 1961, Bergman’s health had been good, and he led an active life. During 1959 and 1960, the Bergmans lived in Austria, where Dr. Bergman did a considerable amount of walking on a daily basis. Bergman testified that his health was excellent when he left Detroit to join the freedom rides. At trial, Dr. Gilroy testified that although he still believed that the beating had caused an injury to Bergman’s vertebral artery and that such injury had ultimately resulted in the cerebellar damage, a literature search had caused him to refine his theory. He testified that the vertebral artery injury he had postulated would not have caused damage during the period of hypotension unless the autoregulatory capability of the vertebral basilar system had been severely impaired. Autoregulation refers to the ability of the brain’s circulatory systems to maintain the proper blood flow despite variations in blood pressure. With impairment of autoregulation, a drop in blood pressure is accompanied by an equivalent diminution of blood flow through the arterial system. Consequently, perfusion of the brain by an arterial system with impaired autoregulation is affected at higher pressures than if autoregulation were functioning. Gilroy concluded that in this case there was, in addition to occlusion of a vertebral artery, a loss of autoregulation in the vertebral basilar system, and that it was this combination of factors that made Bergman’s cerebellum susceptible to damage during the period of hypotension. Since in his opinion a vertebral artery injury could have caused the impairment of autoregulation, he felt that the validity of his theory of causation remained intact. The description of how the beating and vertebral artery injury could have resulted in impaired autoregulation, is somewhat complicated, and largely theoretical. Gilroy testified that one way that blood vessels accommodate changes in blood pressure is by an automatic involuntary muscular response: if the pressure drops, the vessel — essentially a tube of muscle tissue — expands to maintain the same amount of flow; if the pressure increases, the tube constricts. Dr. Gilroy’s theory in this case focused on a second mechanism of autoregulation he described, in which nerve fibers on the blood vessels receive impulses and respond by contracting or relaxing. Dr. Gilroy testified that it has been proved that the nerve fibers take their origin from nerve cells in the brainstem; there, the cells respond to stimuli and send out impulses that result in regulation of the flow through the vessel. According to Gilroy, studies reported in the literature indicate that when the brainstem is damaged almost anywhere in its central pathway of core brain matter, autoregulation is impaired, because of the integral nature of the autoregulatory system there. Such impairment of autoregulation may last for many weeks or months, or as long as a year, Dr. Gilroy stated. He believes that is what happened in this case. According to Dr. Gilroy, this scenario resulted because a blood clot from the occluded or injured vertebral artery had moved up into the brainstem and occluded a small vessel there, causing tissue death (infarction) in the area cut off from blood supply. This event could have occurred either during clot formation at the time of the trauma to the artery, or later during the normal processes of clot dissolution, but in any event within some ten days of the beating. Dr. Gilroy testified that in his opinion, with impaired autoregulation Bergman would have gotten into trouble with a systolic blood pressure of 90 or even higher, while a normal individual would not start to feel faint until that upper pressure dropped to about 60. The medical record reflects that at approximately 5:45 p.m. during the course of the operation, Bergman’s blood pressure dropped to 80/50, from a pressure of 120/80 recorded at the beginning of the operation. I find no blood pressure recorded from 5:45 until shortly after 5:55, contrary to Dr. Gilroy’s testimony that at 5:50 there was a systolic pressure of 60. However, it is clear that there was a period of relative hypotension for some seven minutes prior to the cardiac arrest. Dr. Gilroy opined that damage to the cerebellum began with the fall in pressure, because the autoregulatory system could not respond to allow a sufficient supply of blood to reach that portion of the brain. Bergman felt the effects of the variation in the cerebellum, while a separate undamaged autoregulatory system in the cerebral hemispheres was able to maintain an adequate blood flow to that portion of the brain. The cerebellum continued to sustain permanent injury during the one minute and 45 seconds of cardiac arrest. Dr. Gilroy testified that this total period of almost nine minutes was a long time in terms of brain damage, and that it was the cause of the selective and permanent damage to Bergman’s cerebellum. Gilroy testified that his theory is the only way to explain the severity of Bergman’s brain damage while at the same time accounting for a short period of cardiac arrest and the predominantly cerebellar nature of Bergman’s residual symptoms. He testified that because he can find no other explanation consistent with all the facts, he can state to a reasonable degree of medical certainty that Bergman suffered an injury to his vertebral artery on May 14 that played a direct causal role in the later brain damage. The Government, through its medical experts, took exception to Dr. Gilroy’s theory at every step of the analysis. Drs. Reinmuth and Victor directly contradicted many of the medical principles upon which Dr. Gilroy relied, and disputed the reasonableness of Gilroy’s conclusions, pointing to the lack of objective evidence of vertebral artery injury and brainstem damage. They rejected Gilroy’s conclusion that the picture of predominantly cerebellar syndrome could not have been produced by cardiac arrest alone, and they directed the court’s attention to indications in the medical record of “mild but definite” cerebral deficits. Dr. Reinmuth testified to an entirely different school of thought on autoregulation, stated that autoregulation is not controlled by a center located in the brainstem, and opined that damage to the brainstem would have to have been severe to impair autoregulation. Both Dr. Reinmuth and Dr. Victor were of the opinion that injury to a vertebral artery during the beating was highly unlikely and that if there had indeed been such an injury, it would have been accompanied by symptoms. The Government contends that the most reasonable explanation for Bergman’s condition is that the medical record inaccurately reflects the length of the period of anoxia, and that in fact Bergman must have suffered cardiac arrest for at least three to five minutes. Drs. Reinmuth and Victor believe that the cerebrum suffered the same lack of oxygen as the cerebellum during the operation, causing severe damage in a diffuse fashion. In their opinion, Bergman’s concededly excellent cerebration can be attributed to a strong recovery in the cerebrum and to the great redundancy of cell function within that portion of the brain. Law of Causation In order to prevail on their theory of causation, the Plaintiffs must meet the requisite legal standard of proof. Under the Federal Tort Claims Act, Alabama law controls the question of causation, since the United States’ negligence occurred in that state. 28 USC § 1346(b); Richards v. United States, 369 U.S. 1, 10, 82 S.Ct. 585, 591, 7 L.Ed.2d 492 (1962). The Court has already ruled that the United States’ negligent failure to act was the proximate cause of the beating sustained by Walter Bergman on May 14, 1961. Bergman v. United States, 565 F.Supp. 1353, 1414 (W.D.MI. 1983). Under Alabama law, the United States is responsible for all the reasonably foreseeable consequences of that negligent omission. Watkins v. United States, 589 F.2d 214, 219 (CA 5 1979). Thus, Bergman may recover for his brain damage if it is shown to be a natural and probable consequence of the negligent act or omission which an ordinarily prudent person ought reasonably to foresee would result in injury. Vines v. Plantation Motor Lodge, 336 So.2d 1338, 1339 (Ala.1976). This rule applies equally to a contention that a second injury occurred because of a weakness or disability caused by an original injury. Alabama Farm Bureau v. Henderson, 374 So.2d 355, 357 (Ala.Civ. App.1979). The beating need not be the sole proximate cause in order for Defendant to be held liable for the brain injury. Alabama Power Company v. Taylor, 293 Ala. 484, 306 So.2d 236, 249 (1975); Watkins v. United States, supra. Neither must it be the act nearest in time to the injury, as long as it actively aided in producing the injury as a direct and existing cause. Aggregate Limestone Co. v. Robison, 276 Ala. 338,161 So.2d 820, 822 (1964). Dr. Gilroy readily admits that his theory is constructed not from a history of symptoms which support a diagnosis, but from a series of deductions which he contends are compelled by the facts, and which are almost entirely unsubstantiated by any direct evidence. The logic of Plaintiffs’ case may be summarized as follows: the operation alone cannot satisfactorily explain the facts because the cardiac arrest lasted for only a short time and cardiac arrest alone would not cause the clinical picture Bergman presents; in order to account for these facts, there must have been a preexisting impairment of circulation in the vertebral basilar system susceptible to a reduction in blood pressure; impaired autoregulation and inefficient circulation can result from a vertebral artery injury and brainstem infarction; and the beating could have caused a vertebral artery and a brainstem infarction. Therefore, Plaintiffs reason, it is medically possible that there is a causal relationship between the beating and the brain damage, and since Dr. Gilroy can conceive of no other explanation, it is more probable than not that his theory describes what in fact occurred. Plaintiffs are not foreclosed from sustaining their burden of proof simply because the evidence on causation is circumstantial. E.g., Southern Railway Co. v. Dickson, 211 Ala. 481, 100 So. 665, 669 (1924); City of Bessemer v. Clowdus, 261 Ala. 388, 74 So.2d 259 (1954); Folmar v. Montgomery Fair Company, Inc., 293 Ala. 686, 309 So.2d 818 (1975); Plyworld, Inc. v. St. Paul Fire & Marine Insurance Co., Inc., 351 So.2d 1363 (Ala.1977). But their theory cannot prevail if it rests on speculation or conjecture. Southern Railway Co. v. Dickson, supra; St. Paul Fire & Marine Insurance Co. v. Thompson, 346 So.2d 439, 441 (Ala.Civ.App.1977). Thus it is not sufficient for the plaintiff to show only that the injury could have occurred in the manner alleged. Southworth v. Shea, 131 Ala. 419, 30 So. 774 (1901); Maddox v. Ennis, 274 Ala. 229, 147 So.2d 788 (1962); Peevy v. Alabama Power Company, 393 So.2d 971 (Ala.1981). A “mere possibility” of causation does not satisfy the requirement of proximate cause. Brown Mechanical Contractors, Inc. v. Centennial Insurance Company, 431 So.2d 932, 942 (Ala.1983); Ex parte Travis, 414 So.2d 956 (Ala.1982). At the same time, The plaintiffs here are not required to prove their case beyond a reasonable doubt. They need not negative entirely the possibility that the defendant’s conduct was not the cause. It is generally recognized that it is enough that the plaintiff introduce evidence from which reasonable [persons] may conclude: “ * * * that it is more probable that the event was caused by the defendant than that it was not. The fact of causation is incapable of mathematical proof, since no [person] can say with absolute certainty what would have occurred if the defendant had acted otherwise____” Prosser, Handbook of Law of Torts, 3rd Ed., Hornbook Series, Sec. 41, p. 245, et seq. Swanner v. United States, 309 P.Supp. 1183, 1188 (M.D.Ala.1970). Plaintiffs argue that their theory is consistent with the unique features of Bergman’s condition and the one minute, 45 second cardiac arrest, while the Government’s explanations of the facts are not satisfactory. While the ability of a theory to accommodate the total picture is often persuasive of its merit, see, e.g., City of Bessemer v. Clowdus, supra, the appeal of consistency will not compensate for a medical theory which is lacking. In Dr. Bergman’s case, Plaintiffs’ theory has a certain internal consistency and provides an explanation for what may appear to be a mystery. In its most appealing aspect, it is responsive to the sense one has on a gut level that somehow, given the proximity of events, the beating and the injury to Bergman’s brain must be causally linked. Nevertheless, a thorough examination of the evidence upon which Plaintiffs’ theory rests, fails to persuade me that the proofs tip in favor of Plaintiffs on this factual issue. Specifically, I am unconvinced that it is more probable than not that Bergman sustained a vertebral artery injury from the beating which was capable of seriously damaging autoregulation in the vertebral basilar system without manifesting itself until four months later. For the reasons discussed below, I find that Plaintiffs have failed to cross the fine line between conjecture and a theory which carries a preponderance of the evidence: As a theory of causation, a conjecture is simply an explanation consistent with known facts or conditions, but not deducible from them as a reasonable inference. There may be two or more plausible explanations as to how an event happened or what produced it; yet, if the evidence is without selective application to any one of them, they remain conjectures only. On the other hand, if there is evidence which points to any one theory of causation, indicating a logical sequence of cause and effect, then there is a judicial basis for such a determination, notwithstanding the existence of other plausible theories with or without support in the evidence. Ex parte Travis, supra, 414 So.2d at 959, n. 3, quoting from Southern Railway Co. v. Dickson, supra, 100 So. at 669. Vertebral Artery Injury and Impairment of Autoregulation Dr. Gilroy testified that both the medical literature and his personal experience demonstrate that a vertebral artery can be injured by the kind of trauma Bergman sustained when he was beaten in Anniston. Gilroy cited examples of such traumatic causes as chiropractic manipulation,. football injuries, traction to the neck, yoga, car accidents, fractures, and subluxations, and noted a report of one case in which a man occluded his vertebral artery simply by bending his head back for two hours while painting his ceiling. Despite this testimony, it is clear that vertebral artery injury as the result of a beating, even one as severe as that sustained by Bergman, is a rare occurrence. In fact, there was no testimony specifically relating cases of vertebral artery injury as the result of a beating. Dr. Gilroy stated that in the course of personally performing thousands of arteriograms, he routinely discovered occluded vertebral arteries, but his testimony was merely that “some” of those were from traumatic causes. Dr. Reinmuth conceded that he could not rule out the possibility of a vertebral artery injury given a beating, but he testified that in his opinion such injury was highly unlikely and that vertebral artery injury in general is rather rare. Dr. Victor testified that although he has seen many patients who have been brutally beaten, he has never seen a vertebral artery occlusion in such a case. At best, Plaintiffs proved that it is not impossible that Bergman could have sustained this kind of injury. Even assuming a vertebral artery injury or occlusion, the Government’s experts reject the reasoning by which Dr. Gilroy then posits a brainstem infarction that causes impairment of autoregulation. Dr. Reinmuth discounted Gilroy’s description of autoregulátion and propounded an entirely different one. Instead of the nerve stimulus theory of autoregulation to which Dr. Gilroy and his cited authorities subscribe, according to Reinmuth the most widely studied mechanism and the “standard theory of regulation of blood flow” since 1895, is “metabolic autoregulation.” (TR D 343). Briefly, he explained that metabolic autoregulation functions as the result of the production of acid in tissue at a cell by cell level in the brain, right next to the blood vessels that supply microscopically local territory. The nerve cells burn sugar, producing carbon dioxide and lactic acid, which then interacts with the blood vessel. As the amount of carbon dioxide and lactic acid produced increases (the harder that portion of the brain is working), the blood vessel dilates so that more blood is able to flow through. (TR D 343-344). Under this theory of autoregulation, Dr. Reinmuth testified that he is unaware of any way to destroy autoregulation by one or even two infarcts specifically placed in the brainstem. In order to impair autoregulation, he testified that a very large segment of the brainstem must be seriously damaged. He directly contradicted Dr. Gilroy’s testimony that the autoregulatory system depends on the integrity of the whole, and stated instead that the brain has redundancies to protect against destruction of such vital functions. (TR D 371-372). Dr. Reinmuth knows of no mechanism localized in the brainstem that regulates blood flow there and in the cerebellum. (TR D 401). On direct examination he stated, “If I were to design a method to destroy autoregulation by brainstem lesion, I am not sure that I would know how to go about it. It would be extremely difficult.” (TR D 372). Dr. Gilroy himself recognized the existence of this competing school of thought on autoregulation (see TR D 231), and did not testify that the nerve stimulus theory was widely accepted. He relied on articles which came mainly out of one laboratory. None of these articles were introduced into evidence, and they were not attacked with specificity by Dr. Reinmuth. However, I note that Dr. Reinmuth has extensive and current experience in the area of cerebral blood flow study. He testified that all of his research over 30 years as a neurologist has been in experimental understanding of mechanisms of cerebral circulation, how it is regulated and how it responds to stresses. Dr. Gilroy, while an impressive authority and a credible witness, has not been as extensively involved in the study of cerebral vascular disease. His research concentrated on this area from approximately 1960 to 1968, but after that his focus changed to the fields of neuro-audiology and neuro-imaging of the brain. Dr. Reinmuth’s testimony convinces me that the nerve' stimulus theory of autoregulation and the idea of a center of autoregulatory control in the brainstem, are not widely accepted in the neurological community. I cannot find that Dr. Gilroy’s version of the medical truth is more correct than Dr. Reinmuth’s, solely on the basis that the nerve stimulus theory coincides with Dr. Gilroy's explanation of Bergman’s injury. More importantly, there is no evidence that Dr. Bergman had symptoms during the four months between the beating and the operation that would support Plaintiffs’ theory of vertebral artery injury and brain-stem damage. Dr. Gilroy testified that symptoms could have been absent or minimal, and noted that reports of some neurological changes in Bergman — the foot drop and haziness — could be indicative of such injury. But on cross-examination the only objective evidence he pointed to as proof of impaired autoregulation, was the destruction of the cerebellum. (TR D 258). Dr. Reinmuth and Dr. Victor opined that the lack of direct evidence of vertebral injury and brainstem damage made Plaintiffs’ claims highly unreasonable. Both of the Government’s experts testified that they found no evidence of vertebral basilar insufficiency or brainstem damage in Bergman’s medical record. Dr. Victor, while agreeing with Dr. Gilroy that an artery may be occluded without symptoms, testified that in a 61-year old individual, symptoms such as acute vertigo, nausea, vomiting, facial weakness, inability to use the limbs on one side and a loss of sensation on the other side, would normally be present. Dr. Reinmuth testified that an asymptomatic brainstem infarction simply would not be severe enough to impair autoregulation. There was some testimony from Dr. Gilroy that impairment of the vertebral artery alone might have caused a loss of autoregulatory function in Bergman. On cross-examination, Dr. Gilroy testified that the absence of brainstem damage “might not” affect the validity of his theory. (TR D 249). He went on to say that there is “some evidence which I didn’t talk about which simply interfering with the basilar of the, vertebral basilar system, may lead to loss of autoregulation.” (TR D 249). He explained that people with vertebral basilar insufficiency will have periodic symptoms of reduced blood flow to the brainstem and impaired autoregulation, and stated that vertebral basilar insufficiency “could” “possibly” result from traumatic injury. (TR D 250). Dr. Gilroy testified that this theory of impaired autoregulation from vertebral basilar insufficiency is apparently well-accepted, since articles to that effect have been published. (TR D 250-251). Dr. Reinmuth admitted that if one vertebral artery is injured, that segment might lose its autoregulatory capacity, but he testified that one would expect that the rest of the vertebral basilar system would maintain its autoregulatory response. He did not believe that such an impairment would last longer than a few weeks. (TR D 373). The vertebral basilar insufficiency theory of autoregulatory impairment, raised by Dr. Gilroy only during cross-examination, was not incorporated into his discussion of causation with specific reference to how it may or may not have affected Dr. Bergman, and Gilroy’s testimony suggests that it is no more than speculation. Dr. Gilroy clearly rested his theory on his testimony that the “most likely” event was impairment of autoregulation by damage to the brain-stem. (TR D 224). I cannot ignore the fact that the addition of the concept of autoregulation to the Plaintiffs’ causation theory apparently occurred long after Dr. Gilroy had theorized a vertebral artery injury. In opening and closing statements, Plaintiffs’ counsel suggested that they had two theories of causation, one involving autoregulation and one simply relying on impaired circulation in the vertebral artery. However, a careful review of Dr. Gilroy’s testimony reveals that in fact, autoregulation is essential to his theory of a chain of causation. Gilroy never testified at trial that the impairment of circulation which would have been caused by the occlusion would alone have resulted in the damage to the cerebellum. Rather, his testimony was that this would have been a factor in combination with impaired autoregulation. (TR D 85, 96). He stated that autoregulation is very important in this case (TR D 84), and testified that with impaired autoregulation, ... the effects of variation to blood pressure, of course, would now be felt; whereas, if autoregulation was functioning they would not____ With a fall in blood pressure, the vessels in the, over the cerebellum should have opened up to compensate and allow maintenance of blood flow. Since autoregulation is impaired, they would not do this, and, therefore, the cerebellum would be impaired from a fall in blood pressure. That is what I think happened here. (TR D 87-88). This “refinement” of Dr. Gilroy’s earlier theory takes for granted his original conclusion that there must have been a vertebral artery injury, while admitting that his first analysis contained an important flaw. The concept of a brain-stem infarction that caused impaired autoregulation maintains the internal logic of the theory, but Plaintiffs have effectively failed to re-build the bridge of causation between the cerebellar damage and the beating with this new element in mind. In addition to these weaknesses in Plaintiffs’ autoregulation theory, there is some indication in the evidence that Bergman’s autoregulatory system was not impaired after the beating. Dr. Reinmuth made this observation on the basis of Bergman’s testimony about the strenuous work he engaged in during the summer of 1961, building the switchback trail on his property. In Reinmuth’s opinion, this kind of exertion would have tested Bergman’s ability to respond to blood pressure fluctuations. He explained that vigorous activity of the type described by Bergman would have caused Bergman’s blood pressure to rise, and fluid and salt loss through perspiration followed by rehydration could have caused Bergman’s pressure to fall below normal. According to Dr. Reinmuth, someone without autoregulation would be extremely sensitive to even modest changes in pressure when working in an upright posture, and would feel dizzy and faint. He testified that with impaired autoregulation and an increase in pressure, there would be a high risk of brain hemorrhage. Since Bergman testified that he had experienced no dizziness or other problems that summer, his autoregulatory system must have been accommodating those changes in pressure, Reinmuth testified. Dr. Gilroy opined that impaired autoregulation would not have caused Bergman to exhibit symptoms if his blood pressure had risen, but he did not elaborate on why autoregulation would not be stressed at the high end of the scale. Dr. Reinmuth conceded on cross-examination that there is no specific evidence that Bergman’s blood pressure ever fell below normal between May and September 1961. But he persisted in his testimony that he could posit hypotension as well as hypertension from the kind of strenuous exercise Bergman had described. According to Dr. Reinmuth, autoregulatory mechanisms respond to both increases and decreases in blood pressure, thus affecting circulation with a fluctuation in either direction. While the evidence on this point is not conclusive, I accord Bergman’s lack of symptoms during the summer some weight in evaluating Plaintiffs’ theory. In light of all of the evidence discussed above, I am not persuaded by a preponderance of the evidence that Bergman suffered a vertebral artery injury on May 14, 1961 that resulted in brainstem damage and impaired autoregulation, and that subsequently caused Bergman to suffer severe cerebellar injury. Given that the possibility of an asymptomatic vertebral artery injury from a beating cannot be ruled out, and that Dr. Gilroy’s autoregulation theory is apparently accepted by at least part of the medical community, I am convinced that the injury possibly occurred as hypothesized by Plaintiffs. But this simply is not enough. Moreover, I find that evidence of a mild cerebral deficit, and questions concerning the length of the cardiac arrest, cast serious doubt on the factual premises of a one minute, 45 second period of anoxia, and of isolated cerebellar injury, from which Dr. Gilroy’s entire theory proceeds. This is critical, since Plaintiffs’ argument is that Dr. Gilroy’s theory should prevail because it is not only possible, but the only possibility that fits. Presence of Cerebral Injury Plaintiffs’ theory of causation relies on the premise that Bergman suffered isolated damage to his cerebellum, and that any indications of mild cerebral impairment are inaccurate or not attributable to the operation. I find that testing done in 1975 as part of a reevaluation of Dr. Bergman’s condition reveals slight cerebral deficits that cannot be dismissed out of hand. When he examined Bergman in March 1983, Dr. Gilroy found no problems with Bergman’s intellectual and cognitive functions. Upon testing the cranial nerves, Dr. Gilroy found no abnormalities except for certain problems with eye movement, which he testified could be indications of injury to the brainstem. He found Bergman’s basic sensations normal, although he did not test beyond touch, pain, vibration and position sense, because he felt that given Bergman’s age and the tremor, more discriminating tests would be invalid. Bergman’s deep tendon reflexes were normal and symmetrical and his skull was normal. Dr. Gilroy testified that the examination revealed no findings of cerebral injury, and he concluded that the neurological injury was cerebellar “in almost pure form.” (TR D 61; Ex. 24). The Government’s experts have no quarrel with Dr. Gilroy’s examination, but they disagree with his conclusions, based on certain testing information contained in Bergman’s medical records. Dr. Reinmuth agreed that Dr. Bergman’s cerebration is excellent. He agreed that Bergman’s records indicate that at least since several months after the arrest, he has had severe damage to the cerebellum with at best mild injury to the cerebrum. And Dr. Reinmuth conceded that the progress notes contain indications of a return of cerebral function within a relatively short time after the operation. However, in his opinion this does not mean that the cerebrum was not damaged during the operation. In Reinmuth’s opinion, Bergman had a good recovery, even though a lot of cells did not survive, because of redundancies built into the brain. (TR D 396). Dr. Whelan, a neurologist who saw Bergman on a consultation basis on October 2, 1961 and on several occasions in later years, apparently reached a similar conclusion. He noted in May, 1969 that Bergman “undoubtedly had diffuse neuronal damage at time of cardiac arrest and despite fairly good recovery ... he operates from a decreased brain cell reserve,” although he also observed that time was taking an additional toll on Bergman’s brain. (Ex 2, p 71). Another neurologist, Dr. McHenry, examined Bergman on September 11, 1975. The findings contained in his report are in large measure consistent with those made by Dr. Gilroy on his examination of Dr. Bergman. Dr. McHenry noted that Bergman was mentally alert, and that he had no problem with words or expression. He, like Dr. Gilroy, noted poor elevation of eyes, but otherwise that the cranial nerves seemed intact. He found position and vibration sense were also intact. But, unlike Dr. Gilroy, he went on to note that Bergman did have a problem with two point discrimination and number writing on fingers, hands and feet. Two point discrimination involves touching the patient’s finger with a two-pointed instrument which can be set at graduated degrees of distance between the points; the patient is asked to indicate whether one or two points are felt. The number writing test requires the patient to identify a numeral as the examiner writes it on the patient’s skin without allowing the patient to look. In testing stereognosis, Bergman was required to identify an object by clasping it in his hand, and there McHenry found that Bergman “identifies coins OK.” Dr. McHenry’s impression was “residuals of cerebral anoxia” including cerebellar type ataxia and “possible cortical impairment.” He recommended neuropsychological testing. (Ex. 2, p. 17). Pursuant to that recommendation, Bergman was tested by a psychologist, Dr. Bast, on September 11, 12, and 15, 1975. Dr. Bast found only questionable to mild dysgraphesthesia (number writing problem) on the left hand. But another cortical sensory perceptual exam revealed mild finger dysgnosia on the left hand. (Ex. 2, p. 18). According to Dr. Victor, this reflects some incapacity to recognize the fingers of one’s own hand or tó name and identify the fingers of the examiner’s hand. (TR D 514). Bergman’s scores on the Wechsler Adult Intelligence test showed a verbal IQ of 148, while his performance IQ was 124. Dr. Bast reported that “[sjubtests indicate mild deficits with uptake on immediate memory as reflected by decreased attainment with Picture Arrangement & Digit Span items.” Dr. Bast’s impression was that in addition to the severe cerebellar dysfunction, Bergman showed mild bitemporal involvement, probably with hippocampal foci. He then went on to note, It is difficult to perceive this [patient], who has a very superior IQ, as showing some dementia. However, there is sufficient evidence in the data to indicate that he has lost some of his former capacity with immediate memory functions. In this sense he does show a very mild, static and non-progressive dementia. (Ex. 2, pp. 18-19). Both Dr. Reinmuth and Dr. Victor testified that these findings were indicative of mild cerebral impairment. This conclusion is not inconsistent with the findings made by Dr. Gilroy on his examination of Dr. Bergman, since he did not undertake the sophisticated kind of testing done by Dr. Bast. Dr. Victor explained that only the discriminating testing reported by Dr. Bast would allow Bergman’s mild cerebral abnormalities to be detected. (TR D 484-85). Although it was not specifically noted by Dr. Bast in his report, Drs. Reinmuth and Victor testified that the disparity in Bergman’s verbal and performance IQ scores is also an objective sign of slight injury to the cerebral cortex. (TR D 422, 484-85, 522-23). Dr. Gilroy questioned Bast’s findings of dysgnosia and the slight problem of dysgraphesthesia noted by both Bast and McHenry, pointing out that even the examining doctors did not find a strong indication there. Dr. Gilroy attributed their findings to Bergman’s tremor, which in his opinion would affect the ability to accurately perform these tests as well as two point discrimination. He noted that Bergman had no problem with stereognosis, where the tremor would not be a factor. In Dr. Gilroy’s opinion, the minimal brain damage reported by McHenry and Bast may have been quite normal, given Bergman’s age at the time the testing was performed. He specifically noted that memory problems are not unusual for someone at Bergman’s age. (TR D 271). However, Dr. Victor explained that a mild, static and non-progressive dementia such as that reported by Dr. Bast, is different than the kind of memory loss associated with aging. Dr. Victor was of the opinion that Dr. Bast would have noted it if he had felt the memory loss was due to aging, since that is a discrete, identifiable phenomenon. (TR D 518-20). Dr. Gilroy’s observation that some of the findings by McHenry and Bast are only questionable or phrased tentatively, is well taken. But I do not find that those doctors’ conclusions should be ignored altogether. Both McHenry and Bast found some cerebral involvement, after a significant amount of subtle testing. The Plaintiffs argue that because there was no need to determine the cause of Bergman’s problem at the time these consultations were obtained, the reports may not draw the kind of fine distinctions required in the context of this litigation. However, I note that Bergman’s 1975 admission at Grace Hospital was specifically for the purpose of an intensive reevaluation of his condition. Under these circumstances, I do not believe that mild bitemporal involvement would have been noted if it were only questionable. Moreover, I am convinced that if the findings were affected by Bergman’s trem- or or his advanced age, the reports would have noted that fact. On cross-examination, Dr. Gilroy conceded that Dr. McHenry is a competent neurologist who would have made a notation if his conclusions were questionable because of a tremor. Bast’s report indicates that he did not fail to take considerations of Bergman’s physical symptoms and age into account in evaluating the results of his testing. He observed that Bergman had a problem with severe ataxia on a test dealing with visual motor integration. And in connection with a test of Bergman’s finger tapping speeds, Bast expressly took Bergman’s age into consideration, in his comment that the results were indicative of impaired speech and coordination. For these reasons I cannot accept entirely Dr. Gilroy’s explanation for the findings of mild cerebral impairment. One of the factual premises under which Dr. Gilroy operated was his finding that Bergman had no cerebral injury. (See TR D 63). And while his testimony often referred to Bergman’s injury as “predominantly” rather than “purely” cerebellar, his theory did not account for any damage to the cerebrum. Specifically, he had explained that the one minute, 45 second cardiac arrest would not have caused permanent damage to the cerebrum, and he testified that the portion of the cerebrum supplied by the vertebral basilar system was protected by the Circle of Willis. In addition, the testimony indicated that Bergman’s blood pressure had not dropped sufficiently during the operation to affect the cerebral hemispheres during the period of hypotension, since autoregulation was not impaired in the carotid artery system. In sum, Dr. Gilroy did not attempt to- integrate evidence of mild cerebral deficit into his theory of causation, but relied solely upon his opinion that these findings were inaccurate or attributable to old age or Bergman’s tremor. The Cardiac Arrest and Bergman’s Cerebellar Syndrome The presence of some cer