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February 8, 1983

United States of America, Defendant

The opinion of the court was delivered by: ACKERMAN

ACKERMAN, District Judge

 This is an action brought pursuant to the Federal Tort Claims Act, 28 U.S.C. § 2671, et seq., and the Swine Flu Act, 42 U.S.C. § 247(b). Plaintiffs, Mrs. Miriam and Dr. Ernest Stich, seek to recover damages allegedly suffered as a result of a swine flu inoculation which Mrs. Stich received on November 18, 1976, pursuant to the national immunization program undertaken by the federal government. See The National Swine Flu Immunization Program of 1976, Pub.L. 94-380, 90 Stat. 1113. Specifically, Mrs. Stich contends that she contracted either Guillain-Barre Syndrome ("GBS") or some other condition as a result of this immunization which, in turn, caused her to suffer her injuries. Her husband, Dr. Stich, seeks recovery for loss of consortium and loss of services.

 Under the Federal Tort Claims Act, as incorporated in the Swine Flu Immunization Act, this action is governed by the law of the forum state, here New Jersey, except as otherwise provided. 28 U.S.C. § 1346(b); 42 U.S.C. § 247b(k)(2)(A); Richards v. United States, 369 U.S. 1, 7 L. Ed. 2d 492, 82 S. Ct. 585 (1962).


 This action was filed on April 12, 1978. On May 18, 1978, it was transferred by the Judicial Panel on Multidistrict Litigation to the United States District Court for the District of Columbia for coordinated and consolidated pretrial proceedings pursuant to 28 U.S.C. § 1407 before the Honorable Gerhard A. Gesell. The case was thereafter remanded to this court on February 5, 1980. The Final Pretrial Order of the transferee court, dated November 15, 1979, provides that if plaintiffs establish that Mrs. Stich contracted GBS, they need not establish any theory of liability. If, however, it cannot be established that she has GBS, then plaintiffs must prove negligence or another appropriate theory of liability.

 The Final Pretrial Order also limits the litigants herein to local discovery, meaning only that which is specifically related to her condition. Over seventy depositions were taken during the course of national discovery, many of which were introduced into evidence at trial in this action.

 The trial of this nonjury case was trifurcated. The three phases contemplated in the pretrial order are: Phase I -- Diagnosis and Causation of Miriam Stich's condition; Phase II -- Foreseeability of Risk and Informed Consent; Phase III -- Damages. After thirty-nine days of testimony comprising some 6,390 pages of trial transcript, the trial of Phase I has been completed. The plaintiffs have presented medical testimony through the following witnesses:


Dr. Joseph Gluck, internist and a treating physician of Mrs. Stich


Dr. Howard Medinets, neurosurgeon and specialist in forensic medicine


Dr. Robert Lisak, neurologist


Dr. Charles Poser

 Plaintiffs also presented testimony by deposition of certain doctors drawn from the multi-district discovery proceedings in the consolidated swine flu cases. See In re Swine Flu Immunization Products Liability Litigation, 89 F.R.D. 695, (D.C.D.C.).

 The United States presented medical evidence through the following witnesses:


Dr. Peter Tsairis, neurologist and electromyographer


Dr. Richard Price, neurologist and virologist


Dr. Richard Whitley, virologist and Director of the National Institute of Allergy and Infectious Diseases ("NIAID") Collaborative Anti-Viral Study Group


Dr. Neal Nathanson, epidemiologist and microbiologist

 Defendants also presented testimony through the multi-district depositions, including the following witnesses:


Dr. Barry Arnason, Dr. Paul Wehrle, Dr. Stephen Schoenbaum, Dr. Peter Dyck, Dr. Larry Schonberger, Dr. Henry Retailliau, Dr. Alexander Langmuir, Dr. Jonas Salk, Dr. Frederick Davenport, Dr. Harry Meyer, Dr. David Karzon, Dr. Gordon Meiklejohn, Dr. D.A. Henderson, Dr. David Sencer, Dr. Charles Hoke, Dr. J. Donald Millar, Dr. John Seal, and Dr. E. Russell Alexander.

 The court has carefully considered the live testimony, the deposition testimony, the exhibits submitted, and the arguments of counsel. This memorandum constitutes the court's decision and includes the court's findings of fact and conclusions of law pursuant to Federal Rules of Civil Procedure 52(a). I find that Mrs. Stich has failed to establish by a preponderance of the credible evidence that the condition she is suffering from is GBS, or that it is causally related to the swine flu inoculation which she received. I find instead that the most probable diagnosis of Mrs. Stich's condition is herpes simplex encephalitis ("HSE") of a viral etiology unrelated to the swine flu inoculation she received. See Caputo v. United States, 157 F. Supp. 568, 571 (D.N.J. 1957); Szczytko v. Public Service Coordinated Transport, 21 N.J. Super. 258, 264, 91 A.2d 116 (App. Div. 1952).


 It is undisputed that Mrs. Stich received a swine flu inoculation at Brookdale Community College on November 18, 1976. *fn1" That afternoon she flew to California on a pleasure trip, where she stayed for five days. On November 22, 1976, towards the end of her stay in California, she began to feel ill. She returned home to New Jersey the next day. At that time she had a fever, muscle aches, a headache and noted a general malaise. Her physician husband put her to bed and gave her Keflex and aspirin. The following day, November 24, 1976, she remained ill with a fever of 102 degrees and was in bed, and on November 25, 1976, she was not well enough to prepare the Thanksgiving dinner.

 On November 26, 1976, Mrs. Stich was seen at her home by the family's physician, Dr. Joseph Gluck. Although she still had a fever and complained of a headache and a general loss of well-being, her physical examination at that time was otherwise unremarkable. Her urinalysis and complete blood count were normal, and Dr. Gluck prescribed rest and aspirin.

 On November 27, 1976, Mrs. Stich was taken to the Emergency Room of Riverview Hospital in Red Bank, New Jersey, where she was admitted at 12:00 p.m. Upon examining Mrs. Stich, Dr. Gluck found her condition dramatically changed. He noted that she now had convulsions as well as a fever. She was totally unconscious, and the muscles of all her extremities were in spasm. Her neck was supple, her eyes were roving horizontally without focusing, although they were deviating mainly to the left. Her pupils were equal, small and reacted normally to light. The Babinski and Hoffman reflexes, which are indicative of Central Nervous System ("CNS") pathology, were both abnormal. Mrs. Stich appeared to have normal power in her extremities and she was continent. During her convulsive state, Dr. Gluck noted that Mrs. Stich showed physical signs of decerebration. The family history, which was taken on November 27, 1976 and dictated by Dr. Gluck, indicates the following:


Examination in the past has been without any significant abnormalities other than residual polio affecting both lower extremities, mainly to the left; approximately five days ago, while in California, she noted the onset of malaise, muscle aches, headache and then fever. She flew home and by the next day, had temperature to 102 degrees with marked loss of well-being. There were no other specific symptoms. The illness had the character of a typical acute febrile viral infection.

 Diagnosis on admission by Dr. Gluck was meningo-encephalitis of unknown etiology. Dr. Gluck was unaware until December 10, 1976, that Mrs. Stich had received a swine flu inoculation on November 18, 1976. Dr. Gluck had, however, himself given her an influenza B inoculation on October 25, 1976.

 For the three or four days following her admission to Riverview Hospital, Mrs. Stich's level of consciousness varied substantially, although she never regained full normality. By December 2, 1976, she was totally unconscious and unresponsive, and she remained comatose or semi-comatose for the next three to four months.

 On February 14, 1976, Mrs. Stich was transferred to the Neurological Institute at Columbia Presbyterian Hospital in New York, New York. This transfer was apparently made for the purpose of seeking assistance with the diagnostic treatment of Mrs. Stich's condition, and perhaps to facilitate the performance of a brain biopsy. The medical records from her stay at Columbia Presbyterian Hospital indicate that during this period her vital signs were stable and normal. Although she did not respond to external stimuli, she did occasionally open her eyes and look around her room. No verbalization took place.

 On March 8, 1977, she was again re-hospitalized at Riverview Hospital. By April or May her coma had lightened to the point that she was awake. On June 6, 1978, she was transferred to Morris Hall Rehabilitation Center and remained there until August 15, 1978, when she was again returned to Riverview Hospital. Mrs. Stich currently remains at Riverview.

 As a result of intensive therapy, Mrs. Stich eventually became able to walk with substantial assistance, sometimes feed herself and perform certain other activities of daily living. She remains seriously disoriented, however, and much of her speech is unintelligible. A physical examination by Dr. Tsairis on October 14, 1981, found her spastic in all four extremities. She still exhibited bilateral Babinski reflexes, and could not follow objects or fingers with her eyes. She had a mild left ptosis (drooping of the eyelid) and would attempt to put into her mouth any object that might come into her visual field. As is clear from this summary, Mrs. Stich's residual intellectual impairment is substantial.


 Guillian-Barre Syndrome is a neurologic disorder, inflammatory in nature, which was first described in 1859 by Dr. Landry. It was again described in 1916 by Drs. Guillian, Barre and Stohl. The syndrome characterizes a set of neurologic symptoms, rather than defining a specific organic disorder. To date, medical science has not established the syndrome's exact etiology or cause.

 The extent to which GBS may encompass any ("CNS") involvement remains a controversy within the medical community. As classically defined, GBS is a peripheral neuropathy which results from the demyelination of the peripheral nervous system. *fn2" This demyelination results in a progressive motor weakness of the limbs which ranges from mild weakness to paralysis of every motor muscle. Most typically GBS involves the lower extremities initially, progressing (normally over the course of between a few days and two weeks) upward to affect the upper limbs, face and bulbar muscles. This progressive weakness affects both proximal and distal muscles, and it reaches a plateau in the second or third week after onset as the affected muscles begin to re-myelinate. Over the course of a period ranging from three months to one year, GBS patients generally regain full use of the affected muscles, although there are permanent residual effects in approximately 10% of all GBS cases.

 Plaintiffs urge this court to adopt a much broader clinical definition of GBS. Their position is that GBS may embrace a wider spectrum of neurologic or CNS involvement than suggested by the classical definition, and that GBS does not represent any specific neurologic picture. They argue that GBS properly includes central nervous system disease as well as peripheral nervous system disease, and may affect any or all, or any combination of the parts, of the nervous system.


 While the precise nature of the syndrome may be in dispute, the criteria established for the diagnosis of GBS by the National Institute of Neurological and Communicative Diseases and Stroke ("NINCDS") have been generally accepted by the medical profession, and particularly by neurologists, as an authoritative and accurate description of GBS. *fn3" See 3 Annals of Neurology, (June 1978). Under these criteria, clinical, laboratory and electrodiagnostic data are together evaluated in a non-mechanistic manner to determine whether a diagnosis of GBS is appropriate in a specific case. I find the NINCDS criteria to be an appropriate standard against which to measure the plaintiffs' proofs and adopt them as controlling herein.

 Under the NINCDS criteria, the two features required for diagnosis are:


A. Progressive motor weakness of more than one limb. The degree ranges from minimal weakness of the legs, with or without mild ataxia, to total paralysis of the muscles of all four extremities and the trunk, bulbar and facial paralysis, and external ophthalmoplegia.


B. Areflexia (loss of tendon jerks). Universal areflexia is the rule, though distal areflexia with definite hyporeflexia of the biceps and knee jerks will suffice if other features are consistent.

 I have previously discussed the characteristic monophasic course of progressive motor weakness, plateau, and then gradual improvement that is a diagnostic hallmark of GBS. Areflexia, the second required finding in GBS, is the absence or depression of deep tendon reflexes ("DTRs"). The type of reflex loss finding required to substantiate a diagnosis of GBS is a value less than one-plus or two-plus, which are considered to be in the normal range. This loss of DTRs must occur within days or, at most, a few weeks of the onset of the illness.

 It follows as a corollary to this required absence or depression of DTRs that the related pathological reflexes or signs, such as the Babinski and Hoffman, would be similarly absent. The presence of either these pathological reflexes or of increased DTRs (hyperreflexia) would be an indication of central nervous system disease. Other signs of an overwhelming central nervous system involvement, such as a history of mental confusion, dementia, loss of memory and congnitive functions, delirium and agitation, would suggest a diagnosis other than GBS.

 The NINCDS criteria next list seven clinical features which are strongly supportive of a diagnosis of GBS. Ranked in order of importance, these are:


1. Progression. Symptoms and signs of motor weakness develop rapidly but cease to progress by four weeks into the illness. Approximately 50% will reach the nadir by two weeks, 80% by three weeks, and more than 90% by four weeks.


2. Relative symmetry. Symmetry is seldom absolute, but usually, if one limb is affected, the opposite is as well.


3. Mild sensory symptoms or signs.


4. Cranial nerve involvement. Facial weakness occurs in approximately 50% and is frequently bilateral. Other cranial nerves may be involved, particularly those innervating the tongue and muscles of deglutition, and sometimes the extraocular motor nerves. On occasion (less than 5%), the neuropathy may begin in the nerves to the extraocular muscles or other cranial nerves.


5. Recovery. It usually begins two to four weeks after progression stops. Recovery may be delayed for months. Most patients recover functionally.


6. Autonomic dysfunction. Tachycardia and other arrhythmias, postural hypotension, hypertension, and vasomotor symptoms, when present, support the diagnosis. These findings may fluctuate. Care must be exercised to exclude other bases for these symptoms, such as pulmonary embolism.


7. Absence of fever at the onset of neuritic symptoms.

 The six variants of GBS which have been recognized under the NINCDS criteria are:


1. Fever at onset of neuritic symptoms.


2. Severe sensory loss with pain.


3. Progression beyond four weeks. Occasionally, a patient's disease will continue to progress for many weeks longer than four or the patient will have a minor relapse.


4. Cessation of progression without recovery or with major permanent residual deficit remaining.


5. Sphincter function. Usually the sphincters are not affected, but transient bladder paralysis may occur during the evolution of symptoms.


6. Central nervous system involvement. Ordinarily, Guillian-Barre Syndrome is thought of as a disease of the peripheral nervous system. Evidence of central nervous system involvement is controversial. In occasional patients, such findings as severe ataxia interpretable as cerebellar in origin, dysarthria, extensor plantar responses, and ill-defined sensory levels are demonstrable, and these need not exclude the diagnosis if other features are typical.

 The NINCDS criteria further list cerebrospinal fluid and electrodiagnostic features which are indicative of a diagnosis of GBS:


Cerebrospinal fluid features strongly supportive of the diagnosis


1. CSF protein. After the first week of symptoms, CSF protein is elevated or has been shown to rise on serial lumbar punctures.


2. CSF cells. Counts of 10 or fewer mononuclear leukocytes/mm in CSF.




1. No CSF protein rise in the period of one to ten weeks after the onset of symptoms (rare).


2. Counts of 11 to 50 mononuclear leukocytes/mm in CSF.


Electrodiagnostic features strongly supportive of the diagnosis.


Approximately 80% will have evidence of nerve conduction slowing or block at some point during the illness. Conduction velocity is usually less than 60% of normal, but the process is patchy and not all nerves are affected. Distal latencies may be increased to as much as three times normal. Use of F-wave responses often gives good indication of slowing over proximal portions of nerve trunks and roots. Up to 20% of patients will have normal conduction studies. Conduction studies may not become abnormal until several weeks into the illness.

 Finally, the NINCDS criteria list six features whose presence casts doubt on a diagnosis of GBS:


1. Marked, persistent asymmetry of weakness.


2. Persistent bladder or bowel dysfunction.


3. Bladder or bowel dysfunction at onset.


4. More than 50 mononuclear leukocytes/mm in CSF.


5. Presence of polymorphonuclear leukocytes in CSF.


6. Sharp sensory level. *fn4"


 Applying the NINCDS criteria to the evidence adduced during the first phase of trial, I find that plaintiffs have produced little or no affirmative evidence to support their contention that the proper diagnosis of Mrs. Stich's condition is GBS. In the paragraphs that follow, I will summarize the evidence applicable to each element of the NINCDS criteria, and will assess whether or not it supports plaintiffs' proposed GBS diagnosis.

 I. Features Required for Diagnosis

 A. "Progressive motor weakness of more than one limb."

 At the time of her admission to the Riverview Hospital's Emergency Room on November 27, 1976, four days after the onset of her initial symptoms, Dr. Gluck made several findings relevant to this first criterion. Dr. Gluck's notes of his examination of Mrs. Stich reveal that he found her totally unconscious and convulsing, with muscles of all extremities in spasm, and with clonic convulsions. She had bilateral ankle clonus and normal power in all extremities. A progress note by Dr. Gluck made on November 28, 1976, indicated that Mrs. Stich still had ankle clonus bilaterally and normal power in all extremities.

 Further observations were made in the course of a consultation by Dr. Angelo Scotti on November 30, 1976. Dr. Scotti, finding Mrs. Stich more responsive than she had been (in her prior comatose state), recorded that she had good power in all extremities. This observation was confirmed by Dr. Gluck in a progress note of this same date. A further progress note by Dr. Gluck recorded on December 2, 1976, indicated that Mrs. Stich still had moderate muscle spasticity in all extremities but worse on the left, and that her ankle clonus continued. A consultation performed by Drs. Kreider and Gainsburg on December 3, 1976, found, inter alia that Mrs. Stich's spasticity in her lower extremities continued. Another progress note by Dr. Gluck on February 10, 1977, indicated that Mrs. Stich's right hand and foot were clenched, and that she had a tremor in her left hand, and that her neck and extremities were rigid. Finally, Dr. Gluck testified that for the period of December 1, 1976, through January 27, 1977, Mrs. Stich's comatose and semi-comatose state precluded any testing which could conclusively determine her motor strength or the progressivity vel non of any motor weakness. *fn5"

 I find that this evidence both fails to affirmatively establish Mrs. Stich's progressive motor weakness and is, in fact, incompatible with the requirements of this first criterion. Dr. Gluck's observations of Mrs. Stich's continuing spasticity *fn6" and ankle clonus, his findings of normal power in all extremities as late as November 30, 1976, together with the rigidity of her limbs and the clenching of her right hand and foot, are particularly contrary indications. Plaintiffs have offered no credible affirmative evidence which contradicts the "inescapable conclusion" that plaintiffs have failed to establish the presence of this feature.

 B. "Areflexia."

 The second criterion under the NINCDS "Features Required for Diagnosis" is Areflexia, or loss of tendon jerks. The evidence relevant to this is as follows: Mrs. Stich was found to have ankle clonus on November 27th, 28th, 29th, 30th and December 2, 1976. She was found to have Babinski reflexes and/or positive Hoffman signs at various times throughout her initial admission at Riverview Hospital, including November 27th, December 2nd and February 10th. Hyperreflexia, or hyperactive DTRs, were found on November 30th, December 2nd and December 3rd. Each of these observations is inconsistent with, or rules out the presence of, areflexia. *fn7" Plaintiffs have adduced no affirmative credible evidence to contradict the implication of these observations. *fn8" I must therefore conclude that plaintiffs have failed to meet either of these first two criteria, both of which are characterized by the NINCDS as required features for a GBS diagnosis.

 While the plaintiffs' failure to meet these two criteria would be perhaps sufficient to rule out a diagnosis of GBS, prudence and the special circumstances of this case *fn9" dictate that I evaluate each of the other NINCDS criteria to determine whether they suggest a different conclusion.

  II. Features Strongly Supportive of the Diagnosis

 A. Clinical Features

 The next set of these criteria are those which the NINCDS characterizes as features strongly supportive of a GBS diagnosis. The first of these is progressive motor weakness. The evidence relating to this criterion uniformly fails to establish progression. Mrs. Stich had no symptoms or signs of progressive motor weakness within the ten weeks immediately following her inoculation which are attributable to a cause other than her comatose or semi-comatose state. Her deterioration occurred early and rapidly; during the relevant four-week period her condition must be described as chronic. Once again the conclusion which I reach is that plaintiffs have failed to establish that Mrs. Stich's condition is consistent with progressivity.

 The second clinical feature strongly supportive of a GBS diagnosis is relative symmetry. The evidence relating to this criterion is limited due to the absence of any evidence of motor weakness in Mrs. Stich's limbs. *fn10" Nonetheless, there is some evidence which suggests that symmetry is absent in her case. In particular, the observations by Dr. Pertchik and others that Mrs. Stich had a left gaze preference, *fn11" that her muscle spasticity was worse on the left than on the right, *fn12" that she had left-only wrist and ankle clonus, and that at times she had Babinski and Hoffman reflexes only on the left *fn13" all tend to be incompatible with a finding of symmetry. In the absence of any affirmative evidence, I conclude that this criterion has not been met by plaintiffs.

 The next clinical feature strongly supportive of a GBS diagnosis is "mild sensory symptoms or signs". Mrs. Stich's failure to note any sensation of numbness or tingling or other similar sensations at the onset of her symptoms might be considered to be inconsistent with this particular feature. Other than this, Mrs. Stich's comatose or semi-comatose condition prevented any conclusive determination of her sensory symptoms or signs. Thus, I agree with defendant that this feature neither supports nor casts doubt upon a diagnosis of GBS.

 The fourth feature under the NINCDS criteria is cranial nerve involvement. Here the only evidence which arguably supports a finding of the presence of this feature is Dr. Pertchik's observation on November 27, 1976, that Mrs. Stich had a conjugate gaze preference to the left and that her eyes were roving. This observation is by itself inconclusive, however, because such a symptom could be the result of either cranial nerve or central nervous system involvement. Otherwise, the evidence fails to demonstrate any possible cranial nerve involvement: There is facial weakness noted, no tongue or muscles of deglutition involvement, she swallowed normally, and her pupils were equal, small, and reactive. *fn14" I therefore must conclude that plaintiffs have failed to demonstrate by a preponderance of the credible evidence that Mrs. Stich had any cranial nerve involvement.

 The next clinical feature cited by the NINCDS criteria is recovery. Mrs. Stich has, with therapy, been able to regain only minimal functional abilities, but many of her disabilities are seemingly permanent or chronic, including residual spasticity and general weakness. Further, her recovery, contrary to the usual pattern, did not begin two to four weeks after progression stopped. I find on balance that the evidence is insufficient to find that Mrs. Stich has recovered in accordance with the terms of this feature.

  The sixth of these NINCDS features is autonomic dysfunction. The signs which would support this feature are entirely absent. No unusual vascular signs were noted, nor were tachycardia or other arrhythmias, postural hypotension, hypertension or vasomotor symptoms. I must therefore conclude that plaintiffs have failed to demonstrate that Mrs. Stich manifested this feature.

 The seventh and final clinical feature which under the NINCDS criteria is strongly supportive of a GBS diagnosis is the absence of fever at the onset of neuritic symptoms. Mrs. Stich had a fever from the onset of her earliest symptoms, on November 23, 1976, until at least November 30, 1976. On November 25th she had a fever of 102 degrees, on November 27th it was 104 degrees, on November 28th it was 102 degrees, and on November 30th it was 100 degrees. This data is clearly incompatible with the seventh NINCDS feature.


  Plaintiffs' proofs more closely fit the six variants on the NINCDS clinical features which are strongly supportive of the diagnosis, but a GBS diagnosis is still not demonstrated by a preponderance of the credible evidence.

  The first, fever at onset of neuritic symptoms, is clearly met by the same data which was incompatible with the seventh clinical feature (immediately above). Obviously, a patient who failed to meet one of these features would meet the other, and thus neither finding can be very probative, much less conclusive.

  The second variant, severe sensory loss with pain, has not been established by plaintiffs' proofs. Prior to the date she became comatose, Mrs. Stich's senses remained fully intact; thereafter no sensory testing could be undertaken. Thus, this variant feature has not been met.

  Progression beyond four weeks is the third variant recognized by the NINCDS criteria. It is difficult to fairly determine whether Mrs. Stich's motor weakness progressed beyond the usual four-week period normally associated with GBS because of her comatose and semi-comatose condition. Further, as I have noted above, there is little evidence to support any progresivity in her motor weakness symptomatology, given the sudden and massive nature of the onset of her condition and the overwhelming CNS involvement even in the earliest stages. I must therefore find that plaintiffs have not established by a preponderance of the evidence that this variant is applicable to Mrs. Stich's condition.

  The next variant is cessation of progression without recovery or with major permanent residual deficit remaining. I find that Mrs. Stich's condition fits this variant to some degree, given her residual and chronic functional impairments. I also find, however, that this in and of itself does not confirm a GBS diagnosis. This variant simply allows for a finding of GBS when other features point to such a diagnosis but recovery has not occurred. Such is not the case here.

  Variant five is sphincter function. Again, because of Mrs. Stich's comatose state, it is difficult to determine whether her observed occasional urine incontinence is due to bladder dysfunction (which would be consistent with this variant) or merely the result of her inability to express herself. I therefore find that the proofs regarding this feature are inconclusive.

  Variant six, also known as the Fisher variant, pertains to central nervous system involvement and was the subject of substantial controversy at trial.

  The parties are in agreement that Mrs. Stich's condition involves a substantial CNS component. The extent of that involvement, and more basically whether her CNS manifestations may fairly be linked to a diagnosis of GBS or instead reflect an independent, non-GBS CNS dysfunction, were the subject of much dispute. For the reasons which I will outline more fully below, I find that Mrs. Stich's condition reflects a massive CNS dysfunction and pathology unrelated to GBS, and further that her CNS symptomatology vastly exceeds the type and extent of CNS involvement embraced by Variant Six.

  Variant Six expresses the resolution reached by the NINCDS over the proper role of CNS signs or symptoms in the diagnosis of GBS. What Variant Six means is simply that the predominantly peripheral nature of GBS symptomatology need not exclude some CNS signs; in other words, that some evidence of CNS dysfunction in a patient need not exclude a diagnosis of GBS.

  The NINCDS criteria lists several examples of CNS findings which may occasionally be found in GBS patients, specifically ". . . severe ataxia interpretable as cerebellar in origin, dysarthria, extensor plantar responses, and ill-defined sensory levels . . ." Testimony by Dr. Price also indicated that there is some evidence in GBS cases of trace findings of other CNS involvement such as lymphocytes in the cerebrospinal fluid. All pathological evidence of such CNS involvement under Variant Six should be found, if at all, in the cerebellum rather than the cerebrum. *fn15"

  Findings consistent with Variant Six may not, by themselves, form the basis for a proper GBS diagnosis. Only when a patient presents the recognized typical signs of GBS may the accompanying CNS involvement be reconciled with a GBS diagnosis through the variant. As Dr. Shaumberg has testified, "If someone has a very striking picture of peripheral Guillain-Barre Syndrome, the so-called soft central nervous system findings . . . [don't] bother me." A diagnosis of GBS based overwhelmingly upon Variant Six findings would however transform GBS into an entity not recognized by any substantial body of medical opinion and would be akin to "the tail wagging the dog".

  This is, however, what plaintiffs here attempt. Mrs. Stich's overwhelming, "disastrous" and "explosive" cerebral involvement bears little or no physiological or pathological resemblance to the relatively mild symptomatology expected under Variant Six. Her tragic comatose and vegetative state, the demonstrable destruction of brain matter, dysfunction of cognition and memory, hemiparesis and disabling spasticity all point to massive cerebral involvement, rather than the expected cerebellar. None of the potential cerebellar findings listed under Variant Six were ever found in Mrs. Stich's case prior to the onset of her coma, and no such signs were (or perhaps could have been) found thereafter. Therefore, I must find that, in addition to failing to demonstrate that the required peripheral nervous system features are present, plaintiffs have also failed to establish by a preponderance of the credible evidence that her CNS involvement properly falls within Variant Six.

  Cerebrospinal Fluid Features Strongly Supportive of the Diagnosis

  The first feature under this next category in the NINCDS criteria calls for an elevation in cerebrospinal fluid ("CSF") protein levels after the first week of symptoms. The evidence establishes that there was an elevation in CSF protein, and I conclude that this criterion has been met.

  The second feature in this category involves CSF cells, specifying that counts of ten or fewer mononuclear leukocytes/mm in the CSF are consistent with GBS. The evidence pertaining to this feature is contradictory: On November 27, 1976, Mrs. Stich had a cell count of 200; on December 2, 1976, it was 49; and on December 17, 1976, the count was 0, although on that date there was a count of 372 red cells in the CSF. On balance I find that Mrs. Stich's data fails to meet the requirements for this feature.

  The NINCDS criteria provide for two variants on these CSF features, the first allowing for no CSF protein rise in the period of one to ten weeks after the onset of symptoms, and the other accepting counts of eleven to fifty mononuclear leukocytes/mm in the CSF. Based on the foregoing data, I find that Mrs. Stich's condition may meet the requirements of the second variant (regarding CSF cells).

  Electrodiagnostic Features Strongly Supportive of the Diagnosis

  Under the NINCDS criteria, approximately 80% of all GBS cases will have evidence of nerve conduction slowing or blockage at some point in the course of the illness. Conduction velocity is usually less than 60% of normal, but the process is patchy and not all nerves are affected. The NINCDS criteria suggests that distal latencies may be increased to as much as three times normal.

  No evidence of slowed or blocked nerve conduction was presented by plaintiffs. To the contrary, the only evidence presented which related to nerve conductivity (and to this criterion as a whole) was the testing done by Dr. Lovelace on February 16, 1977. This testing showed that at least at that time Mrs. Stich's nerve conductivity (conduction velocities) were normal. I must therefore conclude that plaintiffs have not met their burden to establish by a preponderance of the evidence that Mrs. Stich's condition included this feature.

  III. Features Casting Doubt on the Diagnosis

  The first feature identified under the NINCDS criteria as casting doubt on a GBS diagnosis is a marked, persistent asymmetry of weakness. The issue of whether Mrs. Stich's condition is marked by such an asymmetry is seriously clouded by her history of polio. The record contains several references to her residual polio, some of which suggests that it affects both lower extremities, with the remainder specifying that it affects primarily (or only) the left lower extremity. Discounting the evidence regarding her persistently greater left lower extremity weakness, I still find a marked persistent asymmetry in her condition, with her various symptomatology evincing greater left-side involvement. Several reports by Dr. Gluck and Dr. Pertchik note greater upper limb reflex abnormality on the left than right, a conjugate gaze preference to the left, tremor of the left hand, and other indications of this asymmetry. I therefore conclude that the presence of this feature casts doubt on a GBS diagnosis here.

  The next two features which under the NINCDS criteria cast doubt on the diagnosis are (a) persistent bladder or bowel dysfunction, and (b) bladder or bowel dysfunction at onset. Incontinence of urine was noted for Mrs. Stich following the onset of her coma, but it is impossible to determine whether this was due to dysfunction or her inability to communicate. For this reason I find the evidence inconclusive as to these two features.

  The fourth feature in this category is a finding of more than fifty mononuclear leukocytes/mm in the CSF. As I have noted earlier, the first measure of Mrs. Stich's CSF cells, on November 27, 1976, revealed that she then had a count of 200 mononuclear leukocytes/mm . Although the count was later found to be lower, I find that this initial high level is evidence which casts doubt on a diagnosis of GBS.

  The final two features which, under the NINCDS criteria, cast doubt on the diagnosis are (a) the presence of polymorphonuclear leukocytes in the CSF, and (b) a sharp sensory level. The absence of any findings bearing on these two features leads me to conclude that they are inapplicable.

  In conclusion, I find that plaintiffs have failed to establish by a preponderance of the credible evidence that Mrs. Stich's symptomatology fits the NINCDS GBS criteria. Specifically, I find that plaintiffs have failed to demonstrate that her condition includes the two features required for a diagnosis of GBS, and that they have similarly failed to demonstrate the applicability of most of the features which are strongly supportive of such a diagnosis. I find further that plaintiffs' evidence of central nervous system involvement in Mrs. Stich's condition does not meet the standard for Variant Six, and that in any event Variant Six findings in and of themselves are insufficient here to sustain a GBS diagnosis, given the lack of other evidence. Finally, I find that several features are present in her condition which, under the NINCDS criteria, cast doubt on a GBS diagnosis, even if all other findings had been typical. Therefore, I must conclude that plaintiffs have failed to sustain their burden of proof as to this diagnosis.


  In the final pretrial order of the multi-district swine flu litigation, the United States stipulated that GBS can be caused by a swine flu inoculation in certain instances. In this case, no doctor who ever either saw Mrs. Stich or reviewed her file prior to this stipulation ever diagnosed her as having GBS. There is no evidence that any doctor even considered that GBS might be the correct diagnosis during this period. Prior to November of 1979, neither Dr. Gluck nor any of the consulting neurologists at Riverview Hospital diagnosed her as having GBS or even included it in a differential diagnosis. At Columbia Presbyterian Hospital, where the physicians and neurologists who examined her had the benefit of many of the most advanced and sophisticated neurological testing procedures, GBS was never even considered to be a plausible diagnosis. Mrs. Stich's medical records simply never established a basis for such a finding.

  Mrs. Stich's condition is, as her medical records so clearly demonstrate, overwhelmingly a central nervous system disease. There is no evidence of any peripheral involvement at any time within the first twelve weeks after she received the swine flu inoculation. All symptoms and signs were of indisputable brain damage which devastated the cerebral area. Plaintiffs have failed to meet their burden of establishing that the few arguable peripheral nervous system findings in this record constitute GBS. Nor have plaintiffs demonstrated that her condition is explainable by the GBS variant which recognizes that in certain limited circumstances, where other signs are typical of GBS, findings which may be cerebellar in origin need not exclude the diagnosis. Plaintiffs' suggestion that the definition of GBS be broadened to include the kind of overwhelming CNS involvement as is found in her condition cannot be accepted, particularly where, as here, the essential signs of GBS are absent.


  Dr. Joseph Gluck

  Mrs. Stich's primary treating physician was Dr. Joseph Gluck. Dr. Gluck, by his own admission, has ministered to her and been a friend of the family for many years. From November of 1976 until August of 1980, one looks in vain for any mention by Dr. Gluck which even remotely suggests a diagnosis of GBS. The record reflects that in the summer of 1980, Dr. Gluck suffered a heart attack. While recovering, he, as plaintiffs suggest, was "afforded the luxury" of conducting "an exceptionally thorough review of the medical literature concerning Guillian-Barre Syndrome." The doctor, as I observed, brought to court a Niagara of articles, many of which he referred to in the course of his testimony. His thesis, based on his readings, is facially attractive: Since many medical writers, including Dr. Guillian himself (in 1953), have recognized that GBS can have CNS features, he opined that Mrs. Stich's case fits neatly into this diagnostic syllogism.

  Defendant has attacked Dr. Gluck's opinion on many grounds: First, that he did not arrive at this opinion until the eve of trial (in September of 1980), thus suggesting, inferentially, that that opinion was colored by a stipulation by the government that it would compensate a causally related GBS. If I felt that Dr. Gluck had persuaded me that his later readings had shed light on this perplexing problem, I would not have been phased by his intensive, albeit tardy, research. However, in listening to Dr. Gluck, and observing him as a witness, I became convinced that I was listening to a physician who had an intense emotional investment in this case. On various occasions he broke down into tears in the course of his testimony. While I am in no way critical of this loss of composure, I do sincerely believe that it reflected a deep personal desire to make up to the Stich family for what he considered to be a serious lapse in medical judgment during the prior three years. Indeed, there were times when I felt that this expert witness had, by choice, transformed himself into an expert advocate. Considering Mrs. Stich's tragic situation, one can well understand his remorse. However, carefully considered, his opinion must be rejected in the face of the overwhelming amount of contrary clinical and other evidence which has been adduced in this case. Considered together, this evidence suggests that Dr. Gluck's failure to diagnose Mrs. Stich's condition as GBS from November 1976 to September of 1980 was not incompetence.

  Dr. Howard Medinets

  Dr. Howard Medinets' opinion as to diagnosis and causation on behalf of the plaintiffs is rejected by this court for somewhat different reasons. Dr. Medinets has been practicing neurology and neurosurgery since 1950. He felt that Mrs. Stich suffered from encephalomyeloradiculopathy. He testified that she had both peripheral nervous system and CNS involvement. Boiled down, it was Dr. Medinets' conclusion that Mrs. Stich's peripheral neuropathy could be classified as a GBS and her CNS pathology as a meningo-encephalitis. While I have considerable regard for Dr. Medinets' qualifications, I find that his opinion as to diagnosis and causation is unpersuasive. For example, Dr. Medinets ruled out Herpes Simplex Encephalitis because of the results of the complement fixation test, the validity and efficacy of which was seriously questioned by the recent research referred to in the testimony of Drs. Price and Whitley (discussed infra). I am convinced that Dr. Medinets was not sufficiently discriminating or meticulous in giving consideration to the various possible causes of Mrs. Stich's condition, particularly those relating to a viral etiology.

  Dr. Charles Poser

  Dr. Charles Poser had no hesitation in causally relating Mrs. Stich's condition to the swine flu inoculation she received or in diagnosing it as GBS. His precise diagnosis was that she had an encephaloradiculoneuropathy. He felt that her condition falls within the spectrum of diseases described in the medical literature as disseminated vasculomyelinopathy, and which could be diagnosed neurologically as GBS. He also had no hesitation in stating that Mrs. Stich's neurological conditions met the requirements of the NINCDS criteria.

  It was obvious to me that while the doctor has had extensive interest in and exposure to GBS, his opinion as to the nature of that condition is a distinctly minority view, and not one shared by an overwhelmingly impressive body of medical opinion. In listening to Dr. Poser, I had the distinct impression that his was a "voice crying out in the wilderness". If I felt that his theory, as applied to the facts of this case, made sense in light of the evidence presented, I would have no hesitation in embracing his rationale. I decline to do so, however, because I find that his general opinion as to the nature of GBS is contradicted by the overwhelming weight of credible medical opinion presented to this court. Secondly, his diagnosis in this particular case is, in my judgment, faulty. I had the distinct impression that Dr. Poser took the pathological picture presented by Mrs. Stich in this case and attempted to mold it to fit his own almost unique theories. A square peg cannot fit into a round hole. Although I was highly interested in his theories, I find that they do not form a sufficient qualitative basis in this case to permit me to conclude that plaintiffs have met their burden of proof.

  Dr. Robert Lisak

  The record will reflect that I questioned Dr. Robert Lisak extensively. His expertise in the field of neurology was conceded by the government. After acknowledging his familiarity with the NINCDS criteria, he acknowledged that his "boss", Dr. Arthur Asbury, (chairman of the NINCDS Committee) had "made them [the criteria] up". It was his opinion that Mrs. Stich had post-immunization encephalomyelitis, and that she also had "involvement of the nerve roots or possibly of the peripheral nerves as well, which would then give her encephalomyeloradiculitis. The radiculitis would be compatible or a part of the Guillian-Barre Syndrome." With respect to her central nervous system condition, it was his opinion that she was suffering from acute disseminated encephalomyelitis (ADEM).

  I think it is fair to conclude that, after extensive questioning on my part, the doctor stated that he felt that Mrs. Stich's condition fit the NINCDS criteria, particularly Variant Six. In this process I had attempted to carefully ascertain that I understood where Dr. Lisak stood with respect to this extremely difficult case. After questioning Dr. Lisak, I felt that the opinion he expressed regarding the diagnosis was couched with considerable hesitancy. He appeared to be far more certain regarding the problem of causal relationship between the inoculation and alleged result than he was with diagnosis. I was quite impressed with the quality of his testimony, yet I retain serious doubts whether his hesitant and perhaps vacillating opinion provides a sufficient basis for plaintiffs to carry the day.


  I was also tremendously impressed by most of the testimony presented by video deposition, which significantly undermined the general theses offered by Drs. Poser and Gluck. While I acknowledge Dr. Neil Nathanson's eminence in the field of epidemiology, it is my opinion that an epidemiological solution to this particular problem is not one which I can adopt, either way.

  In sum, I find that, when carefully evaluated, plaintiffs' essential thesis strains my credulity. The net impression I have is that plaintiffs' expert witnesses made a valiant effort to persuade this court on the issues reserved for this phase of the case. That effort, I find, has failed, for reasons I have expressed and will express later in the body of the opinion.


  As defined earlier, GBS is clearly a demyelinating peripheral neuropathy. As Dr. Medinets testified, demyelination involves the stripping away of the myelin sheath around the nerve, the result being that a demyelinated fiber cannot conduct any nerve impulses at all. Despite the interpretation of the EMG reports in this case by plaintiffs, I find that there is insufficient credible evidence of peripheral nerve involvement in Mrs. Stich's upper extremities at any time. Dr. Medinets noted that slowed nerve conduction, or absence of conduction, does not necessarily mean demyelinating disease.

  And further, the EMG reports of Drs. Lovelace and Anayotis (and the interpretation of these reports by Drs. Tsairis, Price and Goodgold), which I will more fully discuss below, indicate that there is no persuasive evidence of a demyelinating peripheral neuropathy. On the contrary, Mrs. Stich's condition manifested itself overwhelmingly in the central nervous system.

  Dr. Lovelace, in his report dated February 16, 1977, concluded that Mrs. Stich showed evidence of lower motor neuron disease at the anterior horn cell level. That conclusion, as evidenced by the normal conduction velocities on EMG, indicates that plaintiff was suffering a CNS disorder, not a demyelinating peripheral neuropathy. Two factors make this conclusion inescapable. First, there was no evidence of slowed conduction, as motor conduction was found to be normal. Second, the involvement of the nerve was at the anterior horn cell level which is part of the central nervous system, not the peripheral nerves. Thus, because of the lack of findings supportive of a demyelinating peripheral neuropathy, Dr. Lovelace's EMG report is not evidence that Mrs. Stich had GBS; in fact, it supports the contrary conclusion.

  A similar conclusion must be drawn from the report by Dr. Anayotis from March 1980. The most that can be fairly drawn from this report is that some denervation can be identified. There is no basis, however, for finding demyelination of the peripheral nerves. Further, Dr. Price testified that Dr. Anayotis was wrong to base his conclusion on a single conduction velocity (right perineal nerve) that is low normal, not abnormal. Dr. Tsairis found that the denervation that was identified on EMG testing involved both lower extremities was consistent with denervation of some part of the lower motor neuron but not consistent with damage to the motor axon (i.e., not peripheral).

  The Anayotis report also identified fibrillations in several muscle groups. This is not significant, however, because one does not find fibrillations or fasciculations in a demyelinated peripheral nerve; fibrillations, as Dr. Medinets testified, are, rather, a definite indicator of anterior horn cell involvement. In fact, because of the involvement at the anterior horn cell level, any absence of conduction in the peripheral nerve is more likely secondary to a central nervous system condition. In summary, Dr. Anayotis' EMG study, including the F wave response and the conduction velocities, is not compatible with a peripheral neuropathy.

  Both Dr. Lovelace's and Dr. Anayotis' reports were subject to the scrutiny and analysis of Dr. Joseph Goodgold in Dr. Goodgold's deposition testimony on October 27, 1980. Dr. Goodgold, director of the Electrodiagnostic and Neuromuscular Disease Service at New York Hospital and a prominent expert in his field, found that these two reports, even considered together, could not support a diagnosis of GBS. Several factors contributed to this judgment. First, much emphasis was placed by plaintiffs upon the motor conduction velocity of the right perineal nerve from the head of the fibula to the ankle which Anayotis reported as 45 meters/sec or low normal. That measurement, however, is considered and recorded as normal in Dr. Goodgold's laboratory (as well as in Dr. Tsairis' laboratory).

  Further, in referring to the fibrillations identified by Anayotis, Dr. Goodgold testified that he cannot tell one way or the other whether they are evidence of GBS or anterior horn cell disease. In fact, Dr. Goodgold admits that he cannot rule out anterior horn cell disease as the cause because he does not have enough information from Anayotis' report or from Lovelace's report to rule it out. In referring to the inability to obtain conduction velocities in the lower extremities, Dr. Goodgold agreed with Dr. Tsairis that the reason they could not be obtained was "because of the severe atrophy due to extensive denervation in all distal muscles on the needle EMG study", [and not because of peripheral demyelination].

  Dr. Goodgold also found that the fibrillation potentials which Dr. Lovelace found (which plaintiffs suggest is a sub-clinical sign of peripheral nerve involvement) are not reliable because of atrophy and residual weakness due to Mrs. Stich's history of polio. As Drs. Price and Tsairis confirmed, it is known among polio specialists and electromyographers that old polio will produce EMG abnormalities for many years -- greater than twenty and perhaps up to sixty -- after the acute phase of the polio has passed. Mrs. Stich's left leg was clearly involved with polio and muscle loss was the residual deficit. Whether the right leg was also clinically involved is unclear from the medical records, but it is quite likely that the right leg was at least sub-clinically involved with polio. Dr. Tsairis, whose subspecialty is electromyography, testified that he knew of many cases of old polio in which the patient believes only the left leg to be affected, but sensitive EMG studies will show right leg denervation as well. Recent research confirming this phenomenon was also brought to the Court's attention by him.

  Here, I agree with defendant that Mrs. Stich's left leg EMG findings by Dr. Anayotis of fasciculations in March of 1980 were identical to those in the right leg; that the left leg has findings characteristic of old polio supports the proposition that the right leg was also previously involved, leaving a similar deficit at the anterior horn cell level. Polio is, of course, an anterior horn cell disease. The Lovelace EMG finding of a disease process at the anterior horn cell level is consistent with the findings one would expect in the EMG of a muscle affected many years before with clinical or subclinical old polio. Accordingly, the electromyographic findings which have been interpreted as indicative of anterior horn cell disease may indeed arise from the polio involvement that plaintiffs' experts chose to ignore.

  Finally, the Lovelace report is the only arguable evidence of denervation of the facial nerves in this case. It is highly significant that neither Dr. Lovelace nor Dr. Goodgold concluded that this was proof of peripheral nerve demyelination. Lovelace instead identified the involvement at the anterior horn cell level, which, as I pointed out previously, is in the central nervous system. The face fibrillations in the Lovelace report, which are rated at one-plus, are, as Dr. Price testified, minor subclinical nonspecific findings. GBS can never be diagnosed from an isolated finding of fibrillations, which are not tantamount to weakness.

  For all of the above reasons, the EMG evidence fails to prove that Mrs. Stich suffered from a demyelinating condition of the peripheral nerve in 1976 or at any subsequent time. Dr. Goodgold's opinion, that he cannot conclude from these reports that there is evidence of demyelinating peripheral nerve disease to a reasonable medical probability, casts substantial doubt on the plaintiffs' position.


  The record indicates that virtually every treating physician's diagnosis was either viral encephalitis, encephalomyelitis, or encephalitis of unknown etiology. The final discharge diagnosis at Columbia Presbyterian Hospital was also viral encephalitis. After carefully reviewing the evidence, I find that Mrs. Stich's condition is, to a reasonable medical and legal certainty, Herpes Simplex Encephalitis.

  Encephalitis is an inflammation of the brain. Viral encephalitis is the most common form of encephalitis and is usually characterized by localized lesions in the brain. HSE, in turn, is the most frequently found viral encephalitis in humans, and is caused by the herpes simplex virus. This virus is usually benign, but for unknown reasons it may attack the temporal lobe or the inferior part of the frontal lobe, thereafter sometimes extending back into the occipital, parietal and frontal areas.

  In HSE cases the virus typically causes localized involvement first, with affected brain cells becoming swollen and edematous. The disease, as detected by such edema, normally begins in the gray matter, but may spread through the white matter (neural tissue which typically underlies the cortical gray matter, or is gathered into central tracts and peripheral nerves) as the infection progresses. The acute phase of HSE, with the virus infecting the cortex and subcortical white matter, leads eventually to severe necrosis. The host eventually may bring the virus under control, but not before irreversible brain damage is done. Where HSE is untreated, the infection may become bilateral, meaning that the opposite side of the brain may become involved, and the virus may continue its destructive process. *fn16"

  HSE, as a predominantly focal disease, usually produces neurological signs on the opposite side of the body from the sector of the brain which is involved; such signs include central nervous system weakness, focal seizures, one-sided pathological responses, and hemiparesis (implying frontal area involvement) or hemianopsia (implying occipital area involvement). Onset of HSE is typically accompanied by fever and headache, focal neurological symptoms, behavioral disturbances, and altered consciousness. HSE is the most common non-epidemic cause of fatal rapid onset disorder of the central nervous system; it is a devastating condition which is fatal for approximately 75% of all patients. Those who survive suffer a severe neurologic deficit due to destruction of part of the brain. The typical residual disabilities include hemiparesis and disorders of cognition, thought and memory.

  Diagnosis of HSE

  The credible testimony indicates that the only sure method to diagnose HSE is by a brain biopsy of the affected brain material. *fn17" Mrs. Stich, of course, never had a brain biopsy performed, primarily because her transfer to Columbia Presbyterian Hospital occurred too late in the course of her condition to provide the opportunity for a meaningful test. Reliance must therefore be placed instead on the recent advances in the diagnostic tools available for establishing an HSE diagnosis to a medical and legal certainty.

  Primary among the recent diagnostic advances is the work of the National Institute of Allergy and Infectious Diseases ("NIAID") Collaborative Antiviral Study Group, and particularly that of its principal investigator and director, Dr. Richard Whitley. The protocol of the Collaborative Antiviral Study Group is the diagnosis and therapy of HSE. The group began with the participation of thirteen medical institutions, and this number expanded to twenty-two in 1976. By 1981, there were forty-five participating medical institutions throughout the United States, Canada, England and Sweden. The Group has had the benefit of the study of two hundred and fifteen patients presenting signs of encephalitis, each of whom has undergone a biopsy. The results of these studies, first reported in the medical literature in August of 1977 *fn18" and in various scholarly articles thereafter, have provided the medical community with the best available means, other than (or prior to) biopsy, of predicting whether a given patient has HSE. In practice, the Group's findings are regularly employed as the criteria for establishing a tentative HSE diagnosis, which would, in turn, lead to a biopsy procedure to confirm the diagnosis and, if confirmed, admit the patient to an experimental antiviral drug therapy. I adopt the NIAID Collaborative Antiviral Study Group's findings or criteria for the limited purpose of determining whether or not the evidence herein suggests that HSE is the most probable diagnosis of Mrs. Stich's condition. *fn19"

  It has been known for some time that HSE, being primarily a focal encephalitis, may be detected through the use of Computer Axial Tomography ("CAT") and technetium radionucleid-type brain scans and electroencephalographs ("EEGs") which may reveal the location of focal lesions in the brain. The presence of such focal lesions would support the diagnosis of HSE and contraindicate the diagnosis of post-vaccinal encephalitis. The Collaborative Study Group has found that the EEG, brain scan and CAT scan are the three best non-invasion (non-biopsy) tools or studies to correctly predict an HSE diagnosis. Clinical findings alone, such as fever, CSF pleocytosis, consciousness and convulsions, have been found insufficient in and of themselves to predict or confirm such a diagnosis, although they may create the initial suspicion.

   The Collaborative Study Group has recently published its most current research in an article in the Journal of the American Medical Association. See Whitley, et al., Herpes Simplex Encephalitis: Clinical Assessment, Journal of the American Medical Association (January 1982). The essential data included in that article summarizes the Group's experience with 176 patients who presented with signs of focal encephalitis. All of these patients were biopsied at the suspected brain site; as a result, a diagnosis of HSE was confirmed in 101 patients and not confirmed in the remaining 75. The data which the Collaborative Group collected were then analyzed to determine whether there were findings and symptoms which were common to the HSE group as distinguished from the non-HSE group. All tabulations were verified by virologists, neurologists, and biostatisticians, who checked by double-blind methods for the accuracy and proper categorization of the patient data. The resulting findings are reproduced here as Table 1: *fn20" Table 1 Herpes Simplex Encephalitis Diagnostic Assessment Within Three Days of Biopsy EEG Brain Positive Brain Negative Focal 58/73 (81%) 39/66 (59%) * Generalized 44/72 (61%) 41/62 (68%) Spikes 40/70 (57%) 14/58 (24%) * Slow Activity 65/72 (90%) 52/62 (83%) *** Brain Scan Localization 37/74 (50%) 6/44 (14%) * CAT Scan Localization 33/56 (59%) 8/37 (22%) ** Any one or More Assessment of Localization 83/101 (82%) 47/75 (60%) * Two or More Positive Results 31/64 (48%) 9/50 (18%) *


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