Dr James Schaller
tick infection pearls chat free books testimonials main page books and articles schaller health creed free consult testimonies search
menu main page what's new second opinion new patient meet doctor schaller location, travel

Confronting Dubious "Experts"
Trying to Dupe Juries & Judges

***********

Critique of Dr. X's Report:
Errors, Distortions & Concessions by Omission

Summary Impression of Dr. X's Report:

Simply, she seems to feel it is a contribution to justice to:

  • Restate her conclusion repeatedly.
  • Merely repeat the quotes of others who oppose her which fill up much of her report.
  • Make some occasional criticism with no clear relevant point.
  • Misrepresent the position of this expert.
  • Dr. X entirely ignores massive sections of authoritative science which strongly undermine her position, and for which she has no reply or only unreasonable replies.
  • Finally, Dr. X attempts to be authoritative, by dropping in two inapplicable studies, from the 14 million she might have selected. She presents them in a way that shows she is either unable to understand them, or is forcing patient A into these studies when he meets exclusionary criteria for both of them.
  • Finally, she pads her report by merely quoting the DSM-IV extensively (presumably the DSM-IV Text Revision) which offers no argument at all related to this case.
  1. In the first page of her report, Dr. X takes the utterly amazing position that mild head injury is not associated with resulting psychosis.

    Bluntly, the association between all forms of brain trauma and the increase in psychiatric disorders is a fact, and has been considered basic elementary medicine for decades. Specifically, this includes many varieties of psychotic disorders. That this is even a point of controversy in this case is fairly astounding and inappropriate. Dr. X offers no evidence for her position. Below is a small sample of evidence for my position.

    1. Victims of brain trauma have psychosis far in excess of the rest of the population, or what is expected to arise spontaneously in the population. Trauma to the brain increases psychosis and schizophrenia presentations.

      * Achte, et al, as early as 1969 published the results of a study of 3552 brain-injured men, and found 8.9% with psychosis, with younger victims who tended to have milder injuries with a schizophrenia-like presentation at 24%. (Acta Psychiatr Scand).

      * Achte, et al, in 1991 published the results of 2907 brain injury victims and found 26% had various psychotic disorders (Psychopathology).

      * An extensive survey of the literature, done by Davidson and Bagley as early as 1969 reports a full 200% to 300% increase in "schizophrenia symptoms" post head trauma (Current Problems in Neuropsychiatry).

      * Labbate, et al, in 2000, offers an entire section on the treatment of traumatic brain injury related psychosis. Reporting again, that the incidence of psychosis is in excess of expected from the normal population. Further, he explains that many areas of the brain are frequently affected by brain trauma, e.g., the prefrontal and temporal lobes, the thalamus and the basal ganglia. (Current Psychiatry Reports. 2:268ff.)

      * Zhang and Sachdev, in 2003, explain simply and clearly that, "Traumatic brain injury can result in ... severe and chronic psychosis." They explain further, a common expression, "schizophrenia-like psychosis" is much more common after head trauma and looks a lot like schizophrenia (Current Psychiatric Reports. 5:197-201)

      * Wood & McMillan in Neurobehavioral Disability and Social Handicap Following Traumatic Brain Injury present evidence of routine psychiatric disorders after even modest concussions in many patients, which are consistent with many of this patient's functional declines.

      * Parker in Concussive Brain Trauma presents evidence of common brain injuries, even mild ones, which are consistent with many of this patient's functional declines.

      * Smeltzer, et al. Psychotic disorders. In Silver, Yudofsky, Hales, eds. Neuropsychiatry of traumatic brain injury. American Psychiatric Press, 1994:251-83.

      Further references available.
  2. On page two and four of her report, Dr. X quotes Dr. Y and I as reporting on the lack of schizophrenic relatives. She never refutes this repeated comment and so it is conceded. The absence of genetic relatives with schizophrenia, does not support her "blame the Schizophrenia genes" or the family for patient A's current state.
  3. She blames patient A's genes. But no such family history exists. Nevertheless, that does not stop her from rushing in with studies that she forces into this case, which are not relevant and which she appears to never have carefully read. She profoundly misses the key points of her own quoted studies.

    For example, she quotes a study of schizophrenics by Malaspina & Goetz published in 2001 presented in a junk science manner. She offers a flawed presentation of her only main supporting study.

    1. She edits the first line in the discussion section (pg. 444), which says: "This study found a threefold greater rate of reported traumatic brain injury for subjects with schizophrenia ... when the subjects were compared to their never-mentally-ill family members." Yes, and this is the point. A schizophrenia-like presentation is 300% more common when there is brain trauma in people like patient A with no schizophrenic relatives.
    2. Patient A does not fit this study since he does not have schizophrenic family members. In other words, Dr. X is simply throwing a couple academic crumbs at the court, which have little to do with the issues. In checking the actual articles I found errors in accurately presenting them. They have no applicability to the main issues in this case.
    3. Indeed, to be in this study a patient had to have two relatives with clear diagnosed schizophrenia or schizoaffective disorder.

      Since Dr. X never offers the names of patient A's schizophrenic or schizoaffective relatives, the application of this study is zero. Despite the many articles on schizophrenia, she searches out the one that appears to support her point, edits out the crucial inclusion criteria of the study, i.e., having a massive and specific family history of major psychosis in close relatives, and then presents it in a way that appears authoritative. She is either careless or attempting to dupe the court.

      To be very clear: patient A does not have two very clearly documented schizophrenic relatives, so he would not even be allowed in this study!
    4. Schizophrenia is a diagnosis of exclusion and is never assumed. This has been the strong tradition in American and European Psychiatry for decades. Indeed, Dr. X explains in page X of her report, e.g., that to have the diagnosis of schizophrenia, one must exclude "a general medical condition or a general medical condition that is the cause of his symptoms. " The point is that her use of this study involves circular reasoning.

      1. She simply decides that no medical condition occurred.
      2. She avoids any medical qualification and merely labels patient A as "schizophrenic."
      3. Then she uses a study that assumes patient A has schizophrenia apart from medical causes.
    5. This adult study of patients with a patient mean age of 44 years old is questionable, since child psychiatry studies often to do follow adult findings.
    6. The studies other major conclusion reports "schizophrenia genes may increase exposure to head trauma, with head trauma further increasing the risk for schizophrenia." It is agreed that trauma makes virtually all psychiatric conditions increase. This is evident from the wide balance of psychiatric research. We know, for example, that individuals with left frontal strokes (an internal brain trauma) tend to suffer high incidences of major depression, but without the stroke, they would not be depressed. Is Dr. X blaming patient A for the car accident?
    7. Schizophrenic can evolve with many contributions. These include malnutrition, viral infections, dementia, brain deterioration disorders, tumors, syphilis-like infections, strokes, etc. Indeed, genetics function as only one modest contributor when one looks at family studies. Dr. X seems to be saying genes plus trauma equals the fault of the genes.
    8. In actuality, since no major or meaningful family history has been proposed for patient A, then this is not just a misused study, but her point can be fully reversed in the absence of genetic family history. If it is not 2 (genetic family history) plus 2 (trauma) ='s schizophrenia, than it is 0 plus 4 = Psychosis. Or zero genetics plus a traumatic brain injury caused his psychotic disorder.
  4. Misuse of second study. Dr. X reports that the research of "Abdelmalik Housted, " which I assume is correctly spelled P. AbdelMalik and J. Husted, reports "similar conclusions" to her first article described above.

    1. I disagree. A careful reading of the article clearly is in keeping with the wider knowledge of psychosis in explaining that "nongenetic factors" are very important (Page 231). They also say that psychosis, specifically one form of psychosis, i.e., schizophrenia, is caused by "abnormal neurodevelopment." Simply, there are many ways to get to this "abnormal" development, in the same way there are many ways to break an ankle -- including trauma.
    2. The study only looks at 16 children with families that have a "strong genetic predisposition" for schizophrenia. Patient A does not have this so he would not even be allowed in this study. Its application then is meaningless and false.
  5. Dr. X repeatedly quotes the issue of odors and seems to feel this is the first sign of schizophrenia in this approximately XX-y/o boy.

    1. Dr. X has not spent two years studying the unique field of child and adolescent psychiatry as I have, which constitutes a full-time two-year fellowship, and she is forcing adult psychiatry into child and early adolescent psychiatry. All of the events in this case, such as his odor compliant and the effects of the accident, apply to adolescent psychiatry, not adult psychiatry. I am frankly confused why someone with no training in this area, or publications on neurologically or psychiatrically impaired youth, is involved in this case. The reason one is required to practice and study fulltime for two years is so that such simple mistakes are not made, e.g., errors in understanding what early adolescent schizophrenia looks like and how it progresses.
    2. First, I see no comments on the much more obvious, common, and reasonable proposals for his smell complaints -- just that it means he has early schizophrenia. Pediatricians and child psychiatrists rarely think of common smell annoyances as early psychosis as Dr. X proposes, very simplistically.
    3. I offered Dr. X the fifteen basic possible causes for his transient common smell complaints. Surprisingly, she offered no comment on this material. Her silence is surprising since her entire position seems to largely rest on patient A having olfactory hallucinations before the accident.
    4. Patient A had some anxiety over his smell annoyance and sadness at the time he was being worked up. This is reported as a "mental status change" -- an expression so vague, it is useless, and fully within the realm of common early adolescent emotions. Many boys have mental status changes on a weekly or monthly basis. (Even serious mental status changes are comment in adolescents, e.g., many have suicidal thoughts, plans, and feelings, but end up resolving their early life challenges successfully).
    5. In a young early adolescent with emerging schizophrenia, we do not see the picture Dr. X proposes, i.e., with significant olfactory hallucinations, which then entirely depart for years without any anti-psychotic. Child or early adolescent schizophrenia psychosis does not develop this way once it starts to present, i.e., with extended holidays, and this seems to be an error in the application of adult psychiatry to child psychiatry.
    6. Finally, we are asked to believe that patient A developed this single lonely early schizophrenia symptom, in complete isolation from any other sign or symptom that would be associated clearly with schizophrenia.

      In conclusion, Dr. X's complete silence on these points above lend me to believe this "odor complaint" is unrelated to this entire case, and is merely junk science.
  6. Dr. X holds the position that if an early adolescent does not show immediate profound damage to their psychiatric status, they have experienced no injury (pg. x). This position shows ignorance of child and adolescent developmental pathology evolution. It is the kind of position we occasionally see in untrained and out-of-date concussion evaluators, i.e., if you are not found with grossly abnormal trauma, you are sent home.

    1. The facts are that delays in decreased functioning are very common in the literature, and due to many possibilities. For example, subtle neurotransmitter system shifts or other changes in brain tissue, or many intracellular changes are not instantaneous, and these very small changes are at the foundation of many types of psychosis.
    2. Further, delay in brain effects is seen in an analogy to see the point. Psychosis medication removes psychosis. But the effects they have are very staggered. These and other psychiatric medications have their maximal effects in months, seasons or even years after an ideal drug and dose are found. Some studies show brain region tissue sizes shifting over long-term anti-psychotic, lithium or antidepressant use. Meaning, improvement can start or be maximized months or years after treatment, in the same way psychosis from trauma can develop over seasons or years.

    Sample Studies Show that Brain Trauma can have Delayed Psychiatry Effects

    *Violon & De Mol, as early as 1987, in examining 530 patients, found that over 1-10 years, 3.4% developed psychosis. (Acta Neurochirurgica)

    *Sachdev & Smith in 2001, explained that they carefully evaluated 45 patients over ten years and found that the mean time until an onset of a "schizophrenia-like psychosis" was 54.7 months. They explained this onset was usually gradual and not sudden -- as Dr. X seems to imply in her commons on patient A's immediate post accident behavior in the following months (Psychological Medicine. 31:231ff).

    *Zhang et al, explains that the onset of post brain trauma schizophrenia-like psychosis has an onset that is "often gradual." (Current Psychiatric Reports 2003:197ff.)

    In conclusion, Dr. X says (pg. X) that since patient A's classes did not show sudden change and since he could still play football, that he was unaffected by his car accident. Such a position confuses the extensive research on car-related brain trauma with its slow neuropsychiatric changes and an acute massive trauma from a gunshot wound. Her vocabulary and expectations seem grossly uninformed about the effects of non-fatal or non-catastrophic brain trauma, and she seems to see all traumas to the brain as one and the same. I do not see why she cannot make the clear distinction.
  7. Dr. X holds the position that a loss of consciousness is required for brain damage in a car accident. We would suggest this is common in TV shows but inaccurate scientifically. The link of brain damage and consciousness is unfounded scientifically and in common sense situations mentioned below.

    Just using basic common sense, we see many well-known medical events in which a patient is conscious and has brain damage. Simple examples would include events involving: a bicycle, hockey, a fall, football, shaken baby damage, whiplash, boxing and a blood pool in some parts of the brain.

    The studies show even mild brain trauma with no loss of consciousness, can have profound damage, and often has a wide variety of different negative outcomes.

    * Leininger, et al, Neuropsychological deficits in symptomatic minor head injury patients after concussion and mild concussion. Journal of Neurology, Neurosurgery and Psychiatry 1990;53:293ff.

    * Mild Head Injury Interdisciplinary Special Interest Group of the American Congress of Rehabilitation Medicine. Definition of mild traumatic brain injury. Journal of Head Trauma Rehabilitation 1993;8:86ff.

    * Umile, et al, Archives of Phys Med Rehabil 2002;83:1506ff

    * Parker, Concussive Brain Trauma: Neurobehavioral Impairment and Maladaptation. CRC; Boca Raton, 2001.

    *Barth, et al. Neuropsychological sequelae of minor head injury. Neurosurgery 1983:13:529ff

    Further, it is now well established that only mild trauma or mild concussion, with or without loss of consciousness can have significant effects that are not reversible. This was established in the 1980's.

    Alves & Jane. Mild brain injury: damage and outcome. In: Beck, Povlishock, eds. Central nervous system trauma status report -- 1985. Washington, (DC): National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health; 1985. Pg. 255-270.
  8. The Emergency Room Blame Argument -- Ignoring the Many Evaluations Immediately Following the Accident

    1. Dr. X, in her masterly filtering style, yet again blames patient A for the accident because he did not rush to the emergency room. The fact is that many people do not rush to the ER unless they are gushing blood or plan a lawsuit. Adolescents never want to sit around for 3-15 hours. And most parents, along with Dr. X, do not appear to be up on the many studies showing the major effects and delayed effects of even mild concussions. The idea that an ER visit would have found the subtle damage found on a PET scan is unrealistic.
    2. And the evaluations immediately after the car accident were left uncommented upon by Dr. X because they are devastating and clear. They are evaluations by physicians who know the child or specialists. Their reports make it clear that the child certainly met criteria for an entirely new and significant event to the brain.

      1. The patient was evaluated by his family doctor Dr. M, approximately 48 hours or less after the injury, in which head bruising and swelling was noted, along with headaches.
      2. Approximately five weeks later, neurologist Dr. R was asked to evaluate patient A due to unusual thinking and new social withdrawal. [Symptoms classic in adolescent brain trauma -- my comment]. Over the next month, this neurologist determined that he had mild post-concussive syndrome and felt that there was a possibility of cerebral contusion.
      3. Neurologist, Dr. L did a second consultation, in December 19XX, February 19XX and April 19XX. On December XX, 19XX, this physician wrote a letter to patient A's family doctor noting troubles with memory and concentration, a personality change that was marked, and noted that the youth was now tending to stay around the house. His diagnosis included Post Traumatic Encephalopathy, Closed Head Injury, Concussion, and Post Traumatic Headaches.
      4. A Neuropsychological evaluation done by Dr. H on March 19XX found a personality change due to concussion and also memory problems and/or Amnestic Disorder, due to concussion.
      5. In April of 19XX, the patient was placed on Anti-Depressant by his neurologist for mood and functional changes.
      6. The following month patient A began having auditory hallucinations. He was therefore repeatedly admitted to XXX Hospital over the course of May 19XX. He was given a wide range of possible diagnostic labels -- they were merely treating his hallucinations, which is an understandable goal.
      7. He was transferred to the XXXX in June of 19XX, where he stayed for XX days. His discharge diagnosis was rule out Epilepsy, Status Post-Head Trauma, and Psychosis Not Otherwise Specified.
    Conclusion: Patient A's neuropsychiatric problems follow back to the immediate 48 hours following his car accident on XX/XX/XXXX.

Bank Towers, Tamiami Trail, Naples, FL
disclaimer privacy