There is no more important issue for the diagnosis and determination of prognosis after a brain injury than the length and severity of amnesia. Amnesia is defined as the loss of memory for events, both before and after the accident. Loss of memory for events before the accident is called retrograde amnesia, i.e. similar to the use of the term retroactive, i.e. something that relates back to a time prior to the event. Loss of memory for events after the accident is called anterograde amnesia. This also includes problems with new learning. See http://tbilaw.com/AboutMildBrain16.html In non-coma brain injury cases, there is rarely any significant retrograde amnesia, and the term Post Traumatic Amnesia, (“PTA”) is often used generally to describe the loss of memory following an event.
One of the leading text’s in the Field of Brain Injury, Lezak’s Neuropsychological Assessment, now in its 4th Edition, clearly states the prevailing opinion, that it is the length of Post Traumatic Amnesia that is the biggest predictor of outcome after a brain injury. The 4th Edition contains this chart with respect to amnesia:
TABLE 7.1 Estimates of Severity of Injury Based on Posttraumatic Amnesia (PTA) Duration
PTA Duration Severity
________________________________________________________________________
<5 minutes Very Mild
5-60 minutes Mild
1-24 hours Moderate
1-7 days Severe
1-4 weeks Very Severe
More than 4 weeks Extremely Severe
Now the problems with prognosticating brain injury from determinations of PTA is that this measure is rarely properly assessed by treating doctors after a head injury. Lezak explains this dilemma as follows:
“However, difficulties in defining and therefore determining the duration of PTA have made its usefulness as a measure of severity questionable in some cases (Jennett, 1972; Macartney-Filgate, 1990). For example, while it is generally agreed that PTA does not end when the patient begins to register experience again but only when registration is continuous, deciding when continuous registration returns may be difficult with confused or aphasic patients (Gronwall and Wrightson, 1980). Moreover, many patients with relatively mild head are discharged home while still in PTA, leaving it up to the examiner to attempt at some later date to estimate PTA duration from reports by the patient or family members, who often have less reliable memories. These considerations have led such knowledgeable clinicians as Jennett (1979) and N. Brooks (1989) to assert that fine-tuned accuracy of estimation is not necessary as judgments of PTA in the larger time frames of hours, days, or weeks will usually suffice for clinical purposes (e.g., Table 7.1). Length of PTA as more accurate than coma duration in predicting cognitive status two years after injury(D.N. Brooks, Aughton, et al., 1999). Yet failures to discriminate between moderately and severely impaired patients suggest that it may not classify patients with sufficient sensitivity for research (N. Brooks, McKinlay, et al., 1987).”
What does this all mean? It means that someone who is comatose for a week but has a rapid return of memory and a reasonably quick end to PTA may be expected to have a better outcome than someone who is never knocked out but continues to have PTA for more than a month. YES. I DID SAY THAT. Someone without a loss of consciousness can have a worse outcome than someone who is in a coma, if they have a longer period of PTA.
But alas, I am a lawyer, and how do I prove that someone has PTA that persists for weeks after a seemingly routine concussion? If the medical professionals would do their job of follow-up, my job would be so much easier.
I met with a client recently who was amnestic for as much as three months post accident. Among the highlights of what she doesn’t remember is an airline trip to visit a doctor, meeting her lawyer, the last four months of a pregnancy. While not remembering a lawyer might be a good thing, forgetting one of her first airline trips and a significant portion of her pregnancy, are undeniably abnormal. But are these memory gaps clearly documented in her medical records? One month post accident, she is seen by her family doctor, because her significant other is concerned about her memory problems and seizure episodes she is having. The doctor documents the seizure episodes but asks no probing questions about memory or even notes her boyfriend’s concerns about memory.
Why can’t doctors learn how critical documenting amnesia is? Is it so hard to ask questions of a person with Post Concussion Syndrome questions that will test whether that person is imprinting current memories to that person’s long term memory? The brain has a memory mechanism quite analogous to a computer’s RAM conversion to hard drive memory process. If you are creating a document on a computer and lose power or your computer crashes before you save the document, all will be lost and what was held in your computer’s RAM, will not be saved to your computer’s hard drive. Amnesia is the failure of the brain to convert short term memories into long term memory, in essence saving the memory to a different part of the brain.
In order to test for amnesia, it is necessary to ask questions of a person that determine what they remember about a few hours ago, what they remember of yesterday. Why is this so hard? It isn’t hard – it is just that it has never been made to seem important enough. Yet all of 50 steps of the classic neurological exam will tell us far less than simply asking someone what an injured person ate for dinner the night before the follow-up exam.
For more on my thoughts about identifying amnesia, see my YouTube videos at:http://youtube.com/profile?user=braininjuryattorney
Brain Injury and Locked-In Syndrome
In yesterday’s blog, I talked about the exception to my skepticism about miracle recoveries, years post a coma causing event. The exception is in the cases of “locked in syndrome”. The National Institute of Health contains this definition of Locked-Iin Syndrome:
What is Locked-In Syndrome?_Locked-in syndrome is a rare neurological disorder characterized by complete paralysis of voluntary muscles in all parts of the body except for those that control eye movement. It may result from traumatic brain injury, diseases of the circulatory system, diseases that destroy the myelin sheath surrounding nerve cells, or medication overdose. Individuals with locked-in syndrome are conscious and can think and reason, but are unable to speak or move. The disorder leaves individuals completely mute and paralyzed. Communication may be possible with blinking eye movements
Is there any treatment?
There is no cure for locked-in syndrome, nor is there a standard course of treatment. A therapy called functional neuromuscular stimulation, which uses electrodes to stimulate muscle reflexes, may help activate some paralyzed muscles. Several devices to help communication are available. Other treatment is symptomatic and supportive.
What is the prognosis?
While in rare cases some patients may regain certain functions, the chances for motor recovery are very limited.
What research is being done?
The NINDS supports research on neurological disorders that can cause locked-in syndrome. The goals of this research are to find ways to prevent, treat, and cure these disorders.
See http://www.ninds.nih.gov/disorders/lockedinsyndrome/lockedinsyndrome.htm
Why do I feel that locked-in syndrome is an exception to the no hope scenario in long term coma recovery? Because these are cases where the person was fully aware, despite the inability to communicate. What is so tragic when such cases are discovered after the fact, is that the person was there, so to speak, the whole time, just no one was listening. If a PET scan or fMRI had been done, it would have been clear from the beginning that such person’s brain was functioning. Instead, like the character in the anti-war story that galvanized my youth, Johnny Got His Gun, the mind of the survivor was totally isolated.
Another interesting example of a locked in type syndrome is the House episode where it begins with the seemingly persistent vegetative individual driving his wheel chair into a swimming pool. http://en.wikipedia.org/wiki/Meaning_(House_episode)
See also: http://en.wikipedia.org/wiki/Locked-In_syndrome
What is Locked-In Syndrome?_Locked-in syndrome is a rare neurological disorder characterized by complete paralysis of voluntary muscles in all parts of the body except for those that control eye movement. It may result from traumatic brain injury, diseases of the circulatory system, diseases that destroy the myelin sheath surrounding nerve cells, or medication overdose. Individuals with locked-in syndrome are conscious and can think and reason, but are unable to speak or move. The disorder leaves individuals completely mute and paralyzed. Communication may be possible with blinking eye movements
Is there any treatment?
There is no cure for locked-in syndrome, nor is there a standard course of treatment. A therapy called functional neuromuscular stimulation, which uses electrodes to stimulate muscle reflexes, may help activate some paralyzed muscles. Several devices to help communication are available. Other treatment is symptomatic and supportive.
What is the prognosis?
While in rare cases some patients may regain certain functions, the chances for motor recovery are very limited.
What research is being done?
The NINDS supports research on neurological disorders that can cause locked-in syndrome. The goals of this research are to find ways to prevent, treat, and cure these disorders.
See http://www.ninds.nih.gov/disorders/lockedinsyndrome/lockedinsyndrome.htm
Why do I feel that locked-in syndrome is an exception to the no hope scenario in long term coma recovery? Because these are cases where the person was fully aware, despite the inability to communicate. What is so tragic when such cases are discovered after the fact, is that the person was there, so to speak, the whole time, just no one was listening. If a PET scan or fMRI had been done, it would have been clear from the beginning that such person’s brain was functioning. Instead, like the character in the anti-war story that galvanized my youth, Johnny Got His Gun, the mind of the survivor was totally isolated.
Another interesting example of a locked in type syndrome is the House episode where it begins with the seemingly persistent vegetative individual driving his wheel chair into a swimming pool. http://en.wikipedia.org/wiki/Meaning_(House_episode)
See also: http://en.wikipedia.org/wiki/Locked-In_syndrome
Coma Help and Prognosis
My last blog contained an email from one of the charter contributors to http://waiting.com waiting.com was created to provide help for those who were waiting for someone to awake from a coma. With the creation of that page, the phone calls began to come into our office asking perhaps the most terrible question a person can ever ask themselves, at what point do we decide to withdraw life support.
I am not a doctor but a lawyer who spends his life representing people who have survived a brain injury. I have no medical training to qualify me to second guess the advice of a doctor who has properly considered this horrible question, in light of the full diagnostic criteria as it has evolved in current medical science. I wish that physicians would give a fully informed answer to this question. At no time, do family members need a more thoughtful, fully informed discussion. Sadly, the answer in 90% of coma cases is: We Will Just Have to Wait and See.
That is the easy answer of course. It may even be the technically correct answer. After all, there is no predicting when a person will emerge from a coma. But, current medical research does tell us considerably more about coma prognosis than that. The literature contains clear diagnositic criteria, which will help to shed some light on prognosis. Of course, no family really wants to hear the bad news, so saying nothing specific, may be easier for the doctor. But is that the right thing to do?
I believe that hope is important, that hope is essential, but there comes a time, when a family does need to start to deal with the horrible realities of what may lie ahead. What has always frustrated me is why doctors don’t offer the functional imaging option. For more than a decade, researchers have been calling for PET scans or SPECT scans, to help identify whether there is any meaningful brain activity, inside the comatose brain. What is functional imaging? It is a scan that can tell us how much the brain is actually working.
The PET scan and SPECT scan use a radioactively tagged glucose (sugar) molecule. If the glucose is being used to any significant degree, the brain must be working. In the 10 years since the first calls for routine functional imaging in coma cases, the functional imaging technology has grown exponentially. Not only are PET scans now more available and have radically improved quality and resolution, but fMRI has now readily available, at almost any major imaging center. fMRI is actually uses a conventional MRI scanner, but can measure the extent of brain activity, not by the sugar used, but by the oxygenation changes within the brain. A working brain must not only use glucose, it must also use oxygen.
Without any meaningful activity, there is little likelihood of emergence, and even if there is emergence, little chance of a satisfactory recovery. But if there is activity, then more radical measures should be undertaken to stimulate the brain, and more patience is warranted. I have instructed my medical power of attorney to insist on a functional imaging test if I am ever in that position.
We all hear about the news reports of the miracle emergence after 7 years in a coma. For a discussion of what it means to emerge from a coma, click here. I will always remain skeptical of such late emergency stories, unless those people were not truly comatose, but “locked in.” (I will discuss “locked in syndrome” later this week, but essentially that is a state where a person is fully awake, but there neurological damage leaves them incapable of overt communication. Locked In Syndrome is something that could absolutely be determined by a PET or other functional imaging scan, is someone bothered to order the test. ) But where a person is truly comatose, I believe that the longer the coma persists, the less the likelihood of any emergence, and if there is an emergence, little or no chance of a satisfactory recovery. Most of those who have traumatic injuries and do have a satisfactory recovery, have emerged within one month of their injury. Coma’s that persist longer than two months, leave a very marginal chance of a satisfactory recovery.
If the hours and weeks of waiting have gone on to long, it is time to demand better answers and active diagnostic interventions to give some solid answers.
I am not a doctor but a lawyer who spends his life representing people who have survived a brain injury. I have no medical training to qualify me to second guess the advice of a doctor who has properly considered this horrible question, in light of the full diagnostic criteria as it has evolved in current medical science. I wish that physicians would give a fully informed answer to this question. At no time, do family members need a more thoughtful, fully informed discussion. Sadly, the answer in 90% of coma cases is: We Will Just Have to Wait and See.
That is the easy answer of course. It may even be the technically correct answer. After all, there is no predicting when a person will emerge from a coma. But, current medical research does tell us considerably more about coma prognosis than that. The literature contains clear diagnositic criteria, which will help to shed some light on prognosis. Of course, no family really wants to hear the bad news, so saying nothing specific, may be easier for the doctor. But is that the right thing to do?
I believe that hope is important, that hope is essential, but there comes a time, when a family does need to start to deal with the horrible realities of what may lie ahead. What has always frustrated me is why doctors don’t offer the functional imaging option. For more than a decade, researchers have been calling for PET scans or SPECT scans, to help identify whether there is any meaningful brain activity, inside the comatose brain. What is functional imaging? It is a scan that can tell us how much the brain is actually working.
The PET scan and SPECT scan use a radioactively tagged glucose (sugar) molecule. If the glucose is being used to any significant degree, the brain must be working. In the 10 years since the first calls for routine functional imaging in coma cases, the functional imaging technology has grown exponentially. Not only are PET scans now more available and have radically improved quality and resolution, but fMRI has now readily available, at almost any major imaging center. fMRI is actually uses a conventional MRI scanner, but can measure the extent of brain activity, not by the sugar used, but by the oxygenation changes within the brain. A working brain must not only use glucose, it must also use oxygen.
Without any meaningful activity, there is little likelihood of emergence, and even if there is emergence, little chance of a satisfactory recovery. But if there is activity, then more radical measures should be undertaken to stimulate the brain, and more patience is warranted. I have instructed my medical power of attorney to insist on a functional imaging test if I am ever in that position.
We all hear about the news reports of the miracle emergence after 7 years in a coma. For a discussion of what it means to emerge from a coma, click here. I will always remain skeptical of such late emergency stories, unless those people were not truly comatose, but “locked in.” (I will discuss “locked in syndrome” later this week, but essentially that is a state where a person is fully awake, but there neurological damage leaves them incapable of overt communication. Locked In Syndrome is something that could absolutely be determined by a PET or other functional imaging scan, is someone bothered to order the test. ) But where a person is truly comatose, I believe that the longer the coma persists, the less the likelihood of any emergence, and if there is an emergence, little or no chance of a satisfactory recovery. Most of those who have traumatic injuries and do have a satisfactory recovery, have emerged within one month of their injury. Coma’s that persist longer than two months, leave a very marginal chance of a satisfactory recovery.
If the hours and weeks of waiting have gone on to long, it is time to demand better answers and active diagnostic interventions to give some solid answers.
From an Old Contributor to waiting.com
Attorney Johnson:
Hello. Thank you very much for the tbi law website and for the waiting.com page. It helped me a great deal to be able to communicate to others that *there is hope*.
I had forgotten about waiting.com until I asked the “high functioning” TBI online support group to which I belong for some recommendations for someone new to TBI. TBI Law was one of the recommendations.
I don’t know how many people view my and Megan’s story, but if possible, could you please change my contact email address to jodymo@pobox.com ? I hate to think that someone tried to contact me and thought I just didn’t answer because the email address is out of date.
http://www.waiting.com/jody.html
Thank you in advance for your time.
Jody Silvey Goppelt
—–
EDITOR’S NOTE: Twelve years ago, my co-author Rebecca Martin and I created http://waiting.com and its Bridge from Despair. The Bridge from Despair was perhaps the first collection of a series of anecdotal comments from those who had lived thru the ordeal of a loved one in a coma. In an interesting post note, I got this email today from one of its contributors. It is a nice reminder of the efforts we put in at the beginning of our advocacy, when brain injury information on the web was still a new idea.
Hello. Thank you very much for the tbi law website and for the waiting.com page. It helped me a great deal to be able to communicate to others that *there is hope*.
I had forgotten about waiting.com until I asked the “high functioning” TBI online support group to which I belong for some recommendations for someone new to TBI. TBI Law was one of the recommendations.
I don’t know how many people view my and Megan’s story, but if possible, could you please change my contact email address to jodymo@pobox.com ? I hate to think that someone tried to contact me and thought I just didn’t answer because the email address is out of date.
http://www.waiting.com/jody.html
Thank you in advance for your time.
Jody Silvey Goppelt
—–
EDITOR’S NOTE: Twelve years ago, my co-author Rebecca Martin and I created http://waiting.com and its Bridge from Despair. The Bridge from Despair was perhaps the first collection of a series of anecdotal comments from those who had lived thru the ordeal of a loved one in a coma. In an interesting post note, I got this email today from one of its contributors. It is a nice reminder of the efforts we put in at the beginning of our advocacy, when brain injury information on the web was still a new idea.
What is a Mild Brain Injury?
Head injuries (or otherwise called brain injuries) have been traditionally classified into three categories, mild, moderate and severe. Mild head injuries are typically brain injuries that do not involve loss of consciousness for more than 20 minutes. Moderate involve significant loss of consciousness, but not do not involve extended coma. Severe brain injuries are those that involve a coma for a substantial length of time. For our treatment of severe brain injury, see http://waiting.com
The problem with these classifications schemes that define the severity of the brain injury in terms that relate to a period of loss of consciousness, is that they severely understate the risk factors associated with mild brain injury. Mild brain injury, which is also synonymous with concussion, can leave a person completely and totally disabled. Even though a brain injury may not involve a significant disruption of the part of the brain that triggers consciousness, it can involve severe damage to either specific parts of the cerebral cortex, or disruptive damage to the white matter of the brain.
Focal versus Diffuse Brain Damage. Brain injury is usually broken out into two geographic classes, focal and diffuse. A focal brain injury involves damage to a specific area of the brain, and in mild brain injuries, this can be a very small area. Diffuse damage means the damage is spread out throughout the brain, but the pathology in any one area is large enough for specific pathology in that one area to be identifiable.
Mild Focal Injury. Again the term mild here is something of a misnomer. The type of focal injury which would be classified as mild, would typically be a focal injury that does not involve a significant portion of one of the major lobes of the brain, but can still be identified as existing, because it has compromised a specific function of that particular part of the brain. Most of the significant mild focal injuries, involve injuries to the frontal lobes, particularly the underside of the frontal lobes. The reason these relatively small areas of damage can become disabling, is that the underside of the brain hold particularly important functions in terms of adult like behaviors and productivity.
Diffuse Injury. Diffuse injury to the white matter is referred to as diffuse axonal injury. An axon the long skinny wire like part of a neuron, that transmits the electrical impulse from the cell nucleus of the neuron, to the next part of the brain or nervous system, that must receive that signal, for the appropriate function to occur. Neuron’s are microscopic, and axons, even smaller. Typically an axon can only be seen by an electronic microscope. While there are massive numbers of these microscopic axons transmitting signals throughout the white matter of the brain, injury to even thousands of these axons in the same area, may not be concentrated enough pathology for it to show up on even a high resolution MRI. For more information on Diffuse Axonal Injury, click here.
Most of the controversy in brain injury cases involves battles about whether or not a mild brain injury even occurred and if so, whether it was severe enough to leave any last deficits. The reason such controversy exists is that most mild brain injuries do not involve clear cut loss of consciousness. For most of the 20th century, a identifiable loss of consciousness was required in order for there to be the diagnostic possibility of a brain injury. While this issue began to change as considerable research on axonal injury evolved between 1971 and 1990, the significant definition change occurred in 1992, with the publishing by the American Congress of Rehabilitation Medicines definition of Mild Traumatic Brain Injury. See http://subtlebraininjury.com/noloc.html
“It is not necessary to have a loss of consciousness to suffer permanent brain injury.”
Source: Definition of Mild Traumatic Brain Injury Developed by the Mild Traumatic Brain Injury Committee of the Head Injury Interdisciplinary Special Interest Group of the American Congress of Rehabilitation Medicine. J Head Trauma Rehabil 1993:8(3):86-87
In that definition, loss of consciousness was only one of four acute symptoms, that could form the basis of a diagnosis of concussion or MTBI. Those four events are:
Loss of Consciousness (of less than 20 minutes);
A change in mental state;
Amnesia, for events both before OR after the event; or
Focal neurological deficits.
With this 1992 definition, the medical community began to look at brain injury differently, and in subsequent years, the American Academy of Neurology and the CDC, adopted similar definitions. Now, no recognized organization still maintains the Loss of Consciousness is a prerequisite for a diagnosis of brain injury, but there are still holdouts. One of the challenges of being a brain injury attorney, is finding ways to get defense neurologists to admit that what it says in the old textbooks about loss of consciousness, is no longer good medicine or good science.
This discussion here has used the classical term of mild traumatic brain injury. However, this has been used strictly in the context of the definitional scheme that is laid out throughout our three tiered classification of brain injury. I have been since creating the web page http://subtlebraininjury.com in 1999, using the word subtle brain injury© to describe MTBI.
The problem with these classifications schemes that define the severity of the brain injury in terms that relate to a period of loss of consciousness, is that they severely understate the risk factors associated with mild brain injury. Mild brain injury, which is also synonymous with concussion, can leave a person completely and totally disabled. Even though a brain injury may not involve a significant disruption of the part of the brain that triggers consciousness, it can involve severe damage to either specific parts of the cerebral cortex, or disruptive damage to the white matter of the brain.
Focal versus Diffuse Brain Damage. Brain injury is usually broken out into two geographic classes, focal and diffuse. A focal brain injury involves damage to a specific area of the brain, and in mild brain injuries, this can be a very small area. Diffuse damage means the damage is spread out throughout the brain, but the pathology in any one area is large enough for specific pathology in that one area to be identifiable.
Mild Focal Injury. Again the term mild here is something of a misnomer. The type of focal injury which would be classified as mild, would typically be a focal injury that does not involve a significant portion of one of the major lobes of the brain, but can still be identified as existing, because it has compromised a specific function of that particular part of the brain. Most of the significant mild focal injuries, involve injuries to the frontal lobes, particularly the underside of the frontal lobes. The reason these relatively small areas of damage can become disabling, is that the underside of the brain hold particularly important functions in terms of adult like behaviors and productivity.
Diffuse Injury. Diffuse injury to the white matter is referred to as diffuse axonal injury. An axon the long skinny wire like part of a neuron, that transmits the electrical impulse from the cell nucleus of the neuron, to the next part of the brain or nervous system, that must receive that signal, for the appropriate function to occur. Neuron’s are microscopic, and axons, even smaller. Typically an axon can only be seen by an electronic microscope. While there are massive numbers of these microscopic axons transmitting signals throughout the white matter of the brain, injury to even thousands of these axons in the same area, may not be concentrated enough pathology for it to show up on even a high resolution MRI. For more information on Diffuse Axonal Injury, click here.
Most of the controversy in brain injury cases involves battles about whether or not a mild brain injury even occurred and if so, whether it was severe enough to leave any last deficits. The reason such controversy exists is that most mild brain injuries do not involve clear cut loss of consciousness. For most of the 20th century, a identifiable loss of consciousness was required in order for there to be the diagnostic possibility of a brain injury. While this issue began to change as considerable research on axonal injury evolved between 1971 and 1990, the significant definition change occurred in 1992, with the publishing by the American Congress of Rehabilitation Medicines definition of Mild Traumatic Brain Injury. See http://subtlebraininjury.com/noloc.html
“It is not necessary to have a loss of consciousness to suffer permanent brain injury.”
Source: Definition of Mild Traumatic Brain Injury Developed by the Mild Traumatic Brain Injury Committee of the Head Injury Interdisciplinary Special Interest Group of the American Congress of Rehabilitation Medicine. J Head Trauma Rehabil 1993:8(3):86-87
In that definition, loss of consciousness was only one of four acute symptoms, that could form the basis of a diagnosis of concussion or MTBI. Those four events are:
Loss of Consciousness (of less than 20 minutes);
A change in mental state;
Amnesia, for events both before OR after the event; or
Focal neurological deficits.
With this 1992 definition, the medical community began to look at brain injury differently, and in subsequent years, the American Academy of Neurology and the CDC, adopted similar definitions. Now, no recognized organization still maintains the Loss of Consciousness is a prerequisite for a diagnosis of brain injury, but there are still holdouts. One of the challenges of being a brain injury attorney, is finding ways to get defense neurologists to admit that what it says in the old textbooks about loss of consciousness, is no longer good medicine or good science.
This discussion here has used the classical term of mild traumatic brain injury. However, this has been used strictly in the context of the definitional scheme that is laid out throughout our three tiered classification of brain injury. I have been since creating the web page http://subtlebraininjury.com in 1999, using the word subtle brain injury© to describe MTBI.
Brain Injury and Malingering – A Dangerous Deceit
I hope you read past the title, because that was meant as a double entendre. The “Dangerous Deceit” is not that of the brain damaged person, but the deceit of the neuropsychologist who claims to be able to tell if someone is committing a fraud. At its core, to claim someone is a malingerer is to claim that they are lying. In most states, an expert is not able to testify that someone is lying. That is felt to be the province of the jury. Far too many plaintiff lawyers accept such claim at face value and do not challenge this claim with a pre-trial motion.
The more clever defense doctor will not go so far as to outright claim that a plaintiff has malingered, but suggest it, and then to base such suggestion on what the doctor deems to be inconsistent effort throughout the battery of tests. I discussed in my previous blog the problem that fatigue creates in interpreting neuropsychological results, especially claims that someone did not give best effort. If you progressively tire, you invariably will do worse on tests given later in a battery than earlier.
But a progressive decline in test performance is not the only pattern that can be expected in a brain injured person. In my way of looking at it, a significantly brain injured person can be expected to be inconsistent, because virtually every symptom of brain injury can affect how a person feels, thinks and reacts at any given moment. And that symptom can ebb and flow, both within a given test, across a test battery or from one day of testing to another.
Another common problem with malingering tests is that they are based upon the theory that such test is so easy that even a severely brain injured person would pass it. Well that has some superficial merit, but when they are talking about severely brain injured individuals, they are talking about someone who in most cases, had a focal injury that resulted in an increase in intracranial pressure, resulting in a coma. Such people often have a different set of problems, more severe in the focal area of their injury, but with not as severe of problems in other areas. One cannot assume, despite the logic of it, that a person with a severe brain injury will have a worse outcome than someone with a significant concussion. I have written for years about the Miracles and Tragedies of Brain Injury.
The third problem with malingering claims, is that they only look at the few tests in the battery that are considered malingering or effort tests, and ignore the dozens of other tests in the battery that require considerably more effort than the “effort” test. If properly designed, an effort test should look just like all of the others. So if a person was truly malingering, wouldn’t they do poorly on all the tests, not just the “effort” tests. Yet in every single case I have every heard a defense neuropsychologist raise the malingering specter, there were subtests by my client, and usually many, many subtests, where my client did extremely well. If they were malingering, why did they do well on these tests?
Bottom line, all malingering tests are fatally flawed because there is no actual research on people who actually malingered. The research that is done is done on experimental subjects who are told to pretend to be malingered. In my favorite malingering study, the instruction to exaggerate your claims, but in a way not to get caught, was given to an equal number of brain injured persons and non-brain injured persons. In this study, it was only the brain injured persons got caught. In all other studies, the pretend malingerers were instructed to “act” like a malingerer. But a true malingerer would not want to get caught. The realities are that the only time a malingering test is ever likely to catch someone for true exaggeration, it is likely to catch a brain injured person, because they lack the judgment to do it in a way they won’t get caught.
The more clever defense doctor will not go so far as to outright claim that a plaintiff has malingered, but suggest it, and then to base such suggestion on what the doctor deems to be inconsistent effort throughout the battery of tests. I discussed in my previous blog the problem that fatigue creates in interpreting neuropsychological results, especially claims that someone did not give best effort. If you progressively tire, you invariably will do worse on tests given later in a battery than earlier.
But a progressive decline in test performance is not the only pattern that can be expected in a brain injured person. In my way of looking at it, a significantly brain injured person can be expected to be inconsistent, because virtually every symptom of brain injury can affect how a person feels, thinks and reacts at any given moment. And that symptom can ebb and flow, both within a given test, across a test battery or from one day of testing to another.
Another common problem with malingering tests is that they are based upon the theory that such test is so easy that even a severely brain injured person would pass it. Well that has some superficial merit, but when they are talking about severely brain injured individuals, they are talking about someone who in most cases, had a focal injury that resulted in an increase in intracranial pressure, resulting in a coma. Such people often have a different set of problems, more severe in the focal area of their injury, but with not as severe of problems in other areas. One cannot assume, despite the logic of it, that a person with a severe brain injury will have a worse outcome than someone with a significant concussion. I have written for years about the Miracles and Tragedies of Brain Injury.
The third problem with malingering claims, is that they only look at the few tests in the battery that are considered malingering or effort tests, and ignore the dozens of other tests in the battery that require considerably more effort than the “effort” test. If properly designed, an effort test should look just like all of the others. So if a person was truly malingering, wouldn’t they do poorly on all the tests, not just the “effort” tests. Yet in every single case I have every heard a defense neuropsychologist raise the malingering specter, there were subtests by my client, and usually many, many subtests, where my client did extremely well. If they were malingering, why did they do well on these tests?
Bottom line, all malingering tests are fatally flawed because there is no actual research on people who actually malingered. The research that is done is done on experimental subjects who are told to pretend to be malingered. In my favorite malingering study, the instruction to exaggerate your claims, but in a way not to get caught, was given to an equal number of brain injured persons and non-brain injured persons. In this study, it was only the brain injured persons got caught. In all other studies, the pretend malingerers were instructed to “act” like a malingerer. But a true malingerer would not want to get caught. The realities are that the only time a malingering test is ever likely to catch someone for true exaggeration, it is likely to catch a brain injured person, because they lack the judgment to do it in a way they won’t get caught.
Brain Damage Not Malingering
Yesterday’s blog about my frustrations with the refusal of the Wikipedia editor to add my two cents on the interaction between organic injury and emotional problems is symptomatic of a problem that is persuasive throughout neuropsychology: the insurance companies and their alter ego, the defense bar, are polluting the science of brain injury. The toxic words in this equation are malingering, conversion disorder and somatoform disorder. Huge sums of money are being funneled into what is being passed off as neuropsychological research from the insurance industry. The goal: to create peer reviewed literature that says that those with mild brain injury symptomotology are either faking their symptoms or are having an emotional reaction to what they experienced.
This topic is one worthy of several blogs. But essentially, more effort is being put into effort testing research, than almost all of the research that is going into the rest of the field brain injury. And the insurance industry has made it so profitable for neuropsychologists to work on the defense side of forensic cases, that neuropsychologists who went into the field with some sense of a calling, have convinced themselves that the doctrines of malingering, conversion disorder and malingering are real.
What does that have to do with a PTSD issue discussed in Wikipedia? It is a mild version of the same equation. The defense bar has what is correctly identified as a dog bite defense to brain injury cases. A dog bite defense is a multi-layered basis of denial, that each time something is proven, then retreat to the next defense.
You weren’t bitten by a dog; if you were, it wasn’t my dog; it you were bitten by my dog, it was your fault the dog bit you; if it was my dog’s fault you weren’t hurt.
Well in brain injury cases the dog bite defense is this:
There are no deficits, the plaintiff is normal; if there are deficits, then the plaintiff is malingering those deficits; if the plaintiff isn’t malingering, then the deficits are being caused by emotional problems, that the plaintiff had before the injury; if the plaintiff’s deficits didn’t exist before the injury, they are still just an exaggerated case of a somatoform or conversion disorder that a normal person wouldn’t have. If none of those other things don’t work, then call it PTSD (post traumatic stress disorder.)
If you work for the defense, NEVER, NEVER, NEVER, admit that the plaintiff had any permanent organic (meaning actual physical) damage or injury to the brain.
The ways in which these “research” studies are structured, they evaluate the plaintiff’s effort. They claim that their research validates that they can tell whether someone is malingering. That is just so much lying with statistics. No study can possibly tell that. It is impossible to tell what is in the mind of an individual. Neuropsychologists are not mind readers. In a court of law, they are most often not even allowed to comment on the credibility of a plaintiff. When you strip the cover off this claim, what they are really saying is that their super secret methodology (that no plaintiff could ever guess at) is telling them that a plaintiff didn’t give consistent “best effort” throughout the test.
I will blog on this particular topic more in the coming days, but such logic is incredibly flawed for a myriad of reasons. But one simple issue invalidates all effort testing claims: no person with brain damage could be expected to give consistent “best effort” over any battery of tests that last for hours and hours. Every single symptom of brain injury, makes it virtually impossible to maintain consistent effort for hours upon hours. I will later itemize how many of those symptoms effect consistent effort, but one common denominator has such a profound impact on effort that it alone makes effort testing a fraud: FATIGUE. Virtually everyone with brain damage, has fatigue. Fatigue makes you work slower, and progressively slower, the longer you are tested. Fatigue makes you make more mistakes. If you are working progressively slower and with progressively more mistakes, you will not be able to give consistent “best effort.”
Our next blog will examine these effort testing issues in more depth.
This topic is one worthy of several blogs. But essentially, more effort is being put into effort testing research, than almost all of the research that is going into the rest of the field brain injury. And the insurance industry has made it so profitable for neuropsychologists to work on the defense side of forensic cases, that neuropsychologists who went into the field with some sense of a calling, have convinced themselves that the doctrines of malingering, conversion disorder and malingering are real.
What does that have to do with a PTSD issue discussed in Wikipedia? It is a mild version of the same equation. The defense bar has what is correctly identified as a dog bite defense to brain injury cases. A dog bite defense is a multi-layered basis of denial, that each time something is proven, then retreat to the next defense.
You weren’t bitten by a dog; if you were, it wasn’t my dog; it you were bitten by my dog, it was your fault the dog bit you; if it was my dog’s fault you weren’t hurt.
Well in brain injury cases the dog bite defense is this:
There are no deficits, the plaintiff is normal; if there are deficits, then the plaintiff is malingering those deficits; if the plaintiff isn’t malingering, then the deficits are being caused by emotional problems, that the plaintiff had before the injury; if the plaintiff’s deficits didn’t exist before the injury, they are still just an exaggerated case of a somatoform or conversion disorder that a normal person wouldn’t have. If none of those other things don’t work, then call it PTSD (post traumatic stress disorder.)
If you work for the defense, NEVER, NEVER, NEVER, admit that the plaintiff had any permanent organic (meaning actual physical) damage or injury to the brain.
The ways in which these “research” studies are structured, they evaluate the plaintiff’s effort. They claim that their research validates that they can tell whether someone is malingering. That is just so much lying with statistics. No study can possibly tell that. It is impossible to tell what is in the mind of an individual. Neuropsychologists are not mind readers. In a court of law, they are most often not even allowed to comment on the credibility of a plaintiff. When you strip the cover off this claim, what they are really saying is that their super secret methodology (that no plaintiff could ever guess at) is telling them that a plaintiff didn’t give consistent “best effort” throughout the test.
I will blog on this particular topic more in the coming days, but such logic is incredibly flawed for a myriad of reasons. But one simple issue invalidates all effort testing claims: no person with brain damage could be expected to give consistent “best effort” over any battery of tests that last for hours and hours. Every single symptom of brain injury, makes it virtually impossible to maintain consistent effort for hours upon hours. I will later itemize how many of those symptoms effect consistent effort, but one common denominator has such a profound impact on effort that it alone makes effort testing a fraud: FATIGUE. Virtually everyone with brain damage, has fatigue. Fatigue makes you work slower, and progressively slower, the longer you are tested. Fatigue makes you make more mistakes. If you are working progressively slower and with progressively more mistakes, you will not be able to give consistent “best effort.”
Our next blog will examine these effort testing issues in more depth.
Wikipedia and Concussion
I am a lawyer, not a doctor. I carry no academic credentials as an author on brain damage. Yet, brain damage is all I do. All of my cases involve brain damage, and I interact with doctors on both side of the forensic bar, day after day. I can’t prove that it is true, but my guess is that more words of mine are read about brain damage and brain injury worldwide, than any other author. We get 50,000 visitors a month to our websites and our pages are linked on more than 6,000 other places on the internet. http://tbilaw.com is 4176 days old.
Yet, because I am a lawyer, my words only mean anything formally, when I am the one asking the questions, not doing the teaching. Despite this, years ago, I got involved in the definition of concussion on Wikipedia and was delighted that my non-scholarly words were allowed to guide people. If you have been reading this blog, you are well aware at the severe deficiencies in our medical approach to concussion, both from a treatment and a research standpoint. At least on the web, things could be better.
Well today I went back to Wikipedia, because a traffic report indicated that my page on concussion, http://subtlebraininjury.com was no longer linked there. What I found was a technically improved definition, with more than 40 references to scholarly treatment on Mild Traumatic Brain Injury. But alas, we now have a definition that is written by a committee, and a committee that has been too greatly influenced by insurance companies and doctors in their care, who are trying to fight the tide of growing understanding about brain damage following a concussion. Click here for Wikipedia’s definition of concussion.
I found these words there: “Diagnosis of concussion can be complicated because it shares symptoms with other conditions. For example, post-concussion symptoms such as cognitive problems may be misattributed to brain injury when they are in fact due to post-traumatic stress disorder (PTSD).[54] Injured people may suffer PTSD due to emotional trauma from the event, and cognitive effects of MTBI may impair a person’s ability to deal effectively with a traumatic event, potentially increasing the risk of PTSD.[54]“
This reads an awful lot like a defense neuropsychological report, and I can almost guarantee you was authored by someone who makes his living charging insurance companies $500 an hour to write 50 page reports, blaming every legitimate brain damage symptom on pre-injury psychological problems. So, I added my thoughts to the role of PTSD in brain injury diagnosis. It went up, and a minute later it came down. Someone named LeadSongDog, cut my additions, because he said it was unreferenced. Here is what was left:
I cut the following new para by User:Whipesq, as it was unreferenced:
However, PTSD is frequently over diagnosed in Post Concussion situations. Too many medical providers are using PTSD as a grab bag diagnosis to cover symptoms that appear to be more severe than the medical provider concludes they should be, based upon the verified evidence of concussion on the day of the event. Historically, PTSD is a syndrome that grew out of combat type stressors. Few, if any civilian injuries involve the same level of emotional shock (and hypervigilance) which accounts for the combat diagnosis. If, as discussed above, the concussion was under diagnosed on the day of the event, the symptoms may be consistent with a more severe injury than originally believed. The intersection of organic brain damage and emotional issue post concussion is a synergistic battleground within the mind, with both areas at risk for more severe symptoms, because of the interplay between the two. An area of study still in it’s infancy is whether brain plasticity, which has for generations been credited with positive gains in brain recovery, may be partially responsible for the poor recovery from PCS. The hypothesis here would be that during the early PCS period, the combination of cognitive difficulties, synergistically interacting with the stress and frustration of adapting to the trauma, rewires the brain in destructive ways.
The account had just been registered and I wouldn’t want to discourage a new editor. If someone can back it up with cites, some of it might be worth keeping. LeadSongDog (talk) 19:45, 7 March 2008 (UTC)
LeadSongDog is a physicist. I wonder where they taught about amnesia/PTSD/PCS in his education? I wonder if I could bring references from depositions of defense doctors?
I suppose it is fair. Wikipedia is supposed to be the people’s encyclopedia. I wonder how he got elected chair of one of the most important pieces of information on the internet?
Yet, because I am a lawyer, my words only mean anything formally, when I am the one asking the questions, not doing the teaching. Despite this, years ago, I got involved in the definition of concussion on Wikipedia and was delighted that my non-scholarly words were allowed to guide people. If you have been reading this blog, you are well aware at the severe deficiencies in our medical approach to concussion, both from a treatment and a research standpoint. At least on the web, things could be better.
Well today I went back to Wikipedia, because a traffic report indicated that my page on concussion, http://subtlebraininjury.com was no longer linked there. What I found was a technically improved definition, with more than 40 references to scholarly treatment on Mild Traumatic Brain Injury. But alas, we now have a definition that is written by a committee, and a committee that has been too greatly influenced by insurance companies and doctors in their care, who are trying to fight the tide of growing understanding about brain damage following a concussion. Click here for Wikipedia’s definition of concussion.
I found these words there: “Diagnosis of concussion can be complicated because it shares symptoms with other conditions. For example, post-concussion symptoms such as cognitive problems may be misattributed to brain injury when they are in fact due to post-traumatic stress disorder (PTSD).[54] Injured people may suffer PTSD due to emotional trauma from the event, and cognitive effects of MTBI may impair a person’s ability to deal effectively with a traumatic event, potentially increasing the risk of PTSD.[54]“
This reads an awful lot like a defense neuropsychological report, and I can almost guarantee you was authored by someone who makes his living charging insurance companies $500 an hour to write 50 page reports, blaming every legitimate brain damage symptom on pre-injury psychological problems. So, I added my thoughts to the role of PTSD in brain injury diagnosis. It went up, and a minute later it came down. Someone named LeadSongDog, cut my additions, because he said it was unreferenced. Here is what was left:
I cut the following new para by User:Whipesq, as it was unreferenced:
However, PTSD is frequently over diagnosed in Post Concussion situations. Too many medical providers are using PTSD as a grab bag diagnosis to cover symptoms that appear to be more severe than the medical provider concludes they should be, based upon the verified evidence of concussion on the day of the event. Historically, PTSD is a syndrome that grew out of combat type stressors. Few, if any civilian injuries involve the same level of emotional shock (and hypervigilance) which accounts for the combat diagnosis. If, as discussed above, the concussion was under diagnosed on the day of the event, the symptoms may be consistent with a more severe injury than originally believed. The intersection of organic brain damage and emotional issue post concussion is a synergistic battleground within the mind, with both areas at risk for more severe symptoms, because of the interplay between the two. An area of study still in it’s infancy is whether brain plasticity, which has for generations been credited with positive gains in brain recovery, may be partially responsible for the poor recovery from PCS. The hypothesis here would be that during the early PCS period, the combination of cognitive difficulties, synergistically interacting with the stress and frustration of adapting to the trauma, rewires the brain in destructive ways.
The account had just been registered and I wouldn’t want to discourage a new editor. If someone can back it up with cites, some of it might be worth keeping. LeadSongDog (talk) 19:45, 7 March 2008 (UTC)
LeadSongDog is a physicist. I wonder where they taught about amnesia/PTSD/PCS in his education? I wonder if I could bring references from depositions of defense doctors?
I suppose it is fair. Wikipedia is supposed to be the people’s encyclopedia. I wonder how he got elected chair of one of the most important pieces of information on the internet?
Brain Injury Awareness Month Wisconsin Lectures
Mr. Johnson,
I will greatly appreciate your assistance in promoting advertisement of the Brain Awareness Weeks activities, that will take place next week at the Milwaukee Veterans Administration.
We are organizing a few lectures on Traumatic Brain Injury (TBI). These lectures are scheduled in the context of outreach activities of the Milwaukee Chapter of the Society for Neuroscience, to patients and families, as well as the general public and health care providers. Next week is the Brain Awareness Week (http://www.sfn.org/baw/), which provides a great opportunity for educational and outreach activities.
We need to increase the awareness of people on brain diseases and injuries, and inform clinicians, and patients and families about what modern research on brain/nervous system and clinical neuroscience can do for them, and to increase their awareness on resources and support systems.
We have a lot of veterans who have survived Traumatic Brain Injuries, and their suffering has great impact in their own life, and their families’ lifes (not to mention the burden to our health care system, in general).
So, we think that patients, families and health care providers will benefit a lot from hearing a few experts present their experiences, insights, and some pertinent information and helpful material. The Brain Injury Association of Wisconsin is willing to contribute also.
So, we need to advertise the lecture to include an audience as large as possible: This will be of interest to several practitioners involved in the care of veterans with TBI, as well.
These lectures are to be held at the Matousek auditorium.
Monday, March 10, 12-1 pm: “What physical therapy has to offer to patients with Traumatic Brain Injury”. By Jennifer Batie, PT, CJ Zablocki VAMC Dept of Physical Therapy
Tuesday, March 1, 11-12: “Current advances in pain management”. By H.
Shankar, MD, Pain Medicine Specialist, Assistant professor, CJ Zablocki VA Pain Clinic
Thursday, March 13, 12:30-1:30: “Battle mind: Traumatic Brain Injury and post-combat stress”. By Kenneth Lee, MD, National Surgeon, Spinal Cord Injury Unit, CJ Zablocki VAMC
Friday, March 14, 12-1 pm: “Resources and support for people with Traumatic Brain Injury and families”. Will be presented by speakers from the Milwaukee Chapter of the Society for Neuroscience (C. Sarantopoulos, MD, PhD), from the Brain Injury Association of Wisconsin (Pat David, BIA Director – confirmation pending) and the CJ Zablocki VAMC.
Your help will be highly appreciated,
Thanks,
Constantine Sarantopoulos, MD, PhD
President, Milwaukee Chapter of the Society for Neuroscience Director, CJ Zablocki VAMC Pain Clinic Associate Professor of Anesthesiology, and Pharmacology & Toxicology Department of Anesthesiology Medical College of Wisconsin
Dear Dr. Sarantopoulos, MD, PhD:
Thank you for this notification. I will make my best efforts to attend Thursday’s lecture Dr. Lee on TBI and combat stress, as the overlap between organic brain injury and emotional issues is one of my greatest areas of interest.
I will greatly appreciate your assistance in promoting advertisement of the Brain Awareness Weeks activities, that will take place next week at the Milwaukee Veterans Administration.
We are organizing a few lectures on Traumatic Brain Injury (TBI). These lectures are scheduled in the context of outreach activities of the Milwaukee Chapter of the Society for Neuroscience, to patients and families, as well as the general public and health care providers. Next week is the Brain Awareness Week (http://www.sfn.org/baw/), which provides a great opportunity for educational and outreach activities.
We need to increase the awareness of people on brain diseases and injuries, and inform clinicians, and patients and families about what modern research on brain/nervous system and clinical neuroscience can do for them, and to increase their awareness on resources and support systems.
We have a lot of veterans who have survived Traumatic Brain Injuries, and their suffering has great impact in their own life, and their families’ lifes (not to mention the burden to our health care system, in general).
So, we think that patients, families and health care providers will benefit a lot from hearing a few experts present their experiences, insights, and some pertinent information and helpful material. The Brain Injury Association of Wisconsin is willing to contribute also.
So, we need to advertise the lecture to include an audience as large as possible: This will be of interest to several practitioners involved in the care of veterans with TBI, as well.
These lectures are to be held at the Matousek auditorium.
Monday, March 10, 12-1 pm: “What physical therapy has to offer to patients with Traumatic Brain Injury”. By Jennifer Batie, PT, CJ Zablocki VAMC Dept of Physical Therapy
Tuesday, March 1, 11-12: “Current advances in pain management”. By H.
Shankar, MD, Pain Medicine Specialist, Assistant professor, CJ Zablocki VA Pain Clinic
Thursday, March 13, 12:30-1:30: “Battle mind: Traumatic Brain Injury and post-combat stress”. By Kenneth Lee, MD, National Surgeon, Spinal Cord Injury Unit, CJ Zablocki VAMC
Friday, March 14, 12-1 pm: “Resources and support for people with Traumatic Brain Injury and families”. Will be presented by speakers from the Milwaukee Chapter of the Society for Neuroscience (C. Sarantopoulos, MD, PhD), from the Brain Injury Association of Wisconsin (Pat David, BIA Director – confirmation pending) and the CJ Zablocki VAMC.
Your help will be highly appreciated,
Thanks,
Constantine Sarantopoulos, MD, PhD
President, Milwaukee Chapter of the Society for Neuroscience Director, CJ Zablocki VAMC Pain Clinic Associate Professor of Anesthesiology, and Pharmacology & Toxicology Department of Anesthesiology Medical College of Wisconsin
Dear Dr. Sarantopoulos, MD, PhD:
Thank you for this notification. I will make my best efforts to attend Thursday’s lecture Dr. Lee on TBI and combat stress, as the overlap between organic brain injury and emotional issues is one of my greatest areas of interest.
Guidelines for Coma Management
One of the most difficult challenges in being a brain injury attorney and an advocate, is struggling with what to tell people when they call up and their loved one is in a coma. The Brain Injury Law Group is here to a significant degree, because that was one of the challenges we faced when we first started doing web advocacy. We created http://waiting.com in 1997, with a sense of urgency to help those who were waiting for word as to whether their loved one would ever awake. The story of our frustration with the Brain Injury Association’s refusal to accept our offer of help to create such a page, and our decision to do it ourselves, is well explained on that page.
The Brain Trauma foundation is an organization which shares a similar advocacy to help those in a coma, and I received this email from them today, covering the guidelines to assist medical professionals dealing with coma patients. To get to those links, click here: http://www.guideline.gov/whatsnew/newthisweek.aspx#date
What these new guidelines don’t call for, which I believe they should, is the use of funtional imaging, such as PET scans or fMRI to tell the degree to which there is sufficient brain function going on in the comatose person, to predict any reasonable chance of recovery. Coma guidance from doctors is far too much “we will just have to wait and see” and most times, from a very pessimistic outlook. I believe that PET scans and fMRI should be routinely used to give guidance to the family, when they are trying to make that awful decision as to whether there is enough chance of a satisfactory recovery, to keep trying to save the life of the comatose person. We always counsel prayer and inner searching. But when there are tools out there that could be used to provide more meaningful information on what is going on inside of that skull, we believe they should be used. I have instructed the person who is my health care power of attorney to demand that I have a functional imaging test if I am ever in that situation, and there is no valid reason why doctors don’t do the same.
They Brain Trauma Association has guidelines on the following:
Anesthetics, analgesics, and sedatives.
Antiseizure prophylaxis.
Blood pressure and oxygenation.
Brain oxygen monitoring and thresholds.
Cerebral perfusion thresholds.
Deep vein thrombosis prophylaxis.
Hyperosmolar therapy.
Hyperventilation.
Indications for intracranial pressure monitoring.
Infection prophylaxis
Intracranial pressure thresholds.
Nutrition.
Prophylactic hypothermia.
Steroids.
The Brain Trauma foundation is an organization which shares a similar advocacy to help those in a coma, and I received this email from them today, covering the guidelines to assist medical professionals dealing with coma patients. To get to those links, click here: http://www.guideline.gov/whatsnew/newthisweek.aspx#date
What these new guidelines don’t call for, which I believe they should, is the use of funtional imaging, such as PET scans or fMRI to tell the degree to which there is sufficient brain function going on in the comatose person, to predict any reasonable chance of recovery. Coma guidance from doctors is far too much “we will just have to wait and see” and most times, from a very pessimistic outlook. I believe that PET scans and fMRI should be routinely used to give guidance to the family, when they are trying to make that awful decision as to whether there is enough chance of a satisfactory recovery, to keep trying to save the life of the comatose person. We always counsel prayer and inner searching. But when there are tools out there that could be used to provide more meaningful information on what is going on inside of that skull, we believe they should be used. I have instructed the person who is my health care power of attorney to demand that I have a functional imaging test if I am ever in that situation, and there is no valid reason why doctors don’t do the same.
They Brain Trauma Association has guidelines on the following:
Anesthetics, analgesics, and sedatives.
Antiseizure prophylaxis.
Blood pressure and oxygenation.
Brain oxygen monitoring and thresholds.
Cerebral perfusion thresholds.
Deep vein thrombosis prophylaxis.
Hyperosmolar therapy.
Hyperventilation.
Indications for intracranial pressure monitoring.
Infection prophylaxis
Intracranial pressure thresholds.
Nutrition.
Prophylactic hypothermia.
Steroids.