Discussion Topic |
|
This thread has been locked |
jogill
climber
Colorado
|
|
Philosophical discussions like this one should be done without any reference to mathematics. Just because a physical result can be predicted as a function of forward time, and the math involved has the independent variable, t>0, is not an argument that t<0 connects to reality. Can we travel backwards in time? The applications of math have their limitations.
However, I'm no physicist, and probably don't understand the time-reversal arguments in that science.
|
|
jogill
climber
Colorado
|
|
Way beyond my level, but thanks for the link.
In the normal (macro) world an equation like S(t)=√t, giving distance traveled as a function of time, yields a distance along an imaginary axis for t=-1 and an imaginary velocity. But I suppose that could make sense.
|
|
zBrown
Ice climber
|
|
"Someday someone might come along who looks at the mind body challenge in different terms"
The theory holds that the universe in retrospective can shrink to the size of an extremely small “subatomic ball” known as the singularity. Hawking said that the laws of physics and time cease to function inside that tiny particle of heat and energy. The ordinary real time as we know now shrinks infinitely as the universe becomes ever smaller but never reaches a definable starting point. Hawking argued that before the Big Bang, real ordinary time was replaced by imaginary time and was in a bent form. “It was always reaching closer to nothing but didn’t become nothing,” he said. Taking the example of Earth, he said: “One can regard imaginary and real-time beginning at the South Pole ... There is nothing south of the South Pole, so there was nothing around before the Big Bang. There was never a Big Bang that produced something from nothing. It just seemed that way from mankind’s perspective,” Hawking said, hinting that a lot of what we believe is derived from a human—centric perspective, which might limit the scope of human knowledge of the world
So at one time, perhaps, the mind/body problem did not exist and it might safely be removed from ones tick list. Singular notion.
Anyway I've always believed that the alternative minimum tax disappeared as you approach age seventy unless of course you
|
|
WBraun
climber
|
|
Even Hawking is saying that all the gross materialists ever have is dry incomplete speculative knowledge they masquerade as their modern science to mislead themselves and the world .....
|
|
Largo
Sport climber
The Big Wide Open Face
|
|
|
Topic Author's Reply - Mar 6, 2018 - 05:16pm PT
|
Been on the road a bunch this past month but found it amusing once more to check in with this thread and try and summarize what is being said and, most importantly, try and dig into the quagmires and determine what makes the most sense. As usual here, the hard part is making clear the first assumptions and implications of comments that are glibly fobbed off but which on closer inspection are highly debatable. This is especially crucial when the title of “fact” is implied or suggested as being axiomatic to the given position.
One great new twist, in my opinion, recently introjected here by Jstan, was … “ask questions in new ways (is key).”
I would add, “look at first assumptions in new ways.”
To illustrate a first assumption, or guiding principal common to most all investigations of mind, consider the following back and forth I had with John G.
In reference to John’s reports on lucid dreaming, I asked: “If you are wondering if the dreams themselves were "real," what is the metric or criteria for "real?"
John replied: “No wondering on my part. The ‘dreams’ were fabrications of the brain without external stimuli.”
The most obvious problem here is that John didn’t answer the question. But the WAY he did answer betrays his unconscious fealty to his first assumption -- that an ontological question can and should only be answered with a declarative statement pertaining to physical, linear causatio. In this case, his dream is sourced by the brain.
So for John, re Jstan’s directive to ask question in new ways (“is key”), the challenge would be to look at the question again and try and reply without reverting to a linear causal belief that he furthermore believes IS answering the question about what a dream, itself, actually is. This would require him to investigate what his experience WAS, dream included, and how his perception figured into it as well.
Clearly it is easier to toss the question to neuroscience than to investigate the actual nature of his own life. “Actual nature” in this case would, to John, refer to and only to linear causality, which he apparently believes truly answers all questions.
This obvious dodge is exactly what Nagle was driving at when he wrote that inquiries about mind itself are not linear causal questions, but questions about what subjective first person experience is, in and of itself.
The questions is: why is it so prevalent to revert to linear causation to try and answer the “why?” or “what is this?” questions about mind. I believe it boils down to two basic factors.
First, our rational minds are linear machines. Most everything we do depends on tracking the chain of linear causation. I turn the wheel left and it follows that the car goes left. I work to get the money to feed myself. That not only is how we think but also how we interpret and explain reality. Linear causation, coupled with physicalism, is also how we normally “explain” physical reality, “reality” itself being physical … as the narrative goes. In fact, physico-chemical reductionism is hardwired into our brains as an orthodox view, and any resistance to it is regarded as not only scientifically but politically incorrect.
The evidence is strong to support such a view per the physical world. Physical, linear causation and evaluations are the go-to explanatory tools we use to “know,” explain, and make our predictions about external objects and phenomenon. And this method has worked wonderfully – with external objects and phenomenon. But why should it be the knee-jerk mode of inquiry for mind? Again, several reasons, and misconceptions, are involved.
Those beholden to physical causation often refer to phenomenon that in centuries past was attributed to God or spirits or magic, and have since mostly been thoroughly explained in physical, causal terms. This is used as an argument to investigate mind by the same methods, despite the fact that John’s dreams are not observable to any 3rd person perspective as external objects or phenomenon we can objectify via standard means, to say nothing of the fact that science has never been asked to quantify anything remotely like consciousness itself.
In all cases of scientific inquiry, whatever external object or phenomenon was duly quantified, there was never an extra dimension of subjectivity involved. The physical descriptors tell the entire story per what an object or phenomenon IS. There is “nothing it is like” to BEING a quark or tree or White Star. Neither of the three knows it is a quark etc., has a conscious experience and first person perspective of being a tree, etc., or is consciously aware of itself or anything else.
In short, evaluating any known thing or phenomenon in linear causal terms would perforce leave out precisely what we are seeking to understand – mind. That which we experience but cannot observe as an external object or force.
The default for the physicalist is to unconsciously conflate what they believe is the linear causal source of mind, believing that – as it goes with all other physical phenomenon – physical/causal reductionism is the case, the whole case and nothing but the case. Case closed.
Another example of what slaves we are to this mode, consider that oft repeated retort that if we don’t seek and only seek physical causal explanations, we can only appeal to magic and woo. For those appealing to magic, or using it as example of puerile thinking – both are still just as much slave to the linear causal mode, they’ve simply swapped out an observable source/cause with an unobservable one, like "God." They are still thinking in the old ways, even when trying to write off all other views as absurd. They are stuck in a perspective, one that has worked wonderfully on all other "things."
Again, this shows what power the linear causal mode has over our minds, unconsciously running all explanations through this skrim as though no other options exist – valid options being linear causal alone.
This belief can be summarized like this: IF brain (A), THEREFORE mind (B). Hey, if it’s good enough to “explain” a rock or wavelet, then it’s good enough for mind. “You just think there is more involved…” This is neither deep or nuanced reasoning, and it’s certainly not answering Jstan’s call to ask new questions.
Another factor is the strange, and sometimes silly misinterpretations, misrepresentations and insinuations of ANY mode of inquiry that is not about linear causality.
Consider this whopper from Ed:
“Introspection leads you down the rabbit hole (in my opinion) and you come up with silly analogies like kissing your own lips and such. The sort of things that amused us when we were in high school puzzling out the same questions.”
“Rabbit hole” to Ed is almost certainly terrain (like his own experience) where he cannot easily garner linear causal data. At least not in the way he is accustomed to working. Suggestions that he work differently, at least to exercise Jstan’s directive, are ridiculed by assailing analogies he does not understand, but gives the impression that he does, and that they are schoolboy amusements, but not rigorous investigations nohow.
For example, the “kissing your own lips” is a phrase to underscore a plain truth that is strictly not debatable: Nobody can escape their conscious, first person perspective and observe it from a third person vantage. That is, no one can jump outside their own skin, look back and observe the content of THEIR OWN consciousness (thoughts, feelings, sensations, memories, etc.) as external objects or phenomenon.
This simple truth might serve as a starting point for many fruitful inquiries, but according to Ed’s experience and beliefs, such inquires “amused us when we were in high school,” but once he discovered the gold of linear causation, or at any rate, physical causation however you might describe it, introspection by any description is, apparently to Ed, merely doing science with no instruments, since linear causal inquiries are the only means of knowing anything.
Asking questions beyond causality has no argumentative force against certain causal-state identity theorists and some functionalists like Ed, not because of any expertise in doing anything else but seeking physical causes, but because of the overriding force of his unconscious first assumption. In psychological terms, he does not control it, it controls him, and he has the facts to back it up. But nothing remotely novel or insightful about what mind, consciousness, awareness, content, etc. are in any way that is either logically coherent or deepens our understanding of anything but - you guessed it, a search for physical, linear causal "answers."
This is, as Aristotle said, “sticking to a cause at all costs.”
We can only wonder what some of the studied and intelligent minds on this thread would come up with they took Jstan’s challenge, set aside linear causality for a spell, and for example, people like John investigated what his dreams, themselves, actually are – NOT the brain he believes fabricated them, which in fact is another question.
To consider: Mind, resisting the impulse to cram it into a physical causal paradigm. Take Jstan at his word and start asking other questions.
|
|
MH2
Boulder climber
Andy Cairns
|
|
That is, no one can jump outside their own skin, look back and observe the content of THEIR OWN consciousness (thoughts, feelings, sensations, memories, etc.) as external objects or phenomenon.
That depends on what you mean by 'content.'
Did you have to jump outside your own skin to look at EEGs?
How can you be sure that in the future people will not be able to look at the content of their own thoughts, feelings, sensations, memories, etc. as external objects or phenomena?
Examine your own assumptions.
|
|
Largo
Sport climber
The Big Wide Open Face
|
|
|
Topic Author's Reply - Mar 6, 2018 - 05:40pm PT
|
That depends on what you mean by 'content.'
Did you have to jump outside your own skin to look at EEGs?
How can you be sure that in the future people will not be able to look at the content of their own thoughts, feelings, sensations, memories, etc. as external objects or phenomena?
Examine your own assumptions.
As you know, MH2, I spent years looking at EEGs ans qEEGS and other brain mapping instruments and outputs. No one I know doing this work, including the leading dudes at the Brain Institute at UCLA, believe that when they are observing, say, the spiking signal in the High Beta bandwidth, that they are looking at the subjective reality of thinking itself, rather the electric artifact that we associate with thinking. And no one I know says these two phenomenon are selfsame.
When you suggest that in some future date, by way of some future technology, we WILL be able to escape our subjective bubble and observe, from a distance, our own subjective content, this assumes first, that awareness is divisible through some future technology, and can be exported to some point in space where, entirely disembodied, it can observe and objectify.
Of course the empirical evidence is hugely against you. For example, nobody, no other conscious agent, can read your thoughts, feel you feelings, know your sensations themselves. The subjective bubble itself is not observable as subjective phenomenon from any external perspective. So if you somehow escaped your subjective bubble, and were outside of it, you would perforce have no more access to it than I have access to your thoughts from down here in Venice, Ca.
If this were possible, and you could actually escape your subjective bubble and look back, what exactly would you be looking for beyond linear causal phenomenon? How might you make good on Jstan's invitation to ask new questions? What might you ask or look for?
My first assumption is that your thought experiment is logically incoherent and another species of science fiction, with the accent on fiction.
|
|
Ward Trotter
Trad climber
|
|
First, our rational minds are linear machines. Most everything we do depends on tracking the chain of linear causation. I turn the wheel left and it follows that the car goes left. I work to get the money to feed myself. That not only is how we think but also how we interpret and explain reality. Linear causation, coupled with physicalism, is also how we normally “explain” physical reality, “reality” itself being physical … as the narrative goes. In fact, physico-chemical reductionism is hardwired into our brains as an orthodox view, and any resistance to it is regarded as not only scientifically but politically incorrect.
Au contraire mon frere
https://en.m.wikipedia.org/wiki/Nonlinear_system
The first archaic life forms could be said to have had a linear relationship to solar energy.
As life developed into multicellular organisms that relationship became nonlinear.
I think.
|
|
Largo
Sport climber
The Big Wide Open Face
|
|
|
Topic Author's Reply - Mar 6, 2018 - 06:12pm PT
|
The point, Ward, is that linear causation dominates our thinking, especially when trying to "explain" what mind is. For most, it is, IF BRAIN (A), then MIND (B). A came before B, and caused B.
Are there non-linear processes within this and other things and phenomenon? Certainly, but we are still looking at causation, linear or otherwise, as an "explanation" for mind.
What else have you got? If you were to take up Jstan's challenge, what might you look for beyond physical causes, and how might you do so? What questions might you ask?
|
|
zBrown
Ice climber
|
|
Approach to the Patient with Suspected Brain Death
2. Pediatric guidelines for brain death were first published in 1987 and again revised in 2011 by the American Academy of Pediatrics (AAP) and the Child Neurology Society (CNS). The guidelines define the minimum standards that must be met in all clinical situations for brain death to be considered. There are three distinct differences in comparison to the adult guidelines that include apnea test requirements, number of examinations, and an observation period. The guidelines are as follows:
a. Exclusion of confounders
b. Established etiology of coma
c. Ascertain the futility of interventions
d. All clinical prerequisites are met
e. Test for the absence of motor responses
f. Test for absence of brainstem reflexes at all levels
g. Test for conclusive lack of respiratory drive
h. Confirmatory apnea test with PaCO2 ≥60 mm Hg and PaCO2 increase >20 mm Hg from normal baseline value
i. Two separate neurologic and apnea examinations performed by different qualified examiners
j. Interexaminer observation periods of:
(1) 24 hours for term newborns up to 30 days of age
(2) 12 hours for infants and children up to 18 years of age
B. Prerequisites. For each patient, the clinical assessment of brain death should be performed in an orderly and repetitive fashion. A step-by-step approach should be developed by the examiner that creates an unbiased and objectively confident diagnosis. With this approach, prior to examination, the clinician should define a set of prerequisites that rule out all medical and neurologic cofounders that mimic brain death.
1. Coma should be evaluated and assessed early on in the clinical course. Both etiology and irreversibility are key factors in determining the need for a brain death examination. A thorough review of the history, a complete neurologic examination, and adequate assessment of ancillary data are necessary. In approach to the patient, some period of time should be allowed to pass following acute presentation to exclude the possibility of recovery. Some conditions that may mimic brain death and reverse with appropriate management include hypothermia, drug intoxication, basilar artery occlusion, nonconvulsive status epilepticus, Guillain–Barré syndrome, and botulism. The etiology of acute presentations can be established with a variety of objective assessments including examination, neuroradiologic testing, and neurophysiologic testing. The concept of irreversibility is established not only with examination, but by the assurance that all necessary interventions for a given etiology have been performed. Such interventions can include ventriculostomy placement, hematoma evacuation, craniectomy, osmotic diuresis, and intoxication reversal. If these considerations have been met, then consideration of brain death may be necessary.
2. Neuroimaging should be performed and strictly evaluated with every patient suspected of brain death. Typical patterns with cause for concern include mass lesions with hemispheric shift, subdural hematoma with multiple parenchymatous contusions, diffuse subarachnoid hemorrhage, generalized loss of gray–white junction, and diffuse brain edema alone with effacement of the basal cisterns. In specific situations, such as early cardiac arrest, initial computed tomography scans may be normal. In such cases, repeat imaging should be performed to confirm or exclude the presence of advancing pathology. In cases of repeated normal neuroimaging, other confounders including intoxication and metabolic disturbance should be considered.
3. Pharmacologic interventions are a commonly overlooked confounder in the assessment of brain death. A detailed historical and objective examination into the history and administration of sedative, analgesic, and paralytic agents should be performed. It is recommended that all patients undergo a urine and plasma drug screen in addition to an adequate medication reconciliation. Examiners should consider the half-life clearance of all medications administered, and in situations of impaired renal and hepatic function, adjust appropriately. In patients who have undergone therapeutic hypothermia, metabolic clearance rates are slower and should be accounted for during examination. In patients who have received paralytic agents, confirmation of clearance with either facial nerve stimulation or the presence of muscle stretch reflexes is imperative.
4. Metabolic parameters should be adequately assessed in all patients prior to procession of the neurologic examination. Reversible metabolic conditions such as uremia, renal failure, hepatic failure, and hyponatremia should be worked up and treated. The presence of a severe acid–base disturbance may suggest an alternate underlying pathology. Metabolic acidosis is typically seen following drug intoxication. Respiratory acidosis may be seen following sedative and analgesic administration. Consideration of such factors and appropriate reversal should be considered. Finally, absence of all endocrine abnormalities, such as Hashimoto’s encephalopathy, should be confirmed to rule out such confounders that may mimic comatose or brain death states.
5. Physiologic parameters such as blood pressure and core temperature should also be considered in the assessment of brain death. In general, the diagnosis of brain death should never be made in an individual whose core temperature is 80 mm Hg. This can be achieved with either volume resuscitation or vasoactive medications. If overt arterial hypotension and shock are present, the brain death examination should not continue until all morbidities have been treated.
6. Respiratory analysis should be performed to ensure that no spontaneous respirations occur. The absence of physiologic respiratory patterns confirms suspected pontomedullary dysfunction and is necessary when testing apnea. In specific situations, including tidal volume mismatch, triggering of the ventilator may not be indicative of a breathing patient. If some form of ventilatory triggering is present, the examiner should consider further analysis using decreased sensitivity or a pressure support setting to confirm all absence.
C. Neurologic examination. Following confirmation that all prerequisites have been met and all confounders have been excluded, procession with the neurologic examination is warranted. The assessment of brain death should include a detailed evaluation of the following: pupillary response, corneal reflexes, oculocephalic reflexes, oculovestibular reflexes, facial movement, gag reflex, cough reflex, and motor responses.
1. Pupillary responses are the first examination technique in the assessment of brain death, measuring the integrity of the afferent limb of cranial nerve II and the efferent limb of cranial nerve III. The examiner should use a bright light in both eyes to determine the presence or absence of a pupillary response. The typical pupillary patterns associated with brain death are the midposition (4 mm) fixed pupils and dilated (6 mm) fixed pupils. Pupillary dilation, in some cases, is still present in brain death because of intact ascending cervical sympathetic input. With initial assessment prior pupillary trauma or surgery should be distinguished from history. Many drugs are known to influence pupillary size. However, such agents do not inhibit the total contraction or dilation of the ciliary muscle and with careful examination can be excluded.
2. Corneal reflexes assess the integrity of the afferent limb of cranial nerve V and the efferent limb of cranial nerve VII, to elicit a blink response. Such response requires a distinct interplay between cranial nerves and an intact brainstem is vital. The examiner should induce corneal stimulation by squirting water on the cornea or by stimulating with a cotton swab. Stimulation of this pathway should produce a bilateral blink response. Facial trauma and edema may preclude adequate examination. The complete absence of blink response is compatible with brain death.
3. Oculocephalic reflexes assess the functionality of cranial nerves III, IV, and VI. This technique, also referred to as the doll’s eyes technique, requires the examiner to initiate quick turning of the head from midposition to 90 degrees in either direction. Turning of the head should stimulate horizontal ocular movements. The examiner should also observe the eyes initially at rest with the lids open, assessing presence or absence of spontaneous ocular movements. The presence of forced deviation (vertical, horizontal, or skew) and nystagmus at rest would otherwise imply intact brainstem or cortical function. The absence of all ocular movements at rest and with motion is compatible with brain death.
4. Oculovestibular reflexes are used to assess the integrity of cranial nerves III, IV, VI, and VIII. In contrast to the oculocephalic reflex, the oculovestibular reflex requires the use of cold caloric testing with ice water. The examiner should elevate the patient’s head 30 degrees from supine position to ensure verticality of the horizontal canal. Next, a small suction catheter should be attached to the end of a 50-cc syringe filled with ice water and instilled into the patient’s auditory canal. Following injection, 1 minute should be allowed for observation of response, and 5 minutes should be given between examinations of either canal. Instillation of cold water into the tympanum induces an inhibition of the ipsilateral vestibular complex. In a comatose patient, a forced deviation of the eyes would ensue toward the cold stimulus. Certain pharmacologic agents including anticholinergics, tricyclic antidepressants, ototoxic antibiotics (aminoglycosides), and antiepileptics (phenytoin) may diminish such response, but are rarely relevant confounders. In brain death the oculovestibular response is completely absent.
5. Facial movements are a less common examination technique used in the assessment of brain death, but should be considered in all patients. Noxious stimulation should be performed with either deep nail bed pressure or bilateral condylar temperomandibular pressure. Stimulus in a comatose patient should cause activation of cranial nerve VII and elicit a grimace response. Supraorbital pressure may also be applied, stimulating both cranial nerve V and VII. The complete absence of facial grimacing following noxious stimulation is compatible with brain death.
6. Gag and cough reflexes are used to assess the functionality of cranial nerves IX and X. Determination of the gag and cough reflexes in an intubated patient can at times be difficult. The examiner should attempt stimulation by using bronchial suctioning. The catheter should be advanced completely through the endotracheal tube, followed by suctioning pressure for several seconds. In a comatose patient, a cough or gag reflex is typically initiated. Simultaneously, the clinician should also observe for physiologic responses to suctioning including tachycardia and change in respiratory rate. The complete absence of physiologic response and cough reflexes during bronchial suctioning is consistent with brain death.
7. Motor responses are used to assess functionality of the cortical and brainstem pathways required for movement. The examiner should apply a noxious stimulus, such as deep nail bed pressure, sternal rubbing, or condylar temperomandibular pressure, to the patient. In brain death, noxious stimulation should produce no motor response at all. The presence of spinally mediated reflexes to noxious stimulus can be seen, but is not indicative of an intact brainstem. The spinal reflexes can include brief movements of the upper limbs, finger flexion, finger tremors, and arm elevation. Differentiation between normal motor responses and spinal reflexes can be difficult and requires much expertise. Typically repetitive stimulation will cause spinal reflexes to diminish and help the examiner define a response. Fasciculations may also be noted on examination, and are likely due to pathologic anterior horn cells. Plantar reflexes are typically absent in brain death, but may be seen with instances of triple flexion. The absence of all motor movements is consistent with brain death image(Video 34.1).
D. Apnea testing uses the mechanics of oxygen diffusion to assess ventilatory drive and is the most commonly used technique in the assessment of brain death. The apnea test itself, like that of the overall brain death assessment, requires a definable set of prerequisites be met to ensure that performance and interpretation of the test is adequate (Table 34.2). Prior to initiation, the patient must be hemodynamically stable with a SBP >100 mm Hg. The ventilator should then be adjusted to achieve normocapnea (PaCO2 35 to 45 mm Hg) and a consistent positive end-expiratory pressure (PEEP) of 5 cm H2O should be initiated. The patient is then preoxygenated with 100% FiO2 to a goal of PaO2 >200 mm Hg to ensure adequate oxygenation. Once all prerequisites have been met, the ventilator is disconnected and an oxygen insufflation catheter is inserted. After 8 minutes, an arterial blood gas is drawn and the patient is reconnected to the ventilator. The defined criteria for determining brain death with the apnea test includes the absence of all spontaneous respirations, a PaCO2 >60 mm Hg, or an increase in the baseline PaCO2 >20 mm Hg.
In rare instances, complications may arise during the apnea test. The two most common complications include hypotension and hypoxemia. If the patient’s SBP drops below 70 mm Hg, the apnea test should be aborted and the patient should be reconnected to the ventilator. In general, cases of hypoxemia can be avoided by the use of a tracheal insufflation catheter to supply oxygen following disconnection from the ventilator. Cardiac arrhythmias, another concern, are very uncommon and can also be avoided with oxygen supplementation. If the examiner concludes that all criteria for the apnea test have been met, a diagnosis of brain death is confirmed. However, if the patient fails to meet all criteria, further investigation with ancillary testing should be considered.
E. Confirmatory tests. The use of confirmatory tests in the assessment of brain death is reserved for instances when the apnea test cannot be performed, the test itself was inconsistent, or the neurologic examination was unreliable. The current available confirmatory tests aim at the evaluation and interpretation of two distinct categories: cerebral blood flow and neuronal function. Confirmatory tests alone should never be used to diagnose brain death, but rather confirm findings from the neurologic examination. To date, only electroencephalography (EEG), transcranial Doppler (TCD), and cerebral scintigraphy have consensus statements regarding testing in brain death. The use of other ancillary studies including conventional cerebral angiography, and somatosensory evoked potentials (SSEPs) may be considered, but true evidence is lacking. It should also be noted that confirmatory testing may provide false-negative results with an otherwise convincing neurologic examination. The usual explanation in these cases is that testing was performed too early in the determination of brain death, and details that timing of ancillary testing is a crucial concept.
image
1. EEG is the most used ancillary test in the determination of brain death worldwide. Diffuse isoelectric activity is the EEG pattern consistently observed with brain death. Prior to interpretation of the EEG, consensus criteria must be met and consistent throughout the recording (Table 34.3). The overall sensitivity and specificity of EEG in brain death is 90%; however, limitations do exist. Confounders including electrical interference in the intensive care unit, posterior fossa lesions, and preserved subcortical function with ischemic cortex should all be considered. If all stated criteria are not met and a definitive isoelectric pattern is not observed, the EEG may not be considered valuable when assessing brain death.
2. TCD is used in brain death to identify and transmit signals from both middle cerebral arteries (MCAs) and is a validated ancillary test. The sensitivity and specificity are 91% to 99% and 100%, respectively. Performing the exam in the assessment of brain death requires the confirmation of intracranial circulatory arrest on two separate occasions at least 30 minutes apart. The typical pattern seen with cerebrovascular arrest is oscillating flow with early systolic peaks and a high pulsatility index. It should be noted, however, in normal population studies that sonography of the MCAs cannot be obtained in 10% of patients. This limits its use for definitive diagnosis in brain death. The major advantage of TCD is its portability; however, its major disadvantage is interpretive, relying on expertise of the sonographer and the clinician experience. All variables must be taken into account when TCD analysis is considered in the assessment of brain death.
image
3. Cerebral scintigraphy is a dynamic nuclear scan that utilizes radioisotope gamma monitoring to identify cerebral circulation patterns. The tracer isotope is injected into the patient 30 minutes before initiation of the scan. In clinical instances of brain death, the scan will display complete cerebrovascular circulatory arrest at the skull base. Comparison with the spleen or internal carotid arteries should be performed to assess the viability of intracranial tracer uptake. The specificity in brain death is 96%. In certain instances, small amounts of uptake may be seen in cortical venous or subcortical parenchymal structures, rendering the scan inconclusive. Nuclear scanning can also be difficult to obtain institutionally, and with its reported false-positive and false-negative rates, is not a preferred test in the assessment of brain death.
4. Conventional digital subtraction cerebral angiography (DSA) is a dynamic vascular study utilizing contrast injection to visualize the anterior and posterior circulation. In healthy individuals, filling follows normal anatomic and physiologic variables, with internal carotid artery (ICA) and intracranial filling first, followed by external carotid artery filling. In brain death, this normal filling pattern is reversed with extracranial filling occurring first, and arrest of ICA flow at the skull base. This reversal is due to the ICP gradient created at the base following brain death. Of note, DSA has also been shown to correlate quite well with cerebral scintigraphy. To date, no criteria for confirmation of brain death have been established by neuroradiologic societies, implying lack of standardization and perhaps limitation.
5. Electrophysiological studies used in brain death include SSEPs and brainstem auditory evoked potentials (BAEPs). Both studies utilize the generation of electric potentials to assess the functionality and connectivity of specific neural circuits. Several studies have evaluated the use of SSEPs and BAEPs in the assessment of brain death and have found very poor predictive values. With SSEPs, cortical responses are shown to be absent bilaterally in up to 20% of comatose patients. With BAEPs, patients with anoxic ischemic encephalopathy are shown to have absent wave forms, while wave forms are present in brain death. Although certain institutions recommend the use of electrophysiologic studies in brain death, they should truly be reserved for unique instances with otherwise inconsistent confirmatory tests.
ETHICAL CONSIDERATIONS
A. Legal background. Traditionally, the legal definition for death was defined as the complete cessation of all cardiopulmonary function. Early in the literature there was no mention of brain functionality as a definitive criterion. In 1981, the President’s Commission on Bioethics reinterpreted the definition of death as either irreversible cessation of cardiopulmonary function, or irreversible cessation of all brain functions. This Uniform Determination of Death Act was widely adopted by both medical and legal authorities in the United States. All states have also either adopted identical or similar legislation defining brain death as a mortal qualifier. These laws, given their correct use and interpretation, allow a clinician to cease all physiologic support when brain death is confirmed. There are, however, two qualifiers that continue to exist prohibiting termination of resuscitative care. These include preparedness for organ procurement and accommodation of specific family wishes. In three states (California, New Jersey, and New York), law currently protects all family wishes following a diagnosis of brain death, and they must be accommodated regardless of medical opinion.
B. Religious beliefs. Religion in the United States and throughout the modern world plays an integral part in the determination of brain death. Each major religion has long-standing traditions of defining death. Traditional language for most includes the cessation of the beating heart. Over time, however, general acceptance of brain death as a definition of death has been established. Both Christianity and Islam have held international summits that have come to the consensus that no brain function qualifies as death. In Judaism or Jewish Law, brain death is somewhat less defined and divided. Jewish Orthodoxy accounts only cardiopulmonary function as a qualifier, but less-conservative Judaism accepts brain death as a true entity. In general, the qualification of brain death is dependent on religious leaders and their acceptance of both the medical examination and objectivity used to determine diagnosis. In Buddhism, the prolongation of suffering is against standard practice, and brain death is widely accepted. The religious stance of organ procurement is a completely separate topic and again dependent on specific organizations. As an examiner, it is imperative that religious preference is known during the assessment of brain death to accommodate all parties involved.
C. Social background. Family and social support in the initial, intermediate, and late assessment of brain death is vital. Family-centered care and communication go a long way in understanding the diagnosis and willingness to accept death. Studies have shown that only half of families who have undergone an experience with brain death are able to define its criteria and show understanding of the process. Traditional cultural thinking defines the heart as the ultimate living being and the keeper of the soul. With its failure, then and only then is death imminent. A clinician must be able to approach these conflicting beliefs with care and compassion as well as clarity.
Ethnicity also plays an important role in communication and education in brain death. It is crucial to develop a multidisciplinary team approach for the care of the patient and the family that is sensitive to all beliefs and cultures. This will create a unique understanding and sense of respect with the family that may otherwise be lacking. Use of the clergy is also recommended as a safe go-between in the evaluation of brain death.
COMMON PRACTICAL PROBLEMS
A. Examiner qualification. To date, there are no specific studies detailing the accuracy of examination and diagnosis among different specialties. In the majority of tertiary care centers across the United States, the brain death examination is performed by either a neurologist, neurosurgeon, or a critical care physician. Other subspecialties likely participate in other institutions. Legally, all physicians in the United States are allowed to diagnose brain death. There are no adult guidelines recommending qualified examiners; however, the pediatric guidelines allow only for intensivists, neonatologists, trauma surgeons, neurologists, and neurosurgeons. Currently, there exists no standardized competency test to determine qualification. The most common portions of the examination left unchecked are the oculovestibular responses and the apnea test. Moving forward, two separate examinations may need to be considered in the adult population to ensure accurate diagnosis and qualification of examiners. Institutions may also consider implementation of standardized training and evaluation ensuring uniform certification. In general, most physicians do not feel comfortable with or have never performed the brain death examination. Further consideration should be made in the future to allow for only qualified interpretation in the assessment of brain death.
B. Primary brainstem lesion. Acute, destructive lesions to the brainstem can mimic brain death. In primary brainstem lesions, the cerebral hemispheres usually remain intact, precluding a diagnosis of brain death. Typical lesions that will cause catastrophic injury include basilar artery occlusion, pontine hemorrhage, compression from cerebellar hemorrhage, and direct brainstem trauma. In most common instances, a detailed neurologic examination will show some preservation of brainstem function. In most typical brainstem lesions, the medulla oblongata will be spared. The patient will have preserved respiratory drive and lack signs of autonomic failure. In instances when examination is concerning for brain death, patients will pass an apnea test. Ancillary studies such as EEG and intracranial vascular studies will show alpha coma pattern and preserved blood flow, respectively. Generally speaking, brain death examinations in patients with catastrophic brainstem injuries should be reserved for highly qualified clinicians.
C. Spinal reflexes are a polysynaptic, polysegmental reflex that can occur in brain death. Such reflexes are described as slow, short-duration movements that can be diminished by repetitive stimulation. Typical descriptions of such reflexes include triple flexion, finger jerks, head turning, abduction or adduction of the arms, and even attempts at sitting up. The frequency of movements in brain death varies, but has been reported as high as 39%. Review of spinal reflexes compared to complex motor movements has shown no correlation. Typical decerebrate and decorticate motor responses have no clinical correlation with spinally mediated responses, and are thus differentiated. The presence of spinal reflexes on examination does not preclude the diagnosis of brain death. Both experience and careful assessment will allow an examiner to reach a correct conclusion.
D. Difficulty with the apnea test. The final step in the confirmation of brain death is completion of the apnea test. There are several clinical scenarios in which the apnea test may be difficult to ascertain.
1. Chronic CO2 retention is commonly encountered in patients with a history of chronic obstructive pulmonary disease (COPD). It is well documented that chronic hypercapnia (pCO2 50–70 mm Hg) results in a reduction of the chemoreceptor response. In such clinical instances, it is impossible to set target pCO2 values with the apnea test. Although rare, situations may arise where brain death determination is warranted in a patient with COPD. In such cases, the apnea test cannot be reliably performed and further ancillary testing is indicated.
2. Breathing during the apnea test is usually seen in comatose patients with a catastrophic neurologic injury. Brain death exclusively implies that all respiration is absent. Careful re-examination may reveal a cough reflex or other brainstem function that excludes brain death as a diagnosis. In a small number of documented patients, small gasps and agonal breathing have been seen. In such instances a repeat of the apnea test 24 hours later resulted in a positive test. Once the apnea test is positive, breathing effort will not return. If breathing during the apnea test has truly been established, family conversation should switch to determine further goals of care.
3. Termination of the apnea test is a common concern that continues to exist. Factors associated with the need for early termination include insufficient preoxygenation, hypotension, pretest acidosis, and polytrauma. Review of most clinical scenarios demonstrates that patients are inadequately preoxygenated. Additionally, all test prerequisites are not typically met including SBP >90 mm Hg and PEEP supplementation (5 mm Hg) following disconnection from the ventilator. If hypotension occurs during testing, a trial of intravenous phenylephrine may be considered. In situations where adequate oxygenation is difficult to overcome, apnea testing may not be reliable and other investigations should be considered.
E. Cardiopulmonary resuscitation and hypothermia. Therapeutic hypothermia following cardiac arrest has become a standardized practice in most institutions. Brain death occurs in around 5% of patients following arrest. The institution of hypothermia has shown to be beneficial in improving long-term neurologic outcomes and thus utilized today. Most protocols use a combination of benzodiazepines, opioid analgesics, and neuromuscular blocking agents to achieve cooling goals. Such medications are confounders in the examination of brain death and can present a diagnostic challenge. Additionally, hypothermia itself changes the pharmacokinetics of most drugs and delays objective neurologic findings on exam. Some authors recommend delaying a definitive neurologic examination up to 1 week following therapeutic hypothermia compared to the typical 3 days. The clearance of most medications during this time has been shown to be delayed up to five times the norm. Following therapeutic hypothermia it is important that examiners allow for adequate time to pass in order to exclude all major confounders and proceed with assessment of brain death. The use of a checklist prior to examination is highly recommended.
|
|
zBrown
Ice climber
|
|
Post your EEG, you may have died.
|
|
MikeL
Social climber
Southern Arizona
|
|
IF there were anyone who ever wrote narrative, it was Gabriel Garcia Marquez.
|
|
jogill
climber
Colorado
|
|
The first thought that entered my mind upon transiting from normal reality to a Dream (Art of Dreaming variety) was, This is how religion really started!
Our distant ancestors slipped into this mode by accident and found a new world so like the world of everyday, yet so different. Of course, without the knowledge gained over millennia they could only attribute their experiences to supernatural beings - rather than realizing this was the brain performing without sensory input.
And now, we find some wishing to bring back those magical moments of yore and proclaim that such adventures lie outside physical reality in a great Unknown Arena of Metaphysics.
Good luck with that.
;>)
|
|
WBraun
climber
|
|
The next thing you people will say is the muscle is the source of strength.
Yes ..... you dreamers truly are insane .....
|
|
yanqui
climber
Balcarce, Argentina
|
|
I sure hope I don't wind up like that colonel that never gets his pension! Forever waiting for some sign in the mail. Something to worry about if you live in South America, or work for a big US company like United Airlines. Not much magical realism in that scenario, although Marquez once said it was his best work.
BTW, I enjoyed the article about "causation" Largo put up and I see that the smoking duck has turned a bit more thought-provoking with an analogy.
|
|
Ed Hartouni
Trad climber
Livermore, CA
|
|
in reply to the criticism:"the ability to describe with any certainty the role of any particular neuron in the net"
we have:
https://distill.pub/2018/building-blocks/
(I found it best to use Chrome to look at this article, go figure...)
"With the growing success of neural networks, there is a corresponding need to be able to explain their decisions — including building confidence about how they will behave in the real-world, detecting model bias, and for scientific curiosity. In order to do so, we need to both construct deep abstractions and reify (or instantiate) them in rich interfaces [1] . With a few exceptions [2, 3, 4] , existing work on interpretability fails to do these in concert."
it is a first step to an essential tool for any complex programming task, an interface that acts as an interpreter to be used both for understanding how the particular program works, and to aid in "debugging" the program. This is a "linear" interpreter, it will be interesting to see how the idea is generalized and expanded for neural nets.
If we wait long enough, we can ask the neural net to explain how it works... probably with the same result that we find on this thread... only it would happen faster.
|
|
MH2
Boulder climber
Andy Cairns
|
|
For example, nobody, no other conscious agent, can read your thoughts, feel you feelings, know your sensations themselves.
That statement is too broad. Another conscious agent can get an idea of my thoughts, feelings, and sensations from my behaviour: how I move, the noises I make, my facial expressions, and such. Animals can do that.
Humans have created nuanced languages and spoken and written stories that convey much in the way of thought, feeling, and sensation.
Your own left hemisphere reads thoughts, feelings, and sensations from your right hemisphere, and vice versa.
Tatiana and Krista Hogan are two different people with partially joined brains and they apparently share at least sensations and perhaps thoughts and feelings.
I see no reason to rule out all possibility of people making further progress in finding out how the brain generates your sensations, thoughts, feelings, and memories. Just how far the progress can take us can't be judged with the complete certainty you seem to possess. Space travel was once science fiction.
If the corpus callosum can establish communication between your cerebral hemispheres, that sort of connection may be possible to create between the brains of two different people.
Why anyone would want to do that, I can't say.
I think it is much more interesting to study how the brain does its jobs. No great leap into a murky future is needed. There are many basic questions about brain function that we have no good answer to. I believe that we already have good enough ways for sharing thoughts and feelings.
|
|
|
SuperTopo on the Web
|
Let us know!