Posted on 03/30/2005 2:14:34 PM PST by CHARLITE
I'm trying to recall - MS took Terri to California for treatment that involved some manner of "brain implant". Would a sample of brain tissue have been take at the time (1995?).
"...Dr. Grace Fern Thomas, a psychiatrist and an expert in insulin shock therapy, and director of the insulin shock department at the time defendant was at Camarillo, testified as to the procedures on the ward. A precise dosage of insulin was measured for each person at a particular time. At a specific level that patient would go into shock in approximately two hours after the injection. Patients do not progress at the same level. Careful watch must be kept of the pulse, color, blood pressure, general condition, and neurological signs, such as pupillary changes and body motions. When a patient is going into progressive stages of coma he sweats very profusely and breathes very heavily. Saliva is secreted in large amounts, mucous flows freely and mixes with the saliva, and the patient must be carefully watched, turned, or assisted so that he does not aspirate the fluid into his lungs. Otherwise bronchopneumonia may develop, leading to death. The gag reflex and the cornea reflex are lost. Convulsions may occur, and medication is given to prevent this. The extremities may stiffen. At a relatively deep level of coma the Babinski test (scatching the sole of the foot in a certain manner) will cause a reflex known as the Babinski response (toes fan out). The patient must be brought out of the coma within 10-15 minutes thereafter. This is done by administering glucose through gastric tubes, and if this is not effective, glucose is administered intravenously to raise the blood sugar. If the brain is deprived of blood sugar for a prolonged period irreversible brain damage and death may result. As soon as a patient is fed glucose he awakens and is hungry. Only regular insulin was used in the ward because it was the only insulin where the time of coma could be calculated for therapeutic use. Injections began with small doses, very gradually increased over a three-week period..."
He already wanted her dead in his 1993 deposition. Her wedding rings prove it.
Auer RN.
Departments of Pathology and Clinical Neuroscience, Faculty of Medicine, University of Calgary, 3330 Hospital Drive N.W., Calgary, Alta., Canada T2N 4N1.
Hypoglycemia was long considered to kill neurons by depriving them of glucose. We now know that hypoglycemia kills neurons actively from without, rather than by starvation from within. Hypoglycemia only causes neuronal death when the EEG becomes flat. This usually occurs after glucose levels have fallen below 1mM (18mg/dl) for some period, depending on body glycogen reserves. At the time that abrupt brain energy failure occurs, the excitatory amino acid aspartate is massively released into the limited brain extracellular space and floods the excitatory amino acid receptors located on neuronal dendrites. Calcium fluxes occur and membrane breaks in the cell lead rapidly to neuronal necrosis. Significant neuronal necrosis occurs after 30min of electrocerebral silence. Other neurochemical changes include energy depletion to roughly 25% of control, phospholipase and other enzyme activation, tissue alkalosis and a tendency for all cellular redox systems to shift towards oxidation. The neurochemistry of hypoglycemia thus differs markedly from ischemia. Hypoglycemia often differs from ischemia in its neuropathologic distribution, a phenomenon applicable in forensic practice. The border-zone distribution of global ischemia is not seen, necrosis of the dentate gyrus of the hippocampus can occur and a predilection for the superficial layers of the cortex is sometimes seen. Cerebellum and brainstem are universally spared in hypoglycemic brain damage. Hypoglycemia constitutes a unique metabolic brain insult.
PMID: 15542270 [PubMed - in process]
Yes...but I'm eating dinner now, and don't want to offer other alternatives at this point. Let's just say, if Greer did enforce feeding, it would probably be in an other area of the anatomy. I think he likes that sort of power over.
FMCDH(BITS)
As the statutes are currently written, three conditions must apply to authorize the killing by dehydration of a supposedly-PVS person: (1) they must have actually expressed a wish to be starved under such circumstances; (2) they must actually be PVS; (3) they must be incapable of receiving water by natural means.
Although one might argue that #1 is most likely to be false, it is impossible to disprove. Unless one could show that Terri never met Michael's relatives, it would be impossible to prove that she didn't say what they claim. I would posit that #2 and #3 are more relevant because, unlike #1, they could be examined factually and deterministically if a court was interested in actually finding out the truth.
And what if they were true? Does that mean that all "PVS" patients who are correctly diagnosed and have a valid bad prognosis should be killed?
No, but offering the fact that Terri isn't PVS as a reason she shouldn't be killed doesn't imply that that is the only reason.
Terri Schiavo should not be killed precisely because she has severe brain damage and a bad prognosis. Killing her will set an horrific precedent, and hundreds or thousands of lives will be snuffed out in the next several years as that precedent plays out.
Terri is being killed not because she's PVS and can't swallow, but because the Triumvirate knows full well she's not PVS and could swallow.
To my mind, Michael's behavior shows quite clearly that he knows Terri's prognosis (if allowed treatment) is much better than what he lets on. I don't know how much better, but enough better that Michael is willing to go to great lengths to prevent her recovery.
Would induced hypoglycemia, say from insulin injection, result in a different pattern of brain damage than anoxia would?
Not after 15 years.
From my previous post:
"...Hypoglycemia often differs from ischemia in its neuropathologic distribution, a phenomenon applicable in forensic practice. The border-zone distribution of global ischemia is not seen, necrosis of the dentate gyrus of the hippocampus can occur and a predilection for the superficial layers of the cortex is sometimes seen. Cerebellum and brainstem are universally spared in hypoglycemic brain damage. Hypoglycemia constitutes a unique metabolic brain insult..."
(Ischemia = A decrease in the blood supply to a bodily organ, tissue, or part caused by constriction or obstruction of the blood vessels.)
According to this, there may be a discernable difference visible in the brain between hypoglycemia and ischemia (presumably caused by lack of blood supply due to cardiac arrest). Is there a chance we can address this question with existing and available data?
She's being killed not because Michael et al. know there'd be no possibility of recovery, but rather because they can't afford the risk of recovery. The efforts they've expended to prevent her recovery suggest that they believe the risk to be significant.
Of course bulemia can lead to hypoglycemia and potassium lack (Hypokalemia), leading to cardiac arrest and brain damage. There may be no way to sort this out or pin it down to one cause, I fear.
Michael had already decided by 1993 that Terri was never 'coming back'. Why wait until 1997 to remember his wishes, unless he was 'helped to remember' by his new lawyer George Felos?
RN Auer, Y Olsson and BK Siesjo
Thirty-eight male Wistar rats were exposed to insulin-induced hypoglycemia resulting in periods of cerebral isoelectricity ranging from 10 to 60 min. Plasma glucose levels during cerebral isoelectricity ranged from 0.12 mM to 1.36 mM. Control rats were injected with insulin, but hypoglycemia was terminated with glucose at the stage of large delta-wave EEG slowing. After recovery, the rats were allowed to wake up and survive for 1 wk. The number of dying neurons was assessed with acid-fuchsin/cresyl-violet-stained, whole-brain, subserial sections using direct visual counting of acidophilic, cytoclastic neurons. Brains from control rats that were not allowed to become isoelectric showed no dying neurons. Ten minutes of cerebral isoelectricity produced very minimal brain damage. The density of neuronal necrosis was positively related to the number of minutes of cerebral isoelectricity up to the maximum examined period of 60 min, but showed no correlation with the blood sugar levels. The cerebral cortex, hippocampus, caudate nucleus, spinal cord, and, to a lesser extent, cerebellar Purkinje cells were affected. The distribution of neuronal necrosis was not identical with that seen in ischemia, but, rather, suggested a CSF-borne neurotoxin operant in contributing to the pathogenesis of neuronal necrosis in hypoglycemic brain damage. Neuronal death does not occur in hypoglycemia unless the EEG becomes isoelectric, whatever the blood sugar level. Serious brain damage does not occur until electrocerebral silence has been established for at least several minutes. Neuronal death accelerates after 30 min of EEG isoelectricity in the rat.(ABSTRACT TRUNCATED AT 250 WORDS) This article details (at least in a rat brain) the amount of damage caused by induced insulin hypoglycemia as a function of time.
http://carecure.atinfopop.com/4/OpenTopic?a=tpc&s=4754088921&f=6574035662&m=5694054403
posted 01-03-04 11:20 AM
Sorry for being off-topic, but I figured somebody could point me in the right direction.
A cousin of mine was given an accidental dose of insulin (September time frame--hospital admits mistake) and has sustained serious brain damage. EKG and physical response indicate very little brain activity.
Her parents are being told that there is nothing more the hospital can do, and that they should seek a long term care facility. I've been encouraging them to, at the very least, seek out a true expert to evaluate the medical records, or even see the patient for a week to provide some sort of expert prognosis.
My question is: Do the TBI model centers consider admitting or reviewing records for a patient in this condition (sounds like PVS, but I don't have all the information)? I don't know if the TBI centers deal exclusively with traumatic injury and GSW, etc.
Or, would the parents be better off getting an opinion from a coma specialist or maybe even an expert in stroke recovery?
I'm advising them to get the medical records looked at by one of the model centers. My fear is that if they commit her to a long term care facility, the staff will not recognize possible recovery signs or serious complications. Since the injury is so new, I'm strongly encouraging her parents to seek another opinion from an expert.
Any thoughts, Wise? Any facility recommendations?
quote:
--------------------------------------------------------------------------------
Drug-Induced Hypoglycemic Coma in 102 Diabetic Patients
Haim Ben-Ami, MD; Pradeep Nagachandran, MD; Ayelet Mendelson, MD; Yeouda Edoute, MD, PhD
Arch Intern Med. 1999;159:281-284.
Background Hypoglycemic coma is a continuous threat for diabetic patients treated with insulin and/or oral hypoglycemic agents; it may be associated with substantial morbidity and mortality.
Methods We retrospectively reviewed our clinical experience with drug-induced hypoglycemic coma during a 7-year period.
Results The study consisted of 102 patients and included 61 females and 41 males. The median age was 72 years. Ninety-two patients suffered from type 2 diabetes mellitus; 10 patients had type 1 diabetes mellitus. The median lowest blood glucose level was 1.77 mmol/L (32 mg/dL). Drug-induced hypoglycemic coma occurred in 99 patients out of the hospital, while 3 patients developed it during hospitalization. Drug-induced hypoglycemic coma occurred in patients undergoing treatment with insulin, glyburide, and combined therapy with insulin and glyburide, insulin and metformin, or glyburide and metformin. Ninety-three patients had at least 1 of the following risk factors: age older than 60 years, renal dysfunction, decreased intake of energy, and infection. Fourteen patients concomitantly received drugs that potentiated hypoglycemia. Forty patients responded to treatment within the first 12 hours, while 62 patients had protracted hypoglycemia of 12 to 72 hours' duration. Morbidity included physical injuries in 7 patients, myocardial ischemia in 2 patients, and stroke in 1 patient. Death occurred in 5 patients.
Conclusions Hypoglycemic coma is a serious and not an uncommon problem among elderly patients with diabetes mellitus and treated with insulin and/or oral hypoglycemic drugs. Risk factors contribute substantially to the morbidity and mortality of patients with drug-induced hypoglycemic coma. Enhanced therapeutic monitoring may be warranted when hypoglycemic drugs are administered to an elderly patient with the above predisposing factors and potentiating drugs for hypoglycemia.
From the Department of Internal Medicine C, Rambam Medical Center, and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa. ..."
Specific Changes in Human Brain After Hypoglycemic Injury
Background and Purpose Very few reports are available on serial changes in the human brain after severe hypoglycemic injury. The aim of this study was to investigate sequential neuroradiological changes in brains of patients after hypoglycemic coma compared with those after cardiac arrest previously studied with the same methods.
Methods We repeatedly studied CT scans and MR images obtained at 1.5 T in four vegetative patients after profound hypoglycemia associated with diabetes mellitus.
Results In all patients, consecutive CT scans showed symmetrical, persistent low-density lesions with transient enhancement in the caudate and lenticular nuclei and transient enhancement in the cerebral cortex 7 to 14 days after onset. Serial MR images consistently revealed symmetrical lesions of persistent hyperintensity and hypointensity on T1- and T2-weighted images, respectively, in the caudate and lenticular nuclei, cerebral cortex, substantia nigra, and/or hippocampus from 8 days to 12 months after onset.
Conclusions Repeated MR images revealed specific lesions in the bilateral basal ganglia, cerebral cortex, substantia nigra, and hippocampus, which suggests the particular vulnerability of these areas to hypoglycemia in the human brain. We speculate that the localized lesions represent tissue degeneration, including some combination of selective neuronal death, proliferation of astrocytic glial cells, paramagnetic substance deposition, and/or lipid accumulation. The absence of localized hemorrhages on MR images in hypoglycemic encephalopathy is in marked contrast to the presence of regional minor hemorrhages in postischemic-anoxic encephalopathy.
QED
Why? To inherit the millions she's leaving behind?
C'mon. There's no reason for the three of them to lie under oath. Seems to me Michael would have been money ahead to turn Terri over to her parents in 1993, take his $400K loss of consortium check, and say, "Adios". Yes?
I would assume that after hearing the same evidence that Judge Greer heard, a jury (or anyone, for that mattter) would have ruled the same way.
There were six doctors who actually, physically examined Terri.
Two were selected by Michael Schiavo.
Two were selected by the Schindler family.
One was Terri’s GP (also selected by Michael, but whose role was more limited to basic medical needs, illnesses)
And one physician – neurologist – selected by the Court.
These are the only medical examinations that count – from the perspective that they had actual contact.
The two of Michael’s choice and the two of Schindler’s choice pretty much rule each other out. Thus that leaves us with the GP who had no determination in her brain status; and the one neurologist who determined she in PVS.
One physician. Terri’s life is being held bound by the actual examination of One Physician!
How many of us, when faced with a serious condition would leave our lives in the hands of the diagnosis of one physician?
How many of us, would not also want the words of numerous other attending nurses, aids, friends, and family members who actually saw us demonstrate some signs of awareness, ability, sensitivity, and determination – over long periods of time - not want those observations taken into consideration when a legal judgment was being made about letting us live, or die?
If Terri’s alleged statement about not wanting “artificial life support” was true, as a 20 some year old woman did she actually even understand the difference between a feeding tube, and being hooked up to machines that would help her breath or process bodily functions, etc. Who at that age even thinks of feeding tubes?
Yet, also along those lines: Michael won a court case with the contention that Terri had been misdiagnosed (for I suspect previous medical problems) and the Bulimia was not discoverd. That was several years after she had “collapsed,” but before he said he recalled her making the now, life threatening statement. The courts agreed that Terri's heart arrhythmia that caused her collapse was attributed to Bulimia.
What is the psychosis of Bulimia? Bulimia is associated with a personality disorder, particularly of the type that features impulse control issues and rigid thinking (eg, borderline personality disorder). A disturbance in the neuropsychological domain of mental flexibility underlies the spectrum of eating disorders.
Although the act of self-induced vomiting may occur only occasionally and may be of little consequence, a long-term pattern that develops leads to physical problems, i.e. poor overall health, decreased muscle strength, dental erosion, abnormal menses, serious electrolyte abnormalities, cardiac arrhythmias and, even death. It does not happen in six months – it takes a long time. Hence, if Terri was Bulimic, and suffered the heart stoppage, she had endured a long period of “captivity” to the bulimia condition.
The couple was married for two years. It would be safe to conclude then that much of that time she was bulimic, and as most bulimics able to hide that fact quite well.
But the underlying psychosis as typical of bulimics, effected her feeling of self-esteem, desire to be perfect, and as most bulimics state over and over, feeling that death is better than life if they are not thin and perfect – hence they engage in life-threatening behavior: binging/purging, overuse of laxatives, etc. It is almost a “death wish” behavior.
Someone in that state of mind, with that devaluation of self worth, should not be given credibility to a possible statement made about wanting to live or die. They are not thinking rationally. They are under the delusion that unless they are perfect life is not worth living.
Criminals often plead psychological disturbances as a reason to be judged less responsible for their illegal actions. And, oft, judges and juries consider that to be worthy reason for forgiveness.
Shouldn’t Terri have the same opportunity for forgiveness of her alleged statement, if it was made while she was in the grasp of a psychological personality disorder?
Terri’s bulimia was very much the very reason Michael Schiavo won a total of one million plus from the courts. So, which is it: Was she Bulimic and suffering from a personality disorder that affected her judgment about life? Or was she not Bulimic, and capable of making a rational statement that she would rather be dead than live on life support?
The courts cannot rule both ways. Yet, sadly, in the case of Terri, they never considered the psychological aspect. Only the diagnosis of one doctor whose examination never involved or related to any awareness of her mental state at the time of her collapse – only her condition afterward.
God help us from not having the full value of all areas of diagnosis from professionals in a variety of areas of medical expertise, including those who are in regular attendance to our needs, if our life and its worth is being evaluated by the courts.
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