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Thread: Methylprednisolone soon to be replaced as treatment of choice for Acutes???

  1. #51
    Banned Faye's Avatar
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    Quote Originally Posted by Wise Young
    Methylprednisolone is given as an intravenous solution called Solumedrol or methylprednisolone sodium succinate (MPSS). As I understand it, MPSS needs to pass through the liver so that the succinate can be broken off before it starts to act as a glucocorticoid.

    Prednisone is an glucocorticoid that can be given orally. It is usually given when people take longer term oral glucocorticoids. Did Jason receive prednisone for a period of time after the methylprednisolone? It sounds like it, given your description of his "moon-face". If so, I suspect that this may have inhibited his recovery.

    Wise.
    Indeed, courtesy of a misdiagnosis of ADEM, Jason did have prolonged administration of prednisone after the MP IV.( for 4 months until the correct diagnosis of basilar artery occlusion was established at a different hospital via an MRA which should have taken place at the first hospital)

    I know that the second 24 hour course of MP is highly unusual, but it was done just prior to his plasma pheresis treatments to determine if there may be justification for plasma pheresis. The before and after MRI's showed no difference this time.

    The worsening of Jason's condition immediately following a bolus administration of dilantin just 2 hours after presenting to the ER, was significantly due to a lowering of bloodpressure from the dilantin. This lowered bloodpressure prevented what little blood could squeeze by the clot, to get through.

    It's the valium that we know from rat studies to prevent neuro-regeneration. And as you concur the pro-longed administration of prednisone for the first 4 months in rehab also contributed to practically no neurological recovery during that time.

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  2. #52
    Quote Originally Posted by Faye
    Indeed, courtesy of a misdiagnosis of ADEM, Jason did have prolonged administration of prednisone after the MP IV.( for 4 months until the correct diagnosis of basilar artery occlusion was established at a different hospital via an MRA which should have taken place at the first hospital)

    I know that the second 24 hour course of MP is highly unusual, but it was done just prior to his plasma pheresis treatments to determine if there may be justification for plasma pheresis. The before and after MRI's showed no difference this time.

    The worsening of Jason's condition immediately following a bolus administration of dilantin just 2 hours after presenting to the ER, was significantly due to a lowering of bloodpressure from the dilantin. This lowered bloodpressure prevented what little blood could squeeze by the clot, to get through.

    It's the valium that we know from rat studies to prevent neuro-regeneration. And as you concur the pro-longed administration of prednisone for the first 4 months in rehab also contributed to practically no neurological recovery during that time.
    Thanks for the info. I am puzzled by your statement that dilantin reduced blood pressure. Dilantin has actually been reported in several animal studies to be neuroprotective.
    • Rekling JC (2003). Neuroprotective effects of anticonvulsants in rat hippocampal slice cultures exposed to oxygen/glucose deprivation. Neurosci Lett 335: 167-70. Some anticonvulsants show neuroprotective effects, and may be of use in reducing neuronal death resulting from stroke or traumatic brain injury. Here I report that a broad range of anticonvulsants protect cells in hippocampal slice cultures from death induced by oxygen/glucose deprivation (OGD). Hippocampal slice cultures were submitted to 1 h OGD and the resulting cell death was quantified 24 h later using a novel automated fluorescent scanning method. The classical anticonvulsants phenobarbital, phenytoin, ethosuximide, chlordiazepoxide and midazolam all significantly and dose-dependently reduced cell death induced by OGD. The newer anticonvulsants carbamazepine, felbamate, lamotrigine, tiagabine, and oxcarbazepine also had significant neuroprotective effects, but gabapentin, valproic acid (10 mM), levetiracetam and retigabine were not neuroprotective at a concentration up to 300 microM. In conclusion, several classical and newer anticonvulsants have neuroprotective properties in an in vitro model that simulates cerebral ischemia. H. Lundbeck A/S, Biological Research, Department 828, Ottiliavej 9, DK-2500 Valby, Denmark. jre@lundbeck.com http://www.ncbi.nlm.nih.gov/entrez/q..._uids=12531459
    • Hayakawa T, Hamada Y, Maihara T, Hattori H and Mikawa H (1994). Phenytoin reduces neonatal hypoxic-ischemic brain damage in rats. Life Sci 54: 387-92. We investigated the possible protective effect of phenytoin on hypoxic-ischemic brain damage in neonatal rats. Six-day-old rats underwent ligation of the left carotid artery followed by exposure to an 8% oxygen atmosphere for 2.5 hrs. We sacrificed the animals 72 hrs later and assessed the hypoxic-ischemic brain damage histologically. Phenytoin (50 mg/kg), administered intraperitoneally 1 hr before the hypoxia, reduced hypoxic-ischemic infarction in the cerebral cortex and striatum, and attenuated neuronal necrosis in the hippocampus. The plasma concentration of phenytoin after injection was 11.1 +/- 1.9 micrograms/ml (mean +/- S.E.M.) at 1 hr and 22.9 +/- 1.4 micrograms/ml at 4 hrs. Percent volumes of the infarction calculated by dividing the sum of damaged areas by the total area in serial coronal sections were 79 +/- 3% (mean +/- S.E.M.) in vehicle controls versus 13 +/- 6% in phenytoin-treated pups in the cerebral cortex, and 79 +/- 4% in vehicle controls versus 12 +/- 5% in phenytoin-treated pups in the striatum. We semiquantitatively investigated the hypoxic-ischemic change in 5 hippocampal areas: dentate gyrus, CA4, CA3, CA1, and subiculum, in the dorsal hippocampus. Pre-hypoxic treatment with phenytoin reduced hypoxic-ischemic damage in all areas examined. When phenytoin was administered immediately after the hypoxia, there was no difference between vehicle-injected controls and phenytoin-treated pups. These results demonstrate that phenytoin can reduce neonatal hypoxic-ischemic brain damage. Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=8295485


    It has been used for decades to prevent seizures in patients after brain trauma without reports of complications such as hypotension. I therefore did a literature search for any reports of dilantin (phenytoin) causing hypotension and here are several studies reporting from no incidence, to occasional incidence associated perhaps with overdose.
    • Coplin WM, Rhoney DH, Rebuck JA, Clements EA, Cochran MS and O'Neil BJ (2002). Randomized evaluation of adverse events and length-of-stay with routine emergency department use of phenytoin or fosphenytoin. Neurol Res 24: 842-8. Intravenous phenytoin has come under increased scrutiny with the introduction of the prodrug, fosphenytoin. We evaluated adverse events and length-of-stay using parenteral the two drugs in routine emergency department use. Open-label randomization of phenytoin or fosphenytoin in 256 Emergency Department patients prescribed 279 parenteral doses of a phenytoin-equivalent. All phenytoin was administered intravenously, and fosphenytoin was given intravenously or intramuscularly (physician preference). Adverse events and Emergency Department length-of-stay were recorded; re-presentation to the Emergency Department within three months was reviewed for evidence of the purple glove syndrome. Nonparametric statistics were used to analyze the data. Seventy-seven patients received phenytoin and 202 fosphenytoin; 28 (10.0%) received intramuscular fosphenytoin. The mean phenytoin-equivalent dose was similar between the groups. Eighteen patients required reduction in infusion rates because of an adverse event (phenytoin = 6.5%, fosphenytoin = 6.4%; OR 0.9, 95% CI 0.4 2.6; p = 1.0). Adverse events occurred with similar frequency (phenytoin 9.1%, fosphenytoin 15.8%; OR 0.7, 95% CI 0.3 1.4; p = 0.3). The most common events were: pruritis, pain on infusion, and paresthesias. One patient developed hypotension (fosphenytoin); there were no other serious adverse events, including phlebitis. Median Emergency Department length-of-stay was 6.7 h for phenytoin and 5.7 h for fosphenytoin (p = 0.6). In routine Emergency Department use, our data do not support formulary conversion from phenytoin to fosphenytoin, based on the incidence of adverse events or Emergency Department length-of-stay. Departments of Neurology and Neurological Surgery, Wayne State University, 4201 St. Antoine-8D-UHC, Detroit, MI 48201, USA. wcoplin@med.wayne.edu http://www.ncbi.nlm.nih.gov/entrez/q..._uids=12500711
    • Coplin WM, Rhoney DH, Rebuck JA, Clements EA, Cochran MS and O'Neil BJ (2002). Randomized evaluation of adverse events and length-of-stay with routine emergency department use of phenytoin or fosphenytoin. Neurol Res 24: 842-8. Intravenous phenytoin has come under increased scrutiny with the introduction of the prodrug, fosphenytoin. We evaluated adverse events and length-of-stay using parenteral the two drugs in routine emergency department use. Open-label randomization of phenytoin or fosphenytoin in 256 Emergency Department patients prescribed 279 parenteral doses of a phenytoin-equivalent. All phenytoin was administered intravenously, and fosphenytoin was given intravenously or intramuscularly (physician preference). Adverse events and Emergency Department length-of-stay were recorded; re-presentation to the Emergency Department within three months was reviewed for evidence of the purple glove syndrome. Nonparametric statistics were used to analyze the data. Seventy-seven patients received phenytoin and 202 fosphenytoin; 28 (10.0%) received intramuscular fosphenytoin. The mean phenytoin-equivalent dose was similar between the groups. Eighteen patients required reduction in infusion rates because of an adverse event (phenytoin = 6.5%, fosphenytoin = 6.4%; OR 0.9, 95% CI 0.4 2.6; p = 1.0). Adverse events occurred with similar frequency (phenytoin 9.1%, fosphenytoin 15.8%; OR 0.7, 95% CI 0.3 1.4; p = 0.3). The most common events were: pruritis, pain on infusion, and paresthesias. One patient developed hypotension (fosphenytoin); there were no other serious adverse events, including phlebitis. Median Emergency Department length-of-stay was 6.7 h for phenytoin and 5.7 h for fosphenytoin (p = 0.6). In routine Emergency Department use, our data do not support formulary conversion from phenytoin to fosphenytoin, based on the incidence of adverse events or Emergency Department length-of-stay. Departments of Neurology and Neurological Surgery, Wayne State University, 4201 St. Antoine-8D-UHC, Detroit, MI 48201, USA. wcoplin@med.wayne.edu http://www.ncbi.nlm.nih.gov/entrez/q..._uids=12500711
    • Binder L, Trujillo J, Parker D and Cuetter A (1996). Association of intravenous phenytoin toxicity with demographic, clinical, and dosing parameters. Am J Emerg Med 14: 398-401. Previous studies investigating intravenous phenytoin toxicity have been largely anecdotal, and have inferred an association with older patients, cardiovascular disease, and higher doses, concentrations, and infusion rates of phenytoin. This investigation sought to elucidate both the incidence and nature of acute intravenous phenytoin toxicity in emergency department patients, and to identify any demographic, clinical, or dosing associations with toxicity, by analyzing a retrospective case series over 3 years in a municipal teaching hospital. A consecutive series of 164 patients who received intravenous phenytoin loading in the emergency department following acute seizure presentation was identified. Demographic, clinical, and dosing data were collected, and the nature of toxicity was noted. Data were then analyzed statistically for potential associations with toxicity. Eight cases of hypotension and no apnea or arrhythmias were noted in the 164 patients (4.9% incidence). Analysis of demographic, clinical, and dosing data found statistically significant associations between hypotension and both a lower phenytoin dose administered (537 mg in hypotensive patients v 787 mg in normotensive patients, P = .00046) and the presence of abnormal neurological signs at initial presentation (20% incidence when abnormal signs present v 3.5% incidence when absent, P = .026). No other associations were found between toxicity and other variables. This sample size could detect differences ranging from 4% to 11% in complication rate (hypotension) for the various demographic, clinical, and dosing parameters with a statistical power of 80%. It was concluded that the incidence of hypotension from intravenous phenytoin administration in this study population was approximately 5%, and the incidence of apnea and cardiac arrhythmia in this series was 0%. No associations with age, comorbidities, or infusion rates were found, in contrast to other studies. Association of intravenous phenytoin toxicity with lower phenytoin dose is likely related to prompt cessation of the drug once signs of toxicity occur. The possible association of toxicity with abnormal initial neurological signs has not previously been reported and may possibly define a population at risk if validated by prospective research in additional populations. Department of Emergency Medicine, Texas Tech University Health Sciences Center, El Paso, 79905, USA. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=8768165


    Iinterestingly, I found a rat study showing the phenytoin causes hyperglycemia (increase blood sugar) and hypothermia (reduced body temperature in rats).

    • Qi H and Newman GC (1996). Phenytoin-induced hyperglycaemia may confound rat cerebroprotection models. Clin Exp Pharmacol Physiol 23: 893-7. 1. The anticonvulsant phenytoin (PHT) has been used with variable success in animal models of cerebral ischaemia. Although PHT has been reported to alter glucose regulation in man, this potential effect has been largely ignored in animals. Because hyperglycaemia strongly influences the outcome of cerebral ischaemia, we sought to systematically delineate the effects of PHT on serum glucose in several rat strains. 2. We studied the PHT dose-response curve for serum PHT and glucose concentrations and several physiological variables. Phenytoin induces a significant, concentration-dependent hyperglycaemia, even in the ranges commonly used for humans and in animal models. 3. Hypothermia of several degrees was observed during PHT administration, but no hypotension or bradycardia was found. 4. Both hyperglycaemia and hypothermia must be considered when PHT is studied as a neuroprotective agent in animal models. Department of Neurology, State University of New York, Stony Brook 11794-8121, USA. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=8911732


    I just did a literature search on the effects of valium on recovery of function. The rat studies that show this are from nearly 20 years ago:
    • Schallert T, Hernandez TD and Barth TM (1986). Recovery of function after brain damage: severe and chronic disruption by diazepam. Brain Res 379: 104-11. Following unilateral damage to the anterior-medial region of the neocortex (AMC) in rats a sensory asymmetry appeared, but recovered within a week. In a separate group of rats with AMC lesions daily 3-week exposure to diazepam (Valium, 5 mg/kg) beginning 12 h after surgery caused recovery to be delayed indefinitely. The efficiency and speed (as opposed to symmetry) of behavior was not impaired. More than 9 weeks after discontinuation of diazepam (12 weeks postsurgery), recovery was still not apparent. Postmortem analysis ruled out lesion size as a contributing factor. In a second experiment undrugged animals with AMC lesions were allowed to recover for at least 3 weeks before being exposed to diazepam. These animals showed only a transient (2-day) reinstatement of asymmetry despite continuous drug treatment. We conclude that important mechanisms serving recovery of function may be vulnerable during a short period soon after brain damage. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=3742206


    On the other hand, there is a recent study suggesting that Diazepam improves acute stroke outcome in humans
    • Lodder J, van Raak L, Hilton A, Hardy E and Kessels A (2005). Diazepam to Improve Acute Stroke Outcome: Results of the Early GABA-Ergic Activation Study In Stroke Trial. A Randomized Double-Blind Placebo-Controlled Trial. Cerebrovasc Dis 21: 120-127. Background: We tested whether diazepam, a GABA-ergic drug that also inhibits brain nitric monoxide formation, improves acute stroke prognosis. Methods: 880 patients, randomized within 12 h of acute stroke, received diazepam 10 mg or placebo by rectiole, as soon as possible, followed by 10-mg tablets twice daily for 3 days. Primary outcome was independence (Rankin score <3) at 3 months; secondary outcome was complete recovery (Barthel index >/=95 or Rankin score </=1). Results: Intention-to-treat analyses on all 849 patients with full follow-up (50.4% on diazepam): odds ratio (OR) 1.14, 95% CI 0.87-1.49 for primary endpoint, and an OR of 1.26 (0.90-1.76) for complete recovery, both favoring diazepam. Adjusted analyses for all stroke patients (843): OR 1.20 (0.87-1.65), and 1.25 (0.89-1.74), respectively, and for all infarct patients (748): OR 1.31 (0.93-1.85), and 1.46 (1.02-2.09; p = 0.037), respectively. Analyses restricted to cardioembolic infarct patients (200) showed treatment benefit for the primary outcome: OR 2.26, 95% CI 1.07-4.76, p = 0.032, and complete recovery: OR 2.65, 95% CI 1.06-6.59, p = 0.037. About one third of ischemic stroke patients had 'any adverse event', without any difference between treatment groups. In 95 intracerebral hemorrhage patients, frequency of pneumonia and death were higher in the diazepam group than in the placebo group: 35 and 10%, 22 and 12%, respectively. Conclusions: Although point estimates favored diazepam treatment in various analyses, our data did not confirm our primary hypothesis. Diazepam treatment seems beneficial in cardioembolic infarct patients, is safe in acute ischemic stroke, but may better be avoided in intracerebral hemorrhage. Copyright (c) 2006 S. Karger AG, Basel. Department of Neurology, University Hospital Maastricht, Maastricht, The Netherlands. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16340187
    Last edited by Wise Young; 01-01-2006 at 03:25 PM.

  3. #53

    Dilantin loading

    Dilantin is at therapeutic levels neuroprotective , however the potential for hypotension is very high during the initial dilantin load. A patient who is not currently on dilantin therapy would be given a bolus dose followed by blood draw for dilantin level to determine when the patient reaches a therapeutic level. I would like to have a look at the flow sheet used to document that bolus administration of IV dilantin because generally if the drip is infused too quickly the pressure will drop. Very often in the cases of status epilepticus or similar situations, in the ER, a monitored drop in BP is considered accepted risk, however in Jason's case it sounds like it could have been too much of a trade off due to the blockage in the basilar artery which seems to have prevented the blood flow to effectively reach Jason's brain. I do not load dilantin in a patient without continuous vital signs and EKG, and document data every 10 minutes for the duration of the infusion. No one receiving a dilantin load should ever be left alone. Our protocols require the primary nurse to be in the room monitoring and documenting on a flow sheet, as well as a second nurse to verify dosage and drip set up, for patient safety. I am not sure about kids though, but cannot imagine it being much different.

    Mary
    1FineSpineRN

  4. #54
    Banned Faye's Avatar
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    Quote Originally Posted by Wise Young
    Thanks for the info. I am puzzled by your statement that dilantin reduced blood pressure. Dilantin has actually been reported in several animal studies to be neuroprotective. It has been used for decades to prevent seizures in patients after brain trauma without reports of complications such as hypotension.
    Very true. Dilantin has a long reputation of being neuroprotective.

    As with MP, it is the dosage and method of administration that matters.

    In the ER I had observed a worsening of Jason's condition immediately following the bolus administration of dilantin. What had been a series of TIA's ie kicking and screaming for about 1-2 min. followed by lulls of 15-20 min. of peacefulness prior to the dilantin turned into continuous screaming and kicking for hours until he fell into coma from the valium.
    The kicking and screaming bouts in brainstem strokes are well-described by Saposnik et al.:
    Involuntary convulsive-like movements occur in patients with brainstem strokes. These movements vary in nature, frequency, and trigger, including fasciculation-like, shivering, jerky, tonic-clonic, and intermittent shaking movements. Some are interpreted as decerebrate postures or seizures. It is important to recognize this type of motor phenomenon since it may be a diagnostic clue for early diagnosis and treatment of brainstem strokes.....
    These episodes consisted of brief clonic contractions of ...extremities. They were observed in paroxysms lasting for 3 to 5 seconds...
    Convulsive-like movements in brainstem stroke may occur more frequently than reported. Early detection of this motor phenomenon may have practical implications.
    http://www.medscape.com/medline/abstract/11295998


    so months later I researched it and found this:
    Symptoms of a Dilantin overdose include back-and-forth eye movements, slurred speech, stumbling or staggering walk, imbalance, drowsiness, unconsciousness, nausea, vomiting, tremor, low blood pressure, and slow breathing.
    http://www.drugs.com/dilantin.html

    Of course Jason's medical records too showed a significant drop in bloodpressure after dilantin was given.

    In addition it turned out Jason had received a dilantin bolus administration at 200% of the adult dose.

    Dr. Young, thanks for the 2005 study of diazepam/valium admin having positive effects in acute ischemic stroke. Of note though, is the three day administration only, as opposed to prolonged use over a period of four months.

    BTW to complete the picture: at the renowned Children's Hospital Jason was transferred to they added aciclovir to the mix and did two spinal taps which were negative for viral infection.

    As aciclovir has been associated with reversible encephalopathic changes, it should be used with caution in patients with underlying neurological abnormalities, significant hypoxia or ........
    http://www.medsafe.govt.nz/profs/Dat...l/LovirInf.htm
    Last edited by Faye; 01-01-2006 at 05:55 PM.

    "There’s far too much unthinking respect given to authority,” Molly Ivins explained; “What you need is sustained outrage.”
    Kerr, Keirstead, McDonald, Stice and Jun Yan courageously work on ESCR to Cure SCI.

    Divisiveness comes from not following Christopher Reeve's ESCR lead.
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  5. #55
    Banned Faye's Avatar
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    Quote Originally Posted by Duramater
    Dilantin is at therapeutic levels neuroprotective , however the potential for hypotension is very high during the initial dilantin load. A patient who is not currently on dilantin therapy would be given a bolus dose followed by blood draw for dilantin level to determine when the patient reaches a therapeutic level. I would like to have a look at the flow sheet used to document that bolus administration of IV dilantin because generally if the drip is infused too quickly the pressure will drop. Very often in the cases of status epilepticus or similar situations, in the ER, a monitored drop in BP is considered accepted risk, however in Jason's case it sounds like it could have been too much of a trade off due to the blockage in the basilar artery which seems to have prevented the blood flow to effectively reach Jason's brain. I do not load dilantin in a patient without continuous vital signs and EKG, and document data every 10 minutes for the duration of the infusion. No one receiving a dilantin load should ever be left alone. Our protocols require the primary nurse to be in the room monitoring and documenting on a flow sheet, as well as a second nurse to verify dosage and drip set up, for patient safety. I am not sure about kids though, but cannot imagine it being much different.

    Mary
    Thanks Mary.
    Dilantin administration should not be done in a haphazard manner as you so well describe. There were no blood draws to monitor blood levels after administration either.
    Again thanks for your experienced input.

    Faye

    "There’s far too much unthinking respect given to authority,” Molly Ivins explained; “What you need is sustained outrage.”
    Kerr, Keirstead, McDonald, Stice and Jun Yan courageously work on ESCR to Cure SCI.

    Divisiveness comes from not following Christopher Reeve's ESCR lead.
    Young does ASCR.
    [I]I do not tear down CRPA, I ONLY make peopl

  6. #56
    Faye, I am so sorry about the diagnostic fiasco that Jason had to undergo. I have had no experience with brainstem infarcts in a young person although I have seen brainstem strokes in adults. They have seldom been associated with the intermittent agitation (kicking and screaming) that you describe. Thank you for the report of from Saposnik, et al. (2001) which describes the symptoms more like what I have seen. There may be decerebrate posturing (extensor rigidity) and clonic quivering. The fact that Jason was "kicking and screaming" really puzzles me because a serious brainstem stroke should have precluded either of those behaviors.

    Did they give intravenous dilantin? To my knowledge, the side-effects of the intravenous dilantin administration are not due to the dilantin itself but the solvent for the dilantin solution which is alkaline (sodium hydroxide), contains 40% polypropylene glycol, and 10% ethanol. That is one of the reasons why there is preference for fosphenytoin which is a "pro-drug" from of dilantin and is more soluble in saline.
    http://www.surgicalcriticalcare.net/...sphenytoin.pdf

    Wise.

    Quote Originally Posted by Faye
    Very true. Dilantin has a long reputation of being neuroprotective.

    As with MP, it is the dosage and method of administration that matters.

    In the ER I had observed a worsening of Jason's condition immediately following the bolus administration of dilantin. What had been a series of TIA's ie kicking and screaming for about 1-2 min. followed by lulls of 15-20 min. of peacefulness prior to the dilantin turned into continuous screaming and kicking for hours until he fell into coma from the valium.
    The kicking and screaming bouts in brainstem strokes are well-described by Saposnik et al.:

    http://www.medscape.com/medline/abstract/11295998


    so months later I researched it and found this:

    http://www.drugs.com/dilantin.html

    Of course Jason's medical records too showed a significant drop in bloodpressure after dilantin was given.

    In addition it turned out Jason had received a dilantin bolus administration at 200% of the adult dose.

    Dr. Young, thanks for the 2005 study of diazepam/valium admin having positive effects in acute ischemic stroke. Of note though, is the three day administration only, as opposed to prolonged use over a period of four months.

    BTW to complete the picture: at the renowned Children's Hospital Jason was transferred to they added aciclovir to the mix and did two spinal taps which were negative for viral infection.


    http://www.medsafe.govt.nz/profs/Dat...l/LovirInf.htm
    Last edited by Wise Young; 01-03-2006 at 06:03 AM.

  7. #57
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    Quote Originally Posted by Wise Young
    Faye, I am so sorry about the diagnostic fiasco that Jason had to undergo. I have had no experience with brainstem infarcts in a young person although I have seen brainstem strokes in adults. They have seldom been associated with the intermittent agitation (kicking and screaming) that you describe. Thank you for the report of from Saposnik, et al. (2001) which describes the symptoms more like what I have seen. There may be decerebrate posturing (extensor rigidity) and clonic quivering. The fact that Jason was "kicking and screaming" really puzzles me because a serious brainstem stroke should have precluded either of those behaviors.

    Did they give intravenous dilantin? To my knowledge, the side-effects of the intravenous dilantin administration are not due to the dilantin itself but the solvent for the dilantin solution which is alkaline (sodium hydroxide), contains 40% polypropylene glycol, and 10% ethanol. That is one of the reasons why there is preference for fosphenytoin which is a "pro-drug" from of dilantin and is more soluble in saline.
    http://www.surgicalcriticalcare.net/...sphenytoin.pdf

    Wise.
    Yes, the dilantin was intravenous. And thank you for noting the diagnostic fiasco Jason underwent.
    With regard to Sapostic's article, he specifically mentions that the convulsion type movements can vary in nature and frequency:
    These movements vary in nature, frequency, and trigger, including fasciculation-like, shivering, jerky, tonic-clonic, and intermittent shaking movements. Some are interpreted as decerebrate postures or seizures.
    For about an hour or two before the kicking and screaming episodes, Jason had what the nurse and I in the ER indentified as short episodes of the "decerebrate postures", while screaming. ( Obviously, this is where I asked for a neurologist to come in immediately, but none was requested by the ER doc as he was busy treating breathing problems with asthmatic patients etc. in a very busy ER setting)

    You are right though, that most articles refer to low amplitude repetitive movements, whereas the kicking certainly isn't a low ampititude movement.
    The first movements that came back to Jason about 9 months after the stroke were the "stepping reflex of a new born baby".
    The kicking during the acute stage resembled that reflex type pattern.

    As a matter of fact when Jason "walked" into the ER (before I picked him up to carry him in), he walked with an exaggerated "stepping" movement, lifting his legs more than necessary for normal walking. And before that at home, Jason's main symptoms had been shivering.

    WOW, while I just did another search for an article that did describe the repetitive movements like kicking that I had found, I found another article of successful treatment of a boy ( 18 years old)injured in a soccer collision in Chili and published in 1999:
    http://www.alasbimnjournal.cl/revistas/5/mena5.htm

    Excerpt From this Chili case:
    In the posterior circulation, there does not exist a limit as to the amount of time elapse from the beginning of the symptoms to perform thrombolysis, like exists in the anterior circulation of 3-6 hours.....as an anecdotal observation, it may be that neuronal tissue in the pons, which is predominantly axonal, may be less vulnerable to isquemia.
    The article we used in our legal case was a successful treatment of a 11 year old boy injured in a soccer collision in Istanbul or Ankara, Turkey, which was published in the Jan. 1997 issue of Pediatric Neurology, and ironically was THE CURRENT issue, readily available to the pediatric neurologist when Jason arrived at Shands hospital in Gainesville FL, just 16 hours after onset.


    It always amazes me that the US has a reputation of "the best" medical system/care. AND I guess those hyper-extension injuries from soccer collisions are far more "common" than thought.
    Last edited by Faye; 01-03-2006 at 12:24 PM.

    "There’s far too much unthinking respect given to authority,” Molly Ivins explained; “What you need is sustained outrage.”
    Kerr, Keirstead, McDonald, Stice and Jun Yan courageously work on ESCR to Cure SCI.

    Divisiveness comes from not following Christopher Reeve's ESCR lead.
    Young does ASCR.
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  8. #58
    Faye,

    The reason that I am puzzled is because screaming is definitely not a reflexive activity. It requires an intact cerebrum and coordinated control of respiration and the vocal cords, as well as communication with an intact lower brainstem where 10th and 11th cranial nuclei are located. This suggests strongly to me that he did not have a severe brainstem infarct when he was doing this. The fact that he walked into the ER likewise strongly argues against a significant brainstem infarct at that time. Does the MRI scan localize the infarct to any specific location, such as the pons?

    The exaggerating stepping sometimes occur when there has been some compromise of the cerebellospinal tracts. For example, rats that recover from damage to these tracts often show what we call "mud-walking" where they appear to pull their legs too high up when they are stepping, as if they are stepping in deep mud.

    Wise.

    Quote Originally Posted by Faye
    Yes, the dilantin was intravenous. And thank you for noting the diagnostic fiasco Jason underwent.
    With regard to Sapostic's article, he specifically mentions that the convulsion type movements can vary in nature and frequency:

    For about an hour or two before the kicking and screaming episodes, Jason had what the nurse and I in the ER indentified as short episodes of the "decerebrate postures", while screaming. ( Obviously, this is where I asked for a neurologist to come in immediately, but none was requested by the ER doc as he was busy treating breathing problems with asmatic patients etc. in a very busy ER setting)

    You are right though, that most articles refer to low amplitude repetitive movements, whereas the kicking certainly isn't a low ampititude movement.
    The first movements that came back to Jason about 9 months after the stroke were the "stepping reflex of a new born baby".
    The kicking during the acute stage resembled that reflex type pattern.

    As a matter of fact when Jason "walked" into the ER, before I picked him up to carry him, he walked with an exaggerated "stepping" movement, lifting his legs more than necessary for normal walking.

    WOW, while I just did another search for an article that did describe the repetitive movements like kicking that I had found, I found another article of successful treatment of a boy ( 18 years old)injured in a soccer collision in Chili and published in 1999:
    http://www.alasbimnjournal.cl/revistas/5/mena5.htm


    The article we used in our legal case was a successful treatment of a 11 year old boy injured in a soccer collision in Istanbul or Ankara, Turkey, which ironically was published in the Jan. 1997 issue of Pediatric Neurology, when Jason arrived at Shands hospital in Gainesville FL, just 16 hours after onset.

    Excerpt From this Chili case:


    It always amazes me that the US has a reputation of "the best" medical system/care. AND I guess those hyper-extension injuries from soccer collisions are far more "common" than thought.

  9. #59
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    Quote Originally Posted by Wise Young
    Faye,

    Does the MRI scan localize the infarct to any specific location, such as the pons?
    The angiogram ( corrected from MRA as I originally posted in this post) of the turkish boy and Jason's are interchangeable. When my lawyer presented the case, he said it was like the article described Jason's case exactly. BTW, I was the one who supplied my lawyer with that article. Oftentimes it is a client who does much of the "foot" work for them, lawyers simply aren't that eager to waste their money on a case without merit. And many of them don't have the medical expertise well-informed parents have.

    Quote Originally Posted by Wise Young
    The exaggerating stepping sometimes occur when there has been some compromise of the cerebellospinal tracts. For example, rats that recover from damage to these tracts often show what we call "mud-walking" where they appear to pull their legs too high up when they are stepping, as if they are stepping in deep mud.

    Wise.
    Good observation! The exaggerated stepping most likely occured when activity in his middle cerebellar peduncle was compromised as a result of the basilar artery occlusion.

    On MRI there are only two lesions in the middle rostral part of the pons and in the ( right or left, I can't remember) middle cerebellar peduncle.

    And yes you are right, the fact that Jason walked into the ER is not indicative of a significant brainstem infarct. It actually shows that the cortico-spinal tracts in his pons were salvageable had he received prompt and adequate treatment for the basilar artery occlusion that was still developing.
    Last edited by Faye; 01-03-2006 at 01:09 PM.

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    Kerr, Keirstead, McDonald, Stice and Jun Yan courageously work on ESCR to Cure SCI.

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  10. #60
    Hey I am sorry that I am only half-way reading this. Faye you will understand there are three teenagers yelling at me that "we" forgot the x box controllers at their fathers earlier. Am I reading it right that the reason Jason was walking at first is because his infarct was in fact evolving as you were bringing him in? Most of us treat adults. I have seen no evolving strokes in kids but I have in adults. Regardless, its a nightmare and terrible. I will read this thread better tonight after we rectify this "important teenage issue" over here. Take care. Be well,

    Mary
    1FineSpineRN

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