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Thread: ICH suffered by father

  1. #1

    ICH suffered by father

    Dear Dr. Wise

    I am writing to ask you for your opinion regarding what I should do next with my father- in terms of treatment options. My father suffered a severy ICH 8 weeks ago and is in what I am reading to be a vegetative state. I am not getting a lot of information at the hospital he is in.

    He has sleep-wake cycles, reflexive movements only (sometimes to touch), eyes stay open longer and longer and very sluggish response to light stimuli, he grimaces sometimes, the ability to swallow is visible. He is receiving care at the hospital to avoid bed sores, some passive physiotherapy and general nursing care. He has thankfully no other complications.

    What would you recommend at this stage? Should he continue to remain where he is or should I look for rehab programs that help patients in this condition emerge from an unconsious or semi consious state? Are these programs reliable in general? Would you be able to recommend any programs outside the United States?

    Any advice is most appreciated.

  2. #2
    I would encourage you to get him evaluated for a good TBI or severe stroke rehabilitation program (ideally one that is CARF accredited for TBI rehab), although he appears to be very low functioning at this time. If he is making any improvements on his own, he may benefit from such a program. Be sure it is an acute rehabilitation program, not just a sub-acute (nursing home) based program.

    (KLD)

  3. #3
    Quote Originally Posted by Strokepatient View Post
    Dear Dr. Wise

    I am writing to ask you for your opinion regarding what I should do next with my father- in terms of treatment options. My father suffered a severy ICH 8 weeks ago and is in what I am reading to be a vegetative state. I am not getting a lot of information at the hospital he is in.

    He has sleep-wake cycles, reflexive movements only (sometimes to touch), eyes stay open longer and longer and very sluggish response to light stimuli, he grimaces sometimes, the ability to swallow is visible. He is receiving care at the hospital to avoid bed sores, some passive physiotherapy and general nursing care. He has thankfully no other complications.

    What would you recommend at this stage? Should he continue to remain where he is or should I look for rehab programs that help patients in this condition emerge from an unconsious or semi consious state? Are these programs reliable in general? Would you be able to recommend any programs outside the United States?

    Any advice is most appreciated.
    I agree with SCI-Nurse. At the present, there is little that medicine has to offer to patients who are in such a state. There have been some trials of deep brain stimulation but it is unclear whether such stimulation makes a difference. A number of groups are conducting clinical trials of various types of stem cells but the results are not in. Your goal should be to provide the best care for your father possible and hope that he gets better. The chances are low, however. I personally don't know any programs in the United States. Wise.

  4. #4
    I know of several groups in Taiwan, Japan, England, and Germany that are giving G-CSF (a bone marrow stimulating hormone) to patients with severe stroke. This is a well-known and oft-used drug used to increase the number of bone marrow stem cells in blood. For example, G-CSF is given to patients when collecting CD34+ cells from the peripheral blood for the purposes of bone marrow transplants. In any case, this increases the amount of circulating stem cells in his blood stream. However, G-CSF may have several side-effects, including many white cells in the blood and must be given by a doctor who is experienced with its use and can monitor the effects. Here is a list of abstracts of papers on the subject, if you want to talk to his doctors about the therapy.

    • 1. Moriya Y, Mizuma A, Uesugi T, Ohnuki Y, Nagata E, Takahashi W, Kobayashi H, Kawada H, Ando K, Takagi S and Takizawa S (2012). Phase I Study of Intravenous Low-dose Granulocyte Colony-stimulating Factor in Acute and Subacute Ischemic Stroke. Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association Division of Neurology, Department of Internal Medicine, Tokai University School of Medicine, Kanagawa, Japan. BACKGROUND: Granulocyte colony-stimulating factor (G-CSF; filgrastim) may be useful for the treatment of acute ischemic stroke because of its neuroprotective and neurogenesis-promoting properties, but an excessive increase of neutrophils may lead to brain injury. We examined the safety and tolerability of low-dose G-CSF and investigated the effectiveness of G-CSF given intravenously in the acute phase (at 24 hours) or subacute phase (at 7 days) of ischemic stroke. METHODS: Three intravenous dose regimens (150, 300, or 450 mug/body/day, divided into 2 doses for 5 days) of G-CSF were examined in 18 patients with magnetic resonance imaging (MRI)-confirmed infarct in the territory of the middle cerebral artery. Nine patients received the first dose at 24 hours poststroke (acute group) and 9 patients received the first dose on day 7 poststroke (subacute group; n = 3 at each dose in each group). A scheduled administration of G-CSF was skipped if the patient's leukocyte count exceeded 40,000/muL. Patients received neurologic and MRI examinations. RESULTS: We found neither serious adverse event, drug-related platelet reduction nor splenomegaly. Leukocyte levels remained below 40,000/muL at 150 and 300 mug G-CSF/body/day, but rose above 40,000/muL at 450 mug G-CSF/body/day. Neurologic function improvement between baseline and day 90 was more marked after treatment in the acute phase versus the subacute phase (Barthel index 49.4 +/- 28.1 v 15.0 +/- 22.0; P < .01). CONCLUSIONS: Low-dose G-CSF (150 and 300 mug/body/day) was safe and well tolerated in ischemic stroke patients, and leukocyte levels remained below 40,000/muL.

    • Duelsner A, Gatzke N, Glaser J, Hillmeister P, Li M, Lee EJ, Lehmann K, Urban D, Meyborg H, Stawowy P, Busjahn A, Nagorka S, Persson AB and Buschmann IR (2012). Granulocyte colony-stimulating factor improves cerebrovascular reserve capacity by enhancing collateral growth in the circle of Willis. Cerebrovascular diseases 33: 419-29. Department of Internal Medicine, Cardiology and Angiology, Richard Thoma Laboratories for Arteriogenesis, Center for Cardiovascular Research, Charite-Universitatsmedizin Berlin, Berlin, Germany. andre.duelsner@charite.de. BACKGROUND AND PURPOSE: Restoration of cerebrovascular reserve capacity (CVRC) depends on the recruitment and positive outward remodeling of preexistent collaterals (arteriogenesis). With this study, we provide functional evidence that granulocyte colony-stimulating factor (G-CSF) augments therapeutic arteriogenesis in two animal models of cerebral hypoperfusion. We identified an effective dosing regimen that improved CVRC and stimulated collateral growth, thereby improving the outcome after experimentally induced stroke. METHODS: We used two established animal models of (a) cerebral hypoperfusion (mouse, common carotid artery ligation) and (b) cerebral arteriogenesis (rat, 3-vessel occlusion). Following therapeutic dose determination, both models received either G-CSF, 40 mug/kg every other day, or vehicle for 1 week. Collateral vessel diameters were measured following latex angiography. Cerebrovascular reserve capacities were assessed after acetazolamide stimulation. Mice with left common carotid artery occlusion (CCAO) were additionally subjected to middle cerebral artery occlusion, and stroke volumes were assessed after triphenyltetrazolium chloride staining. Given the vital role of monocytes in arteriogenesis, we assessed (a) the influence of G-CSF on monocyte migration in vitro and (b) monocyte counts in the adventitial tissues of the growing collaterals in vivo. RESULTS: CVRC was impaired in both animal models 1 week after induction of hypoperfusion. While G-CSF, 40 mug/kg every other day, significantly augmented cerebral arteriogenesis in the rat model, 50 or 150 mug/kg every day did not show any noticeable therapeutic impact. G-CSF restored CVRC in mice (5 +/- 2 to 12 +/- 6%) and rats (3 +/- 4 to 19 +/- 12%). Vessel diameters changed accordingly: in rats, the diameters of posterior cerebral arteries (ipsilateral: 209 +/- 7-271 +/- 57 mum; contralateral: 208 +/- 11-252 +/- 28 mum) and in mice the diameter of anterior cerebral arteries (185 +/- 15-222 +/- 12 mum) significantly increased in the G-CSF groups compared to controls. Stroke volume in mice (10 +/- 2%) was diminished following CCAO (7 +/- 4%) and G-CSF treatment (4 +/- 2%). G-CSF significantly increased monocyte migration in vitro and perivascular monocyte numbers in vivo. CONCLUSION: G-CSF augments cerebral collateral artery growth, increases CVRC and protects from experimentally induced ischemic stroke. When comparing three different dosing regimens, a relatively low dosage of G-CSF was most effective, indicating that the common side effects of this cytokine might be significantly reduced or possibly even avoided in this indication.

    • Abe K, Yamashita T, Takizawa S, Kuroda S, Kinouchi H and Kawahara N (2012). Stem cell therapy for cerebral ischemia: from basic science to clinical applications. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 32: 1317-31. Department of Neurology, Okayama University Medical School, Okayama, Japan. abekabek@cc.okayama-u.ac.jp. Recent stem cell technology provides a strong therapeutic potential not only for acute ischemic stroke but also for chronic progressive neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis with neuroregenerative neural cell replenishment and replacement. In addition to resident neural stem cell activation in the brain by neurotrophic factors, bone marrow stem cells (BMSCs) can be mobilized by granulocyte-colony stimulating factor for homing into the brain for both neurorepair and neuroregeneration in acute stroke and neurodegenerative diseases in both basic science and clinical settings. Exogenous stem cell transplantation is also emerging into a clinical scene from bench side experiments. Early clinical trials of intravenous transplantation of autologous BMSCs are showing safe and effective results in stroke patients. Further basic sciences of stem cell therapy on a neurovascular unit and neuroregeneration, and further clinical advancements on scaffold technology for supporting stem cells and stem cell tracking technology such as magnetic resonance imaging, single photon emission tomography or optical imaging with near-infrared could allow stem cell therapy to be applied in daily clinical applications in the near future.

    • England TJ, Abaei M, Auer DP, Lowe J, Jones DR, Sare G, Walker M and Bath PM (2012). Granulocyte-colony stimulating factor for mobilizing bone marrow stem cells in subacute stroke: the stem cell trial of recovery enhancement after stroke 2 randomized controlled trial. Stroke; a journal of cerebral circulation 43: 405-11. Stroke Trials Unit, University of Nottingham, Nottingham, United Kingdom. BACKGROUND AND PURPOSE: Granulocyte-colony stimulating factor (G-CSF) is neuroprotective in experimental stroke and mobilizes CD34(+) peripheral blood stem cells into the circulation. We assessed the safety of G-CSF in recent stroke in a phase IIb single-center randomized, controlled trial. METHODS: G-CSF (10 mug/kg) or placebo (ratio 2:1) was given SC for 5 days to 60 patients 3 to 30 days after ischemic or hemorrhagic stroke. The primary outcome was the frequency of serious adverse events. Peripheral blood counts, CD34(+) count, and functional outcome were measured. MRI assessed lesion volume, atrophy, and the presence of iron-labeled CD34(+) cells reinjected on day 6. RESULTS: Sixty patients were recruited at mean of 8 days (SD +/- 5) post ictus, with mean age 71 years (+/- 12 years) and 53% men. The groups were well matched for baseline minimization/prognostic factors. There were no significant differences between groups in the number of participants with serious adverse events: G-CSF 15 (37.5%) of 40 versus placebo 7 (35%) of 20, death or dependency (modified Rankin Score: G-CSF 3.3 +/- 1.3, placebo 3.0 +/- 1.3) at 90 days, or the number of injections received. G-CSF increased CD34(+) and total white cell counts of 9.5- and 4.2-fold, respectively. There was a trend toward reduction in MRI ischemic lesion volume with respect to change from baseline in G-CSF-treated patients (P=0.06). In 1 participant, there was suggestion that labeled CD34(+) cells had migrated to the ischemic lesion. CONCLUSIONS: This randomized, double-blind, placebo-controlled trial suggests that G-CSF is safe when administered subacutely. It is feasible to label and readminister iron-labeled CD34(+) cells in patients with ischemic stroke. CLINICAL TRIAL REGISTRATION: URL: www.controlled-trials.com. Unique identifier: ISRCTN63336619.

    • Prasad K, Kumar A, Sahu JK, Srivastava MV, Mohanty S, Bhatia R, Gaikwad SB, Srivastava A, Goyal V, Tripathi M, Bal C and Mishra NK (2011). Mobilization of Stem Cells Using G-CSF for Acute Ischemic Stroke: A Randomized Controlled, Pilot Study. Stroke research and treatment 2011: 283473. Department of Neurology, Room No. 704, Neurosciences Centre, All India Institute of Medical Sciences, Ansari Nagar, New Delhi 110029, India. Background. There is emerging evidence to support the use of granulocyte colony-stimulating factor (G-CSF) therapy in patients with acute ischemic stroke. Aims. To explore feasibility, safety, and preliminary efficacy of G-CSF therapy in patients with acute ischemic stroke. Patients and Method. In randomized study, 10 patients with acute ischemic stroke were recruited in 1 : 1 ratio to receive 10 mug/kg G-CSF treatment subcutaneously daily for five days with conventional care or conventional treatment alone. Efficacy outcome measures were assessed at baseline, one month, and after six months of treatment included Barthel Index (BI), National Institute of Health Stroke Scale, and modified Rankin Scale. Results. One patient in G-CSF therapy arm died due to raised intracranial pressure. No severe adverse effects were seen in rest of patients receiving G-CSF therapy arm or control arm. No statistically significant difference between intervention and control was observed in any of the scores though a trend of higher improvement of BI score is seen in the intervention group. Conclusion. Although this study did not have power to examine efficacy, it provides preliminary evidence of potential safety, feasibility, and tolerability of G-CSF therapy. Further studies need to be done on a large sample to confirm the results.

    • Boy S, Sauerbruch S, Kraemer M, Schormann T, Schlachetzki F, Schuierer G, Luerding R, Hennemann B, Orso E, Dabringhaus A, Winkler J and Bogdahn U (2011). Mobilisation of hematopoietic CD34+ precursor cells in patients with acute stroke is safe--results of an open-labeled non randomized phase I/II trial. PLoS ONE 6: e23099. Department of Neurology, University of Regensburg, Bezirksklinikum Regensburg, Regensburg, Germany. sandra.boy@medbo.de. BACKGROUND: Regenerative strategies in the treatment of acute stroke may have great potential. Hematopoietic growth factors mobilize hematopoietic stem cells and may convey neuroprotective effects. We examined the safety, potential functional and structural changes, and CD34(+) cell-mobilization characteristics of G-CSF treatment in patients with acute ischemic stroke. METHODS AND RESULTS: Three cohorts of patients (8, 6, and 6 patients per cohort) were treated subcutaneously with 2.5, 5, or 10 microg/kg body weight rhG-CSF for 5 consecutive days within 12 hrs of onset of acute stroke. Standard treatment included i.v. thrombolysis. Safety monitoring consisted of obtaining standardized clinical assessment scores, monitoring of CD34(+) stem cells, blood chemistry, serial neuroradiology, and neuropsychology. Voxel-guided morphometry (VGM) enabled an assessment of changes in the patients' structural parenchyma. 20 patients (mean age 55 yrs) were enrolled in this study, 5 of whom received routine thrombolytic therapy with r-tPA. G-CSF treatment was discontinued in 4 patients because of unrelated adverse events. Mobilization of CD34(+) cells was observed with no concomitant changes in blood chemistry, except for an increase in the leukocyte count up to 75,500/microl. Neuroradiological and neuropsychological follow-up studies did not disclose any specific G-CSF toxicity. VGM findings indicated substantial atrophy of related hemispheres, a substantial increase in the CSF space, and a localized increase in parenchyma within the ischemic area in 2 patients. CONCLUSIONS: We demonstrate a good safety profile for daily administration of G-CSF when begun within 12 hours after onset of ischemic stroke and, in part in combination with routine i.v. thrombolysis. Additional analyses using VGM and a battery of neuropsychological tests indicated a positive functional and potentially structural effect of G-CSF treatment in some of our patients. TRIAL REGISTRATION: German Clinical Trial Register DRKS 00000723.

    • Floel A, Warnecke T, Duning T, Lating Y, Uhlenbrock J, Schneider A, Vogt G, Laage R, Koch W, Knecht S and Schabitz WR (2011). Granulocyte-colony stimulating factor (G-CSF) in stroke patients with concomitant vascular disease--a randomized controlled trial. PLoS ONE 6: e19767. Department of Neurology, Charite-Universitatsmedizin Berlin, Berlin, Germany. agnes.floeel@charite.de. BACKGROUND: G-CSF has been shown in animal models of stroke to promote functional and structural regeneration of the central nervous system. It thus might present a therapy to promote recovery in the chronic stage after stroke. METHODS: Here, we assessed the safety and tolerability of G-CSF in chronic stroke patients with concomitant vascular disease, and explored efficacy data. 41 patients were studied in a double-blind, randomized approach to either receive 10 days of G-CSF (10 microg/kg body weight/day), or placebo. Main inclusion criteria were an ischemic infarct >4 months prior to inclusion, and white matter hyperintensities on MRI. Primary endpoint was number of adverse events. We also explored changes in hand motor function for activities of daily living, motor and verbal learning, and finger tapping speed, over the course of the study. RESULTS: Adverse events (AEs) were more frequent in the G-CSF group, but were generally graded mild or moderate and from the known side-effect spectrum of G-CSF. Leukocyte count rose after day 2 of G-CSF dosing, reached a maximum on day 8 (mean 42/nl), and returned to baseline 1 week after treatment cessation. No significant effect of treatment was detected for the primary efficacy endpoint, the test of hand motor function. CONCLUSIONS: These results demonstrate the feasibility, safety and reasonable tolerability of subcutaneous G-CSF in chronic stroke patients. This study thus provides the basis to explore the efficacy of G-CSF in improving chronic stroke-related deficits. TRIAL REGISTRATION: ClinicalTrials.gov NCT00298597.

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