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    HGH & testosterone

    I am curious i know methlyprednisolone is given for swelling which in my scarce knowledge is just a very fast acting steroid.

    What's the idea of using standard tesosterone with intense therapy? All that tissue regenerating certainly it might assist with good blood flow to injury areas. If your working the lowest muscle areas you can still control.

    Also using Growth hormone at the same time couldn't hurt in my mind. Especaially if your young and healthy.

    Isn't the spinal cord simply not repairing itself because of a damn protein that says no healing? Well taking steroids that modify and slow down protein synthesis might influence those proteins and inhibit spinal nueron growth?

    Who knows just ideas that flow through my mind

    Hi Varian, there are two types of steroids, anabolic steroids - the type taken to increase muscle bulk and corticosteroids which are potent anti-inflammatory agents and immune regulators. Methylprednisone is a corticosteroid, it is given to SCI's during the acute phase to reduce the inflammation caused by trauma or injury to the spinal cord. Testosterone or 'andro' may increase serum testosterone levels but unless your levels are low to begin with, its affects could be deleterious. A general search should answer your questions regarding the use of anabolics as adjuncts to PT, a search for HGH turned up 17 topics, human growth hormone turned up 61 and testosterone 194.



      Testosterone may have beneficial effects on spinal cord injury but for reasons other than you think. But, before anybody goes rushing off to take supplemental testosterone, let me say that there is no evidence that testosterone improve neurological recovery in chronic spinal cord injury. Most of the work has focused on the effects of testosterone on acute spinal cord injury, protection of neurons that have had their axons injured, the peripheral effects of testosterone on sperm production and muscle, and the studies of testosterone levels in men with spinal cord injury. Some recent abstracts that might be of interest are listed below:

      Effects of testosterone on sperm and semen:
      • Huang HF, Li MT, Wang S, Barton B, Anesetti R and Jetko JA (2004). Effects of exogenous testosterone on testicular function during the chronic phase of spinal cord injury: dose effects on spermatogenesis and Sertoli cell and sperm function. J Spinal Cord Med. 27: 55-62. Veterans Affairs Medical Center, East Orange, New Jersey, USA. INTRODUCTION: Exogenous testosterone has been shown to attenuate spinal cord injury (SCI)-related regression of spermatogenesis in the rat. The current experiment investigated the effects of exogenous testosterone in testicular and sperm functions in the rat during the chronic phase of SCI. METHODS: Chronic SCI rats were given subcutaneous implants of testosterone-filled silastic capsules (TC). Northern blot cDNA hybridization was used to measure testicular levels of Sertoli cell- and germ cell-specific transcripts. Western blot and immunohistochemistry were used to determine protein level and cellular localization, respectively, of cyclic adenosine monophosphate-responsive element modulator (CREM) in the testes. Flow cytometry was used to determine sperm viability and mitochondrial potential. RESULTS: Spontaneous restoration of spermatogenesis occurred in 7 of the 8 untreated SCI rats. Although exogenous testosterone restored complete spermatogenesis in all SCI rats, regressed seminiferous epithelium remained in 30% to 70% of tubular cross sections in these rats. These effects were associated with altered responses of germ cell-specific mRNA transcripts to exogenous testosterone, and abnormal cellular distribution of CREM. Sperm of untreated SCI rats exhibited lowered motility, viability, and mitochondrial potential. Implantation of 10 cm of TC worsened sperm motility in sham control and SCI rats, but restored sperm viability and mitochondrial potential in SCI rats. CONCLUSION: Administration of exogenous testosterone to SCI rats during the chronic phase of injury failed to facilitate spermatogenic restoration over that achieved in untreated SCI rats. Abnormalities in postmeiotic spermatogenic differentiation could contribute to these effects, and perhaps the production of sperm with abnormal morphology and/or functions during the chronic phase of SCI.
      • Huang HF, Wang S, Molina CA and Ottenweller JE (2004). Preservation of spermatogenesis in spinal cord injured rats with exogenous testosterone. Relationship with serum testosterone levels and cellular localization of cAMP responsive element modulator. J Androl. 25: 95-103. Veterans Affairs Medical Center, East Orange, New Jersey 07103, USA. The current experiment examined the effects of exogenous testosterone (T) on spermatogenesis in rats with spinal cord injury (SCI) and their relationship with the cellular distribution of a cyclic AMP-responsive element modulator (CREM) in testicular cells. Implantation of T-filled Silastic capsules (TCs, 1-20 cm) resulted in dose-dependent, biphasic changes in testicular T levels and spermatogenesis in SCI rats. However, dose responsiveness of spermatogenesis to exogenous T in SCI rats differed from that in sham control rats. Specifically, implantation of 2-cm TCs enhanced the effects of SCI on spermatogenesis, resulting in total regression of the seminiferous epithelium. Although 3-cm TCs maintained complete spermatogenesis in sham control rats, this regimen failed to support complete spermatogenesis in SCI rats. Although complete spermatogenesis was maintained in SCI rats given 5-20-cm TC implants, various abnormalities persisted. Cellular distribution of CREM remained normal in SCI rats but was altered in those SCI rats that received 3- or 5-cm TC implants. Such effects were associated with reduced CREM proteins in testicular tissues. These results were consistent with altered cAMP signaling and its regulation in testicular cells after SCI and provided possible mechanistic explanations for the effects of SCI on spermatogenesis. CONCLUSION: SCI resulted in changes in the responsiveness of spermatogenesis to exogenous T. These effects were associated with altered cAMP/CREM signaling in testicular cells. Further studies, including a study of the relationship between serum T levels and normalcy of sperm functions and the role of neural-endocrine interactions in mediating the effects of SCI on spermatogenesis and sperm function, are needed so that therapeutic regimens can be designed for clinical use.
      • Huang HF, Li MT, Wang S, Pogach LM and Ottenweller JE (2003). Alteration of cyclic adenosine 3',5'-monophosphate signaling in rat testicular cells after spinal cord injury. J Spinal Cord Med. 26: 69-78. Veterans Affairs Medical Center, East Orange, New Jersey, USA. INTRODUCTION: Earlier studies demonstrated that the effects of spinal cord injury (SCI) on spermatogenesis were associated with altered Sertoli cell responses to treatment with follicle-stimulating hormone (FSH) and/or testosterone (T). Because of the importance of the cyclic adenosine 3',5'-monophosphate (cAMP) signal pathway in hormonal actions on Sertoli cells and spermatogenesis, the purpose of this study was to determine whether cAMP signaling in testicular cells is altered after SCI. METHODS: Rats with SCI were treated with FSH, T, or FSH + T for 7 or 14 days. Northern blot cDNA hybridization was used to measure testicular levels of Sertoli and germ cell-specific transcripts encoded by genes that contain cAMP responsive element (CRE) and/or steroid hormone responsive element (HRE). Cellular distribution of CRE modulator (CREM) was determined by immunohistochemistry. RESULTS: Treatment of sham control rats with FSH or T + FSH for 2 weeks resulted in decreases in mRNAs for CREM and CRE binding protein (CREB). Concomitantly, levels of mRNA for Sertoli cell inhibin alpha and germ cell-specific protamine 1 (Pm-1), transition protein 2 (TP-2), and lactate dehydrogenase C (LDHC) were all reduced. In contrast, identical FSH and/or T treatments resulted in increases in levels of CREM and CREB mRNAs in the testes of SCI rats; these effects were associated with similar changes in mRNAs for inhibin alpha, Pm-1, TP-2, and LDHC. The effects of SCI on CREM expression were corroborated by similar changes in its distribution in testicular cells. CONCLUSION: SCI is associated with changes in FSH and/or T regulation of cAMP/CRE and HRE signaling in testicular cells. These effects may mediate the effects of SCI on spermatogenesis.

      Protection of motoneurons
      • Fargo KN and Sengelaub DR (2004). Testosterone manipulation protects motoneurons from dendritic atrophy after contralateral motoneuron depletion. J Comp Neurol. 469: 96-106. Department of Psychology and Program in Neural Science, Indiana University, Bloomington, Indiana 47405, USA. Dendritic morphology is reactive to many kinds of injuries, including axotomy and deafferentation. In this study, we examined the response of motoneurons in the spinal nucleus of the bulbocavernosus (SNB), an androgen-dependent population of motoneurons in the lumbar spinal cord of the rat, to partial motoneuron depletion. We depleted SNB motoneurons on one side only of the spinal cord by unilateral intramuscular injection of a retrogradely transported form of saporin, and examined the morphology of contralateral SNB motoneurons. Motoneuron morphology was assessed in normal control males, gonadally intact saporin-treated males, and saporin-treated males who had been castrated 6 weeks previously and given testosterone replacement beginning at the time of saporin injection. Untreated castrated males served as an additional control group. Four weeks after saporin treatment, SNB motoneurons contralateral to the saporin injection were retrogradely labeled with horseradish peroxidase conjugated to the cholera toxin B subunit and reconstructed in three dimensions. In gonadally intact males, unilateral motoneuron depletion caused regressive changes in contralateral SNB motoneurons: Soma size and dendritic length were both decreased. However, testosterone manipulation (i.e., castration followed by testosterone replacement) completely prevented the dendritic retraction. These data suggest a therapeutic role for testosterone in preventing, or accelerating recovery from, dendritic atrophy induced by motoneuron injury.
      • Brown TJ, Khan T and Jones KJ (1999). Androgen induced acceleration of functional recovery after rat sciatic nerve injury. Restor Neurol Neurosci. 15: 289-295. Research and Development Service, Hines VA Hospital, Hines, IL 60141, USA. PURPOSE: Testosterone (T) treatment accelerates recovery from facial paralysis after facial nerve crush in hamsters. In this study, we extended those studies to another injury model and asked the following question: Will T treatment accelerate recovery from lower limb paralysis following sciatic nerve crush in the rat? METHODS: Castrated adult male rats received a right side sciatic nerve crush at the level of the sciatic notch, with the left side serving as control. Half the animals received a subcutaneous implant of a propionated form of T (TP), the others were sham-implanted. Weekly testing using the Sciatic Functional Index (SFI), a quantitative measure of locomotion, was done for 7 weeks postoperative (wpo). RESULTS: Between 3 and 5 weeks post-op, the average SFI score of the TP-treated group was higher than controls. This difference was significant at 4 wpo, indicating an accelerated degree of functional recovery. At these timepoints, the differences were attributable to the footprint or paw length and associated with calf muscle reinnervation rather than the toespreading component associated with intrinsic foot muscle rein-nervation. Beyond 5 wpo, there were no differences in the SFI scores. CONCLUSION: The results indicate that, as with facial nerve regeneration in the hamster, testosterone accelerates functional recovery from hind limb paralysis following sciatic nerve injury in the rat. While the responses of spinal motoneurons to injury can differ from those of cranial motoneurons, in this case it appears that they share a similar response to the trophic actions of androgen. This is important in the context of designing therapeutic strategies for dealing with direct trauma to motoneurons resulting from both peripheral and central nervous system trauma, such as spinal cord injury.

      Endocrine profiles after spinal cord injury
      • Naderi AR and Safarinejad MR (2003). Endocrine profiles and semen quality in spinal cord injured men. Clin Endocrinol (Oxf). 58: 177-84. Department of Urology, Military University of Medical Sciences, Tehran, Iran. PURPOSE: To evaluate the hypothalamic-pituitary-testis (HPT) axis, endocrine profiles and semen quality in men with spinal cord injury (SCI). MATERIALS AND METHODS: Fifty-five men with SCI were studied. Serum levels of FSH, LH, testosterone, oestradiol and prolactin (PRL) were determined; the LH-releasing hormone (LHRH) stimulation test and a semen analysis were performed, and testicular volumes were measured. Thirty-six age-matched healthy male volunteers and 34 noninjured infertile men served as controls. RESULTS: Eight SCI subjects had low basal LH, four had low basal FSH, and 16 had decreased basal serum levels of LH and FSH. Of subjects with lower serum levels of gonadotrophins (LH and/or FSH), nine had low serum testosterone and seven had hyperprolactinaemia. Serum levels of oestradiol were similar for all groups. There were increased LH and FSH responses to LHRH in SCI subjects compared to normal controls, but this difference was only statistically significant in SCI subjects with lower than normal serum levels of LH and/or FSH. There was no significant difference in testis volume between SCI subjects and controls. The mean semen volume in SCI subjects was lower than from controls, but the difference was not statistically significant. Sperm motility and percent normal sperm morphology were lower in SCI compared to normal controls but not to infertile control subjects. In total, 51% and 86% of SCI subjects had at least one hormonal or axis abnormality, respectively. CONCLUSION: We conclude that hypogonadotropism in SCI subjects is likely to be secondary to altered neural or hormonal pathways between the hypothalamus and the pituitary gland, and that these endocrine abnormalities may be the mechanisms contributing to impairment of semen quality.
      • Benaim EA, Montoya JD, Saboorian MH, Litwiller S and Roehrborn CG (1998). Characterization of prostate size, PSA and endocrine profiles in patients with spinal cord injuries. Prostate Cancer Prostatic Dis. 1: 250-255. Department of Urology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas, USA. Aims of this study: From cross-sectional and longitudinal population based studies as well as from autopsy studies it is well documented that total prostate volume increases with advancing age. However, it is not well known (1) which factors are ultimately responsible for this growth phenomenon; or (2) at what time in a persons life the growth tends to occur. At present at least a permissive role for testicular androgens is assumed to be involved in growth regulation. Other factors such as growth factors, epithelial-mesenchymal interaction, and the role of intact neural pathways are still poorly understood. We aimed to study a group of men with spinal cord injuries to determine whether the pattern of prostate enlargement would be different in men with partially or completely interrupted innervation of the pelvis and the prostate gland. Materials and methods: Forty-three men from the Spinal Cord Injury (SCI) Service at the VA North Texas Health Care System ranging in age from 27-73 y (mean 51 y) were recruited to participate in this study. Time since SCI ranged from 2-47 (mean 19 y). All patients underwent standardized questionnaire, physical examination, transrectal ultrasonography (TRUS) measurements of total and transition zone volume of the prostate, serum PSA, testosterone (T), dihydrotestosterone (DHT), FSH and LH measurements, some had TRUS guided biopsies taken. Results: By all the measured criteria there were no abnormalities regarding the pituitary-gonadal axis observed in these men. Testicular volume, serum T, DHT and LH were within normal ranges, and when the patients were stratified by age, no differences were identified. There was an age related increase in FSH which has been described in neurologically intact men. Serum PSA increased slightly with advancing age. While total (TPV) and transition zone (TZV) prostate volume increased with age, the groupwise differences by decades of life were not significant. Moreover, when compared to a group of community dwelling men without known prostatic diseases and a clinic cohort of men with BPH, TPV was substantially lower for each decade of life except for men in their 40s, while TZV was substantially lower for men in their 60s. Conclusions: We observed normal age related changes regarding serum PSA and serum FSH without significant changes in other hormonal parameters. All parameters behaved consistent with changes described in neurologically intact populations. However, we did not observe the typical increase in TPV and TZV of the prostate as seen in population, autopsy and clinic patient studies. This interesting finding indicates that factors other than an intact pituitary-gonadal axis and male steroid hormones may be responsible for the normal age related growth of the prostate. Further studies in larger cohorts are needed to corroborate our findings.
      • Safarinejad MR (2001). Level of injury and hormone profiles in spinal cord-injured men. Urology. 58: 671-6. Department of Urology, Division of Urology and Renal Transplantation, Military University of Medical Sciences, Air Force Hospital, Tehran, Iran. OBJECTIVES: To evaluate the level of injury and endocrine profiles in men with spinal cord injury (SCI). METHODS: Seventy-six men with SCI at different levels were studied, using uninjured normal and infertile subjects as controls. RESULTS: Compared with normal controls, the subjects with SCI (50%) had lower serum levels of luteinizing hormone, follicle-stimulating hormone, and testosterone. Subjects with T8-T11 and T12-L5 injury had the highest and lowest incidence of hormonal abnormalities, respectively. All subjects with hyperprolactinemia (n = 5) had T8-T11 injuries. CONCLUSIONS: The results of our study indicate that subjects with SCI have an altered central neurotransmitter tone, and the likelihood of these abnormalities (hypogonadotropism) are higher in men with low thoracic SCI.

      Effect of testosterone replacement therapy on skeletal muscle after spinal cord injury:
      • Gregory CM, Vandenborne K, Huang HF, Ottenweller JE and Dudley GA (2003). Effects of testosterone replacement therapy on skeletal muscle after spinal cord injury. Spinal Cord. 41: 23-8. Department of Physical Therapy, Texas Women's University, Houston, Texas, TX 77030, USA. STUDY DESIGN: Randomized control. OBJECTIVE: To examine the effects of testosterone replacement therapy (TRT) on skeletal muscle 11 weeks after complete SCI. SETTING: Athens, Georgia USA. METHODS: Soleus (SOL), gastrocnemius (GA), tibialis anterior (TA), vastus lateralis (VL) and triceps brachii (TRI) muscles were taken from twelve young male Charles River rats 11 weeks after complete SCI (T-9 transection, n=8) or sham surgery (n=4). Rats received either TRT (two 5 cm capsules, n=4) or empty capsules (n=8) implanted at surgery. Muscle samples were sectioned and fibers analyzed qualitatively for myosin ATPase and quantitatively for succinate dehydrogenase (SDH), alpha-glycerol-phosphate dehydrogenase (GPDH) and actomyosin ATPase (qATPase) activities using standard techniques. RESULTS: SCI decreased average fiber size (49+/-4%) in affected muscles and the percentage of slow fibers in SOL (93+/-3% to 17+/-2%). In addition, there was a decrease in SDH and an increase in GPDH and qATPase activities across the four hind-limb muscles of the SCI animals. Fiber size in the TRI was increased (31+/-2%) by SCI while enzyme activities were not altered. Average fiber size across the four hind limb muscles was decreased by only 30% in TRT SCI animals and their SOL contained 39+/-2% slow fibers. TRT also attenuated changes in enzyme activities. There was no effect of TRT on the TRI relative to SCI. CONCLUSIONS: TRT was effective in attenuating alterations in myofibrillar proteins during 11 weeks of SCI in affected skelatal muscles. SPONSORSHIP: Supported by a grant from The National Institutes of Health (HD-33738) and HD-37645 to KV, and HD-39676 to GAD.
      • Talmadge RJ, Castro MJ, Apple DF, Jr. and Dudley GA (2002). Phenotypic adaptations in human muscle fibers 6 and 24 wk after spinal cord injury. J Appl Physiol. 92: 147-54. Muscle Function Laboratory, Virginia Polytechnic Institute and State University, Blacksburg, Virginia 24061, USA. The effects of spinal cord injury (SCI) on the profile of sarco(endo) plasmic reticulum calcium-ATPase (SERCA) and myosin heavy chain (MHC) isoforms in individual vastus lateralis (VL) muscle fibers were determined. Biopsies from the VL were obtained from SCI subjects 6 and 24 wk postinjury (n = 6). Biopsies from nondisabled (ND) subjects were obtained at two time points 18 wk apart (n = 4). In ND subjects, the proportions of VL fibers containing MHC I, MHC IIa, and MHC IIx were 46 +/- 3, 53 +/- 3, and 1 +/- 1%, respectively. Most MHC I fibers contained SERCA2. Most MHC IIa fibers contained SERCA1. All MHC IIx fibers contained SERCA1 exclusively. SCI resulted in significant increases in fibers with MHC IIx (14 +/- 4% at 6 wk and 16 +/- 2% at 24 wk). In addition, SCI resulted in high proportions of MHC I and MHC IIa fibers with both SERCA isoforms (29% at 6 wk and 54% at 24 wk for MHC I fibers and 16% at 6 wk and 38% at 24 wk for MHC IIa fibers). Thus high proportions of VL fibers were mismatched for SERCA and MHC isoforms after SCI (19 +/- 3% at 6 wk and 36 +/- 9% at 24 wk) compared with only ~5% in ND subjects. These data suggest that, in the early time period following SCI, fast fiber isoforms of both SERCA and MHC are elevated disproportionately, resulting in fibers that are mismatched for SERCA and MHC isoforms. Thus the adaptations in SERCA and MHC isoforms appear to occur independently.