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Thread: SCI & elevated prolactin levels

  1. #1
    Member Becky's Avatar
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    Jul 2001

    SCI & elevated prolactin levels

    After numerous blood tests and and MRI to rule out a growth on the pituitry gland, my doctor has given up on finding why my levels are so high. I just saw the old post about the thyroid & SCI, so now I am thinking that the SCI has something to do with it. Right after my SCI my menstral cycle was off and my prolactin levels were high, but they put me on provera to help start and sent me home. They figured the high levels were from a med. That was about 14 months ago. Then a few weeks ago to my surprise I noticed I am producing milk. At first I thought it was one of the meds I am on, but the doctor ruled that out. Blood tests were fine--only showed the elevated prolactin levels. And the MRI showed nothing. Is it reasonable to associate this with the SCI? Or could there possibly be another explaination?

  2. #2

    empty sella

    I had the same happen to me. I now have an empty sella, which is not supposed to cause any problems.


  3. #3
    Becky, a significant percentage of people have pituitary hormonal imbalances after spinal cord injury. I list several abstracts that summarize some of the findings. The last two papers by Yarkony, et al. and Berezin, et al. are particularly relevant. What medications are you on? One cause is medication induced...

    Cindy. What do you mean by an *empty* sella? The sella refers to the place where the pituitary gland is supposed to be!

    1. Campagnolo DI, Bartlett JA, Chatterton R, Jr. and Keller SE (1999). Adrenal and pituitary hormone patterns after spinal cord injury. Am J Phys Med Rehabil. 78 (4): 361-6. Summary: Current evidence indicates that the neuroendocrine system is the highest regulator of immune/inflammatory reactions. We hypothesized that immune alterations, which were related to the level of injury, found in a cohort of spinal cord-injured subjects may be influenced by altered hormonal patterns postinjury. Therefore, we investigated aspects of both pituitary and adrenal function in the same cohort of spinal cord-injured subjects. We found significant elevations in both cortisol and dehydroepiandrosterone sulfate in chronic spinal cord- injured survivors compared with their able-bodied age- and gender- matched controls. Levels of dehydroepiandrosterone, adrenocorticotropin, and prolactin were not different in spinal cord- injured subjects overall compared with their controls. Both dehydroepiandrosterone sulfate and dehydroepiandrosterone were higher in tetraplegics compared with their controls, but we found no such differences in paraplegics compared with their controls. When the two groups of spinal cord-injured subjects were compared with each other, we also found differences between these two subject groups in dehydroepiandrosterone sulfate and dehydroepiandrosterone (higher in the tetraplegics compared with paraplegics). We found no differences between either group of spinal cord-injured subjects and their controls for adrenocorticotropin, prolactin, or cortisol. These data suggest that some hormonal differences between subjects and their controls may be further related to the level of injury (specifically dehydroepiandrosterone and dehydroepiandrosterone). Finally, we investigated correlations within subjects for the above hormones. Dehydroepiandrosterone sulfate and prolactin were highly correlated (the higher the dehydroepiandrosterone sulfate, the higher the prolactin) but only in the tetraplegic subjects. <> Department of Physical Medicine and Rehabilitation, UMDNJ-New Jersey Medical School, Newark, New Jersey 07103-2406, USA.

    2. Huang TS, Wang YH, Lee SH and Lai JS (1998). Impaired hypothalamus-pituitary-adrenal axis in men with spinal cord injuries. Am J Phys Med Rehabil. 77 (2): 108-12. Summary: Twenty-five men with spinal cord injuries were studied for evaluation of the hypothalamus-pituitary-adrenal axis, using corticotropin- releasing hormone and insulin-induced hypoglycemia. Twenty-five age- matched healthy male volunteers served as controls. Three spinal cord- injured subjects had hyperprolactinemia, three had elevated basal follicle-stimulating hormone levels, one had an elevated basal luteinizing hormone level, and four had hypotestosteronemia. The mean plasma adrenocorticotropin response to corticotropin-releasing hormone of spinal cord-injured subjects was smaller than that of the healthy controls but did not reach a statistical significance. The cortisol response to corticotropin-releasing hormone of the spinal cord-injured subjects was significantly lower than that of healthy controls. However, the difference disappeared if a correction was made for baseline values. Six spinal cord-injured subjects did not have a cortisol response to insulin-induced hypoglycemia, and they had either a minimal or no adrenocorticotropin response. Another 11 spinal cord- injured subjects had a maximal cortisol response to insulin-induced hypoglycemia below the lowest limit of normal, i.e., 0.5 micromol/l. Among these spinal cord-injured subjects, three had a less than 50% increase of plasma adrenocorticotropin after insulin-induced hypoglycemia. These findings are consistent with the notion that spinal cord-injured subjects have an altered central neurotransmitter tone and substantiate the hypothesis that an afferent neural pathway exists between the adrenal and hypothalamus and may modulate stress-induced secretion of adrenocorticotropin. Long-term abnormal adrenocorticotropin secretion may cause mild adrenocortical atrophy and, thereby, a reduced cortisol response. <> Department of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Republic of China.

    3. Huang TS, Wang YH, Lai JS, Chang CC and Lien IN (1996). The hypothalamus-pituitary-ovary and hypothalamus-pituitary-thyroid axes in spinal cord-injured women. Metabolism. 45 (6): 718-22. Summary: Sixteen women with spinal cord injury (SCI) underwent studies of the hypothalamus-pituitary-ovary (HPO) and hypothalamus-pituitary-thyroid (HPT) axes with luteinizing hormone (LH) releasing hormone (LHRH) and thyrotropin (TSH) releasing hormone (TRH) stimulation tests during the early follicular phase. The mean interval from injury to participation in this study was 7.5 years (range, 1.5 to 13.1). All subjects were menstruating regularly. Five (35.7%) SCI subjects who were menstruating before injury had postinjury amenorrhea for 1 to 12 months, and the other nine (64.3%) SCI subjects had no interruption of menstruation after injury. Two SCI subjects whose injury occurred in preadolescence proceeded to menarche without any delay. The amount of menstrual flow was noted to be reduced in nine (64.3%) SCI subjects. Two and three SCI subjects had elevated follicle-stimulating hormone (FSH) and prolactin (PRL) levels, respectively. LH responses to LHRH were significantly higher in the SCI group (P < .001). Ten [62.6%) SCI subjects had enhanced LH responses to LHRH. The mean TSH, PRL, and FSH responses to TRH and LHRH of the SCI group were not significantly different from those of age-matched controls. However, five [31.2%), four [25.0%), and five [31.2%) SCI subjects had enhanced TSH, PRL, and FSH responses to TRH and LHRH, respectively. Six [37.5%) SCI subjects had a delayed FSH response to LHRH. In total, 13 [81.2%) SCI subjects had at least one axis abnormality. These findings are consistent with the hypothesis that changes of central neurotransmitters may occur after SCI. <> Department of Medicine, National Taiwan University Hospital, Taipei, Republic of China.

    4. Cruse JM, Keith JC, Bryant ML, Jr. and Lewis RE, Jr. (1996). Immune system-neuroendocrine dysregulation in spinal cord injury. Immunol Res. 15 (4): 306-14. Summary: Multiple communicative pathways among the nervous, endocrine and immune systems facilitate physiological immunoregulation. Spinal cord injury (SCI) patients have decreased natural (NK cell) and adaptive (T cell) immune function and reduced blood levels of cellular adhesion molecules (CAMs) that participate in immune function and wound healing. We found decreased LFA-1 and VLA-4 on peripheral blood leukocytes in SCI patients and lower levels of CAMs in SCI patients with pressure ulcers than in those without them. SCI might affect immune cells and immune responsiveness by: (1) disrupting the outflow of signals from the sympathetic nervous system to lymphoid tissues and their blood vessels as well as the returning afferent signals from these tissues to the brain; (2) immunosuppression caused by the stressors affecting SCI patients; (3) interrupting returning signals to the CNS from the periphery thereby reducing facilitation of immunoregulatory CNS neurons and decreasing their activity; or a combination of all three. SCI patients may develop dysregulation of the sympathetic nervous system that is intimately involved in immune function. Chronic stress mediates immunosuppression by corticosteroids, catecholamines, endorphins and met-enkephalin. The hypothalamus coordinates the response to stress through the release of soluble products from the sympathetic nervous system and hypothalamic-pituitary-adrenal axis. Whereas the nervous and endocrine systems are not concerned with immunological specificity, they do influence the intensity, kinetics and localization of immune responses. Products of an activated immune system may generate feedback circuits capable of inhibiting, enhancing or regulating neuronal input. Immune system cells can produce neurologically active peptides including ACTH, CRF, growth hormone, thyrotropin, prolactin, human chorionic gonadotropin, endorphin, enkephalins, substance P, somatostatin and VIP. Cytokines are likely important mediators of the HPA response to immune stimuli. <> Department of Pathology, University of Mississippi Medical Center, Jackson 39216, USA.

    5. Huang TS, Wang YH and Lien IN (1995). Suppression of the hypothalamus-pituitary somatotrope axis in men with spinal cord injuries. Metabolism. 44 (9): 1116-20. Summary: Thirty-two men with spinal cord injury (SCI) were studied for evaluation of the hypothalamus-pituitary somatotrope axis, using growth hormone-(GH)-releasing hormone (GHRH) and insulin-induced hypoglycemia. Twenty-six age-matched normal male volunteers served as controls. Six SCI subjects (18.7%) had elevated basal follicle-stimulating hormone (FSH) levels, eight (25.0%) had hyperprolactinemia, and 11 (34.4%) had reduced serum insulin-like growth factor-1 (IGF-1) levels. Twenty SCI subjects (62.5%) had reduced and/or delayed GH responses to GHRH, and eight (25.8%) had reduced GH response to insulin-induced hypoglycemia. Seven of eight hyperprolactinemic SCI subjects showed reduced GH response to GHRH and/or insulin-induced hypoglycemia. These findings are consistent with the notion that SCI subjects have a reduced central dopaminergic tone. <> Department of Medicine, National Taiwan University Hospital, Taipei, Republic of China.

    6. Huang TS, Wang YH, Chiang HS and Lien YN (1993). Pituitary-testicular and pituitary-thyroid axes in spinal cord-injured males. Metabolism. 42 (4): 516-21. Summary: Thirty spinal cord-injured (SCI) males were studied for evaluation of their pituitary-testicular and pituitary-thyroid axes using combined luteinizing hormone-releasing hormone (LHRH) and thyrotropin-releasing hormone (TRH) tests and electroejaculated semen analyses. Thirty age- matched normal male volunteers served as controls. There were four subjects with low serum triiodothyronine (T3) levels, one with elevated serum follicle-stimulating hormone (FSH) level, eight with elevated serum testosterone levels, and 11 with elevated serum prolactin levels. There were significantly elevated luteinizing hormone (LH) responses to LHRH in SCI subjects when compared with normal controls. There were 16 (53.3%) SCI subjects who had exaggerated and/or prolonged LH responses. Among them, six subjects also had elevated FSH responses. There were eight and four subjects whose thyrotropin (TSH) and prolactin responses to TRH were exaggerated, respectively. Marked impaired motility was observed in 56 electroejaculated semen samples from 16 SCI subjects. There was a significant correlation between LH and total sperm count. Our data suggest that there is a reduced central dopaminergic tone in SCI subjects. <> Department of Internal Medicine, National Taiwan University Hospital, Republic of China.

    7. Yarkony GM, Novick AK, Roth EJ, Kirschner KL, Rayner S and Betts HB (1992). Galactorrhea: a complication of spinal cord injury. Arch Phys Med Rehabil. 73 (9): 878-80. Summary: Galactorrhea, a secretion of milk or milk-like products from the breast in the absence of parturition, has been reported to occur in women with spinal cord injuries in association with amenorrhea and hyperprolactinemia. Four cases of galactorrhea in association with spinal cord injury are reported. Galactorrhea developed in four spinal cord injured women who had thoracic paraplegia. The onset of galactorrhea was from one month to five months after injury. Although the onset of galactorrhea may have been related to prescribed medications in all four cases, insufficient data exist to draw conclusions. The three women whose galactorrhea persisted declined treatment and galactorrhea continuing for more than two years in one instance. We conclude that galactorrhea with or without amenorrhea may develop after a spinal cord injury and that spinal cord injured women may have an enhanced sensitivity to medication-induced galactorrhea. <> Department of Rehabilitation Medicine, Northwestern University Medical School, Chicago, IL.

    8. Berezin M, Ohry A, Shemesh Y, Zeilig G and Brooks ME (1989). Hyperprolactinemia, galactorrhea and amenorrhea in women with a spinal cord injury. Gynecol Endocrinol. 3 (2): 159-63. Summary: Six women with a traumatic spinal cord injury (SCI) developed hyperprolactinemia, amenorrhea and galactorrhea. Five of them had thoracic level lesions and 1 had a lumbosacral lesion. Two were postpartum and 1 was pregnant at the time of injury. Transient diabetes insipidus developed in 1 patient. Temporary administration of bromocriptine decreased prolactin levels, caused cessation of lactation and restored ovulatory cycles. The syndrome disappeared spontaneously in all 6 patients. Pituitary stalk concussion resulting from the trauma might cause this phenomenon, with the level of the cord injury playing a role. Being pregnant or early postpartum can predispose women to develop this syndrome. <> Institute of Endocrinology, Chaim Sheba Medical Center, Tel-Hashomer, Israel.

  4. #4
    Originally posted by Wise Young:

    6. Huang TS: [...] elevated serum testosterone levels [...] there is a reduced central dopaminergic tone in SCI subjects
    I was just wondering; can hormonal anomalies like these affect also the mental health, eg cause depression?


  5. #5

    Altered levels of pituitary hormones have profound effects on metabolism, the central nervous system, and the immune system. Several of the pituitary hormones alter thyroid, growth hormones, and corticosteroid levels. They may contribute to neuropathic pain, the presence of chronic fatigue syndrome, osteoporosis, muscle atrophy, infertility, etc. In addition, people with spinal cord injury (particularly cervical spinal cord injury) have very low levels of melatonin which, as you know, regulates sleep cycles. Finally, I have previously (on Cando) worried about the fact that many people with spinal cord injury have abnormal glucose tolerance tests (perhaps because part of the insulin response requires growth hormone). Yes, it may account for mood changes. The big question is why these types of changes occur.

    The hypothalamic-pituitary gonadal axis has been implicated in pain, chronic fatigue, and the sympathic system, as well as the immune system

    We must be careful that we do not blame everything on spinal cord injury. Many drugs affect hormonal balance after spinal cord injury. Drugs that are commonly taken by people with spinal cord injury and that have been implicated to cause prolactonemia include benzodiazepams (valium), tricyclic antidepressants (amitryptyline), H2 histamine receptor blockers (cimetidine), opioids, and even marijuana.

  6. #6
    Member Becky's Avatar
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    Jul 2001
    Thanks for your response Dr. Young.
    I am currently on zoloft, minocycline, coumadin, allegra,ditropan xl, and pericolace. At first I thought it was the zoloft because I read that sometimes antidepressants can cause it, but my doctor said that this particular one does not.

  7. #7

    Dr. Young - Empty Sella

    Empty Sella Syndrome is herniation of the subarachnoid space into the pituitary fossa. It causes pressure atrophy of the pituitary gland. I have seen it referred to an an arachnoidocele.
    It can be caused by surgery, trauma, radiation or sometimes as a birth defect (which has a constellation of various signs)

    Usually there is a small amount of pituitary tissue left and that amount is sufficient enough to provide hormones. Supposedly multi-parious obese women are prone to having it. Most physicians consider it a "nothing" finding.

    One of the deficiencies can be Growth Hormone, which can have cardiac implications, fatigue and lipid problems (This is info I obtained from various sources on the internet) I think I remember something about erectile disfunction in men being a sign.

    I was wondering if all SCI have an empty sella, or perhaps just the cervical ones.


  8. #8
    Cindy, I want to thank you for bringing my attention to this syndrome. I of course had known about this syndrome but had not realized how common it is.

    Although this syndrome is considered a "rare" disorder, my review of the literature (over 700 papers published in the last 30 years) suggest that it may not be so rare. Several studies sugest that 10-24% of people with pituitary disorders may have empty sella syndromes. Of 100 patients who had enlarged sellas, 25% had empty sellas and none of these had pituitary problems.

    Foresti, et al. examined the MRI of 500 patients who were admitted with unrelated neurological conditions (abstract below), overall about 11% of males and 13% of females had the syndrome. However, the incidence increases dramatically with age, so that 40% of females above age 50 and males above age 60 have empty sellas. Even if this particular population of patients, because they had other neurological problems, may have a higher incidence of the empty sellar syndrome, 40% is a high percentage.

    I was unable to find any study that suggested that there is an association of this syndrome with spinal cord injury. It is possible that people with the empty sella syndrome have marginal pituitary function and might have adverse responses to methylprednisolone. I have always been puzzled why some people develop pituitary problems and others do not after spinal cord injury. This is worthwhile following up.

    • Foresti M, Guidali A and Susanna P (1991). [Primary empty sella. Incidence in 500 asymptomatic subjects examined with magnetic resonance]. Radiol Med (Torino). 81 (6): 803-7. Summary: In 500 consecutive patients, aged 11-82 years, who underwent MR imaging of the brain for a variety of conditions not related to pathologic processes of the sellar or juxtasellar regions, the authors detected primary totally empty sella in 28/248 males (11.3%) and in 34/252 females (13.5%). Primary partially empty sella was found in 40/248 males (16.1%) and in 38/252 females (15.1%). A progressive increase in the incidence of the signs of primary empty sella was observed with aging, the increase being more conspicuous in the 5th decade of life in females (37.5%) and in the 6th decade in males (40%). On the whole, signs of primary empty sella were detected in 140/500 cases (38%)--namely, in 9.6% of the subjects under 40 and in 39.9% of those above 40. The incidence of primary empty sella, unrelated to any other clinical condition, seems to support its inclusion into paraphysiologic variants. On the basis of the data reported in literature, the authors consider the factors possibly playing a role in this condition. They seem to be: insufficiency or absence of diaphragma sellae, CSF pressure, and pituitary involution related to aging. < st_uids=1857785> Istituto di Radiodiagnostica, Ospedali Riuniti, Bergamo.

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