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PubMed1985

Modulation of lordosis behaviour in the female rat by corticotropin releasing factor, beta-endorphin and gonadotropin releasing hormone in the mesencephalic central gray.

A possible functional relationship between corticotropin-releasing factor (CRF) and opiate peptide neuronal systems (beta-endorphin, dynorphin1-17 and Met-enkephalin) and their interactions with gonadotropin releasing hormone (GnRH) in the mesencephalic central gray (MCG) for the regulation of lordosis behaviour was assessed in ovariectomized, oestrogen-treated and oestrogen-progesterone-treated female rats. Lordosis behaviour triggered by male mounting was inhibited in a dose-dependent fashion by CRF microinfused into the MCG in both oestrogen-treated and oestrogen-progesterone-treated female rats. This CRF-induced inhibition of lordosis could be overcome by a pre-infusion of naloxone or anti-beta-endorphin-globulin (anti-beta-end-G) directly into the MCG but not by anti-Met-enkephalin globulin (anti-enk-G) or anti-dynorphin1-17 globulin (anti-dynor-G). Supporting data indicate that the facilitation of lordosis behaviour induced by treatment with naloxone or anti-beta-end-G alone but not with anti-enk-G or anti-dynor-G may be due to enhanced GnRH release. This results from the action of these substances in overcoming the inhibition of GnRH secretion mediated specifically by beta-endorphin but not by Met-enkephalin or dynorphin1-17 in the MCG. These studies together with previous data showing that GnRH can overcome the abolition of lordosis by beta-endorphin in the MCG, indicate a close relationship between beta-endorphin (but not Met-enkephalin or dynorphin) and GnRH systems in the MCG in the control of lordosis behaviour. Thus, the inhibition of lordosis by CRF and the complete reversal of this blockade by naloxone or anti-beta-end-G may suggest that CRF could enhance the release of beta-endorphin from fibres in the MCG; beta-endorphin then inhibits lordosis by inhibiting the release of GnRH. However, a direct inhibitory effect of CRF on GnRH release is also likely since anti-CRF-gamma-globulin (anti-CRF-G) infused into the MCG produced a long-lasting facilitation of lordosis which can be blocked by an antagonist analogue of GnRH; in addition, previous studies have shown that GnRH infused into the MCG completely overcame the CRF-induced abolition of lordosis and potentiated lordosis to high levels. These results suggest that there may be functional neuroanatomical relationships between CRF, beta-endorphin and GnRH neuronal systems in the MCG in the control of female sexual behaviour. Neither Met-enkephalin nor dynorphin1-17 appear to participate in such mechanisms.

Animals↗
PubMed1985

Inhibition of the lordosis reflex in rats by intrahypothalamic infusion of neural excitatory agents: evidence that the hypothalamus contains separate inhibitory and facilitatory elements.

In attempts to activate lordosis-facilitating neural mechanisms in the ventromedial hypothalamus (VMH), neural excitatory agents were infused into the medial hypothalamus, and the effects of the infusions on the lordosis reflex and on the electrical activity of VMH neurons were studied. Surprisingly, bilateral intrahypothalamic infusion of glutamate (10 mM, 1.0 microliter/side) into behaving, ovariectomized, estrogen-treated rats displaying moderate lordotic responsiveness did not facilitate lordosis, but instead, resulted in a rapid (within a few minutes) and transient (recovery in about 20 min) inhibition of lordosis. Further experiments showed that this lordosis-inhibiting effect of glutamate was dose-related, and was completely blocked by prior infusion of a local anesthetic, procaine. Infusion of KC1 (1.5 or 15%, 1.0 microliter/side) also induced a dose-related, rapid and transient inhibition of lordosis, that was essentially identical to that induced by glutamate. Kainic acid (0.25 micrograms/0.5 microliter/side) also caused a rapid inhibition of lordosis, but the effect was long-lasting (days). The inhibition of lordosis by these agents was dissociated in time course, presence, and/or severity from effects on non-lordotic behaviors. Electrophysiological studies showed that all three agents tested could excite multiunit activity of the VMH, and that the time courses of these excitations were closely comparable to those of the inhibition of lordosis induced by the respective agents. Altogether, these studies indicated that the excitation of certain medial hypothalamic neurons can inhibit the lordosis reflex. The implied lordosis-inhibiting neural mechanisms are separate from facilitatory mechanism(s), according to differences in latency, duration, and procaine-sensitivity of response.

Animals↗
PubMed1987

Lordosis behavior in males of two inbred strains of guinea pig.

The lordosis behavior of male guinea pigs from inbred strains 2 and 13 was examined. Significantly more isolated gonadally intact males of strain 2 than strain 13 displayed lordosis. Castration did not decrease the display of lordosis. In castrated strain 2 males, those which showed lordosis did not have higher plasma androgen, estrone or estradiol levels than those which did not show lordosis. They also did not differ hormonally from ovariectomized strain 2 females even though strain 2 females never showed lordosis without hormone replacement. Although the lordosis shown by strain 2 males was not related to endogenous gonadal hormone levels, estradiol benzoate (EB) administration facilitated lordosis. EB had no clear effect on lordosis in strain 13 males. Progesterone after EB priming had no further facilitative effect in males of either strain. These results indicate that lordosis is more readily elicited from strain 2 than strain 13 males. Furthermore, lordosis in strain 2 males is not dependent upon gonadal hormones for its display although it is facilitated by EB (but not progesterone).

Animals↗
PubMed2004

Effects of midbrain lesions on lordosis and ultrasound production.

Previous studies suggest the control of lordosis by competing neural systems. A lordosis-inhibiting system is thought to originate in the lateral septum (LS) or preoptic area (POA) and project to midbrain sites, including the ventral tegmental area (VTA) and ventral half of the periaqueductal gray (vPAG). A lordosis-facilitating system is thought to originate in the ventromedial hypothalamus and project to the dorsal half of the PAG (dPAG). To test the generality of this model, we subjected female hamsters to control operations or lesions of the dPAG, vPAG or VTA. Subjects in hormone-induced estrus were observed for lordosis responses to males and manual stimulation and for rates of production of the "ultrasounds" used by hamsters for courtship. PAG lesions of both types depressed ultrasound rate, lordosis initiation and lordosis maintenance. VTA lesions failed to affect ultrasound rate, lordosis maintenance or lordosis responses to males. However, damage to the dorsomedial tegmentum was correlated with deficits in lordosis initiation. These results suggest the concentration in the PAG of mechanisms controlling vocalizations, including the ultrasounds used by hamsters for courtship. They confirm midbrain control of lordosis initiation and maintenance but fail to support any simple specialization of dorsal and ventral areas for these dimensions. They also fail to support a specialization of the dorsal and ventral halves of the midbrain for lordosis facilitation and inhibition, but do suggest several midbrain areas likely to be involved in the first of these functions.

Analysis of Variance↗
PubMed1997

Lumbar lordosis. Effects of sitting and standing.

STUDY DESIGN: The effect of sitting versus standing posture on lumbar lordosis was studied retrospectively by radiographic analysis of 109 patients with low back pain. OBJECTIVE: To document changes in segmental and total lumbar lordosis between sitting and standing radiographs. SUMMARY OF BACKGROUND DATA: Preservation of physiologic lumbar lordosis is an important consideration when performing fusion of the lumbar spine. The appropriate degree of lumbar lordosis has not been defined. METHODS: Total and segmental lumbar lordosis from L1 to S1 was assessed by an independent observer using the Cobb angle measurements of the lateral radiographs of the lumbar spine obtained with the patient in the sitting and standing positions. RESULTS: Lumbar lordosis averaged 49 degrees standing and 34 degrees sitting from L1 to S1, 47 degrees standing and 33 degrees sitting from L2 to S1, 31 degrees standing and 22 degrees sitting from L4 to S1, and 18 degrees standing and 15 degrees sitting from L5 to S1. CONCLUSION: Lumbar lordosis while standing was nearly 50% greater on average than sitting lumbar lordosis. The clinical significance of this data may pertain to: 1) the known correlation of increased intradiscal pressure with sitting, which may be caused by this decrease in lordosis; 2) the benefit of a sitting lumbar support that increases lordosis; and 3) the consideration of an appropriate degree of lordosis in fusion of the lumbar spine.

Female↗
PubMed2005

The impact of total lumbar disc replacement on segmental and total lumbar lordosis.

BACKGROUND: One of the goals of total lumbar disc replacement is restoration of the physiological sagittal alignment. There is little evidence if this goal is reached in vivo and further affects the clinical outcome. METHODS: In 29 patients segmental lordosis and total lumbar lordosis were measured on X-rays pre- and postoperatively. The functional outcome was evaluated prospectively with the Visuell Analogue Scale, Oswestry Low Back Pain Disability Questionnaire and Short Form 36 Health Survey Questionnaire. FINDINGS: Total disc replacement increased segmental lordosis significantly while total lumbar lordosis remained unchanged. Preoperative segmental/total lumbar lordosis was physiological in 52%/91% of the patients. Postoperatively these values changed to 72% for segmental- and 94% for total lumbar lordosis. No difference could be observed in clinical outcome measures in patients with physiological and unphysiological segmental lordosis. INTERPRETATION: Monosegmental total disc replacement increases the segmental lordosis in most of the cases while preserving the total lumbar lordosis which produces a decrease of lordotic angle in the adjacent segment(s). Although short term clinical results are not affected, the segmental lordosis increase and adjacent segment(s) alteration may influence long term outcome.

Adult↗
PubMedDate not supplied

Determining the relationship between cervical lordosis and neck complaints.

OBJECTIVE: To investigate the presence of a "functionally normal" cervical lordosis and identify if this and the amount of forward head posture are related to neck complaints. METHODS: Using the posterior tangent method, an angle of cervical lordosis was measured from C2 through C7 vertebrae on 277 lateral cervical x-rays. Anterior weight bearing was measured as the horizontal distance of the posterior superior body of the C2 vertebra compared to a vertical line drawn superiorly from the posterior inferior body of the C7 vertebra. The measurements were sorted into 2 groups, cervical complaint and noncervical complaint groups. The data were then partitioned into age by decades, sex, and angle categories. RESULTS: Patients with lordosis of 20 degrees or less were more likely to have cervicogenic symptoms (P < .001). The association between cervical pain and lordosis of 0 degrees or less was significant (P < .0001). The odds that a patient with cervical pain had a lordosis of 0 degrees or less was 18 times greater than for a patient with a noncervical complaint. Patients with cervical pain had less lordosis and this was consistent over all age ranges. Males had larger median cervical lordosis than females (20 degrees vs 14 degrees) (2-sided Mann-Whitney U test, P = .016). When partitioned by age grouping, this trend is significant only in the 40- to 49-year-old range (2-sided Mann-Whitney U test, P < .01). CONCLUSION: We found a statistically significant association between cervical pain and lordosis < 20 degrees and a "clinically normal" range for cervical lordosis of 31 degrees to 40 degrees. Maintenance of a lordosis in the range of 31 degrees to 40 degrees could be a clinical goal for chiropractic treatment.

Adolescent↗
PubMed2002

The influence of lumbar lordosis on spinal fusion and functional outcome after posterolateral spinal fusion with and without pedicle screw instrumentation.

The aim of the current study was to examine the correlation between lumbar lordosis, spinal fusion, and functional outcome in patients suffering from severe low back pain, treated by posterolateral spinal fusion with or without pedicle screw instrumentation. One hundred thirty patients were randomly allocated to posterolateral lumbar fusion with or without Cotrel-Dubousset instrumentation. Functional outcome was assessed preoperatively, and 1 and 2 years postoperatively. Lordosis angles of the lumbar spine and fusion rates were assessed at the 1- and 2-year follow-up. No difference in lordosis angle was found between the two groups at any time. Lordosis was unchanged at 2 years compared with preoperative status in both groups. In the instrumented group, nonunion (23%) was followed by a decrease in lordosis at follow-up (p < 0.05). However, in the noninstrumented group, nonunion (14%) resulted in increased lordosis (p < 0.05). No correlation was found between functional outcome and lordosis angle. The current study showed no correlation between functional outcome and lordosis angle either before or after posterolateral spinal fusion. Use of instrumentation did not influence lumbar spinal alignment compared with noninstrumented fusions. The sagittal alignment was stable both 1 and 2 years after solid fusion. The failure mode of instrumented fusions was a reduced degree of lordosis in contrast to an increased degree of lordosis in patients with noninstrumented fusion.

Adult↗
PubMed1997

Effect of anterior wedging of L1 on the measurement of lumbar lordosis: comparison of two roentgenological methods.

OBJECTIVE: To determine whether the choice of either the superior or inferior endplate of the L1 vertebra as the proximal landmark for the measurement of lumbar lordosis could significantly affect the categorization (i.e., hypo- or hyperlordotic or normal) of that lordosis in subjects where the L1 vertebra is wedged anteriorly. DESIGN: Concurrent validity. SETTING: The Anglo-European College of Chiropractic teaching clinic. SELECTION: A total of 260 files were screened from new patient files at the clinic dating from the year 1980 onward. A total of 96 films fulfilled the inclusion criteria, which were: the patient was 20-50 yr old at the time of presentation, and had no evidence of severe degeneration, scoliosis or bony deformity, and the quality of the radiograph was not poor. Wedging of the L1 vertebra in excess of 2 mm was measured in 70 radiographs; these films were used for the two measurements of lumbar lordosis. OUTCOME MEASURES: The lumbar lordosis was roentgenometrically measured on lateral lumbar radiographs. RESULTS: Seventy-three per cent of the X-rays meeting the inclusion criteria showed wedging of the L1 vertebra in excess of 2 mm. Using the Student's t test, the mean lumbar lordosis, measured using the superior endplate of L1 as the proximal boundary for measurement of the lordotic angle, was 52.0 +/- 11.82 degrees and was significantly lower (p < .0001) than the mean lumbar lordosis measured using the inferior endplate of L1, which was 59.06 +/- 12.01 degrees. The Kappa analysis performed to determine the level of agreement in the categorization of the lumbar lordosis using these two methods indicated that, statistically (K = .394), there was poor agreement in the categorization of the lumbar lordosis between the two methods. An intraexaminer reliability study indicated significant intraexaminer agreement using both methods. CONCLUSION: The choice of landmark (i.e., superior or inferior endplate of L1) can significantly affect the value of the lumbar lordosis angle and its subsequent categorization as hypo-/hyperlordotic or normal in patients where this vertebra is wedged anteriorly. In view of the high incidence of this anatomical variant, L1 might not necessarily represent the best choice of landmark for the measurement of the lumbar lordosis. However, further work is necessary to determine which method is the most accurate and to investigate the validity of the suggestion that L2 may be a reasonable alternative.

Adult↗
PubMed1999

Facilitatory and inhibitory effects of beta-endorphin on lordosis in female rats: relation to time of administration.

The purpose of the present study was to investigate the effect of time of beta-endorphin (beta-EP) administration on lordosis in ovariectomized female rats injected subcutaneously (sc) with estradiol benzoate (EB) and progesterone (Prog). Intracerebroventricular (icv) injections of beta-EP and naloxone (NLX), an opioid receptor antagonist, were administered at the various stages of sc steroid hormone priming. Facilitation of lordosis induced by 10 microg beta-EP was observed exclusively within the initial 6 h of estrogen action, after which inhibition of lordosis occurred. At 12 h after EB priming, at the time of sc Prog treatment (or 43 h after EB priming), icv injection of 10 microg beta-EP significantly inhibited lordosis. Lordosis was significantly facilitated by icv injections of 1 and 10 microg beta-EP at the time of sc EB priming, but not by 0.1 microg beta-EP. A dose-response relationship was identified for lordosis in experimental animals receiving icv injection of beta-EP. Lordosis was inhibited by icv injections of 1 and 10 microg beta-EP at 1 h before the test (or 47 h after EB priming). Lordosis was significantly inhibited by icv injection of NLX at all stages. From the present results, it seems that two different mechanisms are involved in endorphinergic modulation of rats' sexual receptivity: (a) the endorphinergic system at the initial stages of estrogen action facilitates the estrogen activation of lordosis; (b) the endorphinergic system at the final stages of steroid action inhibits lordosis. Moreover, there exists a critical time between 6 and 12 h after estrogen priming for endorphinergic mediation to modulate estrogen action.

Animals↗
PubMed1991

Bisexual behavior in the male rat: influence of masculine sexual activity on the display of lordosis behavior.

Sexually inexperienced male Wistar rats (strain WI in our colony) known to very infrequently display spontaneous lordosis behavior (Schaeffer et al., 1990b) were used. A first group was tested four times at 5-day intervals for lordosis with vigorous stimulus males (heterotypic sexual behavior), immediately following testing for masculine sexual activity with highly receptive females (homotypic sexual behavior). A small number of animals displayed lordosis during the first test, but more and more animals displayed this behavior from the first to the fourth test. There was no relationship between the degree of masculine sexual activity--intromission without ejaculation or ejaculation--and the occurrence of lordosis behavior. A second group was tested only once for both masculine sexual activity and lordosis behavior as above and afterwards three times at 5-day intervals for lordosis behavior in the absence of any previous testing for masculine sexual activity. A few animals displayed lordosis during their first test. As compared to the first group, the animals which had not displayed lordosis in the first test never showed lordosis responses in the following tests. It is concluded that both homotypic and heterotypic sexual interactions are required for the display of lordosis behavior in the strain of Wistar rats used in this study.

Animals↗
PubMed1992

The effect of estrogen treatment on scopolamine inhibition of lordosis.

Previous evidence indicates that the cholinergic muscarinic antagonist, scopolamine, inhibits lordosis in female rats. In the experiments reported here, the effects of various doses and repeated administrations of estrogen on the scopolamine inhibition of lordosis were examined. In the first experiment, intraperitoneal injections of scopolamine (1 mg/rat) completely inhibited lordosis in ovariectomized rats primed with low doses of estradiol benzoate (0.25 or 0.5 micrograms for 3 days) and progesterone (500 micrograms). However, scopolamine was significantly less effective in inhibiting lordosis in females primed with a higher dose of estradiol benzoate (25 micrograms for 3 days) and progesterone (500 micrograms). When hormone priming was repeated on subsequent weeks, scopolamine continued to inhibit lordosis in females that received 0.25 micrograms estradiol benzoate but was less effective in females primed with 0.5 micrograms. Scopolamine failed to inhibit lordosis in females treated with 25 micrograms estradiol benzoate on these later tests. In the second experiment, various doses of scopolamine (1, 2, or 4 mg/rat) were administered intraperitoneally to females primed with the highest dose of estradiol benzoate (25 micrograms) and progesterone (500 micrograms). Lordosis was inhibited equally by all scopolamine doses during the first week. As in the first experiment, scopolamine failed to inhibit lordosis at all doses on subsequent weeks of testing. These results indicate that the ability of scopolamine to inhibit lordosis is reduced by increasing the dose or the number of estrogen exposures. Because higher doses of scopolamine failed to restore its inhibitory effect on lordosis an upregulation of muscarinic receptors by estrogen cannot account for the reduced effectiveness of scopolamine.

Animals↗
PubMed1991

Induction of progestin receptors in the mediobasal hypothalamus of gonadally intact male rats primed with estrogen in relation to display of lordosis behavior.

The purpose of this study was to determine whether the effects of estrogen on lordosis behavior in the male rat were related to the number of progesterone (P) receptors in the mediobasal hypothalamus (MBH) and/or dependent on blood P concentration. Two groups of gonadally intact male rats were given five successive doses of 1.0 or 2.5 micrograms estradiol benzoate (EB) and tested for lordosis behavior with a male stimulus at the end of the treatment. One month later they were again injected with EB and sacrificed under the same temporal schedule, but they were not tested for lordosis so as to prevent any emotionally stressful effects of intermale cohabitation. The males given 2.5 micrograms EB more frequently displayed lordosis responses to male mounts than those receiving 1 microgram EB, with a parallel increase in the number of MBH P receptors. The total number of MBH P receptors also appeared to be higher in the animals that displayed lordosis responses (lordosis group) than in those which did not (no lordosis group). In contrast, the display of lordosis behavior was negatively correlated with blood P concentration. Comparing MBH P receptors and blood P values in the EB treated and in nonhormonally treated gonadally intact animals which had been selected for either ability or inability to spontaneously display lordosis behavior, we observed that (1) EB was capable of increasing the number of MBH P receptors in the male rat; and (2) in the absence of EB treatment blood P values were higher in the animals showing lordosis than in those which did not. These data are discussed with respect to observations made in castrated male rats and in ovariectomized females.

Animals↗
PubMed2004

Progestins' actions in the VTA to facilitate lordosis involve dopamine-like type 1 and 2 receptors.

In the ventral tegmental area (VTA), 5alpha-pregnan-3alpha-ol-20-one (3alpha,5alpha-THP) facilitates lordosis. Whether this involves dopamine type 1 (D1) or dopamine type 2 (D2) receptors is of interest. Ovariectomized (ovx) rats with guide cannulae to the VTA were estradiol (E2) primed and pretested for lordosis. Rats were then infused with the D1 (Experiment 1) or D2 (Experiment 2) antagonists or agonists (0, 100, or 200 ng) to the VTA and were retested. After a second infusion of 3alpha,5alpha-THP (0, 100, or 200 ng) or vehicle, rats were tested 10, 60, and 120 min later. In Experiment 3, rats were administered a progestin receptor antagonist, RU38486, systemically or to the VTA 1 h prior to vehicle, SKF38393 and/or 3alpha,5alpha-THP infusions. 3alpha,5alpha-THP infusions increased lordosis over that seen with E2 priming. The D1 antagonist, SCH23390, attenuated 3alpha,5alpha-THP, but not E2-facilitated lordosis. The D1 agonist, SKF38393, augmented 3alpha,5alpha-THP, but not E2-facilitated lordosis. The D2 antagonist, sulpiride, had no significant effects on lordosis. The D2 agonist, quinpirole, prevented 3alpha,5alpha-THP-facilitated lordosis. RU38486 (subcutaneous) inhibited lordosis, whereas infusions to the VTA decreased lordosis produced by SKF38393 and 3alpha,5alpha-THP, but not 3alpha,5alpha-THP alone. Thus, 3alpha,5alpha-THP's actions in the VTA for lordosis may involve D1 and/or D2 receptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2000

Lumbopelvic lordosis and pelvic balance on repeated standing lateral radiographs of adult volunteers and untreated patients with constant low back pain.

STUDY DESIGN: Twenty volunteers and 20 patients with no prior spine surgery had two standing lateral radiographs taken, on the average, 66 months apart and 2 weeks apart, respectively. OBJECTIVES: To first determine the reliability of the measurement techniques used, and then the longitudinal variation between radiographs for the sagittal spinopelvic alignments measured in two stable populations, the one manifesting no back symptoms (volunteers) and the other showing no changes in symptoms (patients). Pelvic morphology also was assessed quantitatively, and significant correlations for the measurements were studied. SUMMARY OF BACKGROUND DATA: There are no published studies on longitudinal variation for measurements of sagittal spinal alignments in asymptomatic control subjects or untreated patients with stable back problems. It may be helpful to know not only how much variation in alignments can be expected between radiographs of the same individual, but also which measurements and measurement techniques offer the greatest clinical reliability and application. METHODS: Each patient in this study reported mechanical type low back pain that was constant in location and character as well as clinically consistent with symptomatic degenerative lumbar disc disease. Each patient and volunteer had 36-inch-long lateral radiographs taken of the entire thoracic and lumbar spine, which included the pelvis. After intervening periods of 1 to 4 weeks (patients) and 5 to 6 years (volunteers), a second radiograph was taken for comparison. Two observers made 24 different measurements on the radiographs including determinations for lumbopelvic lordosis, pelvic balance, and pelvic morphology using the pelvic radius technique. Reliabilities, longitudinal variations, and correlations for the measurements were compared. RESULTS: The most reliable measurements were for pelvic morphology, pelvic balance, and regional lumbopelvic lordosis by the pelvic radius technique. Pelvic morphology was the most constant measurement between individual radiographs. Pelvic morphology and total lumbosacral lordosis were dependent measurements that were complementary in determining total lumbopelvic lordosis. Lumbopelvic lordosis and pelvic balance also had strong correlation, whereas lumbosacral lordosis and pelvic balance were independent measurements. CONCLUSIONS: The pelvic radius technique is recommended for evaluating lordosis to the pelvis because this approach provided not only good measurement reliability on standing radiographs for lumbopelvic lordosis, but also determination of pelvic balance over the hips and the option to assess pelvic morphology quantitatively. Lumbopelvic lordosis and pelvic balance were strongly correlative. This finding, along with higher reliability and lower longitudinal variation on repeated radiographs, indicated greater clinical application for these specific measurements.

Adult↗
PubMed2005

Sagittal alignment of spine and pelvis regulated by pelvic incidence: standard values and prediction of lordosis.

Pelvis and spinal curves were studied with an angular parameter typical of pelvis morphology: pelvic incidence. A significant chain of correlations between positional pelvic and spinal parameters and incidence is known. This study investigated standards of incidence and a predictive equation of lordosis from selective pelvic and spinal individual parameters. One hundred and forty nine (78 men and 71 women) healthy adults, aged 19-50 years, with no spinal disorders, were included and had a full-spine lateral X-ray in a standardised upright position. Computerised technology was used for the measurement of angular parameters. Mean-deviation section of each parameter and Pearson correlation test were calculated. A multivariate selection algorithm was running with the lordosis (predicted variable) and the other spinal and pelvic parameters (predictor variables), to determine the best sets of predictors to include in the model. A low incidence (<44 degrees ) decreased sacral-slope and the lordosis is flattened. A high incidence (>62 degrees ) increased sacral-slope and the lordosis is more pronounced. Lordosis predictive equation is based on incidence, kyphosis, sacral-slope and +/-T9 tilt. The confidence limits and the residuals (the difference between measured and predicted lordosis) assessed the predicted lordosis accuracy of the model: respectively, +/-1.65 and 2.41 degrees with the 4-item model; +/-1.73 and 3.62 degrees with the 3-item model. The ability of the functional spine-pelvis unit to search for a sagittal balance depended both on the incidence and on the variation section of the other positional parameters. Incidence gave an adaptation potential at two levels of positional compensation: overlying state (kyphosis, T9 tilt), underlying state (sacral slope, pelvic tilt). The biomechanical and clinical conditions of the standing posture (as in scoliosis, low back pain, spondylisthesis, spine surgery, obesity and postural impairments) can be studied by comparing the measured lordosis with the predicted lordosis.

Adult↗
PubMed1986

Regulation of lordosis behaviour in the female rat by corticotropin-releasing factor, beta-endorphin/corticotropin and luteinizing hormone-releasing hormone neuronal systems in the medial preoptic area.

The role of corticotropin-releasing factor (CRF) and opiocortin neuronal systems and a possible functional relationship between the two in the control of luteinizing hormone-releasing hormone (LH-RH) activity in the medial preoptic area (MPOA) for the regulation of lordosis behaviour were assessed in ovariectomised oestrogen-progesterone-treated female rats. Lordosis behaviour (assessed as the lordosis quotient) triggered by male mounting was significantly inhibited by either CRF or beta-endorphin infused into the MPOA in animals treated with normal doses of oestradiol benzoate (OEB) (5 micrograms) and progesterone (500 micrograms). Saline-treated animals exhibited high levels of lordosis. The inhibition of lordosis produced by either CRF or beta-endorphin could be reversed by LH-RH microinfusions into the MPOA. While naloxone pretreatment of the MPOA site prevented the inhibitory effects of beta-endorphin, neither the opiate antagonist nor anti-beta-endorphin-gamma-globulin (even in high concentrations) infused into the MPOA was effective in completely preventing the inhibition of lordosis produced by CRF. These findings suggest that the inhibition of LH-RH neuronal activity and lordosis behaviour by CRF may be due to a direct action and may not be the result of activation of beta-endorphin release. The possibility that the two peptidergic systems may act in a synergistic fashion is supported by the data showing that combined CRF-beta-endorphin treatment in the MPOA completely abolished lordosis. This is further supported by the finding that CRF totally abolished lordosis in animals pretreated with anti-corticotropin (ACTH-gamma-globulin although this result could suggest that CRF could preferentially stimulate the release of ACTH in the MPOA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1990

Increased GABAergic transmission in medial hypothalamus facilitates lordosis but has the opposite effect in preoptic area.

The role of gamma-aminobutyric acid (GABA) in mediation of lordosis in the rat has been unclear. We report here that GABA plays a dual role in the mediation of lordosis and has differential effects in the medial hypothalamus (MH) and preoptic area/anterior hypothalamus continuum (POA-AH). Bilateral infusion of the GABAA antagonist bicuculline into the MH of cannulated females primed with estradiol benzoate and progesterone (EB + P) resulted in a marked and transient inhibition of ongoing lordosis. A similar pattern of inhibition was seen in females treated with EB only. In contrast, infusion of the same dose of bicuculline into the POA-AH of sexually receptive females had no effect on lordosis whereas infusion of the GABAA agonist muscimol into this site resulted in a short-term inhibition of lordosis. Furthermore, when females were treated with subthreshold doses of EB + P to induce a low level of lordosis responding, infusion of muscimol into the MH resulted in a significant enhancement of lordosis; infusion of bicuculline into the POA-AH also enhanced lordosis responding as compared to saline-infused controls. These data indicate that increased GABAergic neurotransmission in the MH facilitates lordosis whereas increased GABAergic activity in the POA-AH inhibits this behavior.

Animals↗