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Congenital thoracic lordosis.

The rare spinal deformity of congenital thoracic lordosis is illustrated in five patients. Often this deformity is progressive and may cause severe pulmonary deficits and death. In the two patients most recently treated, early spine fusion (one anterior and one posterior) showed promising results--halting of the progression of deformity and even some amelioration of the lordosis. In two patients in whom active attempts were made to correct the lordosis, the complications were severe--one patient died and quadriparesis developed in the other.

Adolescent↗

The efficacy of cervical extension-compression traction combined with diversified manipulation and drop table adjustments in the rehabilitation of cervical lordosis: a pilot study.

OBJECTIVE: To experimentally investigate the effect of cervical extension-compression traction combined with diversified chiropractic manipulation and drop table adjusting in establishing or increasing cervical lordosis. DESIGN: Blinded, before and after trial with pre- and postlateral cervical radiographic measurement. SETTING: Primary care private chiropractic clinic in Saugus, MA. SUBJECTS: A) Control group--convenience sample who had no health care for 10-14 wk, 30 persons. B) Treatment group 1, nonrandomized control trial, 35 persons, whose pre- and postlateral cervical radiographs were taken 10-14 wk apart and whose radiographs clearly depicted C1 through C7. C) Treatment group 2, nonrandomized control trial, 30 persons, whose pre- and postlateral cervical radiographs were taken 10-14 wk apart and whose radiographs clearly depicted C1 through C7. INTERVENTIONS: Treatment group 1: diversified spinal manipulation, drop table adjustments and cervical extension-compression traction five times per week for 10-14 wk (12 wk +/- 2). Treatment group 2: diversified spinal manipulation and drop table adjustments five times per week for 10-14 wk (12 wk +/- 2). MAIN OUTCOME MEASURES: Anterior head translation millimeters, C2 to C7 absolute rotation angle, angle of C1 to horizontal (atlas plane angle), five relative rotation angles (C2-3, C3-4, C4-5, C5-6, C6-7) and qualitative classification of lordotic configuration. RESULTS: No statistically significant changes existed between the pre- and posttests for the control group except in the C6-7 relative rotation angle. In the treatment group 1, statistically significant differences were found in all X-ray markings. Twenty-nine of 35 members have a lordosis after treatment compared to 11 of 35 before treatment. The C2 to C7 angle changed an average 13.2 degrees, C1 to horizontal changed an average 9.8 degrees, the anterior head translation reduced an average of 6.8 mm, the average relative rotation angle changed: C2-3: 3.1, C3-4: 5.5, C4-5: 4.80, C5-6: 2.7 and C6-7: 1.1. In the treatment group 2, no statistically significant changes existed between the pre- and posttests except atlas angulation to horizontal which increased an average of 3.0 degrees. CONCLUSIONS: A transformation to a lordotic configuration or increase in lordotic configuration occurred and was measured in the majority of treatment group 1 subjects, while no change in the control group and essentially no change in treatment group 2 was measured. Extension-compression traction combined with diversified chiropractic manipulation and drop table adjusting procedures may improve or partially reestablish the cervical lordosis in 10-14 wk of daily care.

Adult↗

Increasing lordosis of the occipitocervical junction after arthrodesis in young children: the occipitocervical crankshaft phenomenon.

Five children were treated before age 6 years with occipitocervical fusion for occipitocervical instability. Long-term (average, 11.8 years; range, 8.4-14.5 years) follow-up revealed increasing lordosis across the fused segment in four of the patients, a finding we here refer to as the occipitocervical crankshaft phenomenon. On average, occipitocervical lordosis increased 1.06 degrees per level fused per year until skeletal maturity. Although such a progression might be expected, to our knowledge this is the first report of its occurrence. Compensatory subaxial motion was able to overcome this increase in all of the patients. We recommend occipitocervical fusion in a neutral or slightly flexed position in the very young child to account for this predictable increase in lordosis.

Arthrodesis↗

Elliptical modeling of the sagittal lumbar lordosis and segmental rotation angles as a method to discriminate between normal and low back pain subjects.

Clinical significance of lumbar lordosis has not been agreed on. Our purpose is to compare lordotic measurements of normal and pain subjects and to test the validity of a new anthropometric model of lumbar curvatures. Digitized radiographic points (body corners) from standing lateral lumbar radiographs were modeled with ellipses in a least-squares method and were used to create segmental angles, a global angle at L1-L5, a Cobb angle from T12 to S1, Ferguson's sacral base angle, and an angle of pelvic tilt. Fifty normal subjects were matched in age, sex, weight, and height with 50 acute pain subjects, 50 chronic pain subjects, and 24 pain subjects with radiographic abnormalities. Of 11 angles, 2 distances, and 2 ratios, statistical analysis was significantly different across groups for 12 of these measurements, with the alternative hypotheses accepted for the other 3 measurements. The lordosis of both normal and low back pain subjects can be successfully modeled with a portion (approximately 86 degrees) of an ellipse, but with different major and minor axis ratios. The normal group's average elliptic lordosis has the smallest least-squares error, approximately 1 mm per digitized point, with (minor axis)/(major axis) ratio = 0.39, L1-L5 global angle = 40 degrees, and Cobb angle = 65 degrees. The chronic and radiographic abnormalities pain groups have an elongated ellipse with hypolordosis, reduced L1-L5 global angle = 29.6-35 degrees, reduced Cobb angle = 57-58 degrees, and elliptic axis ratio = 0.27-0.30. The acute pain group is hyperlordotic with the largest L1-L5 global angle, largest Cobb angle = 70 degrees, largest Ferguson's angle, and largest pelvic tilt angle.

Acute Disease↗

Individual differences among female rats in the timing of the preovulatory LH surge are predicted by lordosis reflex intensity.

In young female rats, we found individual differences in LH surge characteristics that could underlie differences in fertility throughout adulthood and aging. We modified a jugular cannulation technique, which enabled us to characterize four successive proestrous LH surges in regularly cycling female rats. During a surge, the timing and amount of LH were negatively correlated, so that late-onset surges reached a low peak, late in the day. Within a female rat, the timing of the LH surge, but not the blood level of LH, was stable from cycle to cycle. Thus, differences in onset and peak time between successive LH surges within one female were less than differences among females. Moreover, these individual differences in timing of the LH surge were positively correlated with individual differences in lordosis reflex intensity on proestrus. Females with early-onset LH surges had high average lordosis reflex intensity on proestrus. Therefore, lordosis reflex intensity is a nonintrusive behavioral biomarker for individual differences in the timing of the preovulatory LH surge. This relationship between behavior and the preovulatory LH surge may reflect a hormonal basis for variations in reproductive strategies throughout the life span.

Animals↗

Facilitation of the lordosis reflex in female rats by electrical stimulation of the lateral vestibular nucleus.

(1) Electrical stimulation of the lateral vestibular nucleus (LVN) facilitated lordosis reflex responses to somatosensory stimulation, in estrogen-primed female rats. (2) Unilateral LVN stimulation was sufficient for this effect. Currents as low as 10muA could be used. (3) With the stimulus parameters used, the effect develops within 5 min of LVN stimulation and decays within 10 min following cessation of stimulation. (4) Together with previous evidence that LVN lesions disrupt lordosis, these results suggest LVN facilitation of spinal reflex mechanisms for lordosis.

Animals↗

Midbrain distribution of neurons with strong, sustained responses to lordosis trigger stimuli in the female golden hamster.

Midbrain single units in anesthetized female hamsters were examined for pronounced, sustained responses to types of somatic stimuli which control the display of lordosis during periods of sexual receptivity. Units showing strong responses to lordosis trigger stimuli were widely distributed, but tended to be most concentrated in th deep superior colliculus, ventromedial midbrain and central gray, brain regions previously implicated, by other methods, in the control of hamster lordosis.

Animals↗

Leumorphin, a novel opioid peptide, promotes lordosis in female rats.

The actions of leumorphin, a recently characterized endogenous opioid peptide, oppose of most opioid peptides in facilitating lordosis reflex, a major component of female sexual behavior in the rat. Maximal lordosis appeared promptly after infusion of 1 nmol leumorphin into the ventromedial hypothalamus of ovariectomized estrogen-primed rats. This facilitation lasted for as long as 5 h, unless interrupted by midbrain infusion of an antiserum to prolactin. The result is a discovery of a novel substance of remarkable strength in facilitating lordosis, an effect presumably mediated by midbrain release of prolactin.

Animals↗

Development of progesterone-facilitated lordosis in female guinea pigs: relationship to neural estrogen and progestin receptors.

Ovariectomized (OVX), 20-day-old female guinea pigs did not exhibit lordosis following treatment with estradiol benzoate (EB) and progesterone. Behavioral responsiveness to EB and progesterone developed abruptly; by 30 days of age, responses typical of adult females (greater than 9 weeks of age) were observed. In vitro assays of neural steroid receptors were performed to test the hypothesis that a deficiency in the concentration of hypothalamic and/or preoptic area estrogen and/or progestin receptors contributes to the lack of progesterone-facilitated lordosis in juvenile (20-day-old) females. Assay of cytosol progestin receptors in the mediobasal hypothalamus (MBH) and preoptic area (POA) of immature and adult females 40 h after injection of EB confirmed a previous report that the concentration of estradiol-induced cytosol progestin receptors in the MBH of juvenile females was slightly lower than that observed in adults. Furthermore, MBH cell nuclear accumulation of progestin receptors after progesterone injection was markedly lower (i.e. 42%) in immature, as compared to adult females. The concentrations of cytosol estrogen receptors in the MBH and POA did not differ between immature and adult OVX guinea pigs. Also, cell nuclear estrogen receptor accumulation in the MBH after estradiol injection was comparable in immature and adult females. These data suggest that a deficiency in cell nuclear progestin receptor accumulation in the MBH may contribute to the absence of progesterone-facilitated lordosis in estradiol-primed, immature female guinea pigs. This age-related difference in cell nuclear progestin receptor accumulation may be due, in part, to reduced concentrations of estradiol-induced cytosol progestin receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

Estrogen-progesterone and 8-OH-DPAT attenuate the lordosis-inhibiting effects of the 5-HT1A agonist in the VMN.

Ovariectomized rats were treated for 2 consecutive weeks with 25 micrograms estradiol benzoate followed 48 h later with 500 micrograms progesterone. Bilateral infusions of 200 ng 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) into the ventromedial nucleus of the hypothalamus (VMN) inhibited female sexual behavior on the first but not the second week of hormone priming. Such attenuation on the second week of priming did not appear to result from an enhanced receptivity of the female rats since there were no differences in the L/M ratios prior to drug infusion; nor was the attenuation a consequence of infusion-induced VMN damage since neither saline nor 8-OH-DPAT preinfusions prevented the later inhibitory effects of 8-OH-DPAT on lordosis behavior. However, preinfusion with 8-OH-DPAT may have reduced the duration of the inhibition. Hormone priming (without any VMN infusion) also partially attenuated the effect of 8-OH-DPAT. Both hormone priming and treatment with 8-OH-DPAT were required to eliminate the effects of the second 8-OH-DPAT treatment. Thus, the present results suggest that gonadal hormones, alone, slightly attenuate the effects of agonist activation of 5-HT1A receptors involved in the inhibition of lordosis behavior; that agonist activation of 5-HT1A receptors also produces a slight attenuation; but that both treatments together have a robust protective action against the inhibitory effect of a 5-HT1A agonist on female lordosis behavior.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

Suppression of lordosis behavior by the putative 5-HT receptor agonist 8-OH-DPAT in the rat.

The administration of 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), inhibited the lordosis induced by estradiol benzoate or estradiol benzoate plus progesterone in ovariectomized rats. There was no facilitation of lordosis by 8-OH-DPAT in animals pretreated with a threshold dose of estradiol benzoate. The results are consistent with the view that 8-OH-DPAT is an agonist at 5-HT receptors and provide further support for an inhibition role of central 5-HT in the mediation of lordosis behavior.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

Estrogen accelerates the recovery of the lordosis response after its exhaustion induced by cervical probing.

Repetitive flank-perineum palpation combined with probing the vaginal cervix in ovariectomized hormonally untreated rats elicited a mean of 4.2 +/- 0.2 (SEM) successive lordosis responses before the response was exhausted. Two days after a single injection of estradiol benzoate (100 micrograms/kg body wt) in ovariectomized rats, a significantly greater number (7.8 +/- 0.2) of lordosis responses could be elicited before the response was exhausted (P less than 0.01). After this exhaustion, recovery of lordosis responsiveness to this stimulation occurred significantly earlier in the estrogen-treated rats (6 hr) than in the oil-treated rats (60 hr) (P less than 0.01). Several possible mechanisms mediating these effects are proposed.

Animals↗

Nonluteal source of lordosis-promoting progesterone secretion in guinea pigs.

Prepubertal (21-24 days of age), intact female guinea pigs treated sequentially with estradiol benzoate and LH or FSH displayed lordosis behavior. The gonadotropins apparently caused release of progesterone from the ovaries, because lordosis behavior in guinea pigs is activated by sequential action of estrogen and progesterone. These data demonstrate that immature ovaries, completely devoid of corpus luteum tissue, are capable of secreting behaviorally significant concentrations of progesterone when stimulated by gonadotropins. Therefore, the luteal compartment of the guinea pig ovary is not essential for the preovulatory surges of progesterone that coincide with expression of lordosis behavior in adulthood. Likely candidates for sources of preovulatory progesterone in prepubertal females are antral follicle and interstitial gland tissue.

Animals↗

Estrogen and the induction of lordosis in female and male prairie voles (Microtus ochrogaster).

Estrogen elicited lordosis in ovariectomized female prairie voles (Microtus ochrogaster). Treatment with estradiol benzoate (EB) was particularly effective if administered as multiple injections. Very high dose levels were not, in general, any more effective than lower doses. Individual animals typically showed lordosis within 24 to 48 hr following the onset of EB treatment and prolonged treatments did not increase the percentage of females responding to EB. Castrated male prairie voles did not respond with lordosis to repeated daily injections of 10 micrograms EB given for a period of 15 consecutive days.

Animals↗

Serotonin type 2 antagonists inhibit lordosis behavior in the female rat: reversal with quipazine.

The theory that activation of serotonin type 2 (5-HT2) receptors facilitates lordosis behavior in the female rat was tested. The 5-HT2 antagonists pizotefin, cyproheptadine, metitepine, and ketanserin were found to inhibit lordosis behavior in ovariectomized rats that had been primed with estradiol benzoate and progesterone. Pipamperone was ineffective. The 5-HT2 agonist quipazine was ineffective alone, but it reversed the inhibitory effects of pizotefin, cyproheptadine, and ketanserin. It did not reverse the effects of metitepine. The results support the theory of a facilitatory role for 5-HT2 receptors in lordosis behavior.

Analysis of Variance↗

The effect of hysterectomy on hormone-induced lordosis behavior in hamsters.

Ovariectomized-hysterectomized (OH) and ovariectomized-sham hysterectomized (OSH) hamsters were tested for lordosis behavior following treatments including either 1, 5, or 10 micrograms estradiol benzoate (EB) in combination with 0.1, 0.25, and 0.5 mg progesterone. Few animals responded at the 1 microgram dose of EB and there were no differences in latency to the first display of lordosis or in the total lordosis duration among responding animals in the 5 and 10 micrograms EB groups. However, there was significantly more positive tests in the OSH group injected with 5 micrograms EB than in the OH group and this difference approached statistical significance in the 10 micrograms EB groups. The results are compared to similar studies in rats and possible mechanisms for the effects of hysterectomy are discussed.

Animals↗

Effects of septal lesions on lordosis in female hamsters.

The ovarian hormones, estradiol and progesterone, are believed to act at specific sites in the female brain to induce sexual receptivity. Septal lesions which have been comprehensively studied in the rat, were carried out on female hamsters. Lordosis behavior was quantified as an index of female sexual receptivity. Septal lesions were found to cause a significant increase in female sexual receptivity in hamsters primed with 3 or 9 micrograms estradiol benzoate (EB) and 200 micrograms progesterone (P), but low levels of lordosis were not enhanced in septal lesioned female hamsters primed with 1 microgram EB + 200 micrograms P. The facilitation of lordosis seen in septal lesioned hamsters is similar to that observed in female rats. However, our results do not confirm increases in sensitivity to estradiol in the hamster.

Animals↗

VMN lesion deficits in lordosis: partial reversal with pergolide mesylate.

Bilateral lesions of the VMN virtually eliminate estrogen-progesterone stimulated lordosis in the spayed female rat. The present paper demonstrates that some recovery in lordosis is possible following treatment with pergolide mesylate, a potent long acting dopamine agonist. Chronic administration of pergolide mesylate in combination with estrogen and progesterone resulted in significant recovery of lordosis in VMN lesioned female rats. The magnitude of recovery was related to the duration and/or dose of pergolide.

Animals↗