SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The purpose of this study was to investigate the response of the ureterovesical junction (UVJ) to ureteric distension and to bladder filling with the aim of elucidating the mechanism of UVJ antireflux. The study was performed on 13 healthy volunteers [age 41.4 +/- 10.2 (SD) years; nine men, four women]. A ureteric catheter connected to a pressure transducer was introduced into the ureter proper. After recording the ureteric pressure, the catheter was withdrawn to the bladder, and the resting pressures in the UVJ and bladder were registered. The catheter was positioned in the UVJ and a 3F balloon-tipped ureteric catheter was introduced into the ureter proper and filled saline in increments of 1 ml. The pressure response of the ureter and UVJ to ureteric distension was recorded. The bladder was then filled with 400 ml saline at two rates, slow (10 ml/min) and rapid (150 ml/min), and UVJ pressure response was registered. The aforementioned tests were repeated after anesthetizing the UVJ, the bladder musculature surrounding the UVJ and the ureteric wall at the site of the ureteric distension, respectively. Ureteric distension of the lower 2-3 cm effected ureteric pressure elevation (P < 0.05) and a UVJ pressure drop (P < 0.05); no pressure response of the UVJ occurred upon ureteric distension above this level. Slow bladder filling induced an increase in the UVJ (P < 0.01) and vesical (P < 0.01) pressures only when vesical filling reached a mean of 219.6 +/- 79.4 ml and above. Upon rapid vesical filling the pressure response occurred at a smaller volume (136.6 +/- 52.3 ml). The pressure response did not occur when the UVJ was anesthetized. The study showed that lower ureteric distension was associated with a UVJ pressure drop. This reflex relationship, which we call the "ureterovesical junction inhibitory reflex," was reproducible and disappeared on anesthetizing the UVJ or ureter. Vesical filling above a certain volume induced a UVJ pressure increase which was reproducible and disappeared on anesthetizing the UVJ; we call this reflex relationship the "vesicoureteral junction excitatory reflex." These two reflexes seem to regulate the entry of urine from the ureters to the bladder and prevent ureteric reflux during bladder filling. In conclusion, two reflexes are identified that might contribute to the mechanism of UVJ antireflux.
The mechanism by which the ureteropelvic junction (UPJ) regulates the passage of urine from the renal pelvis to the ureter, and prevents urinary backflow from the the ureter to the renal pelvis, is not completely understood. The current communication studies this mechanism in 18 dogs. With the dogs under anesthesia, nephrostomy was done through which two catheters (one pressure and one balloon-tipped) were introduced into the UPJ and the renal pelvis, respectively. Renal pelvis distension with a balloon filled with 1 ml of saline effected a rise of renal pelvic pressure from a mean basal pressure of 4.8 +/- 1.2 cm H2O to 6.9 +/- 2.3 cm H2O (P < 0.05). The basal UPJ pressure of 12.6 +/- 2.7 cm H2O showed no significant change with 1 ml distention of the renal pelvic balloon (P > 0.05). Renal pelvic distension with 2, 3, and 4 ml caused a significant rise of renal pelvic pressure to 8.4 +/- 2.7 (P < 0.05), 10.6 +/- 2.2 (P < 0.01), and 11.8 +/- 1.9 (P < 0.01) cm H2O, respectively, and a significant drop of UPJ pressure to 4.8 +/- 1.2, 4.7 +/- 1.1, and 4.6 +/- 1.2 cm H2O (P < 0.01), respectively. Ureteric distension with a balloon filled with 0.5 ml of saline significantly raised the ureteric pressure from a mean basal value of 4.3 +/- 1.4 cm H2O to 14.7 +/- 3.3 cm H2O (P < 0.01) and the UPJ pressure to a mean of 20.8 +/- 3.8 (P < 0.05). Ureteric distension with 1 and 1.5 ml of saline led to an elevation of ureteric and UPJ pressure which was not significantly different from that observed with distension with 0.5 ml (P > 0.05). In contrast, the UPJ showed no significant pressure change upon distension of the locally anesthetized renal pelvis or ureter, respectively. Likewise, the locally anesthetized UPJ exhibited no significant pressure response to renal pelvic or ureteric distension. The study demonstrates that urine might have to accumulate in the renal pelvis up to a certain volume and pressure so as to effect UPJ opening, which occurs at its maximum irrespective of the distending volume. UPJ opening upon renal pelvic distension postulates a reflex relationship which we call "pelviureteral inhibitory reflex." This reflex is believed to regulate the passage of urine from the renal pelvis to the ureter. Ureteric distension closes the UPJ; we call this reflex action the "ureteropelvic excitatory reflex" as it seems to prevent reflux of urine through the UPJ and thus protects the kidney. The concept that the UPJ acts as a physiologic sphincter is put forward.
The quantitative differences among individuals in the natural reciprocal inhibition of the soleus H-reflex during dorsiflexion were examined, in conjunction with the maximal H-reflex as the test reflex size in each individual. Maximal H-reflex was expressed relative to the maximal M-response (H(max)) when compared among individuals. Analysis showed that with increases in H(max) at rest in each individual, the inhibitory effect was first enhanced, then reached a peak, and was finally alleviated. This pattern was similar to the intraindividual pattern of the inhibitory effect induced by specific conditioning stimulus as a function of the test reflex size.
We labeled interneurons in the L1-L2 and L6-S1 spinal cord segments of the rat that are involved in bladder innervation using transneuronal retrograde transport of pseudorabies virus (PRV) in normal animals and in animals with selected nerve transections. Preganglionic neurons were identified using antisera against choline acetyltransferase (ChAT). In some experiments we labelled parasympathetic preganglionic neurons (PPNs) in the L6-S1 spinal cord by retrograde transport of Fluorogold from the major pelvic ganglion. We identified bladder afferent terminals using the transganglionic transport of the anterograde tracer cholera toxin subunit b. We present anatomical evidence for two spinal pathways involved in innervation of the bladder. First, in the intact rat, afferent information from the bladder connects, via interneurons in L6-S1, to the PPNs that provide the efferent innervation of the bladder. The afferent terminals were located mainly in close apposition to interneurons located dorsal to the retrogradely labeled PPNs. Second, using L6-S1 ganglionectomies or L6-S1 ventral root rhizotomies we limited viral transport to the sympathetic pathways innervating the bladder. This procedure also labelled interneurons (but not PPNs) with PRV in the L6-S1 spinal cord in a location very similar to those described in the intact rat. These interneurons also receive bladder afferent terminals but we propose that they project to sympathetic preganglionic neurons, most of which are in the L1-L2 spinal segments. Based on this anatomical evidence, we propose the existence of two spinal reflex pathways involved in micturition: a pathway limited to a reflex arc in the pelvic nerve (presumably excitatory to the detrusor muscle); and a pathway involving the pelvic nerve and sympathetic nerve fibers, some of which may travel in the hypogastric (presumably inhibitory to the detrusor muscle).
Explore the source record for details and available documents.
The sensitivity of soleus H-reflexes, T-reflexes, and short-latency stretch reflexes (M1) to presynaptic inhibition evoked by a weak tap applied to the biceps femoris tendon or stimulation of the common peroneal nerve (CPN) was compared in 17 healthy human subjects. The H-reflex was strongly depressed for a period lasting up to 300-400 ms (depression to 48 +/- 23%, mean +/- SD, of control at a conditioning test interval of 70 ms) by the biceps femoris tendon tap. In contrast, the short-latency soleus stretch reflex elicited by a quick passive dorsiflexion of the ankle joint was not depressed. The soleus T-reflex elicited by an Achilles tendon tap was only weakly depressed (92 +/- 8%). The H-reflex was also significantly more depressed than the T-reflex at long intervals (>15 ms) after stimulation of CPN (H-reflex 63 +/- 14%, T-reflex 91 +/- 13%; P < 0. 01). However, the short-latency (2 ms) disynaptic reciprocal Ia inhibition evoked by stimulation of CPN was equally strong for H- and T-reflexes (H-reflex 72 +/- 10%, T-reflex 67 +/- 13%; P = 0.07). Peaks in the poststimulus time histogram (PSTH) of the discharge probability of single soleus motor units (n = 53) elicited by an Achilles tendon tap had a longer duration than peaks evoked by electrical stimulation of the tibial nerve (on average 5.0 ms as compared with 2.7 ms). All parts of the electrically evoked peaks were depressed by the conditioning biceps femoris tendon tap (average depression to 55 +/- 27% of control; P < 0.001). A similar depression was observed for the initial 2 ms of the peaks evoked by the Achilles tendon tap (69 +/- 48%; P < 0.001), but the last 2 ms were not depressed. Conditioning stimulation of the CPN at long intervals (>15 ms) also depressed all parts of the electrically evoked PSTH peaks (n = 34; average 65%; P < 0.001) but had only a significant effect on the initial 2 ms of the peaks evoked by the Achilles tendon tap (85%; P < 0.001). We suggest that the different sensitivity of mechanically and electrically evoked reflexes to presynaptic inhibition is caused by a difference in the shape and composition of the excitatory postsynaptic potentials underlying the two reflexes. This difference may be explained by a different composition and/or temporal dispersion of the afferent volleys evoked by electrical and mechanical stimuli. We conclude that it is not straightforward to predict the modulation of stretch reflexes based on observations of H-reflex modulation.
Explore the source record for details and available documents.
Due to the complexity of applying a well-defined stretch during human walking, most of our knowledge about the short latency stretch reflex modulation in humans is based on H-reflex studies. To illuminate the difference between the two methodologies, both types of reflexes were evoked in the same subjects, same experiment. Stretch reflexes were evoked via a stretch device capable of evoking stretch reflexes of the human soleus muscles during walking. H-reflexes were elicited by an electrical stimulation of the tibial nerve at the popliteal fossa at the knee. A significantly different modulation of the two reflexes was found in the late stance where the stretch reflex decreased in relation to the H-reflex. This was consistent with the unloading of the muscle spindles during the push-off in the late stance, suggesting a complex alpha-gamma coactivation, if any, at this time of the step. The soleus stretch reflex and H-reflex were compared during the stance phase of walking and sitting at matched soleus activity. No difference was found in the amplitude of the stretch reflex. However, there was a significant decrease of the H-reflex during the stance phase of walking, consistent with a task-specific presynaptic mediated reflex control. It is proposed that the short latency stretch reflex during walking is not sensitive to such a presynaptic inhibition.
The relation of the degree of grasp-reflex asymmetry to the strength of right- and left-hand grasp-reflex strength and body weight was studied in human newborn. In the total sample (N = 103), the right minus left (R-L) reflex strength was found to be positively linearly related to the grasp-reflex strengths from the right and left hands in FS-subjects; the correlation was higher for the right hand than the left hand. In FS+ subjects (N = 17), there was not a significant correlation between R-L and right-reflex strength; left-reflex strength was found to be negatively linearly related to the R-L reflex strength. In FS- subjects, the right- and left-reflex strengths showed a positive linear correlation with body weight. In FS+ subjects, only the left-reflex showed a positive linear correlation with body weight. The R-L reflex tended to be positively correlated with body weight in FS- subjects and negatively correlated in FS+ subjects. In females (N = 58), the relation of R-L to right and left reflex was similar to that for the total sample. There was no significant correlation between grasp reflex and body weight in FS- females. In FS+ females (N = 8), there was a positive linear correlation between the right grasp-reflex and body weight; the left grasp-reflex did not show such a significant correlation. The R-L grasp-reflex strength was not correlated with body weight in females.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVE: To compare the ability of pediatric residents to differentiate an asymmetric from a symmetric red reflex in patients with anisometropia and microstrabismus using the Brückner reflex and the Medical Technology Innovations (MTI) photoscreener. METHODS: A prospective, masked, case-control study was performed. Twelve pediatric residents evaluated 10 study patients and 6 control subjects in a masked manner in 2 separate sessions, using the Brückner reflex or the MTI photoscreener, evaluating for asymmetric (abnormal) or symmetric (normal) red reflexes between the 2 eyes. Each study patient had asymmetric red reflexes and the amblyogenic risk factor of anisometropia or microstrabismus. Each control subject had symmetric red reflexes. RESULTS: The pediatric residents had a mean correct score of 82% (69%-100%) using the MTI photoscreener versus a mean correct score of 65% (44%-81%) using the Brückner reflex (McNemar test: alpha < 0.01). The sensitivity of the MTI photoscreener evaluation was 89% in comparison to 61% for the Brückner reflex. The specificities for the MTI photoscreener versus the Brückner reflex were similar at 69% and 71%, respectively. CONCLUSIONS: Pediatric residents were better at detecting asymmetric red reflexes in patients with anisometropia and microstrabismus when evaluating MTI photoscreener photographs than when evaluating the red reflexes by the Brückner reflex. The MTI photoscreener may be a more sensitive method than the Brückner reflex to screen for the common amblyogenic risk factors of anisometropia and microstrabismus by easier detection of red reflex asymmetry.
OBJECTIVE: To investigate the effect of ipsilateral quadriceps-electrocutaneous stimulation on the T-reflex and the H-reflex of the soleus muscle, and to examine the interactions in human cutaneous sensation - the soleus motoneuron pathway. METHODS: The T-reflex and H-reflex tests were performed bilaterally on 50 able-bodied adults with a standardized technique using the soleus muscle. The reflexes were conditioned by electrocutaneous stimuli applied to the ipsilateral quadriceps using the optimal transcutaneous electrical nerve stimulation (TENS) machine (3 x perception, intensity 15-30 mA). The conditioning stimuli were followed by reflex tests by 30-50 ms (conditioning A) and 80-100 ms (conditioning B). The latency and amplitude of the T-reflex and H-reflex were measured before (control) and after conditioning stimuli (A and B) and at sham (placebo). RESULTS: There were no significant differences between the right and left sides and between the control and placebo in both T-reflex and H-reflex. There were significant differences in both latency and amplitude of the T-reflex only between control and conditioning A. There were no significant differences between control and conditioning tests in the H-reflex. CONCLUSIONS: The above results suggest that supraspinal center and cutaneous fusimotor reflexes, which increase the sensitivity of the soleus muscle spindle, mediate the observed motoneuron excitability changes.
The facilitatory effectiveness of spindle afferent feedback is controlled by modulation of segmental reflex excitability such that the level of muscle activation is appropriate for the task. Phase-dependent modes of reflex modulation have been well-characterized. We hypothesized that segmental reflex excitability of the triceps surae was also modulated in a manner associated with the activation history of the spindle afferents and the segmental reflex pathway during isometric contractions, standing and stepping. In the first experiment. pairs of soleus (S) H-reflexes were evoked 80 ms apart with equal strength stimuli at rest and while subjects isometrically contracted their S against loads of 10%. 20%. and 50% of their maximum voluntary efforts. The percent depression of the second H-reflex relative to the first was used as a measure of the effect of reflex activation history. At rest, the second H-reflexes were depressed an average of 73% relative to the first. The degree of depression was progressively reduced as the plantarflexion torque increased. In the second experiment, paired H-reflexes were obtained from the S and medial (MG) and lateral gastrocnemii (LG) muscles while subjects were standing and during the stance phase of step initiation. The degree of depression of the second H-reflex during standing ( > 78%) was similar in magnitude to that produced at rest in Experiment I. At the end of the stance phase of stepping. depression of the second H-reflex of all three muscles was reduced to less than 25%. We conclude that the segmental reflex excitability is modulated as a function of the reflex activation history during these tasks.
OBJECTIVES: Human withdrawal reflex receptive fields (RRFs) were assessed for 4 different electrical stimulus intensities, ranging from below the pain threshold (PTh) to up to two times the PTh intensity (0.8x, 1.2x, 1.6x, and 2.0xPTh). METHODS: Thirteen subjects participated, and the reflexes were recorded in a sitting position. The stimuli were delivered in random order to 12 positions distributed over the foot sole. Tibialis anterior (TA), gastrocnemius medialis (GM), vastus lateralis (VL), and biceps femoris (BF) reflexes were recorded. Further, knee and ankle joint angle changes were recorded. RESULTS: The strongest reflexes were seen in the TA compared with the other 3 muscles. Dorsi-flexion dominated distal to the talocrural joint corresponding to the TA receptive field area. An expansion of the RRF for the TA and GM was seen when increasing the stimulus intensity from 0.8xPTh to 1.2xPTh and from 1.2xPTh to 1.6xPTh, indicating a gradually increasing reflex threshold towards the border, where TA contraction is inappropriate in a withdrawal reaction. For the BF and VL, the borders of the RRF areas were not detected. By integrating the reflex size within the RRF (i.e. the reflex volume), gradually increasing reflexes for increasing stimulus intensity were seen in all 4 muscles tested, most clearly in the TA and GM. The subjective pain intensity correlated to the reflex volume for the TA, GM, and BF. CONCLUSIONS: In conclusion, the highest reflex sensitivity was seen in the centre of the RRF, while the stimulus intensity needed for eliciting a reflex increased towards the receptive field border. Within the RRF, stronger reflexes were evoked for increasing stimulus intensity. The limit in the size of the receptive field size for the TA and GM supports a modular withdrawal reflex organisation.
The effect of cutaneous tactile stimulation on motoneuron excitability was studied in 20 normal subjects and in patients of hemiplegia (n = 14) and paraplegia (n = 15) by plotting H-reflex recovery curves during application of twin pulses alone ("basal" H-reflex recovery curve), and twin pulses synchronized with electrical stimuli evoking tactile sensation in skin over the lateral border of the small toe. The "basal" H-reflex recovery curves from normal subjects showed a significant lateral asymmetry of motoneuron excitability, with an even distribution of subjects showing greater excitability on the left and right sides. However, there was no relation between handedness and the side with greater excitability. The cutaneous stimulation produced a highly significant inhibition of the H-reflex recovery between 600 and 6000 ms, with the maximum inhibition recorded at 1000 and 2000 ms, at which time even a complete inhibition of the test H-reflex was observed in some instances. The effect of cutaneous stimulation before 600 ms was statistically insignificant. The amount of cutaneous inhibition of H-reflex recovery showed a lateral asymmetry. The side with greater motoneuron excitability showed more cutaneous inhibition of the H-reflex recovery. A comparison of the H-reflex recovery at higher frequencies of cutaneous stimulation with that at basal frequency showed a slight but statistically insignificant difference in the amount of cutaneous inhibition of the H-reflex recovery. In hemiplegics, the "basal" H-reflex recovery curves showed greater motoneuron excitability on the affected side as compared to those of the unaffected side or controls, with the late inhibitory phase being completely obliterated. A similar pattern was also observed in paraplegics. Significantly, the lateral asymmetry of motoneuron excitability observed in the control group was absent in paraplegics. The cutaneous stimulation failed to produce any significant effect on the H-reflex recovery curves either in the affected side of hemiplegics or in both sides of paraplegics. The significant long latency inhibition of the H-reflex recovery curve produced by cutaneous tactile stimulation is a new finding.(ABSTRACT TRUNCATED AT 400 WORDS)
Explore the source record for details and available documents.