By F. Ilja. Western New England College.

We wish to know if we may conclude that these data are not from a normally distributed population with a mean of 80 and a standard deviation of 6 2.5mg ditropan overnight delivery. The sample available is a simple random sample from a continuous population distribution cheap 2.5mg ditropan visa. Critical values of the test statistic for selected values of a are given in Appendix Table M buy ditropan 5 mg cheap. The procedure purchase ditropan 2.5mg overnight delivery, which is similar to that used to obtain expected relative frequencies in the chi-square goodness-of-fit test, is summarized in Table 13. This particular software program has a nonparametric module that contains nearly all of the commonly used nonparametric tests, and many less common, but useful, procedures as well. Note that it provides the test statistic of D ¼ 0:156 and the exact two-sided p value of. Advantages and Disadvantages The following are some important points of comparison between the Kolmogorov–Smirnov and the chi-square goodness-of-fit tests. The Kolmogorov–Smirnov test does not require that the observations be grouped as is the case with the chi-square test. The consequence of this difference is that the Kolmogorov–Smirnov test makes use of all the information present in a set of data. It will be recalled that certain minimum sample sizes are required for the use of the chi-square test. As has been noted, the Kolmogorov–Smirnov test is not applicable when parameters have to be estimated from the sample. The chi-square test may be used in these situations by reducing the degrees of freedom by 1 for each parameter estimated. The problem of the assumption of a continuous theoretical distribution has already been mentioned. When the assumptions underlying this technique are not met, that is, when the populations from which the samples are drawn are not normally distributed with equal variances, or when the data for analysis consist only of ranks, a nonparametric alternative to the one-way analysis of variance may be used to test the hypothesis of equal location parameters. A deficiency of this test, however, is the fact that it uses only a small amount of the information available. The test uses only information as to whether or not the observations are above or below a single number, the median of the combined samples. Several nonparametric analogs to analysis of variance are available that use more information by taking into account the magnitude of 13. Perhaps the best known of these procedures is the Kruskal–Wallis one-way analysis of variance by ranks (8). The Kruskal–Wallis Procedure The application of the test involves the following steps. The observations are then replaced by ranks from 1, which is assigned to the smallest observation, to n, which is assigned to the largest observation. When two or more observations have the same value, each observation is given the mean of the ranks for which it is tied. The ranks assigned to observations in each of the k groups are added separately to give k rank sums. When there are three samples and five or fewer observations in each sample, the significance of the computed H is determined by consulting Appendix Table N. When there are more than five observations in one or more of the samples, H is compared with tabulated values of x2 with k À 1 degrees of freedom. One of the outcome variables examined was the count of eosinophil cells, a type of white bloodÀÁcell that can increase with allergies. Can we conclude that the three populations represented by the three samples differ with respect to eosinophil cell count? We can so conclude if we can reject the null hypothesis that the three populations do not differ in eosinophil cell count. The distributions of the values in the sampled populations are identical except for the possibility that one or more of the populations are composed of values that tend to be larger than those of the other populations. Critical values of H for various sample sizes and a levels are given in Appendix Table N. The null hypothesis will be rejected if the computed value of H is so large that the probability of obtaining a value that large or larger when H0 is true is equal to or less than the chosen significance level, a. When the three samples are combined into a single series and ranked, the table of ranks shown in Table 13. The null hypothesis implies that the observations in the three samples constitute a single sample of size 15 from a single population. If this is true, we would expect the ranks to be well distributed among the three groups. Consequently, we would expect the total sum of ranks to be divided among the three groups in proportion to group size. Table N shows that when the nj are5,5,and5,the probability of obtaining a value of H ¼ 9:14 is less than. We conclude that there is a difference in the average eosinophil cell count among the three populations. The letter t is used to designate the number of tied observations in a group of tied values. In our example there are no groups of tied values but, in general, there may be several groups of tied values resulting in several values of T. Note also that the effect of the adjustment is to increase H, so that if the unadjusted H is significant at the chosen level, there is no need to apply the adjustment. More than Three Samples/Large Samples Now let us illustrate the procedure when there are more than three samples and at least one of the nj is greater than 5. We wish to determine, by means of the Kruskal–Wallis test, if we can conclude that the average net book value of equipment capital per bed differs among the five types of hospitals. The ranks of the 41 values, along with the sum of ranks for each sample, are shown in the table. Solution: From the sums of the ranks we compute " 2 2 2 2 2 12 ðÞ68 246 124 159 264 H ¼ þ þ þ þ À 341þ 1 41 41 þ 1 10 8 9 7 7 ¼ 36:39 Reference to Appendix Table F with k À 1 ¼ 4 degrees of freedom indi- cates that the probability of obtaining a value of H as large as or larger than 36. We conclude, then, that there is a difference among the five populations with respect to the average value of the variable of interest. Output: Kruskal–Wallis Test: C1 versus C2 Kruskal–Wallis Test on C1 C2 N Median Ave Rank Z 1 5 28. All elderly subjects were living at home and able to carry out normal day-to-day activities. The following table shows vitamin B-12 levels for 50 subjects in the young group, 92 seniors, and 90 subjects in the longeval group. May we conclude, on the basis of these data, that the populations represented by these samples differ with respect to vitamin B-12 levels? A total of 53 students from three separate preschool classrooms participated in this study. Students were given a measure of phonemic awareness in preschool and then at the end of the first semester of kindergarten. The improvement scores are listed in the following table as measured by the Yopp–Singer Test of Phonemic Segmentation. The following table gives the information for six guinea pigs in each of the three treatment groups. May we conclude, on the basis of these data, that the number of alveolar cells in ovalbumin-sensitized guinea pigs differs with type of exposure? Such a need may arise because the assumptions necessary for parametric analysis of variance are not met, because the measurement scale employed is weak, or because results 13. A test frequently employed under these circumstances is the Friedman two-way analysis of variance by ranks (9,10). This test is appropriate whenever the data are measured on, at least, an ordinal scale and can be meaningfully arranged in a two-way classification as is given for the randomized block experiment discussed in Chapter 8. Nine other physical therapists were asked to rank the stimulators in order of preference. The observations appearing in a given block are inde- pendent of the observations appearing in each of the other blocks, and within each block measurement on at least an ordinal scale is achieved. For our present example we state the hypotheses as follows: H0: The three models are equally preferred.

Decreased compliance 390 Pathophysiology: increased intravesical pressure secondary to decreased accommodation of detrusor cheap ditropan 5 mg fast delivery. Neurological: loss/reversal of accommodation reflex—conus medullaris or peripheral order ditropan without a prescription. Underactive bladder (decreased intravesical pressure) Symptomatic: overflow incontinence/retention 1 order ditropan 5 mg with amex. Pathophysiology: decreased contractility—neural efferent or myogenic/decreased afferent stimulation order ditropan 2.5 mg with visa. Detrusor myopathy Pathophysiology: decreased contractility secondary to smooth muscle damage. Pharmacological inhibition Pathophysiology: decreased contractility secondary to receptor blockade of neural efferents or afferents. Loss of sense of fullness/urge incontinence without appreciation of “desire to void. Decreased bladder outlet and pelvic floor sensation Pathophysiology: denervation, myopathy, behavioral, pharmacological causing decreased ability to identify/contract/coordinate. Increased sensation of the bladder/bladder outlet Pathophysiology: neuropathic, inflammatory, mucosal permeability defect, psychogenic, afferent amplification. Increased sensation of the pelvic floor/bladder outlet Pathophysiology: neuromuscular myalgia, neuropathic, inflammatory, psychogenic. The overactive outlet: Failure to empty the bladder may be due to elevated outlet resistance or to impaired contractility of the bladder. The most commonly observed clinical etiology of elevated outlet resistance is iatrogenic, obstruction following incontinence surgery. Neurogenic outlet obstruction, commonly seen following injury to the suprasacral spinal cord, is due to a loss of coordination between the bladder and sphincter (detrusor sphincter dyssynergia). The paradoxical failure of the outlet to relax during voiding may result in anatomical obstruction to flow or to inhibition of the initiation or completion of the detrusor contraction. Contraction of the pelvic floor or sphincter is a normal response for bladder inhibition but, when pathological, may be classified as pseudodyssynergia (voluntary or behavioral) or true dyssynergia (neurogenic). The relaxation of the urethral sphincter during voiding and dyssynergic activity in spinal cord injury has been documented. It is not known whether the specific anatomical areas of the urethra or pelvic floor (sphincter urethra, compressor urethra, urethrovaginal sphincter, bulbocavernosus, anal sphincter, levator complex) act in unison, individually, or at all in detrusor 391 inhibition in normal subjects. Therefore, the central and peripheral nervous systems mediate bladder control through complex voluntary pathways and reflex arcs. Central efferent control of the bladder smooth musculature is mediated by afferent activity from the detrusor musculature and bladder mucosa (facilitatory) and the reflex and voluntary contractions of the pelvic floor and sphincter musculature (inhibitory). The underactive bladder: Traditional concepts of detrusor underactivity have focused on either efferent innervation or myogenic dysfunction. By contrast, contemporary views emphasize the importance of the neural control mechanisms, particularly the afferent system, which can fail to potentiate detrusor contraction, leading to premature termination of the voiding reflex. To void efficiently, a feedforward mechanism by which urinary flow in the urethra helps to enhance and maintain adequate contractile function of the bladder until the bladder is empty is required. Sensory information is fed back to the motor system at several levels of control between the end organ and brain cortex. These sensors themselves can be damaged, for example, through an effect of ageing or ischemia. In addition, impairment of innervation can lead to decreased information transfer via either the sensory or motor nerves. A functional disruption of higher central nervous regulatory systems can lead to functional abnormal voiding [44]. During the initial phase of bladder emptying, the pelvic floor and external sphincter relax in order to decrease urethral resistance and facilitate low pressure flow. In addition, this relaxation decreases the reflex inhibition of bladder contractility. Relaxation is followed by a detrusor contraction, which continues until voiding is completed. When emptying failure is secondary to bladder dysfunction, it may be a result of either detrusor smooth muscle pathology or insufficient neural stimulation of the detrusor. Insufficient neural stimulation may occur at the neuromuscular level (pharmacological), with nerve impairment (neuropathy), or with alterations in central control of micturition (conus medullaris, spinal column, or brain). The impairment of detrusor contractility by the absence of pelvic floor relaxation is evident in spinal cord disease (failure to empty following adequate sphincterotomy in the spinal cord patient due to incomplete detrusor contractions) and Parkinsonism (failure to empty secondary to pelvic floor bradykinesia). Mixed–combined disorders: Disorders of the bladder and outlet during storage and emptying may occur alone and in combination. In addition, the elderly females or patients with neurological diseases may demonstrate detrusor overactivity (hyperreflexia) with impaired contractility (poorly sustained contraction). Sensory disorders: Afferent neurons from the bladder and urethra are of major importance during both the storage and emptying phases, both initiating the voiding reflex and sustaining the voiding drive during bladder emptying. Somatic activity may inhibit the emptying reflex by voluntary contraction of the external sphincter or pelvic floor—and although not established in humans, may provide inhibitory activity during bladder filling. Traditional classification systems have focused on motor rather than sensory activity. Disorders of bladder and bladder outlet sensation may result from central or peripheral denervation, from psychological causes, or from pharmacological agents such as pain medications. The role of decreased sensation in the function of the pelvic floor and the interaction between the pelvic floor and bladder with relation to the sensory pathway on the micturition reflexes await further investigation. The pudendal nerve is responsible for the innervation of pelvic floor structures as well as of the genital skin, urethral mucosa, and anal canal. Proprioceptive information of the periurethral musculature and sensory innervation of the levator ani muscles are also mediated by the pudendal branches. Increased sensation or pain attributed to the bladder is a major clinical challenge. The symptoms of urinary frequency, urinary urgency, and suprapubic pressure often result in diagnostic evaluations and therapy for bladder disorders, even in the absence of definitive findings of mucosal or smooth muscle abnormality. Pain that may originate from fascial, muscular, or neurological etiologies within the pelvic floor should be included in the differential diagnosis of the patient with urethral or bladder syndromes. Traditionally, sensory signaling in the urinary bladder has been largely attributed to direct activation of bladder afferents. There is substantive evidence that sensory systems can be influenced by 392 nonneuronal cells, such as the urothelium, which are able to respond to various types of stimuli that can include physiological, psychological, and disease-related factors. The corresponding release of chemical mediators (through activation of a number of receptors/ion channels) can initiate signaling mechanisms between and within urothelial cells, as well as other cell types within the bladder wall including bladder nerves. However, the mechanisms underlying how various cell types in the bladder wall respond to normal filling and emptying and are challenged by a variety of stressors (physical and chemical) are still not well understood. Alterations or defects in signaling mechanisms are likely to contribute to the pathophysiology of bladder disease with symptoms including urinary urgency, increased voiding frequency, and pain [45]. These systems can be clearly illustrated with the functional areas of the bladder and outlet on the vertical and axis the functions of filling/storage and voiding/emptying on the horizontal. The reader is encouraged to incorporate these systems into their own clinical algorithms and critique and modify them based on additional evidence or “opinion. The standardisation of terminology of lower urinary tract function: Report from the standardisation sub-committee of the international continence society. Analysis of the standardisation of terminology of lower urinary tract dysfunction: Report from the standardisation sub-committee of the International Continence Society. Pelvic floor muscle function and urethral closure mechanism in young nullipara subjects with and without stress incontinence symptoms. Female stress, urge, and mixed urinary incontinence are associated with a chronic and progressive pelvic floor/vaginal neuromuscular disorder: An investigation of 317 healthy and incontinent women using vaginal surface electromyography. Pelvic floor muscle training is effective in treatment of female stress urinary incontinence, but how does it work? Standardization of terminology of pelvic floor muscle function and dysfunction: Report from the pelvic floor clinical assessment group of the International Continence Society. An integral theory and its method for the diagnosis and management of female urinary incontinence.

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An example of this methodology is shown in Figure 11-137 cheap ditropan 2.5 mg visa, in which single extrastimuli delivered up to local refractoriness (170 msec) failed to influence the tachycardia purchase ditropan 5 mg. Double or triple extrastimuli can also be delivered such that each extrastimulus interacts with the site of impulse formation to varying degrees before termination generic ditropan 5mg with mastercard. However buy on line ditropan, without controlling the degree to which each impulse interacts with the tachycardia circuit, it becomes difficult to interpret (particularly quantitatively) the significance of the response aside from whether or not the tachycardia was terminated. For example, if three extrastimuli are used, the first two extrastimuli should be delivered at coupling intervals above those that induce resetting, and the third can be used to interact with the tachycardia. In this case, only the third extrastimulus would interact with the tachycardia as a single perturbation. Entrainment of ventricular tachycardia: explanation for surface electrocardiographic phenomena by analysis of electrograms recorded within the tachycardia circuit. This assumes import because many investigators immediately turn to “burst” pacing to terminate tachycardias (even if the patient is hemodynamically stable), and the initial stimulus is delivered at various coupling intervals from the tachycardia for each burst. These factors can lead to a situation in which tachycardias may be reset, terminated, and reinitiated without the investigator knowing it. C: When the first extrastimulus is placed at 190 msec, an interval when no resetting occurred, and a second extrastimulus is then placed at 340 msec, resetting of the tachycardia is produced. The sum of the coupling intervals of the two extrastimuli and the return cycle is 1,000 msec. This is 50 msec earlier than expected, thereby confirming that the tachycardia was reset. Once ensuring synchronization, the investigator should employ a series of paced beats delivered at cycle lengths beginning just shorter than the tachycardia cycle length, then decreasing the cycle length until the tachycardia is terminated. At each cycle length, the response to a variable number of extrastimuli should be assessed (i. By using these techniques, the ability to reset, entrain, and/or demonstrate overdrive acceleration, suppression, or termination can be assessed and evaluated and compared to the respective responses of known triggered and reentrant rhythms. However, approximately 25% of tachycardias (particularly those with cycle lengths <300 msec) will not be able to be terminated by rapid pacing and/or will be accelerated to different tachycardias and will require 322 323 324 325 cardioversion. This results in fully compensatory pauses surrounding the delivery of single or multiple extrastimuli. The tachycardia circuit or the site of origin is “relatively” protected by these physiologic factors, which are unrelated to the tachycardia mechanism. This in no way implies protection of the tachycardia mechanism from responding to an increased number of extrastimuli or extrastimuli delivered at a shorter cycle length and/or closer to the tachycardia origin. Occasionally, simultaneous stimulation from both right and left ventricles fails to influence the tachycardia 336 (Fig. This suggests that the tachycardia circuit is relatively protected by external factors that limit access of stimulated impulses to the tachycardia, particularly if it occurs in an area of a large aneurysm. The term concealed perpetuation is used when extrastimuli not only fail to influence the tachycardia but are followed by pauses that exceed the tachycardia cycle length or that occasionally are interrupted by sinus captures before the 336 next tachycardia beat (Fig. The long pause following the second extrastimulus is due to the inability of the impulse from the reentrant circuit to depolarize the remainder of the ventricles, which have been just activated and captured by the second extrastimulus. The significance of manifest and/or concealed perpetuation is that its presence can be used to demonstrate the extent of ventricular myocardium not required for the tachycardia. As shown in Figure 11-139, occasionally this can be observed with simultaneous stimulation in both ventricles. This phenomenon suggests that the tachycardia mechanism requires only a small area of the ventricle. In a similar fashion, intermittent capture of the His–Purkinje system during the tachycardia suggests that it, too, is not necessary to maintain the arrhythmia, regardless of where the His deflection is located during the tachycardia (Figs. Occasionally, one may observe continuous ventricular capture by ventricular pacing that does not influence the tachycardia (Fig. In most instances, ventricular pacing is begun late in diastole at a rate slightly different from the tachycardia rate. In all such cases, one must demonstrate that ventricular pacing at this cycle length did not terminate and reinitiate the tachycardia. This must be distinguished from continuous resetting of the tachycardia circuit, which will be described subsequently. As noted earlier, sinus captures, occurring either spontaneously or in response to atrial stimulation, can occur without influencing tachycardia. The demonstration that neither the proximal His–Purkinje system nor the majority of ventricles are required to sustain the tachycardia, and that supraventricular captures can occur without influencing the tachycardia, suggests that the tachycardia must occupy a relatively small and electrocardiographically silent area of the heart. Resetting of Ventricular Tachycardia Resetting of a sustained rhythm is the interaction of a premature wavefront with the tachycardia resulting in advancement or delay of the original rhythm. As noted in the preceding paragraphs, extrastimuli delivered at long coupling intervals and/or pacing at slow heart rates approximating those of the tachycardia may fail to interact with the tachycardia, resulting in a fully compensatory pause producing manifest or P. To reset a tachycardia, the impulse must be able to reach the tachycardia site of origin and find it excitable. In the case of a reentrant arrhythmia, an excitable gap (temporal and spatial) must exist between the leading edge of the tachycardia impulse and the wave of refractoriness following the impulse. The temporal excitable gap is the interval of excitability in milliseconds between the head of activation of one impulse and the tail of refractoriness of the prior impulse. The spatial excitable gap is the 311 distance occupied by the excitable gap in millimeters at any moment of time. The size of the spatial gap can vary greatly depending on the conduction velocity and refractoriness that determine the length of the excitable gap. It is impossible to assess the conduction velocity and refractoriness at any point in the circuit (which certainly must vary) with current technology. This is one of the limitations in interpreting accuracy of measurements of the excitable gap. This results in a pause, during which a sinus capture occurs subsequently followed by resumption of the tachycardia. The presence of pauses in excess of the tachycardia cycle length and the sinus capture without influencing the tachycardia defines concealed perpetuation. Continuing activity at the site of origin within the aneurysm is seen despite biventricular capture. Termination occurs when collision with the prior impulse antidromically is associated with orthodromic block (Fig. In the case of a reentrant arrhythmia, the range of coupling intervals over which resetting occurs can be considered a measure of the duration of the temporal excitable gap existing in the reentrant circuit. Overdrive pacing can be used to produce entrainment (or continuous resetting) of the reentrant 1 123 315 319 320 326 327 328 334 335 336 circuit. The entire zone of coupling intervals over which resetting occurs should also be evaluated as a measure of the duration of the excitable gap in the case of reentrant rhythms. The entire extent of the fully excitable gap would be the zone of coupling intervals from the onset of resetting until termination. Site specificity for resetting is another factor that may help discriminate mechanisms because rhythms that are due to triggered activity or automaticity do not exhibit site specificity. As stated in preceding paragraphs, triggered activity may be reset to produce flat return cycles at 100% to 110% of the cycle length of the triggered activity or a decreasing return cycle with a direct relationship to the coupling interval. A: A schematized reentrant circuit with an entrance and an exit is shown with the impulse circulating within the circuit. The solid part of the impulse represents tissue that is totally refractory, and the stippled area represents tissue that is partially refractory. B: Resetting is produced by a premature stimulus, which enters the circuit to collide retrogradely (antidromically) with the preceding tachycardia impulse. At the same time, the stimulated impulse can conduct antegradely (orthodromically) because the tissue is fully excitable. The stimulated impulse then continues to traverse the reentrant circuit to reset the tachycardia. C: Termination occurs when the stimulated impulse collides retrogradely with the preceding tachycardia impulse and blocks antegradely owing to encroachment on the refractory period of the preceding wavefront. When more than a single extrastimulus is delivered, the relative prematurity should be corrected by subtracting the coupling interval(s) from the P. To account for any cycle length oscillation we require at least a 20-msec shortening of the return cycle to demonstrate resetting (Fig.

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This bone articulates a convex and the ulnar distal facet has a convex and a concave segment buy ditropan with mastercard, concave facet distally with the second metacarpal discount 5 mg ditropan with mastercard. In 34% which enables spiral movement during ulnar devia- of cases purchase ditropan 5 mg without a prescription, it also articulates with the third metacarpal buy 2.5mg ditropan visa. Pisiform The pisiform as a sesamoid bone inserts into the trique- Capitate trum with a flat facet. It is around scribed ossification of a tendon caused by pressure or 24mm long and around 16mm wide. The distal radial aspect has there is thus an incongruity because the convex joint a slightly concave facet to the second metacarpal and a head (in the shape of a curved arch) is much larger than convex surface to the trapezoid. All of the joint surfaces are fully phoid abuts the lower end of the radius while the lunate covered with cartilage. The triquetrum is in contact with the ulnar collateral liga- ment of the wrist joint on the ulnar side beyond the ulno- Hamate 256 carpal disc. It is around About 48 to 50% of compressive stresses transferred 21mm long and around 16mm wide. On the palmar aspect in the distal area, fossa, and 12 to 15% through the ulnocarpal disc. Proximally, there may be a con- arm extended, the delicate ulna is less often damaged vex facet to the lunate on the radial aspect (in 65% of than the much more robust radius. The tally, there are two more joint surfaces toward the fourth and fifth metacarpals, respectively. Joints In the proximal radiocarpal joint, these carpal bones form an ovoid or ellipsoid joint (▶Fig. The two a bones together form the proximal biconcave socket, in the first place, from the bifaceted radial surface (scaphoid and lunate facets) and, in the second place, from the con- cave surface of the ulnocarpal disc (ulnar notch233). Three-quarters of this surface corresponds to the radius and one-quarter to the ulna. The distal ovoid convex joint head is formed by the scaphoid, lunate, and triquetrum and is covered with hya- line cartilage. These bones are held together by short liga- ments (scapholunate and lunotriquetral ligaments), which are fully enclosed by these carpal bones and there- b fore give the false impression that the cartilage covering is uniform. This stability of of around 15 to 25°, and ulnar deviation of around 40 to the distal carpal row also impacts the palm (which is a 50°. Midcarpal Joint Carpal Joints Over the course of evolution, the carpus lost contact to the ulnar styloid process, which enabled the hand to have The individual carpal bones are flexibly interconnected a stable torsional movement. Owing to the different bony formations formed from the proximal and distal row of the carpal and the rigid interosseous ligament connections, func- bones (▶Fig. The greatest mobility occurs in the proximal row The scaphoid begins radially with a convex curvature, between the lunate and scaphoid in the form of rotation across from which a socket formed by the trapezium and movements. Toward the ulnar aspect, the capitate is also an independent intercarpal joint with a thin rigid and hamate protrude against it, similar to a joint head. In terms of function, the triquetrum is centered, Both bones are embedded in the socket formed by the stabilized and also guided by the pisiform229 and counter- scaphoid, lunate, and triquetrum. These additional ris muscle and the extensor retinaculum running palmar- joint surfaces can trigger degenerative processes. The entire carpus is a concave structure and forms the shape of a palmar arch, namely the carpal tunnel (space for the tendons of the hand and the median nerve). The carpus is stabilized by several muscles and, in particular, by its complex ligament system. The aspects facing the joints are covered by a synovial membrane, while the lateral aspects have a fibrous layer. This is also true for the stronger 10 palmar ligaments compared to the weaker dorsal liga- ments, which have more densely packed collagen Fig. The carpal articular surfaces are slightly con- with another carpal bone, more or less directly or indi- vex and the bases of the metacarpals are concave. In a dynamic ring system of carpal bones that is under con- similar fashion, the third metacarpal juts into the space stant tension. These bones must be held together tightly between the trapezoid and capitate with its styloid proc- by ligaments,229 which are also important components of ess in a conical manner. A Y-shaped ligament of the third meta- classified this ligament system into superficial, middle, carpal (attached to the capitate and hamate), as well as and deep layers (three-layer structure200). The radial aspect of brachial fascia and radiates into the dorsal fascia of the the latter muscle is attached to the flexor retinaculum hand without any sharp delineation (▶Fig. On the radial side, it is around 15mm form and hook of hamate) and the radial eminences of wide, in the center around 26 mm, and on the ulnar side the wrist (tubercle of trapezium and tubercle of scaphoid) around 20 mm. This layer is fused to the joint capsu- form an aponeurosis that is positioned between the the- le of the distal radioulnar joint, extends below the nar and hypothenar muscles. They also play a key role in physiological pres- sor carpi ulnaris muscle without direct contact with the sure distribution in the carpus. The mobility of the bone during pronation and supi- posed of three groups of ligaments. The ensuing arises from the palmar border of the radial styloid process six osteofibrous tendon compartments serve to provide and extends in an oblique direction across the carpal passage for the extensor tendons of the thumb, wrist, and articular space toward the scaphoid tubercle and toward fingers. The extensor retinaculum prevents bowstringing the sheath wall of the tendon of the flexor carpi radialis and extensive radial and ulnar lateral slipping of the 229 78 188 229 muscle up to the trapezium. The These ligaments run in a thin, superficial layer above a palmar ligaments are thicker than the dorsal liga- strong, thick, deep intracapsular fibrous layer. In a wider sense the radial styloid process, or broad-based from the volar of the term, the scaphotrapeziotrapezoid ligament also lip of the radius, and are divided into three fibrous tracts: belongs to the ligaments of the “distal V”231 and the deep the radioscaphocapitate ligament, and the long and short layer of the ligament system. The radioscaphocapitate ligament connects the scaphoid with the trapezium and the runs across the waist of the scaphoid and spans the distal trapezoid. The main function ligaments run in a flat and somewhat oblique direction of this palmar ligament complex is to hold the scaphoid toward the lunate. The long and short radio- ulnotriquetral ligaments, they form the palmar “proximal lunate ligaments, together with the ulnolunate ligament V” (▶Fig. The long part of the radiolunate liga- ments tightens during radial and ulnar deviation160 and is ▶ Radioscaphocapitate ligament. The ulnar side of the distal group of V-shaped ligaments is formed by a ligament with an ▶ Ulnolunate ligament and ulnotriquetral ligament. They originate on the palmar radioulnar lig- hamate, and terminates on the palmar side of the distal ament and proceed to the anterior horn of the lunate third of the scaphoid. In many cases, the central fibers to the lunate ▶ Function of the palmar “proximal V” ligament. The are absent, which creates a weak point in the wrist (the function of the proximal V-shaped ligament (▶Fig. Together ligaments cover the middle carpal column, the lunate is with the dorsal intercarpal ligament, it forms the dorsal stabilized by the dorsal radiotriquetral ligament and the V-shaped ligaments (▶Fig. While the two liga- capitate is stabilized by the dorsal intercarpal ligaments, which hold the two bones in colinear alignment. The dorsal radiotri- with the radiolunotriquetral ligament on the palmar side, quetral ligament arises from the dorsal border of the the dorsal V-shaped ligament prevent the carpus from radius, immediately distal to Lister’s tubercle (dorsal sliding along the radial joint surface, which slopes to the 160 ulnar side. Its course crosses the proximal scaphoid pole and the posterior horn of the lunate and ultimately dion, viz. The ligament is about 20mm long; proximally it is 5 mm wide configuration permits extensive movement while ensur- and distally around 5mm wide. This ligament originates ments it is therefore among the most important carpal structures providing stability. More- Summary over, they coordinate and center individual carpal bones All in all, the V-shaped ligaments provide the functional and thus contribute to physiological transfer of force. The distal V-shaped ligament stabilizes the capitate and decelerates the scaphoid, while the proximal V- The palmar V- and the dorsal V-shaped ligaments work shaped ligament helps to regulate the proximal transfer in synergy to stabilize radial and ulnar deviation, with of force between the ulna and the carpus and stabilizes individual ligaments alternating as agonists and antago- nists. A tear in the dorsal V predisposes to ulnar 231 capitate to the triquetrum, lunate, and scaphoid. As aligned toward each other on both sides and between described above, as the key element of stabilization for the skeletal elements (e. These small liga- to regulate pressure in the carpus and operates as an mentshaveamembranousattachmenttothearticular important decelerator of radial deviation.

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