Abstract | Introduction | Methods and Materials | Primary Diagnostic Acupoints | Results | Discussion | Summary | Acknowledgements | References | Table 1 | Table 2 | Table 3 | Diagram 1 | Graph 1 | Graph 2 |
Objective: A study was conducted to define the relationship between oriental Channel imbalance and pain of the equine hindlimb. Methods: A single observer using traditional manual palpation of the Acupuncture Channels examined 185 lame and muscle-sore horses from a general equine practice in Virginia. He evaluated and grades the six hindlimb Channels with particular emphasis on the reactivity of three transpositional acupoints, BL18, BL19, BL20, and five traditional veterinary acupoints YaoZhong, ShenShu, XieQi, FengMen, and FuTu. All lame patients were evaluated with western methods to establish an anatomical diagnosis. All non-lame horses with Channel imbalance were treated with an intraarticular anaesthetic, intraarticular cortisone, methylprednisolone acetate, or a hyaluronate and triamcinalone combination. The medications were injected into the three compartments of the stifle joint, tarsometatarsal and distal inter-tarsal joints, metatarsophalangeal joint, or the distal interphalangeal joint. The joint injections were conducted in sequence, distal to proximal, until a definitive change in Channel imbalance had occurred. Chi Square analysis was used to assess different frequencies of Channel imbalance and the sites responsible for that imbalance, with P< 0.05. Results: Channel imbalance was only indirectly associated with extra-articular pathology. Intraarticular structures of three joints of the distal hindlimb, the distal tarsus, metatarsophalangeal, and distal interphalangeal, accounted for all the observed abnormal, referred diagnostic acupoints. In the examined population, Channel imbalance was significantly more frequently related to the distal tarsus than the hind fetlock, and both of these were significantly more frequently involved than the distal interphalangeal joint. Channel imbalance relating to the dorsal aspect of the digit was significantly more frequent in metatarsophalangeal lameness than in distal tarsal lameness. Neither the stifle nor midback pain was directly associated with projected, as opposed to local, Channel imbalance. If projected Channel imbalance could be defined as the presence of reactive acupoints not in the immediate vicinity of the local site of pain, then the projected acupoints detected in stifle lameness or back pain were associated with the tarsus or the hind fetlock. Conclusions: The sites of hindlimb pathology resulting in Channel imbalance were intraarticular, and they were located within the distal tarsal, the metatarsophalangeal and the distal interphalangeal joints. Channel diagnosis reflected intraarticular inflammation of only these three joints, and further diagnostic procedures were required to establish a definitive western diagnosis. The presence of Channel imbalance should be used to determine pattern differentiation in Traditional Chinese Veterinary Medicine.
Oriental Channel Diagnosis (CD) is widely used by veterinary practitioners of acupuncture (AP) to address many painful conditions of the distal extremities of horses. In CD, traditional palpation techniques can be used to evaluate the classical veterinary acupoints as well as the transpositional Channel system popularised by the International Veterinary Acupuncture Society (IVAS) (1, 2). In CD, Channels having abnormally reactive acupoints are referred to as "unbalanced." Having determined the presence of abnormally reactive acupoints, the practitioner then uses knowledge of the theoretical course of the Channel combined with the case history, to diagnose the probable anatomical site of the pathology affecting the Channel. In the hindlimb there are six Channels, which are named for the internal organs Kidney (KI), Urinary Bladder (BL), Liver (LV), Gall Bladder (GB), Spleen (SP), and Stomach (ST). Traditionally these Channels have been linked as the pairs: KI/BL, LV/GB, and SP/ST.
Few attempts have been made to establish the precision of CD in the hindlimb. Many authors have stated that pathology affecting the stifle as opposed to the tarsus could be determined by the use of CD (3, 4, 5). There is a wide diversity of opinion as to the significance of the presence of unbalanced Channels (6, 7, 8). In previous studies by this author, reactive acupoints on AP Channels related to the forelimb corresponded only to traumatic intraarticular inflammation of the distal interphalangeal, proximal interphalangeal, metacarpophalangeal, and carpal joints (9, 10). In order to relate a specific Channel imbalance to joint pathology, the source of Channel imbalance must originate from the joint in question. If the discernible imbalance can be markedly changed by intraarticular medication, then the source of that imbalance must be within the treated joint. The immediate source of Channel imbalance in the diagnosis of hindlimb pain can be defined by the use of intraarticular medications.
During 1996 and 1997, 159 equine hindlimb lameness (at least Gd I\IV) 11 cases, as well as 92 non-lame but back and hindleg sore horses with Channel imbalance, were examined. The population of examined horses consisted of racing Thoroughbred horses as well as Warmblood and Thoroughbred hunters, jumpers, and combined training horses. Diagnosis of the anatomical sites of lameness was based upon traditional western methods of examination, observation, hoof testers, nerve blocks, diagnostic ultrasound, thermography, radiography and nuclear scintigraphy. CD as well as western methods of diagnosis were used. If intraarticular anaesthesia did not result in complete improvement of the lameness, peripheral blocks were used to localise the site. All lame horses that had Channel imbalance were treated with mepivicaine hydrochloride a injected intraarticularly in one or more of the following joints, the distal interphalangeal, the metatarsophalangeal, the tarsometatarsal, the distal intertarsal, the lateral femorotibial, the medial femorotibial or the femoropatellar. Sore horses with Channel imbalance were treated by the injection of methylprednisolone acetateb in the distal tarsus or a hyaluronate triamcinalonec combination in the metatarsophalangeal or distal interphalangeal joints. After joint injection with mepivicaine hydrochloride the Channels could be evaluated within eight minutes. The other medications required twenty-four hours. The joint responsible for the referred Channel imbalance was determined in all cases.
All horses were examined with traditional oriental techniques of digital palpation at key diagnostic acupoints. After every physical examination each acupoint was evaluated on a scale graded I to IV with respect to excess reactivity: Grade (Gd) I = normal sensitivity, Grade (Gd) II = slightly sensitive to palpation, Grade (Gd) III = a painful response to deep palpation and Grade (Gd) IV = a severely painful response to palpation manifested by swift evasive or kicking behaviour by the horse. A record was kept of the number of Gd III and Gd IV acupoints with respect to the six Channels that govern the hindlimbs. A Gd III or Gd IV acupoint indicated Channel imbalance. After each nerve or joint block the Channels were re-examined. Chi Square analysis was used to assess the frequencies of Channel imbalance, with P< 0.05.
Eight primary diagnostic acupoints (Back Shu-Association Points) were used for hindlimb Channel diagnosis. These were: LV-BL18; GB-BL19 and GB20; SP-BL20; ST-YaoZhong; KI-ShenShu and BL-XieQi, and BL10. These 6 Channels represent six spatial divisions of the equine hindlimb. Diagram 1 shows the diagnostic sites used for the equine hindlimb and their locations are as follows.
The following findings were made after physical examination, joint medication, and evaluation of the effects of joint medication on the reactivity of the Channels. The results were recorded for the presence of imbalance for each of the six hindlimb Channels (KI, BL, LV, GB, SP and ST). Channel imbalance was present in 9/20 cases of stifle lameness that occurred during the study. Table 2 shows that the imbalance was due to either the distal tarsus (7/9) or the hind fetlock (2/9). It summarises the AP patterns associated with intense midback pain in 18 horses during that same period of time. The tarsus accounted for all (12/12) referred pain patterns emanating from the hindlimb. The following results were significant (Table 1), Chi Square = P <0.05.
Channel imbalance was most frequently associated with distal tarsal pain and this should not be surprising given that the distal tarsus is the most frequent site of hindleg lameness (29, 30). However, joint inflammation inducing Channel imbalance should not be equated with lameness. Frequently the Channel imbalance of the tarsus is a manifestation of other lameness distal or proximal to the tarsus itself. Four examples of non-tarsal pathology that can result in secondary tarsal related Channel imbalance are hindleg hind suspensory desmitis, stifle lameness, midback pain and front fetlock synovitis. In an unpublished group of eight horses with hindleg proximal suspensory desmitis, seven had Channel imbalance associated with the distal tarsus while the eighth had no Channel imbalance (31). In these horses the Channel imbalance could be eliminated with intraarticular anaesthesia of the distal tarsus, but a subsequent infiltration block of the high suspensory area of the hindleg was required to achieve soundness. The conclusions of this study were that there was no Channel imbalance directly associated with the extra-articular high suspensory lameness, and that the Channel imbalance observed was related to intraarticular structures of the distal tarsus and thus was a secondary phenomenon.
Similarly in horses with intense midback pain and concomitant Channel imbalance, the imbalance could be alleviated by treatment of the distal tarsi (Table 2), but in primary back pathology a midline nidus of sharp pain would remain just anterior to the last thoracic vertebra. Since intense midline pain can be quite difficult to treat, it would be clinically useful to be able to recognise the relative contribution of the components of referred back pain by the use of intraarticular medications. In cases of intraarticular stifle lameness, the tarsus was also the most prominent source of Channel imbalance (Table 2). Given an unknown lameness with a Channel imbalance, a logical diagnostic approach would be to attempt to find the source of Channel imbalance and lameness at the same time. The tarsus and the hind fetlock, being the most probable sources of Channel imbalance, would be blocked first. In the cases of stifle lameness all Channel imbalances were eliminated by blocking the distal tarsus or the hind fetlock before an intraarticular block of the stifle was attempted. Thus it would seem that stifle lameness, either intraarticular or extra-articular, presents with Channel imbalance that reflects distal structures rather than the stifle itself. This finding is consistent with an analogous situation in the front leg. In shoulder lameness with Channel imbalance, the imbalance is due to articular structures of the distal forelimb, i.e. the carpal, metacarpophalangeal, and distal interphalangeal joints (32).
It could be argued that pain source above the tarsus could induce an alteration of the kinematics of the gait of the hindlimb, thus causing an abnormal positioning of the tarsus and a subsequent low grade joint inflammation. A case in point would be that of Channel imbalance in Thoroughbred racehorses with fetlock inflammation. In one study fifty percent of the horses with front fetlock Channel imbalance had hindleg Channel imbalance as well (33). Since the current paper has shown that the tarsus is by far the most common source of hindlimb Channel imbalance, one could assume that the greatest source of hindlimb Channel imbalance in the horses with front fetlock derived Channel imbalance was the distal tarsus. Furthermore a percentage of horses with front fetlock and hock derived combination Channel imbalance could be cleared of all imbalance by treating the front fetlocks alone (34). Less frequently the converse will be true in Thoroughbred racehorses. Therefore, in the absence of lameness, the injection of one or two specific joints can be quite useful in determining the relative importance of individual joints when the AP Channels would indicate that a number of different structures were contributing to the overall clinical presentation. That is to say that in a non-lame horse presented with Channel imbalance affecting both front and hind limb Channels, the most important contributor (s) to the imbalance could be determined by treating either an anterior or posterior pair of joints and subsequently evaluating the response to treatment.
Thus after considering the role of the tarsus in the cases of high suspensory desmitis, midback pain, front fetlock synovitis and stifle lameness, one must conclude that the presence of Channel imbalance of tarsal origin can in no way be assumed to indicate that the tarsus is the primary source of pain. The clinician must take care to differentiate between primary tarsal disease, pain or lameness of the distal tarsus that is completely eliminated by intraarticular therapy, and secondary tarsal inflammation leading to Channel imbalance. The presence of secondary tarsal Channel imbalance may be the only immediate clinical manifestation of more serious underlying structural abnormality in the non-lame horse.
In this study of Thoroughbred and jumping horses the incidence of Channel imbalance related to the hind fetlock was 25 percent. This number is comparable with a published value of 32 percent found in one study of hindleg lameness in racing Standardbreds (35). Pain from the hock, stifle and hind fetlock is often difficult to differentiate especially in fractious and subclinically lame individuals, but to add complications multiple joint involvement is a real possibility. Metatarsophalangeal joint related Channel imbalance differs from that of the tarsus in that there is a significantly increased incidence of ST Channel imbalance evidenced by reactivity at the traditional acupoint, YaoZhong. The conventional placing of the transpositional site of the ST Shu Point is just caudal to the last rib. Some adjustments would seem to be logical in the placing of acupoints when transposing the human Channels to the horse. Acupoints that reflect internal organs are not necessarily the best indicators of Channel pain. For instance, it has been accepted that the Shu Point for the KI Channel, as opposed to the KI organ, is just lateral to the lumbosacral space (36). This placing would be the site identical to that of the traditional veterinary acupoint, ShenShu. If the transpositional KI Shu Point is to be shifted caudally from the midlumbar site, then to maintain a consistent spatial relationship the ST Shu Point should also be moved caudally to a midlumbar site. Support for this arrangement comes in the significantly increased percentage of hind fetlocks that were unbalanced at YaoZhong. The most common sites of distal tarsal pathology would be dorsomedial, medial and plantar corresponding to LV, SP, KI, and BL as opposed to the dorsal aspect of the hind fetlock that would be affected by hyperdorsiflexion of that joint. Hyperdorsiflexion would result in inflammation of the dorsal aspect of the joint, which is governed by the ST Channel. The neurological supply of the hind fetlock differs from that of the front fetlock in the greater importance of the dorsal sensory innervation of the hind joint supplied by the deep peroneal nerve (37). The TH Channel would reflect the dorsal aspect of the front fetlock. The only published incidence of TH Channel imbalance in fetlock dysfunction was 26% (38) as opposed to the high incidence of 81% ST imbalance in the hind fetlock. How does the point reactivity correlate with demonstrable lameness? (Table 3). How can the clinician apply this information? In this study 58% of all lame horses had reactive acupoints in excess, and in 62% of these lame horses CD imbalance was indicative of the site of the lameness. Even though mepivicaine hydrochloride would be required to confirm the diagnosis, a reasonable guess as to the site of pain could be stated before diagnostic anaesthesia. Can we extrapolate the distribution of Channel imbalance in lame horses to the general population of lame and non-lame horses? In Traditional Chinese Medicine the six hindlimb Channels are linked in the following pairs: KI/BL, LV/GB, and SP/ST. The incidence of occurrence of imbalance of these pairs in the general population of lame and muscle sore horses was KI/BL > LV/GB > SP/ST. However, in the presence of intraarticular lameness there was no difference in the incidences of Channel imbalance with the sole exception of a significantly greater SP/ST reactivity associated with the hind fetlock vs. the tarsus. This latter finding is consistent with the overall population. It would seem logical that in pain sufficient to cause lameness, intraarticular inflammation may be more widespread. The result would be a more generalised Channel activation and, thus, eliminating the more subtle range of Channel reactivity in non-lame horses. The presence of reactivity of some Channels as opposed to others should give the examiner an index of suspicion of the more important sites of intraarticular inflammation i.e. the dorsal aspect of the hind fetlock vs. the medial and plantar aspect of the hock.
In a population of lame and muscle-sore horses having Channel imbalance involving either the tarsus or the hind fetlock, the percentage of Channel imbalance follows a predictable frequency with KI/BL > LV/GB > SP/ST. Imbalance of the tarsus was significantly more common than that of the hind fetlock. Both of these were more frequent than imbalance of the hind distal interphalangeal joint. In lame horses the SP/ST Channels were more frequently unbalanced in pain of the hind fetlock than in distal tarsal pain. Channel Diagnosis is never a substitute for lameness diagnosis, but it does provide a useful screening technique for commonly observed joint pain of the distal extremity.
The author would like to thank Lydia L. Donaldson VMD, Ph.D. for statistical analysis and criticism, Jennifer A. Fuhrman VMD, Paul Stevens DVM, and Yann-Ching Hwang DVM, Ph.D. for criticism and Phil Rogers MVB, MRCVS for editorial help.