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Original Research |
1 Division of Radiology, A-21, Cleveland Clinic Foundation, 9500 Euclid Ave.,
Cleveland, OH 44195.
2 Department of Orthopedic Surgery, Cleveland Clinic Foundation, Cleveland,
OH.
Received January 10, 2007;
accepted after revision March 28, 2007.
Address correspondence to M. P. Recht
(rechtm{at}ccf.org).
Abstract
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SUBJECTS AND METHODS. A prospective study of all patients referred for ankle and foot MRI examinations was performed. Six hundred two patients were included in the study: 387 females and 215 males. All images were evaluated for the presence of selective fatty atrophy of the ADQ muscle. The clinical notes on all patients with findings of ADQ atrophy were analyzed for descriptions of symptoms leading to the MR examination, the presence of symptoms that might be related to nerve entrapment, and the influence on clinical management related to the MR finding of ADQ atrophy.
RESULTS. Thirty-eight of the 602 patients had selective fatty atrophy of the ADQ, 29 females and nine males. Only one patient had a clinical diagnosis of possible nerve entrapment before MR examination. MRI findings of ADQ atrophy altered clinical management in only one patient.
CONCLUSION. Selective fatty atrophy of the ADQ is not a rare finding on MR examination of the foot and ankle, being seen in 6.3% of all studies and in 7.5% of all studies in females. The clinical relevance of selective ADQ atrophy seen on MRI is uncertain.
Keywords: abductor digiti quinti muscle atrophy first branch of the lateral plantar nerve heel pain MRI musculoskeletal imaging orthopedic surgery
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Entrapment of the first branch of the lateral plantar nerve is postulated to occur in one of two places: as the nerve passes between the deep fascia of the abductor hallucis muscle and the medial caudal margin of the medial head of the quadratus plantae muscle or where the nerve passes just anterior to the medial calcaneal tuberosity [6, 7] (Fig. 1). In the radiology literature, selective atrophy of the ADQ muscle has been reported as a late pre-sumptive marker of entrapment of the first branch of the lateral plantar nerve [8]. In a retrospective study, ADQ atrophy was seen in 2.1% of patients undergoing MRI of the foot and ankle [8]. Observing in our practice that ADQ atrophy in patients undergoing MRI of the foot and ankle is not rare, we performed a prospective study of patients undergoing foot and ankle MRI to determine the prevalence of selective ADQ atrophy, identify associated abnormal MRI findings in patients with ADQ atrophy, and examine the clinical symptoms of patients found to have ADQ atrophy. We are not aware of any previous prospective study of consecutive patients for evaluation of ADQ atrophy and its clinical implications.
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The clinical notes on patients with MR findings of ADQ atrophy were analyzed by two experienced foot and ankle orthopedic surgeons for descriptions of the symptoms leading to the MR examination, the presence of symptoms that might be related to entrapment of the first branch of the lateral plantar nerve, and alterations of clinical management related to the finding of ADQ atrophy. The clinical symptoms and signs used to indicate nerve entrapment were burning neuritic medial heel pain and radiation either proximally or distally and reproduction of this symptomatology with palpation over the proximal aspect of the abductor hallucis muscle. Although other findings in the foot can overshadow some of the clinical examination findings of nerve entrapment, neuritic pain has very distinctive features of burning pain and is often unrelated to weight bearing. The institutional review board approved this study and no informed consent was required.
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The 38 patients with ADQ atrophy had a number of other abnormal findings on MRI. Twenty patients had plantar calcaneal enthesophytes (53%) (Fig. 4A, 4B), 14 patients (37%) had plantar fasciitis (Fig. 4A, 4B), eight patients (21%) had ankle and foot arthropathy, seven patients (18%) had Achilles tendinopathy, four patients (11%) had peroneal tendinopathy, four patients (11%) had posterior tibialis tendinopathy, three patients (8%) had osteochondral defects of the talar dome, two patients (5%) had had prior plantar enthesophyte resections, two patients (5%) had findings related to prior open reduction and internal fixation of ankle fractures, and one patient (3%) had a tarsal coalition. Eight patients with ADQ atrophy were excluded from the study because of multiple-muscle atrophy: two patients had diffuse muscle atrophy of the foot; two patients, atrophy of the ADQ, flexor digitorum minimi brevis, and intrinsic muscles of the lateral aspect of the forefoot; two patients, atrophy of the ADQ, flexor digitorum minimi brevis, intrinsic muscles of the lateral aspect of the forefoot, and abductor hallucis; and two patients, atrophy of the ADQ and abductor hallucis (Fig. 6).
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The other patients had a variety of symptoms including nonspecific heel pain, pain suspicious for plantar fasciitis, and symptoms consistent with tendon abnormalities. Six patients had diabetes mellitus. Although diabetes can predispose to muscle atrophy, patients with diabetes were included in the study because all patients with multiple-muscle atrophy were excluded from the study. For only one of the patients with ADQ atrophy detected on MRI did clinical management change because of the MR finding of ADQ atrophy and that patient underwent electromyography (EMG).
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The nerve courses plantar from its origin deep in relation to the abductor hallucis muscle. The nerve changes from a vertical to horizontal direction at the inferior margin of the abductor hallucis. As it courses laterally, the nerve lies anterior to the medial calcaneal tuberosity and between the quadratus plantae dorsally and the plantar fascia and flexor digitorum brevis muscle on its plantar aspect. The nerve continues laterally and penetrates the proximal aspect of the ADQ. Although early anatomic drawings depicted the nerve relatively distal to the calcaneal tuberosity, more recent studies have shown that the nerve actually is located more posteriorly, being located on average 5.5 mm anterior to the medial process of the calcaneal tuberosity [12].
Entrapment of the first branch of the lateral plantar nerve was first proposed in 1940 by Roegholt [13] and has subsequently been confirmed by several authors [1, 6, 7, 9, 14-17]. The site of entrapment has been postulated to occur in one of two places: either at the point where the nerve changes direction at the inferior margin of the abductor hallucis where it is compressed between the abductor hallucis and medial aspect of the quadratus plantae or slightly more distal where the nerve passes anterior to the medial calcaneal tuberosity [6, 7].
Muscle hypertrophy, particularly in competitive athletes, has been postulated to be a predisposing factor for entrapment at the first site [7]. Predisposing factors for entrapment at the second potential site include "an increase in mass of any tissues in this area" including inflammatory changes around a plantar spur, the flexor digitorum brevis muscle, or the plantar fascia [6]. Obesity and a hyper-pronated foot have also been implicated as causative factors of nerve injury at the second potential compression site [7].
Although entrapment of the first branch of the lateral plantar nerve has been implicated as the causative factor in up to 20% of patients with chronic heel pain, it is believed to be one of the most overlooked causes of heel pain [1]. The differential diagnosis of nerve entrapment includes plantar fasciitis, heel pain syndrome, fat pad disorders, seronegative sponyloarthropathies, and calcaneal stress fractures. The diagnosis of nerve entrapment is primarily a clinical diagnosis, although electrodiagnostic abnormalities may be present [9, 18]. The major clinical finding differentiating entrapment of the first branch of the lateral plantar nerve from other causes of heel pain is maximal tenderness over the course of the nerve in the area of entrapment, typically located on the plantar medial aspect of the foot, anterior to the medial aspect of the calcaneus [9]. Associated findings may include paresthesias with nerve compression and motor weakness of the ADQ. There is no associated cutaneous sensory deficit, consistent with the lack of cutaneous innervation by the first branch of the lateral plantar nerve.
Treatment of entrapment of the first branch of the lateral plantar nerve is conservative therapy including nonsteroidal antiinflammatory agents, orthotics, and steroid injections [7]. Isolated neurolysis can be performed in patients who do not respond to conservative therapy [7].
Entrapment and compression of nerves have been found to produce characteristic MRI findings. Although there are no MR muscle signal changes immediately after denervation, prolongation of both T1 and T2 relaxation times occurs within 15 days [19-21]. These changes are presumed to be due to increased extracellular water content and decreased muscle fiber volume. Chronic (> 1 year) changes of muscle denervation are manifested as atrophy and fatty replacement, which are irreversible changes [22].
A previous retrospective study suggested that atrophy of the ADQ muscle is helpful in confirming the diagnosis of entrapment of the first branch of the lateral plantar nerve [8]. In that study, 10 of 476 patients (2.1%) undergoing MRI of the foot and ankle had ADQ atrophy. Nine of the 10 patients with atrophy were females. Atrophy was associated with obesity, the presence of a heel spur, and complex and multifocal abnormalities in the hindfoot and ankle. Our study found a higher prevalence of ADQ atrophy (6.3%) than this previous study. This increased prevalence may be due to the prospective nature of our study and that we actively sought ADQ atrophy rather than relying on a retrospective review of MR reports in which ADQ atrophy was not a primary focus of the study or report.
The majority of patients with ADQ atrophy in our study were female (76%), which is consistent with the prior study. The reason for the female preponderance is uncertain, although it may be explained by differences in footwear that may lead to altered mechanics or to other conditions, such as plantar enthesophytes and plantar fasciitis, that have been implicated as causative factors for nerve entrapment [6]. The most common associated findings were plantar enthesophytes and plantar fasciitis.
Ankle and foot arthropathy was also frequently seen in patients with ADQ atrophy. Whether there is a relationship between arthropathy and ADQ atrophy is unclear. The possibility that the arthropathy was either a result of or a causative factor of heel pronation, a factor implicated in nerve entrapment, cannot be excluded because no measure of heel pronation was available. Two patients with ADQ atrophy also had selective atrophy of the abductor hallucis muscle. These patients were not included in our study because the combination of muscle atrophy may be caused by nerve entrapment or compression more proximally involving both the lateral and medial plantar nerves. However, a study showed aberrant innervation to the abductor hallucis from the first branch of the lateral plantar nerve in 15% of patients [5]. Therefore, coexistent atrophy of the ADQ and abductor hallucis muscles could be caused by entrapment of the first branch of the lateral plantar nerve, although we chose to exclude two such patients from our statistical study group.
Interestingly, none of the 38 patients with selective ADQ atrophy nor seven of the eight patients with multiple-muscle atrophy presented with a possible diagnosis of nerve entrapment. Retrospective review of the clinical records in these patients revealed that six patients had symptoms that could have been consistent with nerve entrapment. One of the 45 patients underwent EMG based on the MRI findings, and the EMG study was interpreted as showing "no evidence of tarsal tunnel syndrome." None of the remaining 44 patients without clinical suspicion of nerve entrapment had their clinical management altered by the MR finding of ADQ atrophy. The lack of specific treatment directed to nerve entrapment may have had to do with the fatty atrophy of the ADQ, which by MRI criteria reflected a chronic process.
It is uncertain why most patients with ADQ atrophy had no symptoms attributable to nerve entrapment. We speculate that once fatty atrophy has developed, symptoms of entrapment of the first branch of the lateral plantar nerve are not manifest. It is interesting and somewhat surprising that all the patients with ADQ atrophy had MRI findings of chronic entrapment with fatty atrophy. No patients showed muscle edema within the ADQ, which would be expected in patients with acute or subacute entrapment. It is possible that the chronic nature of the nerve entrapment in our patients led to the lack of symptoms. In fact, ADQ atrophy may have been an incidental finding in these patients rather than the cause of the symptoms that led to the MR examination. This might also explain the fact that the finding of ADQ atrophy had no effect on clinical management in these patients.
There are several limitations with this study. First, a control group matched for age and sex was not studied, although this may be impractical because it would require more than 600 asymptomatic patients to undergo MR examinations. In addition, MRI findings in the 556 patients without ADQ atrophy were not tabulated. Therefore, the significance of the associated findings seen on the MR examinations in our patients with ADQ atrophy is unclear. In addition, because of the large number of referring physicians, it was not possible to have each of the patients reexamined by each physician looking for symptoms of nerve entrapment—specifically, tenderness over the expected area of entrapment.
In summary, fatty atrophy of the ADQ is a not a rare finding on MR examination of the foot and ankle, being seen in 6.3% of all studies and in 7.5% of studies in females. Only one patient presented with the clinical suspicion of nerve entrapment, although a retrospective study of clinical records revealed six additional patients had symptoms compatible with nerve entrapment. Only one of the patients had their clinical management altered by the finding of ADQ atrophy, which may be a reflection of the chronicity of the nerve entrapment in our patients.
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